# data[].attributes.body
Corinne Passman

Folic Acid

When a patient hears folic acid (vitamin B9), the first thing they probably think of is it’s value for pregnant women and their baby. But what exactly does folic acid do during pregnancy? And, does it have value outside of pregnancy? Dr. Lucy Wills initially discovered Folic Acid’s benefits from a pregnancy lens, explaining its initial benefit being associated with pregnancy. She found that folic acid helped reduced anemic symptoms that pregnant patients experienced during terms in 1931. It was many years letter before it was discovered the folate (a derivative of folic acid) was isolated from brewer’s yeast. But, from my literature review, I found that folic acid not only reduces the risk of neural tube defect in pregnant women, but has value in so many different medicinal areas as well as many other indications. Folic acid is also recommended for cancer patients, especially colon cancer, as it is such an essential compound involved in many biochemical processes. There is also value for folic acid in patients with depressive disorders, since many of the cofactors that are in deficit with depression are derivatives of folic acid. Studies suggest that because SAM is a derivative of folic acid, folic acid can serve as an antidepressant or be taken in support with another antidepressant to augment its effects. Another potential application of folic acid is as an anticonvulsant for epilepsy as it’s metabolism might be directly linked to antiepileptic action of the anticonvulsant drugs. Folic Acid’s mechanism of action is that of a cofactor enzyme involved in DNA and RNA biosynthesis. It helps to supply methyl groups to the methylation cycle, so it is essentially a carbon donor. Folic acid is important in the synthesis of thymine specifically, especially as the cell divides, particularly with the synthesis of new red blood cells. Side effects from taking folic acid are rare; however, they do sometimes occur. These side effects include things such as fever, weakness, reddened skin, shortness of breath, trouble breathing and tightness in chest. Since, folic acid was not easily found in food, it has since been added to flour-based products such as cereals, bread, cookies, crackers and other bakery items with a federal regulation to do so. Supplements are also highly recommended for at-risk groups as well. With such wide range of benefits of folic acid, I think many patients would benefit from either including more folic acid in their diet or taking a folic acid supplement.

# data[].attributes.body
Iron is transported by the divalent metal transporter 1 (DMT1) across the endolysosomal membrane to enter the macrophage. It can then can be incorporated into ferritin and be stored in the macrophage or carried of the macrophage by ferroportin. This exported iron is oxidized by the enzyme to ceruloplasmin to Fe3+, followed by sequestration by transferrin for transport in the serum to various sites, including the bone marrow for hemoglobin synthesis or into the liver. Iron combines with porphyrin and globin chains to form hemoglobin, which is critical for oxygen delivery from the lungs to other tissues. Approximately 5 – 10% of dietary iron is absorbed, and this absorption rate increases to up to 30% in iron deficiency states. Oral iron supplements are absorbed up to 60% via active and passive transport processes. Gastrointestinal absorption of iron occurs via strict regulation by the enterocyte and duodenal cytochrome and ferric reductase enzymes. The hormone hepcidin heavily regulates iron absorption and distribution throughout the body. The median time to maximum serum concentration (Tmax) is generally 4 hours after administration. Between 2-8 hours post administration, average serum iron concentrations fluctuate by 20%, according to one study. Bioavailability of iron depends on whether it is administered in a film coated tablet or enteric coated tablet. One pharmacokinetic study in healthy volunteers revealed a 30% bioavailability for enteric coated tablets. The AUC of enteric coated tablets varied between a lower limit of -46.93 to 5.25 µmol*h/l. Cmax is higher for film coated tablets, ranging from 3.4 to 22.1 µmol/h/l. It is advisable to take ferrous sulfate with ascorbic acid, as this practice may increase absorption. Avoid antacids, tea, coffee, tea, dairy products, eggs, and whole-grain bread for at least an hour after taking ferrous sulfate. Calcium can decrease iron absorption by 33% if taken concomitantly. About 60% of iron is distributed the erythrocytes. The remainder of the iron is found in muscle tissues (as a part of myoglobin), and in a variety of different enzymes, as well as in storage form. Most stored iron is in the form of ferritin, which can be found in the liver, bone marrow, spleen and, and muscle. Iron crosses the placenta and is also found in breast milk. The protein binding for ferrous sulfate is equal to or greater than 90%. It is bound to transferrin and ferritin, ferroportin, myoglobin, and other enzymes.

# data[].attributes.body
Montelukast

Montelukast is used to help prevent breathing difficulties in adults and children that are six years or older. The target of montelukast is cysteinyl leukotriene receptor 1, which is an antagonist for the bronchoconstriction of individuals with and without asthma. Arachidonate 5-lipoxygenase is another target that catalyzes the first step in leukotriene biosynthesis and thereby plays a role in the inflammatory processes. Montelukast’s mechanism of action works by blocking the action of leukotriene D4 in the lungs resulting in decreased inflammation and relaxation of smooth muscle. Montelukast was discovered by Merck for the maintenance and treatment of asthma and relieving allergy symptoms. A few side effects of montelukast are body aches or pain, difficulty breathing, dryness or soreness of the throat, headache, pain or swelling of the ear, stomach pain, swollen glands in the neck, or trouble swallowing. The molecular weight of this particular drug is 586.184 g/mol. Montelukast is also known for not having any heterocycles involved in its structure. However, Motelukast does include a carboxylic acid group. Something interesting about this drug is that you can take it while you are pregnant because there are no known negative interactions involved with pregnancy. However, it is suggested that you do not drink alcohol while taking this drug. Because asthma symptoms are known to get much worse at night, it is suggested to take this medication before bedtime. Although Montelukast typically tends to improve patients’ conditions after the first use, some people had to wait an entire week before seeing positive results in their symptoms. While Montelukast is not an antihistamine or steroid, it is often used in combination therapy with an antihistamine or steroid for the best results. Montelukast is also known for being a very well tolerated drug mostly because it only showed adverse drug reactions in 14 of 6,158 patients that take it, and of these 14 people, none of the adverse drug reactions were severe or serious. Something important to remember about this drug is that it just controls the symptoms of asthma and allergies, it does not cure them completely. Because of this, even if you are feeling well, you should not simply stop taking this medication, and you should never stop taking this medication without speaking to your primary care physician about this choice first. An alternative drug that is similar to Montelukast is Zyrtec that is available over the counter and by prescription.

# data[].attributes.body
Loratadine, more commonly known as Claritin, is a second generation antihistamine used to temporarily relieve the symptoms of hay fever (allergy to pollen, dust, or other substances in the air) and other allergies. These symptoms include sneezing, runny nose, and itchy eyes, nose, or throat. Loratadine is also used to treat itching and redness caused by hives. Like other 2nd generation antihistamines, loratadine is selective for peripheral H1 receptors. Loratadine does not penetrate effectively into the central nervous system and has poor affinity for CNS H1-receptors which is what made this drug so popular because it was non-sedating. These qualities or Loratadine result in a lack of CNS depressant effects such as drowsiness, sedation, and impaired psychomotor function. Loratadine exerts its effect by targeting histamine H1 receptors. The H1 Histamine receptors are found on the surface of epithelial cells, endothelial cells, eosinophils, neutrophils, airway cells, and vascular smooth muscle cells and other cells. Loratadine mechanism of action is that it binds to these H1 histamine receptors which favor the active form, meaning loratadine can be classified as an inverse agonist because it binds to these H1 histamine receptors and helps to reduce or prevent any of the histamine related effects. Loratadine undergoes extensive first pass metabolism in the liver and is primarily metabolized by CYP3A4, CYP2D6, CYP1A1 and CYP2C19. Loratadine, being a second generation antihistamine, has very few adverse effects but there still are some that have been reported. These occasional side effects include insomnia, headache, fatigue, drowsiness and rash. Symptoms of loratadine overdose include gastrointestinal side effects, drowsiness, increased heart rate, and headache. Loratadine only needs to be administered once daily, orally. The history of Loratadine began in 1937 when a Swiss-Italian pharmacologist, known as Daniel Bovet, discovered a substance that could block the effect of histamines in guinea pigs. That research, which helped him win a Nobel Prize 20 years later, paved the way for the development of the first antihistamine drugs. Researchers and scientists were in search of an antihistamine drug that did not make you drowsy or was “non-sedating.” Charles Magatti and his team began by taking a sedating antihistamine and, through a series of chemical reactions, began removing the components of the drug that gave it the sedating effect. After around 30-40 tries, they came up with a compound that did not have the sedating effect. Magatti added a chlorine to boost the potency and then Loratadine, more commonly known as claritin, was born.

# data[].attributes.body
Diclofenac

Diclofenac is a drug used to manage pain and treat inflammatory conditions. Specifically, this drug is a nonsteroidal anti-inflammatory drug (NSAID) and is used to reduce symptoms of osteoarthritis or rheumatoid arthritis and treat mild to moderate pain. In order to produce its effects, diclofenac targets cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) and inhibits the activity by reducing the synthesis of PGE2, thromboxanes, and other prostanoids. This is important as prostanoids are key players in the inflammatory response. Because this is an NSAID drug, patients who are allergic to aspirin or NSAIDs should not take this medication. Diclofenac can lead to increased risk of heart attack and stroke, as well as bleeding in the stomach and intestine, which can ultimately lead to death. Therefore, this medication is not recommended for long-term use, at high doses, or for patients with heart disease. Before being prescribed this medication, it is crucial to determine if the patient has a history of heart disease, high blood pressure, ulcers, asthma, liver disease, kidney disease, and if he or she is a smoker. These factors can lead to adverse effects so gathering this information ensures safety. Furthermore, if a pregnant patient takes diclofenac, especially during the last 20 weeks, the baby could have kidney and liver problems with increased chances of complications throughout the pregnancy. With that being said, diclofenac should not be taken when pregnant and there are safety risks associated while breastfeeding. This medication can be extremely helpful, but there are serious side effects associated with the drug that are crucial to be aware of. The most common side effects include nausea, vomiting, stomach pain, indigestion, dizziness, headache, itching, increased blood pressure, swelling, and pain in the arms or legs. Additionally, this medication can cause severe adverse reactions like hives, difficulty breathing, swelling in face and throat, blistering, and peeling skin. There are also drug-drug interactions that can affect the patient’s condition and therapy. For instance, heart or blood pressure medications, other forms of diclofenac, blood thinners, other NSAIDs, and antidepressants can alter the effects of diclofenac. There are numerous different brands of diclofenac with different amounts of diclofenac, meaning there could be different uses for this drug. Diclofenac is not approved for use by any patient that is under the age of 18 years old. The lowest dose that is effective should always be used. Overall, it is imperative to take diclofenac exactly as the doctor prescribes.

# data[].attributes.headline
Brendan Luechtefeld - Hydralazine Hydrochloride

# data[].attributes.subject
Brendan Luechtefeld - Hydralazine Hydrochloride

# data[].attributes.body
[PLEASE NOTE] - I broke up each section to make it easier for everyone (you and I included) to distinguish the different sections/topics of the drug.

What I've Learned -
- I've learned that this is a antihypertensive tablet whose major effects are on the cardiovascular system. It is famous for being able to treat hypertension and more importantly heart failure. Whilst mostly still not understood, it lowers blood pressure by causing peripheral vasodilation (it relaxes vascular smooth muscle). It achieves this by interfering with calcium movement in vascular muscle cells, preventing constriction. This causes hypotension, which is met with the heart increasing heart rate and stroke volume to compensate. The medicine is rapidly absorbed orally (1-2 hours), can increase plasma levels when taken with food, and is rapidly metabolized and excreted via urine. One very interesting fact about this medication is that it is normally not used as a primary drug to treat hypertension on its own. Its effects cause sympathetic stimulation, causing all sorts of side effects, often worsening the situation. For this, hydralazine is administered with beta blockers and a diuretic, which both work to decrease the following sympathetic response.

Indication -
- Hydralazine Hydrochloride is a medication used to treat high blood pressure and heart failure, by exerting vasodilatory effects on the body. This does this by blocking the movement of calcium ions in vascular muscles, preventing constriction. This medication is used commonly in people with preexisting heart conditions, as well as in pregnant women (however, see adverse reactions for more info).

Target Interaction -
- This medication targets "resistant arterioles", acting directly on them by acting as a vasoconstriction repressor, via inhibition of inositol trisphosphate-induced Ca²⁺ release from the sarcoplasmic reticulum in arterial smooth muscle cells. To simplify, it stops specific calcium ion release from the SR of muscle cells, blocking that muscle cell from constricting. This all ends with a decrease in peripheral resistance, which lowers blood pressure.

Mechanism of Action -
- As said before, hydralazine hydrochloride works by inhibiting inositol trisphosphate-induced Ca²⁺ release from the sarcoplasmic reticulum in arterial smooth muscle cells. What this does is stops smooth muscle cells from contracting in the arterioles, decreasing peripheral resistance, leading to decreased blood pressure.

History of Discovery -
- Hydralazine's antihypertensive abilities were discovered in 1945 by scientists working for Ciba (a chemical company), who were working to find a cure/treatment for malaria (FDA approved by 1953).
- This was one of the first antihypertensive drugs ever to be able to be taken by mouth.

Side Effects -
- effect identical to systemic lupus erythematosus including glomerulonephritis.
- Increases the risk of myocardial infarction due to ischemia, as well as a numbness or tingling feeling in appendages.
- Possible teratogenic effects, although all studies were done in animals, and none in pregnant humans (do not breastfeed while on this medication, it gets excreted in milk).
- Overdosage, whilst no antidote exists, is not known to be fatal, and causes hypotension, tachycardia, headache, and generalized skin flushing.

# data[].attributes.body
Elaina Vitale
Propranolol Hydrochloride

Propranolol Hydrochloride is a non-selective β-adrenergic receptor antagonist. This is also more commonly known as a beta-blocker. This drug is used in the treatment of hypertension, chronic angina pectoris, cardiac dysrhythmia, and essential tremors. It helps treat these conditions by being a beta-blocker: blocking the action of epinephrine and norepinephrine. It achieves this by competitively blocking both β1 and β2 adrenergic receptors, which ultimately suppresses vasodilation and changes in heart rate in the patient, helping them to return to normal, homeostatic conditions. Because of this ability to slow heart rate, patients with sick-sinus syndrome, bradycardia, and heart blocks that are not being treated with pacemakers should not take this medicine. Those with asthma should also stay away, as it can affect breathing patterns. Propranolol Hydrochloride can also be administered to patients after they have suffered heart attacks to increase their chances of survival as well as prevent excessive chest pain and migraines. Some studies have shown this medication to decrease the production of melatonin in the body, which could throw off your body’s circadian rhythm and interfere with normal sleep cycles. Melatonin also plays a role in managing immune function and cortisol levels, so one would need to pay attention to their symptoms to ensure this does not happen to them. Dr. Sir James Black and his team of researchers developed Propranolol in the mid 1960’s, and this was the first beta-blocker drug ever. His discovery of beta-blockers is considered one of the most important medical advancements in the 20th century. He originally created these drugs to ease the pain and symptoms for patients that have had heart attacks or any kind of heart abnormality. It wasn’t long after this medication reached the market though that it was discovered to have other important abilities like prolonging life post-heart attack, lowering blood pressure, and correcting rhythm issues. Propranolol Hydrochloride has no heterocycles, but includes phenol, secondary amine, secondary alcohol, and ether functional groups. Some side effects of this drug include dizziness or light-headedness, cold extremities due to lower blood supply to the fingers and toes, nausea, or trouble sleeping. There are a few extreme side effects that are more rare but should still be a concern. These include muscle weakness, hallucinations, memory loss, and blood sugar changes. Unlike many medications, this can be used safely in pregnant women. Propranolol Hydrochloride has been used to treat tachycardia in the mother and fetus, as well as reducing pregnancy-induced high blood pressure and anxiety. Overall, Propranolol Hydrochloride is a great option for a medication and is generally safe and effective.

# data[].attributes.body
Methylphenidate is a drug that has the following structure: C14H19NO2. Methylphenidate is a racemic mixture that consists of two isomers. The d-isomer is the pharmacologically active drug.  The molecular weight of my drug is 233.31 g/mol. Methylphenidate contains a heterocycle called piperidine. Piperidine is an organic, heterocyclic amine that consists of a ring of five carbons and one amine group. Methylphenidate contains several functional groups which consist of an ester group, phenyl group, and secondary amine group. Ritalin is the brand name of this drug and it belongs to a class of drugs called stimulants, often used to treat attention deficit hyperactivity disorder, which is the indication of this drug. The mechanism of action or drug target of methylphenidate is not exactly known, but it is thought that the mode of therapeutic action consists of the drug, methylphenidate, blocking the reuptake of norepinephrine and dopamine into the presynaptic neuron. This makes the drug a central nervous system stimulant because it allows more norepinephrine, which helps modulate hyperactive behavior, to be available in the central nervous system, thus lessening the symptoms of attention deficit hyperactivity disorder. Since the exact mechanism of action is theorized and not finite, neither is the role of the drug, for example, whether it is considered an agonist or antagonist. However, it is thought that methylphenidate is an indirect antagonist that facilitates the action of the dopamine type 1A receptor. In addition, it is theorized that methylphenidate is an agonist of the serotonin type 1A receptor. This means that methylphenidate is thought to have a mechanistic action that targets three different neurotransmitters, dopamine, norepinephrine, and serotonin. Methylphenidate was synthesized by Leandro Panizzon at Ciba’s laboratories in Basel in 1944. The first indication for methylphenidate was an analeptic for reversal of barbiturate, induced coma. The drug earned the name Ritalin because Leandro Panizzon tested the drug on his wife, whose nickname was Rita. The side effects of methylphenidate include nervousness, irritability, difficulty falling asleep, dizziness, nausea, vomiting, loss of appetite, and weight loss. In addition, excessive sweating, mood changes, fast heart rate, dry mouth, and headache are noted. More serious, long-term side effects of ritalin include heart disease, high blood pressure, seizure, irregular heartbeat, abuse and addiction, and skin discolorations. It should be noted that methylphenidate is considered a Class II substance under the Controlled Substance Act. A second indication for methylphenidate is narcolepsy for adults, while it is recommended for children of at least six years old and adults with ADHD.

# data[].attributes.body
Tizanidine (Zanaflex) is a small molecule that has a molecular weight around 253.711g/mol.  Originally approved by the FDA in 1996 iIt is a benzothiadiazole and is a member of imidazoles. Tizanidine is a usually reserved for when there is particular need for pain relief because it has a short duration of action. It's effectivness is similiar to baclofen or diazepam, It is a fast-acting drug used for the management of muscle spasm, which may result from the effects of acquired brain injuries, spinal cord injury or other musculoskeletal injuries. This drug is an oral drug changing the way you take it with regard to eating, can cause an increase in side effects or a decrease in therapeutic effect. It has a bioavalibility of around 40%. This drug is known to cause fetal harm in pregnant women and alcohol should be avoided when using this drug. Tizanidine works as an agonist at alpha2-adrenergic receptor sites. Tizadine also has other effects, specifically on blood pressure and heart rate, it has been found that Tizanidine lowers both and is patients are at risk for tachycardia and high blood pressure if that stop taking the medication to quickly.  Spasticity is an increase in muscle accompanied by uncontrolled, repetitive contractions of skeletal muscles which are involuntary. The patient suffering from muscle spasticity may have reduced mobility and high levels of pain, contributing to poor quality of life and problems performing activities of personal hygiene and care. Tizanidine reduces spasticity by causing presynaptic inhibition of motor neurons via agonist actions at Alpha-2 adrenergic receptor sites. Excitatory amino acids like glutamate and aspartate that lead to muscle spasm are reduced. The anti-nociceptive and anticonvulsant activities of tizanidine may also be attributed to agonist action on Alpha-2 receptors. Tizanidine also binds with weaker affinity to the Alpha-1 receptors, explaining its slight and temporary effect on the cardiovascular system.  Tizanidine shows a stronger action on polysynaptic reflexes, which involve several interneurons (relay neurons) communicating with motor neurons stimulating muscle movement.Tizadines common side effect include, dry mouth, tiredness, weakness, dizziness, urinary tract infection, constipation, vomiting, trouble speaking, runny nose, sore throat, vision problems. Since this is an oral drug it can interact with other medications, vitamins, or herbs you may be taking. An interaction is when a substance changes the way a drug works. This can be harmful or prevent the drug from working well.

# data[].attributes.body
My assigned drug for this semester was Quetiapine Fumarate (Seroquel). Quetiapine Fumarate is a psychotropic agent and is in the chemical class of dibenzothiazepine derivatives. It is indicated for the acute treatment of bipolar disorder, adjunctive therapy of major depressive disorder, and schizophrenia. Off-label uses include agitation/aggression associated with dementia, agitation and/or delirium, delusional infestation, generalized anxiety disorder, OCD, PTSD, psychosis associated with Parkinsons, and monotherapy for major depressive disorder. It can be administered as an oral tablet, an oral extended release tablet, or through a nasogastric/enteral tube.

Seroquel has a black box warning of increased mortality in dementia patients and an increased risk of suicidal thoughts and behaviors. Because of this, it is not approved for patients younger than 10 years of age or in patients with dementia-related psychosis. Some other common adverse reactions include increased blood pressure, decreased HDL levels, increased appetite, decreased hemoglobin, and many nervous system effects (agitation, dizziness, drowsiness, extrapyramidal reaction, fatigue, headache, and withdrawal syndrome). Disease-related contraindications include cancer, GI motility, hepatic impairment, seizures, and urinary retention.

Quetiapine Fumarate (C25H29N3O6S) has a molecular weight of 883.09 g/mol. It has 14 hydrogen bond acceptors and 4 hydrogen bond donors. The LogP value is 2.91. The functional groups found in Quetiapine Fumarate include hydroxyl groups, carboxylate ions, and ethers. The heterocycles in Quetiapine Fumarate are dibenzothiazepine and piperazine.

The proposed mechanism of action for Quetiapine Fumarate is that it is involved with both dopamine and serotonin antagonism. Specifically, it antagonizes serotonin activity mediated by 5-HT 1A and 5-HT2 receptors. With a lower affinity, this agent also reversibly binds to dopamine D1 and D2 receptors in the mesolimbic and mesocortical areas of the brain. It also binds to other alpha-1, alpha-2 adrenergic and histamine H1 receptors.

Seroquel was developed by AstraZeneca, approved in 1997 for schizophrenia, and was heavily marketed. During development, Seroquel showed efficacy in the treatment of schizophrenia and bipolar disorder. Testing included binding and functional assays using rat and human tissues, as well as positron emission tomography (PET) studied in monkeys and humans.  Postmarketing, there were many concerns about the safety of Seroquel regarding its effects on the heart. In 2000 (three years after marketing), researchers began looking into these effects. In 2006, the FDA asked AstraZeneca to stop circulating an ad minimizing the side effects of the drug. In 2009, the FDA cited Astrazeneca for mismarketing Seroquel stating the Seroquel was not approved for treatment of MDD. Later studies showed efficacy for long-term treatment of bipolar disorder and major depressive disorder.

# data[].attributes.body
Zolpidem was used in Europe starting in 1988, and it was brought to market there by Synthelabo. Synthelabo and Searle together bring it to the US market , and it was approved in the United States in 1992 under the brand name "Ambien". Some other brand names for zolpidem are Ambien CR, Edluar, Intermezzo, Zolpimist. Zolpidem is a Schedule IV controlled substances. Its DEA Code is #2783. Zolpidem is the drug that are using to treat insomnia (sleep problem). This medicine will help you fall asleep. This drug is not approved for children to use. Patients who are under 18 cannot use this drug. This drug also should be avoided in individuals 65 and over. It is available in tablet or spray form. Zolpidem is used for short-term only. If this medication is used for a long time, it may not work well as normal. Patients should not suddenly stop using this drug. If you do so, you may have nausea, vomiting, flushing, stomach cramps, nervousness, shakiness, etc. The molecular weight of Zolpidem Tartrate is 457.5 g/mole, and its formular is C23H27N3O7. There are two Heterocycles attached in Zolpidem Tartrate, which are Imidazole and pyridine. Three Functional groups of Zolpidem Tartrate are Amide, Alkanes, methylphenyl. Zolpidem is a GABA - A receptor agonist of the imidazopyridine class. Zolpidem increases GABA effects in the central nervous system by binding to GABA - A receptors at the same location as benzodiazepines. This drug is a nonbenzodiazepine Z drug which acts as a sedative and hypnotic. The excretion of zolpidem in breast milk represents 0.004 to 0.019% of an admin dose. Zolpidem may cause a severe allergic reaction such as hives, breathing, swelling, etc. Zolpidem also contain lactose, so patient with lactose allergic need to be careful. CT scans have shown that the use of the drug actually does dramatically increase the activity in the frontal lobe of the brain in some patients in a minimally conscious state. Patients who are using this drug need to stop consuming alcohol.  You may have some side effects while you are using Zolpidem such as depression, anxiety, aggression, agitation, confusion, unusual thoughts, hallucinations, memory problems, chest pain, irregular heartbeat, short of breath, trouble breathing or swallowing, etc. Patients should not drive after consume Zolpidem because it may cause dizziness or severe drowsiness. The recommended initial doses of this medicine for women and men are different. So that, patients should not share this drug with each other. Woman usually have lower dose. Sometime, this medication can cause addiction. Overdose can lead to coma or death.

# data[].attributes.body
Apixaban

Apixaban is an anticoagulant, or blood thinner, which is used to treat various health problems resulting from blood clots throughout the body. Some diseases that apixaban can help treat are heart attacks, strokes, deep vein thrombosis, and pulmonary embolism. It is administered as a 2.5 milligram tablet to be taken by mouth two times a day or 5 milligram tablet to take once a day, and it can be taken with or without food. Its appearance is a white to pale or yellow powder. One enzyme in the body that can cause blood clots is Coagulation Factor Xa; apixabam works to prevent blood clots by directly, selectively, and reversibly inhibiting both free and bound Factor Xa. Another target of Apixabam is prothrombinase, an enzyme that produces thrombin in the body to regulate homeostasis through coagulation. When clotting causes diseases, Apixaban inhibits prothrombinase to prevent the formation of thrombin, which prevents clots from forming. One side effect is increased bleeding, which when administered incorrectly can cause serious injury or even death. Additionally, if the usage of Apixabam is discontinued without replacing it with another anticoagulant drug, the chances of strokes can increase. Some drug to drug interactions can occur when taking Apixabam because of its binding ability to both CYP3A4 and P-gp. Drugs that inhibit CYP3A4 and P-gp increase risk of bleeding when interacting with Alpixabam, and inducers of CYP3A4 and P-gp increase the risk of stroke. It is not recommened that patients who are pregnant, nursing, or have prosthetic heart valves take Apixabam, as enough studies have not been done to understand its exact effect on those patients. Apixaban has a molecular weight of 459.497 gram per mole. Some functional groups and heterocycles present in this drug include benzene rings, aryl groups, amides, ethers, and pyrazole. Apixaban is the generic name for this drug, but it also goes by its brand name Eliquis. The Food and Drug Administration received the New Drug Application for Apixabam on November 29, 2011. This application emphasized its use in patients with atrial fibrillation, and its goal was to prevent strokes and systemic embolism. The New Drug Application was not approved until over a year later on December 28, 2012. On July 11, 2013, a Supplemental New Drug Application was submitted to the Food and Drug Administration for Apixabam to be used for Deep Vein Thrombosis after knee or hip replacement surgery. This application was approved on August 21, 2014.

# data[].attributes.body
MW: 505.31 g/mol
Heterocycles: triazolopiperazine ring system
Functional groups: triazole, piperazine, amino group, triflourobenzene ring, amide.

Targets: Sitagliptin is an anti-diabetic drug that is taken to treat type II diabetes. Type II diabetes is an illness where the body does not make enough insulin, or the insulin that it makes does not function properly, leading to hyperglycemia, or increased blood sugar levels. Sitagliptin treats this illness by inhibiting the enzyme dipeptidyl peptidase-4 (DPP-4). Under normal conditions, DPP-4 degrades certain hormones, called incretin hormones, that are released following a meal to stimulate insulin secretion from the pancreatic β-cells. Thus, DPP-4 plays a key role in regulating incretin hormone function. When Sitagliptin inhibits DPP-4 activity, it increases the half-life of the incretin hormones, thus allowing increased insulin secretion by the pancreatic β-cells as well as reduced glucagon secretion by pancreatic α-cells. As a result, blood glucose levels decrease. It is also important to note that since incretin hormones are released only following a meal, DPP-4 inhibitors do not cause hypoglycemia.
Sitagliptin is a non-substrate-like inhibitor of the DPP-4 enzyme, making it an allosteric inhibitor (noncompetitive inhibition).
This drug was first approved by the FDA on October 17, 2006, and is sold under the brand name "Januvia". It is sold in the form of tablets, and is administered orally. It comes in 3 different concentrations - 25 mg, 50 mg, and 100 mg. The pharmaceutical company that manufactures and sells this medication is Merck & Co.
It is also important to note that this medication is intended to be taken as an adjunct to diet and exercise to improve gylcemic control in type II diabetic patients.
Administration of this medication can be done with or without meals. Recommended storage for this medication is 20°C to 25°C (68°F to 77°F).
Some of the main adverse reactions to keep in mind when taking this medication are arthralgia (pain in joints); some dermatologic reactions like rashes, itching, and peeling skin with or without fever; hypersensitivity reactions; kidney problems, and pancreatic events.
Some other important information to note about this medication is that it is rapidly absorbed by the gut, has a 38% protein binding ability, is an active drug that is metabolized by CYP3A4, is 87% bioavailable, and has a half-life elimination of 12.4 hours. This medication is also commonly administered within the US (it is the 88th most commonly prescribed medication), with more than 88 million prescriptions.

# data[].attributes.body
Bupropion is an antidepressant that is used to treat and prevent depression in patients with major depressive disorder and seasonal affective disorder (SAD) which can be called winter depression. It can be used to help people stop smoking by reducing cravings and other withdrawal effects. Bupropion is also used off-label for the management of Attention/Deficit-Hyperactivity Disorder (ADHD) in adults with comorbid bipolar depression to avoid mood destabilization caused by typical stimulant mediations used for the treatment of ADHD. It is a norepinephrine and dopamine reuptake inhibitor. It exerts its pharmacological effects by weakly inhibiting the enzymes involved in the uptake of the neurotransmitter’s norepinephrine and dopamine from the synaptic cleft, therefore prolonging their duration of action within the neuronal synapse and the downstream effects of these neurotransmitters. More specifically, it binds to the norepinephrine transporter (NET) and the dopamine transporter (DAT). It lacks any clinically relevant serotonergic effects, typical of other mood medications, or any effects of histamine or adrenaline receptors. Because of this it results in more tolerable side effects, and it is less likely to cause sexual side effects, sedation, or weight gain compared to SSRIs or TCAs. When it comes to smoking cessation, it is thought to be involved in the reward pathways associated with nicotine, and through the antagonism of the nicotinic acetylcholinergic receptor (AChR) thereby inhibiting the effects of nicotine. The stimulatory effects produced by bupropion in the central nervous system are like nicotine’s effects, making low doses of bupropion a suitable option as a nicotine substitute. In addition, Bupropion does not inhibit monoamine oxidase and it has been found to be essentially inactive at the serotonin transporter (SERT), however both bupropion and its primary metabolite hydroxybupropion have been found to block the function of cation-selective serotonin type 3A receptors (5-HT3Ars). It became FDA approved in the United States in 1989. Initially, a three times daily immediate-release formulation was required, a twice-daily sustained-release formulation followed in 1996, and in August 2003, a once-daily extended-release formulation was introduced. Bupropion is now approved for use in over 50 countries for treatment of major depressive disorder and/or as an aid to smoking cessation, with over 40 million patients receiving treatment. Its brand names include Alpenzin, Bupeprion, Contrave, Forfivo, Wellbutrin, and Zyban. Some serious side effects of bupropion include seizure, confusion, changes in mood or behavior, blurred vision, irregular heartbeat, or manic episodes. Other common side effects include dry mouth, sore throat, stuffy nose, ringing in ears, nausea, vomiting, nervous or anxious feelings, insomnia, sweating, tachycardia, agitation or confusion, rash, weight loss increased urination, headache, or muscle/joint pain.

# data[].attributes.body
Prednisone is an oral steroid typically used to treat patients dealing with inflammation such as arthritis. Prednisone is also in the subgroup of corticosteroids. It is also used to treat those with breathing issues, skin issues, cancers, immune systems disorders, and severe allergies. It can also be used in conjunction with antibiotics for certain infections. Prednisone is primarily considered an agonist though it does cause inhibitory responses. Prednisone is a prodrug that must be metabolized into its active form, prednisolone, in order to be used by the body. Corticosteroids bind to glucocorticoid receptors and inhibit the release of inflammatory signals into the body. This includes the actions involved in the inflammatory response such as increased permeability to inflammatory cellular components. This decreased permeability also decreases the migration of leukocytes. Leukocytes are the one of the main sources of the inflammatory response in the body. Another result of prednisone use is decrease of vasodilation in the capillaries. It also promotes the increase of anti-inflammatory signals such as changing electrolyte concentrations. Prednisone also inhibits neutrophil apoptosis. Corticosteroids inhibit phospholipase A2 decreasing the formation of arachidonic acid derivatives. Long term effects can inhibit NF-Kappa B and other inflammatory transcription factors and promote anti-inflammatory genes like interleukin-10. It does this by migrating into the nucleus and binding to gene promoter regions associated anti-inflammatory genes. Different dosage regiments are indicated for different levels of need from inflammatory responses to necessity of immunosuppression. Prednisone’s invention, production, and use was patented by Arthur Nobile in 1950. Before the invention of prednisone, cortisone and hydrocortisone were used but these had higher risk of adverse affects, but Nobile used bacteria to oxidize these products into prednisone and prednisolone which had better health outcomes. As with any medications, prednisone can have adverse affects including adrenal suppression, cardiovascular events, CNS issues, infections, hyperglycemia, and dermatological problems. Prednisone as well as prednisolone are mainly metabolized and cleared from by the body by the oxidative action of cytochrome p450 enzymes in the liver. Prednisone is an immunosuppressive drug; therefore its use is wanted against in conjunction with live vaccinations which could greatly increase adverse affects of vaccine. It is also recommended against with patients experiencing systematic fungal infections. There is a low likelihood of overdosing on prednisone although one would experience severe symptoms and possibly death, but there are issues associated with the long term use of prednisone. Overall, prednisone is a wonder drug that has significantly impacted the medical industry.

# data[].attributes.body
Caroline Kreh
Escitalopram Oxalate

Escitalopram oxalate (brand name Lexapro) is a selective serotonin reuptake inhibitor (SSRI) indicated for the treatment of major depressive disorder and generalized anxiety disorder. Its off-label uses are for the treatment of various eating disorders, obsessive compulsive disorder, panic disorder, post-traumatic stress disorder, and more. As an SSRI, escitalopram is a non-competitive antagonist which binds to SERT (serotonin transporter) to prevent the reuptake of serotonin into the presynaptic neuron, which increases the activity of serotonin. Escitalopram was developed in the late 1990s in a relatively short amount of time, just 3.5 years. This is because it is the (S) enantiomer of citalopram, which was already extensively studied by the laboratory which developed escitalopram, Forest Laboratories (in collaboration with Lundbeck). There are several significant adverse effects associated with escitalopram, including a black box warning regarding increased suicidality, particularly in children and young adults. As such, it is not approved in children 12 years of age or younger. Other serious and significant side effects include mania, bleeding, fractures, hyponatremia, ocular effects, QT prolongation, serotonin syndrome, and sexual dysfunction. Mania is a side effect due to the potential for patients with bipolar disorder to be misdiagnosed as having unipolar depression. Antidepressants would, in turn, create the potential for a manic period to be activated. Another serious side effect, serotonin syndrome, presents in a variety of ways, with serious cases potentially causing coma. It is frequently caused by the concomitant use of multiple serotonergic drugs; this demonstrates the vital importance of thoroughly and accurately accounting for all of a patient’s medications. Another way that serious side effects or treatment failure can be caused is through a lack of pharmacogenomic consideration. A prominent enzyme involved in the metabolism of escitalopram is CYP2C19. The gene encoding CYP2C19 is highly polymorphic. A poor metabolizer may experience a simulated overdose and serious side effects including serotonin syndrome; an ultrarapid metabolizer may experience treatment failure, which is an extremely serious outcome when treating a disease such as major depressive disorder. As such, a poor metabolizer will often start at a significantly lower dose, such as 50% of the typical starting dose; an ultrarapid metabolizer will likely benefit from an alternative therapy not metabolized by CYP2C19. Dosing for this medication is often started at a low dose, such as 5-10 mg orally once per day, and titrated up by 5-10 mg gradually every 2-3 weeks to higher doses as needed by the patient. It is preferable to start at a lower dose so that the patient utilizes the minimum effective dose to avoid serious side effects. Maximum dose varies by indication, but monitoring with ECG is recommended at high doses due to the risk of QT prolongation.

# data[].attributes.body
Aspirin, a nonsteroidal anti-inflammatory drug (NSAID), was discovered in 1897 by Felix Hoffman, who worked for Bayer in Germany. Hoffman modified salicylic acid, which is found in plants such as willow trees and myrtles, to create acetylsalicylic acid, which he then named aspirin. This drug was the first in its class to be discovered. Aspirin is an enzyme inhibitor, with a molecule weight of 180.16 g/mole, which contains a carboxylic acid, ester, and an aromatic group. Aspirin is non-selective and irreversibly inhibits both forms of COX by acetylating the hydroxyl of a serine residue. Low doses (around 71 to 81 mg/day) are sufficient to irreversibly acetylate serine 530, inhibiting the activity of the enzyme cyclooxygenase, COX-1. Intermediate doses (around 650 mg to 4 g/day) inhibit COX-1 and COX-2, blocking prostaglandin production, and have analgesic and antipyretic effects. Aspirin is used to treat mild to moderate pain, fever, inflammation, migraines, menstrual cramps, sprains, toothaches, arthritis and reducing the risk of major adverse cardiovascular events. Aspirin is also used to help reduce blood clots in patients who have just had surgery. Aspirin is commonly used in combination with dipyridamole to create antiplatelet drugs. This works by preventing excessive blood clotting and reduce the risk of stroke in at risk patients, but the FDA recommends only using aspirin in this way under the supervision of a doctor. A doctor may recommend a daily low-dose of aspirin for people who have heart or blood vessel disease, poor blood flow to the brain, high cholesterol or blood pressure, and diabetes. However, for people who do not have serious cardiovascular issues, the risks of long-term aspirin use can outweigh the benefits. The most common side effects of aspirin are nausea, vomiting, heartburn, and stomach cramps. Other adverse events that could occur are bleeding disorders, high blood pressure, asthma, stomach ulcers, and liver or kidney disease. Doctors recommend pregnant women should not take high doses of aspirin. There are many drugs that aspirin can interact with. Some of those are anti-inflammatory painkillers, such as diclofenac, selective serotonin reuptake inhibitors and other antidepressants, warfarin, and methotrexate. Aspirin is not recommended for people under the age of 18 unless instructed by a doctor. Aspirin is available as an over-the-counter drug and a prescription. Common brand names are ascription, aspergum, Bayer, and aspirtab. The dosage forms can be available as extended-release capsules, liquid filled capsules, and tablets: chewable and enteric coated.

# data[].attributes.body
The molecular weight of Ropinirole hydrochloride is 296.83 g/mol. It contains γ-lactam and indole heterocycles as well as amide (secondary amine and ketone) and tertiary amine functional groups. Ropinirole hydrochloride is a non-ergoline dopamine agonist used to treat the symptoms of Parkinson’s disease (PD) as well as Restless Legs Syndrome (RLS). These symptoms include stiffness, tremors, muscle spasms, and poor muscle control. The discovery of this drug’s utility in RLS is an example of successful drug repurposing. Ropinirole hydrochloride can also reduce some of the side effects caused by selective serotonin reuptake inhibitors (SSRI’s) or antipsychotics such as Parkinsonism syndrome and erectile dysfunction. The exact mechanism of action is unknown; however, it is believed to be related to the ability to selectively stimulate dopamine D₂ receptors within the caudate-putamen system of the brain, affecting body movement. On the other hand, some sources claim that it acts as a D₂, D₃, and D₄ dopamine receptor agonist with highest affinity for D₃. It is metabolized primarily by cytochrome P450 CYP1A2, forming SK&F-104557 and SK&F-89124. Both of these metabolites are renally excreted. Ropinirole hydrochloride was approved for medical use in the United States in 1997 and sold under the brand name Requip. Mayo Clinic lists confusion, dizziness, drowsiness, fatigue, nausea, hallucinations, swelling of the legs, and unusual body movements as the most common side effects. REQUIP (ropinirole) may interact with levodopa, ciprofloxacin, fluvoxamine, metoclopramide, omeprazole, or estrogen. It is unknown whether REQUIP (ropinirole) passes into breast milk or if it could harm a nursing baby; however, it may reduce breast milk production. Ropinirole Tablets, USP are available containing ropinirole hydrochloride, USP equivalent to 0.25 mg (white, round, and unscored tablet), 0.5 mg (yellow, round, and unscored tablet), 1 mg (green, round, and unscored tablet), 2 mg (orange, round, and unscored tablet), 3 mg (lavender, round, and unscored tablet), 4 mg (grayish beige, round, and unscored tablet), or 5 mg (blue, round, and unscored tablet) of ropinirole. The maximum recommended dose is 24 mg per day for PD and 4 mg per day, taken one to three hours before bedtime, for RLS. While Requip is short-acting and usually taken three times a day, Requip XL is an extended-release tablet that only needs to be taken once a day. Requip XL is only used to treat PD (not used for RLS). This medication should be stored at room temperature as well as protected from moisture and light.

# data[].attributes.body
Kima Barannik
Valsartan
I have learned a lot of information about this drug, Valsartan is a nonpeptide, orally active, and specific angiotensin II antagonist acting on the AT1 receptor subtype. Angiotensin II is the principal pressor agent of the renin angiotensin system, with effects that include vasoconstriction, stimulation of synthesis and release of aldosterone, cardiac stimulation, and renal reabsorption of sodium. Like I said, Valsartan is an angiotensin II receptor blocker (ARB) and because of that it works by blocking a substance in the body that causes blood vessels to tighten. It relaxes the blood vessels and lowers blood pressure. A lower blood pressure will increase the supply of blood and oxygen to the heart. Its formula is C24H29N5O3, and it’s molecular weight is 435.5. There are a few side effects with this drug: it can cause blood pressure to drop too low. This can cause dizziness, lightheadedness, and headache. One may have a higher risk if they are dehydrated or take high doses of diuretics. It may also cause an increase in potassium levels. The risk may be higher if one may have kidney problems or heart failure. A doctor should check potassium levels with blood tests before allowing one to take this medication. In general the most common side effects include dizziness (17% vs 9% ), low blood pressure (7% vs 2%), and diarrhea (5% vs 4%). Less common side effects include joint pain, fatigue, and back pain (all 3% vs 2%). Stopping valsartan can also cause serious side effects such as someone's blood pressure spiking. This may increase someone's chance of a heart attack or stroke. If not taken on schedule: one's blood pressure may not improve or may get worse. Valsartan controls high blood pressure and heart failure but it does not cure them. The blood pressure may decrease during the first two weeks of the treatment, but it may take up to four weeks for one to notice the full benefit of valsartan. Valsartan was first patented by Novartis Pharmaceuticals in Europe in 1996 and then in 1997 approved in the United States. Novartis originally manufactured valsartan blood pressure medication under the brand name Diovan. The drug generated $5.7 billion worldwide in 2011. The patent was taken off in the USA in 2012, when valsartan was distributed as a generic. Valsartan alone and in combination with other drugs is sold by 30 companies in the US market.

# data[].attributes.body
Furosemide is a loop diuretic that is primarily used to treat hypertension, which is high blood pressure, and its brand name is Lasix.  It is used for edema secondary to various clinical conditions, such as congestive heart failure exacerbation, liver failure, renal failure, and high blood pressure.  Furosemide’s molecular weight is 330.74 g/mol, which is classified as a small molecule, and contains many important functional groups and heterocycles.  The functional groups in furosemide are sulfonamide, benzene, carboxylic acid, and amine groups, and its heterocycle is furan.  Furosemide mainly works by inhibiting electrolyte reabsorption from the kidneys and enhancing the excretion of water from the body.  Specifically, it works to increase the excretion of Na⁺, which is sodium, and water by the kidneys by inhibiting the reabsorption from the proximal and distal tubules, as well as the loop of Henle, which is why it is a loop diuretic.  It works directly on the cells of the nephron and indirectly modifies the content of the renal filtrate.  Ultimately, it increases the urine output by the kidney.  When it is bound to proteins, it is delivered to the kidneys and secreted by active secretion by nonspecific organic transporters expressed at the luminal site of action.  The diuretic effect is achieved through the competitive inhibition of sodium-potassium-chloride cotransporters, known as NKCC2, expressed along the tubules in the nephron, preventing the transport of sodium ions for reabsorption.  It exerts direct vasodilatory effects, which results in its therapeutic effect against pulmonary edema, and it may also open potassium channels in resistance arteries.  Vasodilation leads to reduced responsiveness to vasoconstrictors, such as angiotensin II and noradrenaline, and decreased production of endogenous natriuretic hormones with vasoconstricting properties.  It also leads to increased production of prostaglandins with vasodilating properties.  While Furosemide has all of these different effects on the body, its main mechanism of action is independent of its inhibitory effect on carbonic anhydrase and aldosterone.  Furosemide has a fast onset and short duration of action, and it has been used safely and effectively in both pediatric and adult patients.  Its use is particularly beneficial in clinical settings where a drug with higher diuretic potential is required.  Its formulations include oral, intravenous, and intramuscular administrations.  Oral furosemide is indicated alone for management of mild to moderate hypertension or severe hypertension in combination with other antihypertensive medications.  Intravenous furosemide is indicated in acute pulmonary edema when a rapid onset of diuresis is desired.  Its side effects include frequent urination, excessive thirst with dry mouth, headaches, dizziness, and muscle cramps.

# data[].attributes.headline
Jaycie Keylon- Tamsulosin Hydrochloride 

# data[].attributes.subject
Jaycie Keylon- Tamsulosin Hydrochloride 

# data[].attributes.body
Tamsulosin Hydrochloride is the generic for Flomax. It is a selective alpha-1-Adrenergic Blocking Agent. It is used for benign prostatic hyperplasia. It facilitates the reduction of urinary obstruction in hypertensive (or normotensive) patients with symptomatic BPH. The obstruction is due to mechanical compression of the urethra by the hypertrophied prostate and contraction of the prostate by sympathetic stimulation. Tamsulosin hydrochloride does not shrink the prostate, but relaxes the muscles in the prostate and the bladder. This relieves symptoms of BPH. symptoms of BPH include difficulty in urination, weak urine stream, and the need to urinate frequently. This medication is not used to treat high blood pressure. It may result in a sudden drop in blood pressure, which could result in dizziness or fainting. The higher the initial dose it, the more likely adverse events related to blood pressure are. During the first few doses, be aware of the risk of fainting and be in a situation that reduces chance of injury upon falling. It is administered orally once daily, 30 minutes after the same meal each day. The medication needs to be taken at the same time every day to increase efficacy. If the medication is not taken for several days, the prescribing doctor needs to be contacted and the dose may need to be adjusted. This medication takes up to 4 weeks to improve symptoms. If symptoms do not improve after 4 weeks, the prescribing doctor needs to be contacted and the dose may need to be adjusted. The capsules are not to be crushed, opened, or chewed. Doses need to be adjusted with the liver and kidney impaired. Side effects of the drug include headache infection, back pain, chest pain, dizziness, increased cough, blurred vision, and more. Tamsulosin Hydrochloride has a drug interaction with cimetidine and should be used with caution. It distributes in the extracellular fluids in humans. This drug binds to the alpha-1-adrenergic receptors on the prostate and the bladder trigone, resulting in decreased urinary outflow resistance in men. It has a higher affinity for alpha-1A-adrenergic receptors located in nonvascular smooth muscles. It was invented as a sulfamoylphenethylamine derivative that selectively reduced intra-urethral pressure in the prostate. Tamsulosin hydrochloride was invented and developed by Astellas and has been marketed in 90 countries. It was first launched in Japan. It has been available in the United States since 1997. It has a 20 to 38 fold greater affinity for alpha-1A-adrenergic receptors than for alpha-1B receptors.

# data[].attributes.body
Sam Saraceno
Citalopram

Citalopram is defined as an antidepressant medication and selective serotonin reuptake inhibitor. It is indicated for the use of major depressive disorder, also known as unipolar. Can be prescribed after a physician's advanced physical assessment on patients mood and should continue to be monitored once one the medication, Citalopram. The target interaction that occurs in Citalopram is its capability of being a SSRI, selective serotonin reuptake inhibitor. Citalopram is stated as a racemic bicyclic pthalene derivative. Its mechanism of action consists of Citalopram selectively stopping the reuptake of serotonin in presynaptic neurons causing an increase of serotonin levels in the brain. However, Citalopram seems to not have a notable effect on norepinephrine or dopamine levels in the brain. CItalopram has one component that has the biggest impact on the stopping of serotonin reuptake. This is the S-enantiomer. By increasing the levels of serotonin in the brain, Citalopram can help to improve moods and relieve symptoms of depression. Once Citalopram is first started it is expected to observe effects within 1 to 2 weeks. With the continuation of Citalopram improved results (mood) can be seen 4 to 6 weeks after initial dose. Citalopram was first discovered in August 1972 by Klaus P Bøges. A “5-bromo- 4- fluoro- derivative” was used to create the first sample of citalopram. After this it showed to be a potent SSRI that could help treat serotonin reuptake. It was then also proven to be an option for clinical development. The drug was then approved by the FDA on July 17, 1998 almost 26 years later, after the first sample was made. It was first approved for treatment of major depressive disorder but was later also approved for treatment of panic disorders. Once on the market Citalopram became a very well known and used antidepressant. Even though it was the 5th SSRI released to the drug market it became a popular treatment for major depressive disorder. One factor that made many favor Citalopram over other SSRIs was its good bioavailability, tolerability, long-term use and has favorable drug metabolism and pharmacokinetics properties. Citalopram can cause many common side effects such as nausea, dry mouth, drowsiness, fatigue, diarrhea or constipation, loss of appetite, etc. It also can cause some more serious adverse reactions such as, activation of mania or hypomania, risk of bleeding, fragility fractures, QT prolongation, serotonin syndrome, sexual dysfunction, withdrawal syndrome as well as suicidal thinking and behavior. Citalopram also has a Black Boxed Warning for, suicidality and antidepressants, which discusses how antidepressants such as Citalopram can increase the risk of suicidal thinking and behavior.

# data[].attributes.body
Budesonide, specifically oral inhalation, is a corticosteroid used for the treatment of asthma per the FDA. Off-label uses include chronic obstructive pulmonary disease and eosinophilic esophagitis, allergies, Crohn’s Disease, ulcerative colitis, and hay fever. Budesonide is available orally, or more commonly in an inhaler form. Budesonide Solution is also available for nebulizer systems. While capsules are indicated for patients with Crohn’s Disease, a nasal spray is available for patients with hay fever or upper respiratory infections. Budesonide should be stored at room temperature. Budesonide’s mechanism of action includes controlling the rate of synthesis: it decreases the movement of leukocytes and fibroblasts. Budesonide also reverses the capillary permeability and lysosomal stabilization in order to prevent or control inflammation. Onset of action for Budesonide is two to eight days for nebulization, and twenty-four hours for inhalation. Peak effect is four two six weeks for nebulization and one to two weeks for inhalation. Excretion of Budesonide is sixty percent in urine and feces as metabolites. Patients should not take budesonide if they are allergic to milk proteins, which are present specifically in the Pulmicort Flexhaler. The more probable adverse reactions include otitis media and a respiratory infection. More rare adverse reactions include syncope, dyspepsia, and nasopharyngitis. Budesonide is a substrate of the metabolic enzyme CYP3A4. CYP3A4 metabolizes budesonide into its two metabolites, 6beta-hydroxybudesonide and 16alpha-hydroxyprednisolone. If a patient has hepatic impairments such as cirrhosis, systemic availability of Budesonide is more than doubled post-oral ingestion. Budesonide has a very wide therapeutic index. Budesonide’s targets include glucocorticoid receptors (agonists) and Annexin 1 (substrate). Budesonide is 85-90% protein bound in plasma. While the possibility of overdosing on budesonide is rare, prolonged acute high dosing may lead to hypercorticism and adrenal axis suppression. Side effects from taking budesonide may include respiratory infections, coughs, and headaches. Furthermore, nosebleeds are common as well as throat and nose irritation. Severe side effects include nausea, vomiting, bone and joint pain, and respiratory issues. If a patient is discontinuing Budesonide, it is recommended to gradually taper the dose. Levels to monitor include pulmonary function, bone mineral density, and asthma symptoms. Budesonide was originally patented in 1973. In 1981, Budesonide was approved to be sold in inhaler form to treat allergies. In recent events, Budesonide has been approved as treatment for COVID-19 on a case by case basis. Furthermore, budesonide in conjunction with formoterol create the symbicort inhaler, which is a maintenance therapy of asthma.

# data[].attributes.body
Human Insulin is used for patients who have type 1 and 2 diabetes. Its major target is the liver, skeletal muscle, and adipose tissue. Insulin promotes glucose to transport through the membrane of those target cells by regulating the metabolism of carbohydrates, fats, and protein. It is a peptide hormone and considered to be the main anabolic hormone of the body converting small molecules to large molecules inside the cells. Insulin reduces blood sugar levels when it enhances glucose uptake and metabolism in cells. Beta cells will signal alpha cells to secrete glucagon into the blood when glucose is low and decrease secretion when glucose is high. This primary mechanism is called glucose homeostasis. The discovery insulin was by Sir Frederick G. Banting, Charles H. Best, and JJR Macleod at the University of Toronto in 1921. It began with isolating the clusters of cells in the pancreas called islets. These were the cells that were destroyed in type 1 diabetes. With this understanding, the scientists tried to extract insulin from ground up pancreas cells which were unsuccessful. This led to insulin being removed from a dog's pancreas. On January 11, 1922, insulin was first used in a boy and he showed no obvious signs of side effects. Today, there are many forms of insulin. It varies from personal needs and lifestyles. Humalog and Novolog are often used to treat diabetes. When injecting insulin, it can be injected in a few places such as abdomen, upper arms, thighs, and hips. The abdomen is the most effective way of injecting insulin into the body. It should be done two inches away from the belly button while pinching the injection site. The patient should hold the injection for about seconds. Also, the injection sites should be rotated to prevent irritation and discomfort. Those with diabetes will use a blood glucose monitor to record their levels. This should be done few times a week. Their levels before a meal should be between 80- 130 then after a meal it should be less than 180. For patients who are trying to become pregnant should use rapid acting insulin analogs. Patients who are pregnant should carefully monitor their diabetes for it can affect the fetus. When using insulin, interactions with current medications should be reviewed for there are many medications that interact with insulin. Some common side effects of insulin are dizziness, weight gain, hunger, sweating, and tingling in hands.

# data[].attributes.body
Clonazepam is the medicine I was assigned, and here are some facts I discovered about it from my study. Clonazepam was invented by Hoffman La Roche in 1964, at a time when benzodiazepines were displacing barbiturates as the preferred sedative drug. Clonazepam was originally promoted as a therapy for epileptic seizures and became available for medical prescription in 1975. In 2013, Tennessee passed the first U.S. law requiring pharmacies to limit benzodiazepine dispensing to a 30-day prescription. According to the National Institute on Drug Abuse, the number of deaths from benzodiazepines overall, increased more the 400% between 2002 and 2015. Clonazepam is a member of the benzodiazepine family of drugs. It's used to treat epilepsy-related seizures or fits, involuntary muscular spasms, panic disorder, and restless legs syndrome. Clonazepam is only available with a prescription. It is available in the form of tablets and a liquid that patients must ingest. Both a GABA-A receptor agonist and a GABA-B receptor agonist aids GABA-A activity by increasing the frequency of chloride channel opening, which causes hyperpolarization of neurons and reduced firing, resulting in calming effects on the brain by lowering cell excitability. Clonazepam is an agonist for the GABA-A receptor. Dizziness, tiredness, changes in salivation, stuffy or runny nose, skin rashes, blurred vision, and loss of appetite are all common Clonazepam adverse effects. Some people have more serious side effects, such as shallow breathing, a racing heart, a loss of judgment, easy bruising, or urinary problems. Clonazepam withdrawal-induced catatonia has been reported seldom. Pregnant women should avoid using it because it has been linked to birth abnormalities, fetal dependence, and withdrawal. And, like most sedative medications, Clonazepam should never be used with alcohol as it has a synergistic effect. Constant sleepiness, chronic sore throat, diarrhea, lack of appetite, numbness or stiffness, fainting spells, tremors, cognitive impairment, nightmares, paranoia, violent mood swings, and rising tolerance are all signs that someone is abusing the drug (needing to take more Klonopin to get the same effect). Headaches, nausea, heavy perspiration, dizziness, hallucinations, seizures, depression, and suicidal thoughts are among the symptoms of withdrawal. Blurred vision, acute confusion, dizziness, muscle weakness, breathing difficulty, impaired reflexes, and excessive exhaustion or loss of consciousness are all signs of an overdose. Because of its addictive potential, Clonazepam is not generally recommended for long-term use. Anyone receiving a prescription should consider it a temporary measure while taking time to learn alternate coping skills and possibly find other medications without the abuse potential.

# data[].attributes.body
Pravastatin sodium is a statin medication which  indicated treatment for the prevention of cardiovascular disease. This drug therapy is indicated administrative along with a restricted diet in saturated fat and cholesterol in addition to exercise to optimize the effect of medication.. Pravachol is an example drug of pravastatin sodium. Treatment for reducing the risk of hypercholesterolemia, reducing the mortality rate of stroke, and reducing the elevated LDL and many more diseases in terms of cardiovascular.Due to the agreesive reaction niacin, which leads to skeletal muscle effects. Considering when dispense dose strengths and frequency of drug. It is recommended for using maximum 40 mg by mouth once daily, in order to avoid side effect happening severely. This medication also offered for children diagnosed with primary dysbetalipoproteinemia who not responding to diet but using with cautions.

Pravastaton acts as an lipoprotein-lowering along with two pathways. First is competitive HMG-CoA, which is reductase inhibitor,  playing a role in decreasing cholesterol level through reversible inhibition which in intracellular membrane. the inhibitory mechanism of action produces a reduction in cholesterol synthesis which in order has been observed to increase the number of LDL receptors on cell surfaces and an enhancement in receptor-mediated metabolism of LDL and clearance.Furthermore, decreasing in Cholesterol leading to increase of LDL receptors. Pravastatin Sodium assist the elimination within circulating LDL, it also prevent the production of LDL by inhibit the synthesis of its precursor in the liver. The effect of pravastatin has been shown to significantly reduce the circulating not only total cholesterol, LDL cholesterol, but also apolipoprotein B. Pravastatin is listed into statin drug group which is first discovery by Sankyo Pharma Inc. Pravastatin initially idetified in fungus which called Penicilium citrinum in the 1970s. Pravastatin sodium was first sold in Japan and became worldwide in 2005. FDA approve this drug in 2006 for using in the US. Pravastatin sodium under thousands patients through clinical trials to identify the adverse effect and toxicology level of the medicine. Some severe side effect of 40 mg, once daily randomized and placebo controlled are heartburn, headache. In addition to that, lack of energy, fever, loss of appetite or skin rash and itching are considered to uncommon to this drug. Following by short-tem clinical trials the most commonly reported adverse effect is musculoskeletal pain, nausea and vomiting, upper respiratory infection, diarrhea and headchae.

# data[].attributes.body
Pregabalin

Pregabalin was first synthesized as an anticonvulsant in 1990 by the chemist Richard Silverman at the Northwestern University in Evanston, Illinois. The drug molecule was shaped so it could be transported into the brain to activate a certain enzyme. This enzyme was supposed to increase the inhibition of GABA and block convulsions. It received approval to be sold in the USA by the FDA in 2004. Pregabalin drug indication usage is mainly for neuropathic pain associated with DPN, PHN, and spinal cord injuries. It can also be used in patients with fibromyalgia or to treat patients older than four years of age who experience partial onset seizures. This drug is orally bioavailable and can be taken by mouth via capsules. This means the drug is absorbed in the intestines by active transport through a large amino acid transporter such as LAT1. Even though this drug crosses the blood brain barrier and enters the central nervous system, it still requires a transport because of its low lipophilicity. The mechanism of action of pregabalin is unknow. However, it is known that the drug will selectively bind to alpha2delta (A2D) subunits in the presynaptic voltage calcium channels of the central nervous system. The binding inhibits the influx of calcium which stops the release of neurotransmitters from the presynaptic nerve terminals. This will cause a decrease in neuronal excitability. Although it is a GABA analogue, the drug does not bind to any GABA-A or GABA-B receptors. Therefore, the GABA neurotransmitter is in not altered in the nervous system. Pregabalin also undergoes very little metabolism when going through the body. It is eliminated by the kidneys through urine in its unchanged form.  It has a short half-life and will therefore need to be administered around two to three times per day to keep the needed therapeutic levels. The functional groups associated with the structure of the drug are amines and carboxylic acids. Its structure is very similar to GABA. This drug does not have any heterocycles. Serious side effects surrounding Pregabalin are allergic reactions, suicidal thoughts, swelling of hands/ legs/ feet, muscle pain, weight gain and or dizziness. Common side effects are sleepiness, trouble concentration, dry mouth, dizziness, swelling, blurry vision, and weight gain. There are no known serious side effects in women who are pregnant.

# data[].attributes.body
Cetirizine, more commonly referred to as Zyrtec, is a second-generation antihistamine that reduces the natural chemical histamine in the body. Histamine can produce symptoms of sneezing, itching, watery eyes, and a runny nose. Cetirizine is used to treat these symptoms by binding to histamine receptors and preventing them from affecting. As an H1-receptor antagonist, it will reduce and suppress the expressions of the allergic reaction caused by histamine. The mechanism of action of Cetirizine is that it competes with histamine for H1-receptor sites on effector cells in the gastrointestinal tract, blood vessels, and respiratory tract. The allergic reaction is caused by macrophage migration, and this receptor suppresses this macrophage migration. Cetirizine is also used to treat allergic reactions, itching, and swelling caused by hives. If your hives do not reside or improve after three days of treatment, or if your hives last more than six weeks, contact your doctor. It will minimize or eliminate the effects of symptoms of reactions caused by dust and pollen. The functional groups contained in Cetirizine are aromatic hydrocarbon, halogenated aromatic hydrocarbon, tertiary amine, ether, carboxylic acid, and hydrocarbon. The heterocycle it has is the piperazine, and its molecular weight is 388.9 g/mol. The side effect of looking out for is that I can cause impairment in thinking and reactions. It can also cause sleepiness, dry mouth, headache, and abdominal pain. The degree of sleepiness is generally less than first-generation antihistamines. The medicine can be taken with or without food and comes in. There are different dosage forms of Cetirizine. It can be used as a tablet, IV, or eye drops. Since Cetirizine is an oral drug, it will undergo extensive first-pass metabolism in the liver. Cetirizine should be used with caution when it comes to patients with hepatic or renal impairment. It can also cause CNS effects which could cause CNS depressions, including sedated state, drowsiness, and fatigue. Serious side effects could include aggression and angioedema. Cetirizine is present in breast milk, so it is not recommended to breastfeed while taking Cetirizine. It was patented in 1981 and used in 1987. The person who discovered the first antihistamine was Dr. Daniel Bovet. He was an Italian pharmacologist and discovered antihistamines by experimenting on guinea pigs and found a substance that blocks allergic reactions. His discovery of antihistamine led to the development of more antihistamine drugs, eventually leading to Cetirizine. The discovery of antihistamines would allow a better quality of life for everyone.

# data[].attributes.body
Ranitidine, more commonly known as Zantac 75, is a medication used to treat ulcers, and in more serious cases, stomach ulcers, Gastroesophageal Reflux Disease GERD, and Zollinger-Ellison syndrome. The medication can be administered orally, intramuscularly, and intravenously. At one point in time, the drug was believed to have a carcinogen in it and it had resulted in recalls. Side effects of taking ranitidine include headaches and burning upon injection. Some serious side effects involved with the drug include bradycardia, pneumonia, and some stomach cancers. Ranitidine is generally regarded as safe to take if you are pregnant or planning to become pregnant. Ranitidine has been found in breast milk and exhibits peak concentrations at 5.5 hours after the dose has been given.

Ranitidine has a molecular weight of 314.404 grams per mol. Ranitidine has a furan heterocycle and features an ether, thioether, amine, and nitro functional group. The mechanistic role of ranitidine is to act as an enzyme inhibitor, by reversibly binding to the H2 as needed. This means that the drug helps to inhibit histamine receptors which result in a decrease in the secretion of gastric acid. Overall, this leads to the inhibition of histamine's ability to bind to the receptor, which causes a reduction of total gastric acid secretion. It is important to note that Ranitidine does not change gastric volume, but instead increases gastric PH, making it less acidic and more basic. Ranitidine exhibits 50% oral absorption and 15% protein binding properties. Ranitidine takes 55-65 minutes to onset. The half-life of ranitidine in the human body is generally 2.0-2.5 hours in a patient with normal creatine clearance, and 30%-70% are excreted by the kidneys.

Although Ranitidine was originally discovered in England in 1976, it was first used commercially in 1981. A fun fact about Ranitidine is that it is on the World Health Organization’s List of Essential Medicines. Another interesting fact is that it is the 53rd most prescribed medication in the United States. Some additional medical uses include relieving heartburn, it can be used alongside NSAIDs. It is important to administer this drug overnight as the increase in gastric and duodenal pH promotes healing overnight when the stomach and duodenum are empty.

Some rare adverse reactions to the drug that few patients may experience include, skin rashes, hair loss, vasculitis, thrombocytopenia, neutropenia, anemia, pneumonia, hepatitis, jaundice, eosinophilia, hepatotoxicity, high immunoglobulin E values, malaise, dizziness, somnolence, insomnia, and cancers.

# data[].attributes.body
Ciprofloxacin is an antibiotic, which inhibits gyrase in bacteria. Founded by Bayer Pharmaceuticals in the 1980s, it has become one of the world’s most prescribed antibiotics. Its original brand name was Cipro. Bayer, a German based company, discovered it in 1981. In 1987, the Food and Drug Administration approved its use in the United States until its patent expiration in 2004. Then its use was greatly expanded to generics and the market for this drug increased. Its indications are for gram-negative and positive bacteria and related infections, especially those in the urinary tract. Other diseases that ciprofloxacin treats include acute uncomplicated cystitis in women, chronic bacterial prostatitis, anthrax, and lower respiratory infections such as pneumonia. It is a member of the fluoroquinolone drug class, which were discovered in the 1960s as a derivative of chloroquine (an antimalarial drug). Ciprofloxacin targets topoisomerase II (DNA gyrase) and topoisomerase IV (both Type II topoisomerases) in bacteria, which are necessary for DNA replication, repair, and transcription. Topoisomerase prevents the supercoiling of DNA during replication, which is why ciprofloxacin’s mechanism of action is important to inhibit the bacteria from growing. Because of this mechanism of action, drug resistance can occur when bacteria develop gyrase mutations. Generally, ciprofloxacin is prescribed to be dosed twice a day at regular intervals. It has dosage forms that include tablets, extended-release tablets, and solutions. It is recommended to avoid calcium-rich products such as dairy when taking this medicine, as calcium tends to bind to it. Another point to consider is that ciprofloxacin can increase sunlight sensitivity and cause burning and skin damage. It is recommended to avoid direct sunlight and tanning begs while on this medication. Ciprofloxacin also experiences drug-drug interactions with the muscle relaxer tizanidine because ciprofloxacin increases plasma levels of tizanidine when taken together. This can cause over-dose symptoms such as drowsiness, dizziness, slurred speech, and confusion. When taken orally, ciprofloxacin can cause some side effects such as dizziness, nausea, trouble sleeping, and headaches. Its molecular weight is 331.346 grams/mol, which keeps it well under Lipinski’s Rule of Five molecular weight requirement. This helps justify that this drug has a high bioavailability of 70-80%. The structure of the molecule includes the piperazine and quinoline heterocycles and functional groups of carboxylic acid, ketone, alkene, amines, alkyl, benzene, and a fluorine halide. Overall, ciprofloxacin is a very important drug that has kept the world safe from numerous strains of bacteria for years.

# data[].attributes.body
Meloxicam is a nonsteroidal anti-inflammatory drug (NSAID).  Meloxicam is the generic form of Vivlodex and Mobic.   It is used to reduce hormones that cause inflammation and pain in the body. It is also used to help treat tenderness, swelling, and stiffness. Most adults use meloxicam to treat rheumatoid arthritis and osteoarthritis but can also be used in children who are at least 2 years old for juvenile rheumatoid arthritis. Meloxicam comes as a tablet and suspension. It is usually taken once a day with or without food. It is best to take the medicine at the same time each day. If the patient misses their dose for the day, take it as soon as possible unless it is just a few hours from next dose. This medicine should be kept at room temperature. The medicine comes in a 7.5mg and 15mg strength. Meloxicam is a benzothiazine that is piroxicam in which the pyridin-2-yl group is replaced by a 5-methyl-1,3-thiazol-2-yl group. Meloxicam’s mechanism of action is to inhibit prostaglandin synthetase (cyclooxygenase 1 and 2) enzymes, which leads to a decreased synthesis of prostaglandins. Prostaglandins sensitize neuronal pain receptors; inhibition of their synthesis will lead to analgesic and inflammatory effects.  Meloxicam preferentially inhibits COX-2, but also exerts some activity against COX-1, causing gastrointestinal irritation.

Meloxicam was developed and marketed by the German pharmaceutical company Boehringer-Ingelheim. Meloxicam was initially made in standard animal models of inflammation at a time when its improved pharmacologic profile in relation to other nonsteroidal anti-inflammatory drugs (NSAIDs) could not be explained. The subsequent discovery of COS-2 provided a reasonable hypothesis. Meloxicam was investigated in several in vitro test systems in which it consistently demonstrated preferential COX-2 inhibition. These observations suggested that meloxicam would have a COX-1-sparing effect in vivo.

Meloxicam was developed during the early 1970’s and was patented in 1977. Then it was approved for medical use in the United States in 2000.  Side effects may include the any skin rash, which should be consulted with a doctor no matter how mild the rash is; shortness of breath; swelling or rapid weight gain; signs of stomach bleeding, liver or kidney problems, upset stomach, nausea, vomiting, heartburn; diarrhea, constipation, dizziness; or cold symptoms, flu symptoms. The black box warning warns about Nonsteroidal anti-inflammatory drugs (NSAIDs) cause an increased risk of serious cardiovascular thrombotic events, including myocardial infarction and stroke, which can be fatal. Overdosing on meloxicam can cause organ failure or serious heart problems.

# data[].attributes.body
Metronidazole
Metronidazole is an antibiotic that belongs to the nitroimidazole antibiotic class. It is very common drug and is often seen in the generic version under the name Flagyl.  It can be used to treat a variety of different bacterial and parasitic infections. Examples of the type of infections Metronidazole can treat  are GI infections, trichomoniasis, giardiasis, and amebiasis. It also has some off-label uses including bite wound infections, Crohn disease, etc. The antibiotic consists of a heterocyclic Imidazole and the functional groups primary alcohol and tertiary amine.  The targets of this drug are believed to be protozoal DNA and anaerobic bacterial DNA.  The mechanism of action for this drug is not fully known for every type of host, but it is believed that metronidazole diffuses into an organism, stops protein synthesis by interacting with DNA, and then causes strand breakage in DNA resulting in the DNA losing its helical structure. The breakage of DNA causes cell death in organisms. The mechanism of action can be defined as a four step process. The Mechanism of action begins  with entry into the organism by diffusion across cell membranes of anaerobic/aerobic pathogens. Then, intracellular transport proteins participate in reductive oxidation by altering the chemical structure of pyruvate-ferredoxin oxidoreductase. The reduction of metronidazole will cause a concentration gradient to be formed. The concentration gradient will promote free radicals that are cytotoxic. Once the free radicals are formed, interactions with intracellular targets occur. These interactions happen when cytotoxic particles interact with a host cell DNA that results in DNA breakage. Then, the cytotoxic products are broken down. Metronidazole can be given in various forms including capsules, tablets, topical, and IV forms. It comes with a black box warning that indicates it may be carcinogenic. The risks for developing cancers while taking this drug though have been proved by studies to be low. Other adverse effects that can be seen while using this drug are headaches, nausea, and vaginitis. Patients taking metronidazole should not consume alcoholic beverages. Consuming alcoholic beverages with this medication can lead to toxicity and cause reactions such as flushing, tachycardia, palpitations, and nausea. Overall, Metronidazole is an effective medication against protozoal and bacterial infections in not only humans but dogs as well. Having a variety of uses, it is a very common drug. Because it is able to treat a variety of infections, Metronidazole is a very important drug.

# data[].attributes.body
Ibuprofen is in the nonsteroidal anti-inflammatory drug class (NSAID). Ibuprofen is a weaker anti-inflammatory than other NSAIDs. It is available OTC in low doses but over 800 mg requires a prescription.

Trade names include Advil, Motrin, and Nurofen and is available as a generic medication as well.

The IUPAC name of Ibuprofen is isobutylphenylpropionic acid. Ibuprofen chemical formula is C¹³H¹⁸O2 and has a molar mass of 206. 285 gmol⁻¹. The chirality of Ibuprofen is a racemic mixture. The S-enantiomer is the more pharmacologically active enantiomer. Ibuprofen is insoluble in water, but very soluble in organic solvents such as alcohol, methanol, acetone, and dichloromethane.
The discovery of Ibuprofen was in 1961 by Stewart Adams and John Nicholson in the UK. It was derived from propionic acid by a research team at Boots Group. It was discovered when research was taking place to find a safer alternative to aspirin.

It is used to treat pain, fever, and inflammation. Including painful menstrual periods, migraines, and rheumatoid arthritis. It can also be used after surgery to relieve pain, for post-vaccination fever, and pain from kidney stones.

It can also be used to close a patent ductus arteriosus in premature babies. It is even used to decrease the inflammation of acne. Routes of administration include by mouth, rectal, topical, and intravenous.

Ibuprofen begins to work within an hour of administration and within the second hour, 99% of the drug is bound to plasma proteins. Most of ibuprofen is metabolized and eliminated with 24 hours through urine and biliary excretion.

Common side effects are heartburn and a rash. Nausea, dyspepsia, diarrhea, constipation, headache, dizziness, salt and fluid retention, and high blood pressure are also common side effects.

Infrequent adverse effects include gastrointestinal bleeding is another side effect. Ibuprofen has an increase of risk of heart failure, kidney failure, and liver failure. Low doses do not appear to increase risk of heart attack, higher doses usually do. Ibuprofen can also have a side effect of worsening asthma. Ibuprofen should not be taken during pregnancy.

Contraindications of Ibuprofen are dietary supplements that help prevent platelet aggregation such as ginko, garlic, ginger, coumarin, and red clover.

Ibuprofen works in by inhibiting the production of prostaglandins by decreasing the activity of the enzyme cyclooxygenase (COX).

The metabolism of Ibuprofen takes place in the liver and targets the CYP2C9 gene.

The bioavailability of Ibuprofen by mouth is 80-100% and 87% when administered rectally.

# data[].attributes.body
The assigned drug that I had for this semester was Warfarin. Warfarin, also known as Coumadin, was named after the funding agency, Wisconsin Alumni Research Foundation (WARF.) Warfarin was discovered in Wisconsin when a cow died from a supposed hemorrhagic disease. Determined that moldy hay contained the compound coumarin that gets oxidized to dicoumarol. Now, Warfarin is the most commonly used oral anticoagulant. The scientific indication of Warfarin is the treatment for preventing thrombotic disorders. Warfarin’s mechanism of action is that it inhibits Vitamin K-dependency. Warfarin acts by inhibiting vitamin K epoxide reductase (VKOR) which limits the availability of reduced vitamin K and therefore prevents the formation of functionally mature vitamin K-dependent clotting factors. The antagonist inhibits the enzyme vitamin K epoxide reductase, which catalyzes the γ-carboxylation of the vitamin K- dependent coagulation clotting factors. This ultimately lessens the amount of active vitamin K available to act as a cofactor in the formation of glutamic acid residues within the clotting factors mentioned above. These actions make the clotting factors inactive and unable to act in clotting. Warfarin is often used empirically, which means, when an initial dose is prescribed, it is adjusted sometimes depending on the measurements over time. Some people who are prescribed Warfarin may respond differently to warfarin based on their heredity or genetic make-up. Warfarin is highly efficacious and is limited by a narrow therapeutic index and patient variability. What I learned about Warfarin is to figure out the correct therapy of Warfarin on each patient, doctors use the International Normalized Ratio (INR). The INR measurements measure the time it takes blood to clot. On a chart, patients on anticoagulants should have an INR between 2.0 - 3.0. If the patient’s number is lower than 2 then there is a clotting risk, thromboembolism. If the patient’s number is higher than 3 then the clots are too slow and increase the risk of uncontrolled bleeding. I also learned that for each different strength (dose) Warfarin has a specific color that correlates to the strength. For example, Warfarin 2mg is a lavender color tablet and Warfarin 4 mg is a blue tablet. Side effects of Warfarin are pain, swelling, bleeding from a cut that does not stop in the usual amount of time, nosebleeds or bleeding from your gums, coughing up or vomiting blood or material that looks like coffee grounds, unusual bleeding or bruising, pink, red, or dark brown urine, red or tarry black bowel movements, headache, dizziness, or weakness.

# data[].attributes.body
Venlafaxine has a molecular formula of C17H27NO2 and has an average mass of 277. 402 g/mol. The structure of venlafaxine consists of an ether, tertiary amine, and a tertiary alcohol. When venlafaxine is combined with hydrochloride, it becomes a beneficial medication. Its new molecular weight is 313.87 g/mol. Venlafaxine hydrochloride, also known as Effexor, is a novel antidepressant drug that was first developed in the early 1980s by researchers at Wyeth Pharmaceuticals. During the research, it was found that venlafaxine hydrochloride is a white to off-white crystalline solid with a solubility of 572 mg/ml in water so they are made into tablet form. The oral medicine was initially introduced as an immediate release formulation and was approved by the FDA in 1993 but it later evolved into extended-release which was approved by the FDA in 1997. By 2007, the generic formulation of venlafaxine immediate-release entered the market. The approved indications by FDA include major depressive disorder, generalized anxiety disorder, social anxiety disorder, and panic disorder. Venlafaxine is a bicyclic phenyetilamine derivative and is considered a serotonin-norepinephrine reuptake inhibitor (SNRI). This drug was synthesized to address the problem that experts believe have stemmed from imbalance among neurotransmitters. This drug acts by blocking the reuptake of mainly serotonin and noradrenaline, the two chemicals in the brain that transmit nerve signals, at the presynaptic terminal by inhibiting the uptake pumps 5-HT and NE2. In addition to that, it also does affect the reuptake of dopamine to a lesser extent. By doing so, that results in more transmitters at the synapse and ultimately increases the stimulation of postsynaptic receptors. Having that said, venlafaxine is a potent serotonin antagonist. The drug essentially works by regulating the levels of serotonin and norepinephrine. However, like all drugs, there are side effects that may occur while taking this medication. In fact, there is a block box warning for suicidal thoughts and behaviors in patients under the age of 25. Therefore, it is necessary to be mindful of the dosage regimen. The common side effects may include nausea, headaches, anxiety, insomnia, drowsiness, loss of appetite, dizziness, sweating, dry mouth, and weight loss. There also has been indications of increased blood pressure therefore blood pressure should be monitored. Also, it is essential to note that it could be detrimental when Effexor is taken with MAOIs therefore the concomitant use of Effexor with MAOIs is contraindicated.

# data[].attributes.body
Enalapril Maleate

The generic drug Enalapril, also sold under the brand name of Vasotec, Renitec, Enacard, Kadril and others. They are the ACE inhibitor medications that treat patients with conditions of high blood pressure, diabetic kidney disease and heart failure. It has been proven to protect the function of the kidneys in hypertension, heart failure, and diabetes, and may be used in the absence of hypertension for its kidney protective effects.

Tracing back to the discovery of enalapril, Squibb first developed the first lead compound, captopril, but it had some adverse effects related to it. Later on, Merck & Co. modified the captopril and developed enalapril as a competing prodrug. It was patented in 1978 and came into medical use in1984. And it is also one of the top 200 drugs.

Enalapril has a molecular weight of 376.4 g/mol. Within the structure, the only heterocycle it contains is pyrrolidine. There are several functional groups such as ester, carboxylic acid, and amide. The mechanism of action is that the active metabolite of enalapril competitively inhibits the ACE (Angiotensin-converting enzyme) to hinder the production of angiotensin II, a key component of the renin-angiotensin-aldosterone system that promotes vasoconstriction and renal reabsorption of sodium ions in the kidneys. Enalapril has an L-proline moiety as a part of the molecule which is responsible for the oral bioavailability of the drug. It is also a prodrug, which means it has to be metabolized to be active. The ether part of the molecule will split during the metabolism and the carbon will become a carboxylate, which will interact with the Zn+2 site of the ACE Enzyme.

Enalapril is normally taken on an oral route. It comes as an oral tablet and an oral solution. Usually, patients take enalapril once or twice a day. Sometimes doctors might suggest you to take the enalapril before bedtime because it could cause dizziness in the patients. Other common side effects such as dry, tickly cough, lightheaded, headache, diarrhoea, mild skin rash and blurred vision might occur. For pregnant patients, some evidence suggests it will cause injury and death to a developing fetus. Patients are advised not to become pregnant while taking enalapril and to notify their doctors immediately if they become pregnant. In pregnancy, enalapril may result in damage to the fetus's kidneys and resulting oligohydramnios (not enough amniotic fluid). Enalapril is secreted in breast milk and is not recommended for use while breastfeeding.

# data[].attributes.body
Hydroxychloroquine

Hydroxychloroquine has been heard of a lot lately by many people because of the COVID pandemic. In the beginning it was thought that this drug could potentially be used to treat COVID-19. The FDA even authorized emergency use of it for a little while. It was used so much that there became a shortage of this drug. However, after investigating the effects it had on COVID, it was concluded that it does not help treat the coronavirus. Even though it does not help with our current pandemic, it is used to treat malaria, lupus, rheumatoid arthritis, and some other autoimmune disorders. The way that it works to treat malaria is that it kills the organism causing malaria. In lupus and rheumatoid arthritis, it suppresses the activity of a person’s immune system to treat these disorders. Hydroxychloroquine targets Toll-like receptor 7 and Toll-like receptor 9 by acting as an antagonist. It depresses the activity of these receptors. It also targets a human’s DNA and Angiotensin-converting enzyme 2. The mechanism of this drug is still unknown. It is known that it can come together in lysosomes and other human organelles to raise the pH, but the exact way that it works is still not known. Hydroxychloroquine has many drug-to-drug interactions, so if a person experiences any side effects, they should consult their doctor immediately. Some of Hydroxychloroquine’s side effects include headache, dizziness, loss of appetite, nausea, diarrhea, stomach pain, vomiting, rash, yellowing of the eyes, unusual mood changes, and many others. Some of these are mild, but there are also more serious side effects. These include blurred vision, muscle weakness, seeing light flashes, etc. If these side effects continue, they can lead to something as serious as death. Hydroxychloroquine goes by the brand name Plaquenil, and it has a molecular weight of 335.9g/mol. The history of Hydroxychloroquine dates back to World War II. Quinacrine was first being used as an antimalarial drug, but it had terrible side effects such as yellowing of the skin. After much research, chloroquine was developed. Chloroquine was derived from the original drug of Quinacrine, but it had less side effects. A few years later Hydroxychloroquine was introduced in 1955. It was originally supposed to be used only to treat malaria, but because so many people were using it, they discovered that it could help with lupus and rheumatoid arthritis. Overall, Hydroxychloroquine was a major breakthrough and has been very helpful over the years.

# data[].attributes.body
Celecoxib is used to treat pain or swelling, specifically for patients with arthritis, and it is considered an analgesic or nonsteroidal anti-inflammatory drug (NSAID). Celecoxib is the generic name, while CeleBREX and Elyxyb are the brand names for this medication. Celecoxib works by binding to cyclooxygenase-2 (COX-2) enzyme which is responsible for synthesizing prostaglandin. Because there is a decrease in prostaglandin synthesis, a decrease in inflammation occurs and this is why Celecoxib is considered an anti-inflammatory medication. Celecoxib is able to bind to the COX-2 enzyme at a distinct hydrophilic side pocket. Because this pocket is different than the active binding site, Celecoxib is considered a selective noncompetitive inhibitor. Another important characteristic of Celecoxib is its ability to bind to COX-2 without inhibiting the COX-1 enzyme. Because Celecoxib selectively binds to COX-2, it does not interfere with platelet formation, as seen in many other NSAIDs that also bind to the COX-1 enzyme. Celecoxib has 2 boxed warnings, one for serious cardiovascular risk, and the other for serious gastrointestinal risk. Celecoxib, and NSAIDs in general can increase the risk of gastrointestinal adverse effects like inflammation, GI bleeding, ulceration, and GI perforation. Celecoxib also increases the risk for serious cardiovascular events including myocardial infarction and stroke. A patient should report the following symptoms to their doctor: coughing up blood, unable to pass urine or experiencing kidney problems, increased heartbeat or high blood pressure, shortness of breath, chest pain, or weakness that occurs on one side of the body. While the following symptoms are not serious, some patients do experience constipation, diarrhea, heartburn, dizziness, or throat irritation. Celebrex was approved in 1998 to treat symptoms of osteoarthritis and adult rheumatoid arthritis. It gained this approval after clinical trials were performed by G.D. Searle & Co. and Pfizer Inc. which demonstrated it as an effective nonsteroidal anti-inflammatory drug. Celecoxib was able to be developed after the COX-2 isoform was discovered in 1991. This discover lead to the potential to develop anti-inflammatory drugs, while also avoiding gastrointestinal complications that were due to inhibiting the COX-1 enzyme. In 1999, the FDA added a warning to Celecoxib that mentioned it’s interaction with warfarin which could cause severe bleeding. Additionally, in 1999, Celecoxib was approved by the FDA to treat familial adenomatous polyposis. In 2005, Celecoxib was approved for ankylosing spondylosis treatment and in 2006, it was approved for treatment of juvenile rheumatoid arthritis.

# data[].attributes.body
Naproxen is an non-steroidal anti-inflammatory drug (NSAID). It is used as an over the counter and a prescription strength pain reliever. It helps with pains such as headache, muscle aches, swelling, stiffness, and tenderness, menstrual pain, toothaches, and common colds. Naproxen can also help with conditions such as gout, rheumatoid arthritis, osteoarthritis, tendonitis and much more. Naproxen comes in a variety of dosage forms. In higher forms, a prescription may be necessary and lower dosages may be purchased over-the-counter. In the over-the-counter form of Naproxen called Aleve, you can take this medication up to 3 times per day. The most common form of this medication is a tablet that is taken by mouth. Naproxen is available as tablets, liquid capsules, rectal suppository and also in a liquid form. The target interaction for naproxen is prostaglandins. Naproxen inhibits the enzyme that produces this and it stops the inflammation, and ultimately the pain, from happening. The mechanism of action for naproxen is that it reversibly inhibits COX-1 and COX-2 enzymes. They do this as a non-selective coxib. This is what inhibits the prostaglandins from causing pain throughout the body. Naproxen was formed when Syntex got together with Procter & Gamble. It was sold under the names Anaprox and Naprosyn. However, when the FDA approved the drug for over-the-counter purchases the name was changed to Aleve. It was patented in 1967 but was not approved for sale in the United States until 1976. While widely used, there are still a number of side effects that are caused by Naproxen. Naproxen can cause stomach bleeding with signs involving vomiting blood, having bloody or black stool, and severe stomach pain. Naproxen can also cause heart problems and stroke or make those with these problems worse. The signs of these happenings are pain in the chest, difficulty breathing, weakness on one side of the body, slurring of speech, and swelling of the legs. Liver problems also may occur with dark urine, feeling tired, and yellowing of the skin or eyes. Those who are pregnant should also be careful taking these in the last few months of their pregnancy due to the fact that Naproxen is able to cross the placenta and increases the likelihood of miscarriage. It is also recommended to use with caution in those who have high blood pressure as it may increase the likelihood of heart attack and stroke. Naproxen can also cause sodium and fluid retention in patients who suffer from edema.

# data[].attributes.headline
Connor Pennington: Lisdexamfetamine Dimesylate (Vyvanse) 

# data[].attributes.subject
Connor Pennington: Lisdexamfetamine Dimesylate (Vyvanse) 

# data[].attributes.body
Lisdexamfetamine Dimesylate, or more commonly known as vyvanse, is a pro-drug of dextroamphetamine. The mode of therapeutic action in Attention-Deficit/Hyperactivity Disorder (ADHD) is not known. Amphetamines are thought to block the reuptake of norepinephrine and dopamine into the presynaptic neuron and increase the release of these monoamines into the extraneuronal space. The parent drug, lisdexamfetamine, does not bind to the sites responsible for the reuptake of norepinephrine and dopamine in vitro. I have learned a great deal about the drug Lisdexamfetamine Dimesylate throughout my time studying it, and have actually had interest in the drug before learning about it since many of my ADHD friends are on this drug.

Indication:
The indication for Lisdexamfetamine Dimesylate as stated is a treatment for Attention-Deficit/Hyperactivity Disorder in adults and in children aged 8 years old and older. It is a type of adderall that stimulates people with ADHD.

Mechanism of Action:
“The therapeutically active metabolite of LDX is d-amphetamine. Although the precise therapeutic mechanism by which d-amphetamine relieves the symptoms of ADHD is not known, inhibition of dopamine and norepinephrine reuptake and release of these monoamines into extraneuronal space are thought to be involved.”

Side effects:
Common side effects to Lisdexamfetamine Dimesylate are anorexia, vomiting, anxiety, weight loss, headaches, nervousness, and dry mouth. It shares many side effects with adderall, and should only be used in patients that have ADHD.

Target Interaction:
Amphetamines are thought to block the reuptake of norepinephrine and dopamine into the presynaptic neuron and increase the release of these monoamines into the extraneuronal space. The parent drug, lisdexamfetamine, does not bind to the sites responsible for the reuptake of norepinephrine and dopamine in vitro.

History and discovery of drug:
“Stimulants have been used to treat symptoms of ADHD for more than 50 years, and in 2006, a treatment algorithm developed by the Texas Consensus Conference Panel on Pharmacotherapy of Childhood ADHD confirmed the use of these agents as a first-line treatment.”

“Lisdexamfetamine was developed by New River Pharmaceuticals, who were bought by Takeda Pharmaceuticals through its acquisition of Shire Pharmaceuticals, shortly before it began being marketed. It was developed with the intention of creating a longer-lasting and less-easily abused version of dextroamphetamine, as the requirement of conversion into dextroamphetamine via enzymes in the red blood cells delays its onset of action, regardless of the route of administration.

On 23 April 2008, the FDA approved lisdexamfetamine for treatment of ADHD in adults. On 4 August 2009, Health Canada approved the marketing of 30 mg and 50 mg capsules of lisdexamfetamine for prescription use.”

Citations:

Goodman, David W. “Lisdexamfetamine Dimesylate (Vyvanse), a Prodrug Stimulant for Attention-Deficit/Hyperactivity Disorder.” P & T : a Peer-Reviewed Journal for Formulary Management, MediMedia USA, Inc., May 2010, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2873712/.

“Lisdexamfetamine.” Wikipedia, Wikimedia Foundation, 20 Nov. 2021, https://en.wikipedia.org/wiki/Lisdexamfetamine.

“Side Effects of Vyvanse (Lisdexamfetamine Dimesylate), Warnings, Uses.” RxList, RxList, 2 Nov. 2021, https://www.rxlist.com/vyvanse-side-effects-drug-center.htm.

# data[].attributes.body
Hydroxyzine, also known in the US as the brand name drug Vistaril, is a small molecule drug that is primarily used as an antihistamine in order to treat allergies and the associated symptoms of those allergies such as itching and the formation of itchy welts. It can also be used in order to treat anxiety, and it has some sedative effects. It is available to be taken orally as capsules, tablets, or syrups, and it may also be administered intramuscularly. It primarily acts as a potent and selective inverse agonist of the H1 or histamine receptor, deriving its antihistamine and sedative effects. A factor which likely contributes to its anxiolytic effects is its weak antagonistic activity toward serotonin receptors as other antihistamines lacking such have not been found to be effective in the treatment of anxiety. Similarly, another factor likely tied to its anxiolytic effects is that hydroxyzine is capable of crossing the blood brain barrier. Considering the effect of hydroxyzine, individuals taking it will generally begin experiencing effects within half an hour, and the peak plasma concentration is generally reached within 2 hours. Maximal plasma concentrations are based on dosage initially administered with doses of 25 milligrams having a maximum plasma concentration of approximately 30 nanograms per milliliter; compared to intramuscular injections, oral bioavailability is approximately 80%. It’s oral bioavailability mirrors its relatively small molecular size, low number of hydrogen bond acceptors and donors, and its logP of less than 5. It is extensively metabolized to cetirizine, a fairly active metabolite, by alcohol dehydrogenase, and it is also metabolized to various dealkylated metabolites by several CYP enzymes. Following this, the usual half life of hydroxyzine in the human body is approximately 12 hours, though it may range by up- or downwards by 5 hours. Very little of the original hydroxyzine is excreted unchanged in the urine though a majority of the cetirizine metabolite is excreted unchanged. Though it has useful effects, there are situations where it should not be used. It should generally be avoided in those with Q-T prolongation as it may exacerbate any cardiovascular events that occur as well as the elderly because it may result in over-sedation. Similarly, it should be avoided in those with hepatic and renal impairment as that may result in the failure to metabolize and clear the drug, leading to possible over-exposure and further adverse effects. There are also a variety of drug interactions to consider, and it should be avoided with certain substances such as alcohol.

# data[].attributes.body
Oxycodone, also known as Oxycontin, is indicated for the management of pain, ranging from pain levels of acute to chronic,  when the use of an opioid analgesics is appropriate. The medication is available in immediate and extended release form, including capsules and tablets. This medication serves to provide relief from daily, around the clock, long term pain. Capsules are prescribed when alternative treatments are inadequate in adults. Tablets are prescribed when alternative treatment options are inadequate in adults and opioid-tolerant pediatric patients ≥11 years of age who are already receiving and tolerating a minimum daily opioid dose of at least 20 mg oxycodone orally or its equivalent. The target interaction for oxycodone is opioid receptors on the nerve cells. This drug interacts with the brain in order to change how the body feels by altering the response to pain. One of the main receptors for this medication is the mu receptor, which suppresses pain. The mechanism of action for the drug oxycodone includes binding to an opiate receptor in the central nervous system. Once binding to the opiate receptor,it then inhibits ascending pain pathways. This creates an alteration of the perception to the response to pain stimulated in certain areas of the body. As a result, it produces generalized central nervous system depression creating the illusion that the body is no longer experiencing pain in the current moment.Oxycodone was first developed and synthesized in the year of 1916 by Germans researchers, from opium derived thebaine. Its original intention was for the management of pain. From the start of things, the pharmacological class is opioid. In the year of 1995, the FDA approved the drug as Oxycontin. This drug was later patented in 1996 by Purdue Pharma L.P. The original drug was available in 10mg, 20mg, 40mg and 80mg tablets. It later developed capsules for various reasons. For usage in the United States, the drug became available and hit the markets in the year of 1996. There are a variety of side effects that are common when taking oxycodone. The most common side effects include weakness, nausea, vomiting, headache, trouble sleeping, itching, lack of appetite, diarrhea, and dry mouth. Even though this includes a small portion of side effects, there could be more severe side effects including severe dizziness that could lead to passing out, confusion, and much more. If experience, it is recommended that the primary healthcare physician be contacted immediately.

# data[].attributes.body
My assigned drug for the semester was Tramadol Hydrochloride, brand name Ultram. Tramadol hydrochloride was first discovered and synthesized in Germany in nineteen sixty two and then introduced as tramadol in nineteen seventy seven before being made available in the United States in nineteen ninety five. Upon approval in the United States, tramadol was not considered an opiate until cases of addiction and abuse arose leading to its reclassification in twenty fourteen. Tramadol is a centrally acting opioid agonist and SNRI that is indicated for the management of pain that is severe enough to require an opioid analgesic because other forms of treatment did not yield sufficient pain relief.  Tramadol is structurally similar to codeine and morphine but unlike morphine tramadol has not been shown to cause histamine release. Tramadol is known to have good tolerability and multimodal mechanism of action with roughly one tenth of the potency of morphine making it a lower risk opioid option. Tramadol acts differently from other opioids because it acts as a μ-opioid agonist as well as affecting serotonin and norepinephrine to activate descending pain inhibitory pathways which mimics the effects of other SNRIs such as duloxetine and venlafaxine. Tramadol is a racemic mixture of two active enantiomers, (+)-tramadol and its metabolite are agonists of the μ-opioid while (+)-tramadol also serves as a serotonin reuptake inhibitor and (-)-tramadol serves as a norepinephrine reuptake inhibitor. These separate pathways in which tramadol act are considered to be synergistic as well as complementary allowing tramadol to better modulate the perception of pain and improve the response to pain. Among these targets of action, tramadol has also been shown to affect several other pain modulators in the central nervous system, non-neuronal inflammatory markers, and immune mediators. Due to the wide umbrella of targets tramadol can act upon, tramadol has proven to be effective on pain types from neuropathic to pain associated with labor and because tramadol acts similar to an SNRI it has shown antidepressant, anxiolytic, and anti-shivering effects as well. As with many other opioids, tramadol carries a risk of tolerance, dependence, and abuse. When used in higher doses or when accompanied by other opioids there is an increased risk of dose related overdoses, respiratory depression, and death, but because of tramadol’s SNRI effects there is risk of seizures and serotonin syndrome when used with other serotonergic medications. Tramadol can also produce dizziness, somnolence, nausea, constipation, sweating, and pruritus just as seen with many other opioids.

# data[].attributes.body
Atorvastatin was originally synthesized in 1985. Statins are a class of prescription medicines that have been used for decades to lower low-density lipoprotein or bad cholesterol in the blood. Medicines in the statin class include Atorvastatin, fluvastatin, lovastatin, pitavastatin, pravastatin, rosuvastatin, and simvastatin. Atorvastatin became known as Lipitor in 1996. It was approved by the FDA based on four clinical trials. It was developed by the Parke-Davis Company, which was acquired by Warner-Lambert and then Pfizer. Atorvastatin is used to decrease the number of fatty substances such as low-density lipoprotein (LDL) cholesterol (bad cholesterol) in the blood and increase the number of high-density lipoproteins (HDL) cholesterol (good cholesterol) in the blood. Atorvastatin is in a class of medications called HMG-CoA reductase inhibitors. It works by inhibiting the HMG-CoA enzyme which is responsible for the synthesis of cholesterol. Accumulation of cholesterol and fats along the walls of your arteries decreased blood flow and oxygen supply to the heart and other major organs. Atorvastatin lowers your blood level of cholesterol and fats. which prevents heart disease, strokes, and heart attacks. The possible side effects may include diarrhea, heartburn, gas, joint pain, loss of appetite, and difficulty swallowing or breathing. Atorvastatin comes as a tablet to take by mouth. It is usually taken once a day with or without food. Serious drug interactions can occur when certain medicines are used together with atorvastatin. It is extremely important to let your doctor know all other medicines you use and any medicine you start or stop using. Avoid eating foods that are high in fat or cholesterol. Atorvastatin will not be as effective in lowering cholesterol if you do not follow a cholesterol-lowering diet plan. Atorvastatin may pass into breast milk and could harm a nursing baby. Females should not breastfeed while they are taking this medication. Atorvastatin can also cause a condition that results in the breakdown of muscle tissue leading to kidney failure. This condition is more common in older adults and in people who have kidney disease or poorly controlled hypothyroidism (underactive thyroid). Minimize drinking alcohol. It can raise triglyceride levels and may increase the risk of liver damage.
Grapefruit and grapefruit juice may interact with atorvastatin and lead to potentially dangerous effects. Avoid drinking more than 1 liter per day of grapefruit juice while taking this medication.

.

# data[].attributes.body
Paroxetine (brand name Paxil) is one of six FDA approved selective serotonin reuptake inhibitors (SSRI). It was first marketed in the US almost thirty years ago in 1992. It is used to treat anxiety, depression, obsessive compulsive disorder (OCD), panic disorder, posttraumatic stress disorder (PTSD), premenstrual dysphoric disorder, and vasomotor symptoms of menopause (hot flashes). Some of the potential significant adverse reactions include the activation of mania or hypomania, bleeding risks, serotonin syndrome, sexual dysfunction, and suicidal thinking or behavior. Paroxetine has a black boxed warning on the package insert for increased risk of suicidal thoughts and behaviors. This is a common warning among antidepressants. Serotonin is a neurotransmitter that stabilizes mood and feelings of well-being. The disorders paroxetine is indicated for are related to depleted serotonin levels. SSRIs like paroxetine target the sodium dependent serotonin transporter (SERT). Paroxetine inhibits the transporter and therefore inhibits the reuptake of serotonin molecules from the synaptic cleft back into the presynaptic vesicles. This causes increased levels of serotonin to produce the medication’s antidepressant effects. Paroxetine was also mentioned during the CNS unit of our pharmacogenomics course. Paroxetine is metabolized from an active drug to inactive metabolites through the CYP2D6 enzyme. The 2 family of CYP enzymes is highly polymorphic, therefore paroxetine is susceptible to pharmacogenomic issues with different patient phenotypes. For example, a poor metabolizer should consider a different antidepressant or a 50% dose reduction from what would be considered a normal dose for a normal metabolizer to prevent increased levels of active paroxetine in the patient. In terms of molecular composition, paroxetine has one heterocycle we covered in class (piperidine) and two other functional groups we covered (ether and benzene). Its molecular weight is 329.37g/mol. It has one hydrogen bond donor and four hydrogen bond acceptors. Based on those characteristics and Lipinski's rule of 5, we can conclude the drug is orally bioavailable. Lipinski’s rule of 5 is taken one step further with the following stricter guidelines for CNS penetration: molecular weight less than or equal to 400 g/mol, hydrogen bond donors less than or equal to 3, hydrogen bond acceptors less than or equal to 7, and the logP less than or equal to 5. Even without knowing the logP, we can assume paroxetine is able to cross the blood brain barrier because it meets at least three out of the four guidelines. This makes logical sense that the drug is able to enter the nervous system because paroxetine is an antidepressant that works in the CNS.

# data[].attributes.body
Finasteride

Finasteride is a steroid-like medication that only pertains to males because it is not approved for use among women and pediatric patients. The brand names of finasteride include Propecia and Proscar. Finasteride is a small molecule drug approved for benign prostatic hyperplasia (BPH) by the FDA in 1992. In 1998, the FDA approved finasteride for male pattern baldness (androgenic alopecia). It might be puzzling to some people how it is approved for two completely different conditions, but it becomes clear once we look at the mechanism of action. Finasteride inhibits the enzyme 5-alpha-reductase. This enzyme works to metabolize testosterone into dihydrotestosterone. This secondary hormone is in charge of prostate growth and hair loss in males. Once the patient takes finasteride, they block this enzyme which in turn increases testosterone production. An increase in testosterone production causes a decrease in prostate size and an increase in hair on the scalp. Finasteride is taken orally and undergoes extensive hepatic metabolism through the CYP3A4 enzyme. The volume distribution of finasteride was 76 liters. Portions of finasteride are excreted through both the urine and feces. It also has a half-life ranges from 3 to 16 hours. Finasteride may interact with other medications, so it is essential to gather a detailed medication history from the patient. Finasteride does contain a few contraindications, such as hypersensitivity and pregnancy. Pregnant women or those thinking about becoming pregnant should not handle finasteride in any way. If they do, it may cause problems for the male fetuses in the development of their external genitalia. Finasteride should be stored at room temperature and protected from any kind of moisture. This medicine can be taken with or without food. The tablet must be taken whole as the patient cannot crush or break the tablet. Serious side effects include breast changes such as breast lumps, breast pain and tenderness, and 🤬 discharge. The most common side effects of finasteride include impotence, loss of interest in sex, swelling in the hands or feet, dizziness, weakness, headache, runny nose, or skin rash. After the patient has stopped taking finasteride, the sexual side effects may continue. Luckily, only a few men have ever reported side effects, and most of the side effects stopped once the patient stopped taking the medication. However, if a patient does experience side effects, they should exercise regularly, eat vitamin and mineral-rich foods, decrease alcohol consumption, and decrease smoking to mitigate the side effects.

# data[].attributes.body
Lovastatin was discoverd in 1978 by Alfred Alberts along with his coworkeers at Merk Research Labatories. They discovered a potent inhibitor of HMG-CoA reductase or 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase from a fermentation broth of Aspergillus terreus. Lovastatin caused an increase in drug repurposing of naturally occuring statins to make them more effective. An example of this is shown through the Merck group. They decided to add a ester side-chain to Lovastatin, making it 2.5 times more effecicious resulting in the drug Simivastin. Lovastatin became the first approved statin in the United States in 1987 hitting a peak annual sale of more than $1 billion dollars.

Lovastatin is a fungla polketide employed as a cholesterol-lowering drug. This drug is used in patients who are experiencing high levels of LDL or low density lipoproteins. These high levels can cause occlusion in the blood vessels leading to stroke, myocardial infraction, and other devastating cardiovascular events. The mechanism of Lovastatin is binding to reductase in the liver, causing inhibition of the conversion of HMG-CoA to mevalonate. Melavlonate is  precursor of cholesterol, is the main target for all -statin drugs. This process of inhibition is due to the Lovastatin’s competive antagonist properties. When Lovastatin binds, it prevents the ability of the natural chemical to proceed. Overall, this will cause the patients low density lipoprotein level and triglyceride levels to decrease, while the high density lipoprotein or HDL levels to increase. The ability to increase those HDL levels allows for the absorption of other cholesterols, which can be carried to the liver and disposed of. While this drug is a great medicaiton to be prescribed to hyperlipidemic patients, it does have some pharmacogenetic issues. Since the drug is a CYP3A4 metabolized drug, inhibitor and inducers of this enzyme can cause further issues for the patient. An inhibitor of the CYP3A4 enzyme such as grape fruit juice can cause the failure to eliminate Lovastatin. This will lead to a buildup increasing the toxic effects of the drug. On the other hand, if you have CYP3A4 inducers, the drug is being eliminated to quickly, causing a decrease in efficacy. Lovastatin also has been shown to have side effects like abdominal pain, headache, diarrhea, and an increase in liver enyzmes. Major side effects that need to be known if shown are rhabdomyolysis and hepatotoxicity. These events have significant life-altering effects that could possibly lead to death if not treated in time.

# data[].attributes.body
Glipizide is an oral medication that is taken by patients to treat type two diabetes. This drug is a generic drug of the brand name, Glucotrol. It is a small molecule with an average atomic weight of 445.535.  The main focus of this drug is to sensitize pancreatic beta cells and stimulate insulin release. This is how it controls blood sugar levels in patients with type two diabetes. It is a second - generation sulfonylurea. The initial blood glucose lowering effect occurs about 30 minutes after administration of the medication. The duration of the effectiveness lasts for around 12 to 24 hours. The main actions occur at the pancreas. This is where insulin release is stimulated, therefore it is important for the medication to act there. In addition to the action at the pancreas, it also acts at some extrapancreatic locations. For example, it promotes insulin signaling effects on the liver, muscles, or fat cells. There are some side effects that may occur in some patients because of where in the body the drug is targeting, and these include weight gain and the rise in risk of developing hypoglycemia. The signs of hypoglycemia include a cold clammy feeling, hunger, fast heartbeat, blurred vision, slurred speech, and many others. There are also some effects with the chronic use of glipizide. This includes a possibility of down-regulation of the sulfonylurea receptors on pancreatic beta cells. This is because these are the target for the grug, glipizide. This could lead to a reduced effect on insulin secretion. There is no black box warning for this medication. The mechanism of action starts by taking the medication orally. When the medication reaches the cellular level, it binds to a sulfonylurea receptor, and this inhibits the adenosine triphosphate dependent potassium channel. This stabilizes the potassium efflux. This eventually causes the influx of calcium and this stimulates insulin secretion. The effect of the drug is similar to glucose, but the difference is glipizide only stimulates phase 1 release of insulin. Glipizide is a second generation drug. This class of drug, sulfonylureas, was first discovered in France. They were discovered by a researcher who was working on drugs for typhoid fever. When the drugs were being tested on animals, they discovered something very important. The animals were presenting with symptoms of hypoglycemia (low blood sugar). After this observation, it was decided that these drugs could be used for the treatment of diabetes.

# data[].attributes.body
The assigned drug that I had for this semester was amoxicillin. It has a molecular weight of 365.40 g/mol and belongs to the aminopenicillin antibiotic group. Amoxicillin is well known to be a penicillin-derived antibiotic and is used as an antibiotic to treat many different types of bacterial infections. These infections consist of tonsilitis, bronchitis, pneumonia, gonorrhea, ear, nose, throat skin, dental abscesses as well as chest infections. It was originally discovered in1958 and was made available for medical use in 1972 by a group of scientists at Beecham Research Laboratories. Through their discovery, we were able to learn the differences between ampicillin and amoxicillin. The mere difference between ampicillin and amoxicillin is in their structure. Amoxicillin has an additional hydroxyl group on the benzene ring in comparison to ampicillin’s structure. With that amoxicillin is more lipid-soluble as well as kills bacteria quicker than ampicillin.

Amoxicillin became well known as a beta-lactam antibiotic that targets both gram-positive/negative bacteria, cocci, aerobes, anaerobes, and listeria monocytogenes.  Some specific gram-negative bacteria that amoxicillin targets consist of salmonella, shigella, E-Coli, proteus, and H. influenza. Amoxicillin’s mechanism of action is that it"inhibits bacterial cell wall synthesis by binding to one or more of the penicillin-binding proteins, which in turn inhibits the final transpeptidation step of peptidoglycan synthesis in bacterial cell walls, thus inhibiting cell wall biosynthesis. Bacteria eventually lyse due to the ongoing activity of cell wall autolytic enzymes while cell wall assembly is arrested”.

Amoxicillin is a drug that is susceptible to degradation because some bacteria produce beta-lactamase, which makes them resistant to beta-lactam antibiotics, such as amoxicillin and penicillin. This is why on occasion amoxicillin is found to be combined with clavulanic acid. Clavulanic acid is a beta-lactamase inhibitor that helps in preventing amoxicillin from being susceptible to degradation.

Amoxicillin is a medicinal drug that is better absorbed when taken orally because it diffuses easily into tissues and body fluids. This drug is available for oral administration in the form of capsules, chewable, tablets, syrup, and pediatric suspension.  Amoxicillin is a drug that is not available over the counter and must be prescribed by the doctor to most adults/children. The common side effects associated with amoxicillin consist of headaches, abdominal pain, nausea, vomiting, diarrhea, and/or skin rashes. Amoxicillin also tends to have adverse interactions with certain medications such as warfarin, methotrexate, oral contraceptives as well as allopurinol.

# data[].attributes.body
Duloxetine was first patented in 1986 after being originally created by the pharmaceutical company Eli Lilly. It was first made as a racemic mixture, but the (+) enantiomer showed an increased ability to prevent serotonin reuptake in rat trials so production focused on it. The drug was initially denied approval for a New Drug Application due to concerns of hepatotoxicity, especially when combined with alcohol. However, in 2004 the drug was approved by the FDA for neuropathic pain and depression, and the drug was given the brand name of Cymbalta. In later years, the FDA approved duloxetine to treat generalized anxiety disorders as well as different forms of chronic pain such as fibromyalgia or pain caused by chemotherapy. In other countries, the drug is also approved to treat stress urinary incontinence. It is not approved to treat that in the USA, but it is often used as an off label treatment.

Duloxetine is a serotonin and norepinephrine reuptake inhibitor, and it does this by blocking the transporters which uptake those chemicals. By inhibiting the norepinephrine transporter, it also slightly blocks the reuptake of dopamine in the prefrontal cortex which lacks dopamine reuptake transporters.This leaves more serotonin, norepinephrine, and dopamine around to be picked up by their receptors which can alleviate chronic pain and symptoms of depression. Duloxetine is an active drug which is metabolized primarily by the CYP1A2 and CYP2D6 enzymes in the liver and is then excreted in urine. Duloxetine should be used with caution in anyone who is a poor metabolizer or an ultrarapid metabolizer of the drug due to the higher risks of toxicity or of lessened effect respectively. The drug is also contraindicated in people who take other MAOIs, especially any other antidepressant as it can lead to serotonin syndrome. Duloxetine also should not be taken by people with certain forms of glaucoma or anyone taking thioridazine as duloxetine can increase the concentration of thioridazine in plasma.

While Duloxetine is considered quite safe, it does have some negative side effects. Like all antidepressants, duloxetine has a black box warning for increased risk of suicidality. The drug can also trigger manic symptoms in people with bipolar disorder. Other serious side effects include hepatotoxicity and increased bleeding risk, and it also can cause some less severe side effects such as sexual dysfunction, insomnia, dry mouth, and general stomach issues.

# data[].attributes.body
Amitriptyline is a tricyclic antidepressant indicated for relief of symptoms of depression, specifically endogenous depression. It is also used off-label for treatment of neuropathic pain, prevention of migraine and tension headaches, and insomnia as well as irritable bowel syndrome, cyclic vomiting syndrome, bladder pain syndrome, etc. Some common side effects include: nausesa, change in appetite, mouth pain, itching, constipation or diarrhea, breast swelling, decreased urination, and decreased sex drive. The FDA issued a black box warning for increased suicidal idealation or behavior in adolescents. Due to risk of severe side effects such as seizures, changes in vision, hallucinations, etc, some brand name formulations of amitriptyline were taken off the market although the generic form is still available.

Amitriptyline was discovered in the late 1950s by scientists at Merck and was originally proposed during the clinical trials phase as a medication for schizophrenia. It is a tertiary amine and is derived from a hydride of dibenzo[a,d][7]annulene. However, one of the researchers proposed testing it as an antidepressant and it was found to have similar properties to the first tricyclic antidepressant, imipramine, after success with treating patients. It was eventually approved by the FDA in 1961 as an antidepressant. It soon became more popular than its precursor due to its stronger effect and more effective marketing campaigns by Merck to raise clinician’s awareness of depression as a clinical cause. In the early 1960s, Roche and Lundbeck were also able to independently develop and market amitriptyline due to the patent only applying to the chemical synthesis and not the drug itself.

Amitriptyline acts by increasing synaptic concentration of serotonin and norepinephrine from inhibiting reuptake of these neurotransmitters. It acts specifically upon the presynaptic neuronal membrane pump, blocking the norepinephrine transporter (NET) or serotonin transporter (SERT) at presynaptic terminals. In addition, due to constant stimulation of these receptors, it may downregulate the amount of these receptors. The prolonged activity of serotonergic and adrenergic neurons is thought to lead to its antidepressant activity. An increased concentration of norepinephrine in the posterior grey column of the spinal cord is thought to contribute to its analgesic effects for pain and headaches. Increased activity of alpha-2 adrenergic receptors due to the increased presence of norepinephrine can also increase GABA concentration in the spinal interneurons. Lastly, amitriptyline has a small blocking effect on sodium channels, which may also contribute to its analgesic effects.

# data[].attributes.body
My assigned drug for this semester was Topiramate. Topiramate is a drug that treats and prevents seizures and migraine headaches that was discovered in 1979 by Bruce Maryanoff and Joseph Gardocki, but it was not approved by the FDA until December 24, 1996. Some of the non-FDA uses of Topiramate include treatment for alcohol dependence, eating disorders, essential tremor, obesity, and type two diabetes in obese. The drug is a sulfamate-substituted monosaccharide and a derivative of D-fructose. Topiramate is one of the few drugs that does not have a clear mechanism of action, but potential properties are a blockage of voltage-dependent sodium channels, an augmentation of gamma-aminobutyrate acid activity at some subtypes of the GABA-A receptors, antagonism of AMPA/kainite subtype of the glutamate receptor, and inhibition of the carbonic anhydrase enzyme, particularly isozymes II and IV. The molecular weight of Topiramate is 339.36 g/mol and the functional groups that can be found in the drug include Sulfonamide and ether. Topiramate has orphan drug status for the treatment of Lennox-Gastaut syndrome, which is a type of epilepsy caused by the abnormal development of the cerebral cortex. The drug was found to be most soluble in alkaline solutions containing sodium hydroxide or sodium phosphate, where the pH is 9 to 10. Prior to initial therapy, a baseline serum bicarbonate level in all patients. Some of the serious side effects of topiramate usage is Erythema multiforme, Steven-Johnson syndrome, hyperammonemia, metabolic acidosis, liver failure, Glaucoma, myopia, Nephrolithiasis, and suicidal thoughts. The contraindications of topiramate use include metabolic acidosis with concomitant metformin use and recent alcohol use within six hours prior or six hours after topiramate use. Topiramate tablets are available in 25, 50, 100, and 200 mg tablets, each color coated to represent their strengths. Like all drugs, overdosage is possible with topiramate. A few of the signs and symptoms of topiramate overdosage include convulsions, drowsiness, and abdominal pain. Hemodialysis is one effective mean to remove the topiramate from the body. It is recommended that patients that experience blurred vision, visual disturbances, or periorbital pain seek immediate medical attention. It is also advised that healthcare professionals closely monitor patients taking topiramate, especially pediatric patients, because of decreased sweating and increased body temperature. When ending treatment, it is recommended to do so gradually to minimize seizures. Topiramate can be found in the United States under the names Qudexy XR, Topamax, Topiragenm, Trokendi XR, and Eprontia.

# data[].attributes.body
My assigned drug this semester was Atenolol, also known by its brand name Tenormin and Tenoretic. It is a synthetic beta-1 selective blocker that is used to treat high blood pressure and irregular heart beats, called arrhythmias. It can also be used to treat severe chest pain that is caused by angina. Atenolol can be used as a preventative for future heart disease, strokes, and heart attacks. This drug works by blocking epinephrine, which leads to the heart pumping slower and less forcefully. Some of the common side effects of taking atenolol include difficulty breathing, cold hands/feet, blurred vision, dizziness, faintness, lightheadedness, shortness of breath, wheezing, and tightening in the chest. This drug is orally available in 25, 50, and 100 mg tablets. It is also available as an intravenous infusion. About half of the oral dose is absorbed by the gastrointestinal tract, and the unabsorbed amount is excreted in feces. It undergoes little metabolism by the liver. The amount of atenolol that is absorbed is excreted renally. This indicates that patients with impaired renal function must be monitored closely while taking atenolol. The peak concentration in the blood occurs around 2 to 4 hours after oral ingestion. However, with an IV infusion the peak concentration is reached in about 5 minutes. Atenolol can also cross the placental barrier, and therefore could cause harm during pregnancy. There is also caution around nursing mothers that are taking atenolol, because it can cause the baby to have bradycardia. Atenolol should also be used with caution in patients that are diabetic or have thyroid disease, because it can mask the symptoms of hypoglycemia and hyperthyroidism. The inactive ingredients included in atenolol are magnesium stearate, microcrystalline cellulose, povidone, and sodium starch glycolate. It can be taken with or without food. Atenolol is a small molecule drug with a molecular weight of 266.3361. The chemical formula is C₁₄H₂₂N₂O₃. Atenolol should be stored at room temperature and in a light resistant, tightly sealed container. This drug should not be taken with reserpine and monoamine oxidase inhibitors (MAOIs), because it can cause an increased effect. This could lead to an increase in lightheadedness or slow the heart rate more than it should. Suddenly stopping atenolol could cause heart attack and irregular heart rhythms. Atenolol is not an over the counter medication, which means it is only available by prescription from a physician. Back in 2017, there was a shortage of atenolol, because there was such a low supply of the active ingredient!

# data[].attributes.body
My drug for the semester is Azithromycin, which is commonly known as Zithromax or Z-Pak. Azithromycin is antibiotic used to treat many bacterial infections, such as respiratory, skin, ear, eye, and sexually transmitted infections. Namely, it is used to combat bacterial conjunctivitis, or “pink eye”, and streptococcal pharyngitis or “strep throat”. Azithromycin’s off-label uses include acne vulgaris in adults with moderate to severe acne, Babesiosis, Bronchiectasis (noncystic fibrosis), Bronchiolitis obliterans syndrome, Campylobacter gastroenteritis, cat scratch disease, cesarean delivery preoperative prophylaxis, chlamydia trachomatis infection, Cholera, chronic obstructive pulmonary disease, gonococcal infection, Lyme disease, syphilis, and many more. It can be prepared for several avenues of administration: oral tablet, oral tablet extended release, oral suspension, and intravenous infusion.

Significant adverse reactions for azithromycin include QT prolongation, polymorphic ventricular tachycardia, Clostridioides difficile infection, cholestatic hepatitis, hepatocellular hepatitis, mixed cholestatic/hepatocellular hepatitis, angioedema, urticaria, anaphylaxis, and delayed hypersensitivity reactions. Other common side effects are diarrhea, nausea, chest pain, palpitations, headache, vaginitis, fatigue, and dizziness. A major contraindication to azithromycin is hypersensitivity to macrolide antibiotics, and prolonged use of this drug may cause fungal infection or mask pre-existing infection symptoms. Notable drug interactions include digoxin, clarithromycin, warfarin, coumadin, jantoven, amiodarone, amisulpride, bedaquiline, BCG, pimozide, bilastine, cholera vaccine, and mizolastine.

Azithromycin has a molecular weight of 749.0 g/mol. This drug involves various functional groups, such as alcohol, ether, ester, emine, and acetal groups. Additionally, it includes a complex heterocycle called tetrahydropyran.

Azithromycin’s primary function is as an inhibitor of bacterial protein synthesis. Its primary targets are 23S ribosomal RNA of enteric bacteria and protein-arginine deiminase type 4. Azithromycin reversibly binds to the 23S rRNA of the bacterial 50S ribosomal subunit. This binding greatly interferes with the movement and transpeptidation of protein creation in harmful bacteria throughout the body. Additionally, it prevents the complete formation of the 50S ribosomal subunit. A significant advantage of macrolide antibiotics, such as azithromycin, is their extremely high affinity for binding bacterial ribosomes. This key characteristic is why azithromycin can be used on such a large range of infections and diseases. Azithromycin is also highly stable at a low pH, allowing for a longer half-life and activity within the body.

Azithromycin was discovered by a pharmaceutical company based in Croatia called Pilva in 1980. This team of researchers utilized rational drug design by manipulating structural-activity relationships to develop azithromycin from erythromycin. Azithromycin’s advantage over its counterpart is a basic nitrogen on the macrocyclic ring. Pilva patented it in 1981. In 1986, Pilva signed an agreement with Pfizer, which granted them exclusive rights to sell azithromycin in the United States and Western Europe. Pilva still claimed sales in Central and Eastern Europe by marketing it as Sumamed in 1988. In 1991, Pfizer coined the brand name Zithromax. The patent protection of the drug ended in 2005.

# data[].attributes.body
Cephalexin is an antibiotic that is used to treat bacterial infections. Most commonly cephalexin can be used to treat infections caused by susceptible bacteria such as pneumonia, strep throat and, like other antibiotics, cannot be used to treat any viral infections. It has a molecular weight of 347.39 g/mol. It also contains no heterocycles and five functional groups consisting of a ketone, sulfide, carboxylic acid, alkene and arene. It was developed in 1967, originally marketed as Keflex and Ceporex, and marketed in 1969. It is also listed by the WHO on its list of essential medications. Cephalexin works to kill gram negative and gram positive bacteria by preventing synthesis of the cell wall by bacteria which prevents them from surviving. Specifically, it inhibits the cross linking reaction between N-acetyle muramicacid and N-acetylglucosamine in the cell wall which ultimately leads to cell lysis and elimination of the bacteria. Cephalexin is an antibiotic that belongs to a class called cephalosporins. These Cephalosporins are a class of beta-lactam antibiotics. It was among the first cephalosporins to be discovered and marketed. The first compounds of the cephalosporin group were isolated from cephalosporin-producing fungus that were first discovered by Giuseppe Brotzu in 1948. He discovered this fungus from a sewage outfall off of the Sardinian coast in Italy. Further investigation was done to create the natural compounds that, while not potent enough on their own, would create the basis for future discoveries of cephalosporin derivatives by Sir Edward Abraham and Guy Newton in England around 1958. Sir Edward abraham actually conceived the idea of what the structure would be for one of the initial compounds while on a skiing trip and developed the compound (ultimately becoming cephalosporin C which was much more potent against Staphylococcus aureus strains) with the help of Guy Newton. It is one of the most widely prescribed and commonly used antibiotics and is used for the treatment of superficial infections resulting from minor wounds. Common side effects from cephalexin include nausea, diarrhea, vomiting, heartburn, stomach pain, rectal or genital itching, dizziness, extreme tiredness, agitation, confusion, headache, and joint pain. Serious side effects include watery or bloody stools, rash, itching, hives, swelling of the throat, difficulty breathing or swallowing, wheezing, returning fever, and hallucinations. There are also several major drug interactions with cephalexin which are the tuberculosis vaccine, cholera vaccine, and typhoid vaccine.

# data[].attributes.body
Cyclobenzaprine is generic for brand name Flexeril that is a skeletal muscle relaxer used for muscle spasms. This is an orally bioavailable drug that helps relieve muscle pain in patients. It's molecular weight is 275.4 g/mol and has an amine functional group. It is a 5-HT2 receptor antagonist that relieves muscles spasms through the central nervous system. This is thought to happen through the brain stem, but it does not perform any direct action on the neuromuscular junction or muscle at all. Because it's structure is similar to tricyclic antidepressants, cyclobenzaprine has been known to cause serotonin syndrome when taken with other drugs that interact with serotonin. This is a serious level of toxicity that can occur from the build up of too much serotonin in the body and can lead to death. From the pharmacokinetics stand point, cyclobenzaprine is proven to be linear at the standard doses with a steady state of three to four days. The immediate action of cyclobenzaprine taking affect is one hour and has a lasting duration in the body from 12 to 24 hours depending on the patient's metabolism. This drug is metabolized by the cytochrome P450 isoenzymes CYP3A4, CYP1A2 and CYP2D6 in the liver. The side effects include nausea, dry mouth, dizziness, constipation, heartburn and extreme tiredness. It is best not to take this drug while driving until you know how it effects your body since it can make you drowsy. Avoid taking opioids with cyclobenzaprine due to the high potential to cause heavy sedation that can lead to severe health problems. If you notice your stomach hurting after taking cyclobenzaprine, it is best to take it with food on your stomach to help absorb the drug and lessen the gastrointestinal pain. The maximum dose in patients 15 years and older is 30 mg per day. Any patients younger than 15 years are not recommended to take cyclobenzaprine due to lack of efficacy and safety in that age group. Even though it is not FDA approved due to not having the safety or efficacy proved yet, cyclobenzaprine can be used for patients with fibromyalgia as an off label use. There are no known adverse effects to taking this drug while pregnant or breastfeeding. Cyclobenzaprine was first used in humans in 1973, but first discovered in 1961 and initially studied to be used as an antidepressent due to its similar structure to tricyclic antidepressants. The difference between cyclobenzaprine and the tricyclic antidepressant amitriptyline is one double bond.

# data[].attributes.body
Benazepril Hydrochloride or better known as just Benazepril is a medication used to treat hypertension or high blood pressure, heart failure, and diabetic kidney disease. It is also used for calcium-channel blockers and thiazide diuretics. This is why the drug is also available as the combinations Benazepril/hydrochlorothiazide and Benazepril/amlodipine. It is sold under the brand name Lotensin and is mostly used to treat high blood pressure. Benazepril HCl is also available as a generic version. It is taken orally and it comes in multiple dosage strengths. It is an ACE inhibitor and works by targeting angiotensin II receptors and decreasing renin-angiotensin-aldosterone system activity. This is relaxing the blood vessels so that blood can flow more easily. Some common side effects include feeling tired, dizziness, cough, and light-headedness with standing. Serious side effects may include kidney problems, hypotension, or low blood pressure, high blood potassium, and angioedema, or swelling of the lower layer of skin and tissue just under the skin or mucous membranes. Use while pregnant or thinking of becoming pregnant could harm the baby so it is not recommended but using it while breastfeeding is safe. Benazepril was patented in 1981 by chemist Mahesh Dasai and came into medical use in 1990. It was the 130th most commonly prescribed medication in the United States, with more than 5 million prescriptions. Benazepril HCl is a prodrug and must be metabolized to form the active drug Benazeprilat. Its OCH₂CH₃ group must be metabolized in order to inhibit the ACE enzyme to form Benazeprilat. The bulky cyclic structures are resistant to hydrolysis. A special thing to note about this molecule is that the nitrogen within the ring makes the bulky cyclic structure especially harder to break down and can account for the drug pharmacokinetic profile, in which the duration of action is 24 hours. You can take this medication with or without food as directed by your doctor, usually once or twice daily. If you have the suspension version instead of the tablets it is prudent you shake the bottle well before each use and carefully measure out each dose. The dosage you receive is based on your medical condition and response to prior treatment. But for children is also based on weight. It is crucial to take this medication every day to get the most benefit from it. Most people with high blood pressure won’t feel sick.

# data[].attributes.body
Estradiol

Estradiol is a nuclear hormone, which acts on receptors present inside the cell, and works by binding to subtypes of the estrogen receptor: estrogen receptor alpha (ERα) and estrogen receptor beta (ERβ). It can activate or deactivate transcription in the nucleus. Once interacted with a target receptor, it can enter the nucleus of the cell and induce formation of messenger RNA. This mRNA interacts with ribosomes and produces specific proteins which exterts the effects of estradiol. It also exerts potent agonism of G Protein-coupled estrogen receptor (GPER), which is recognized an important regulator of this drug's rapid effects. In layman's terms, it acts on restogen receptors to relieve vasomotor systems and urogenital symptoms. It is an antagonist that weighs 272.4 g/mol and has no heterocycles. It's functional groups include a phenol and alcohol. It was discovered in the early 1920s by researchers Edgar Allen and Edward Doisy. They conducted an experiment demonstrating that ovarial follicles contain and produce what they called the primary ovarian hormone. This was later renamed estrogen. They extracted estrogen from the ovarian follicles of hogs and proved its isolation through a measurement renamed as the Allen-Doisy test. These research finding helped develop clinical application of estrogen. This led to the birth control pill, prevention and treatment of breast cancer, menopausal hormone therapy, prevention and treatment of osteoporosis, vaginal estrogen therapy, and others. Estradiol's main use is to treat menopause symptoms and can also treat low estrogen levels in women with ovarian failure. It has also been indicated for great cancer and prostate cancer. The main side effects of Estradiol has many side effects. These include, cramping, anxiety, bloating, bleeding, breast tenderness, nausea, and vomiting. Some of the more serious side effects with estradiol are heart attack symptoms such as chest pain or pressure and also signs of a stroke, such as sudden numbness and slurred speech. Side events of high estrogen in men are erectile dysfunction, enlargement of breast, fatigue, water retention, and insomnia. Estradiol is a mainly female hormone and is a synthetic form of estrogen. It is the strongly type. However, in men it is essential for modulation libido, erectile function, and spermatogenesis. The main function of estradiol is to mature and maintain the reproductive system. Increased levels cause the maturation and release of the egg and thickening the lining of the uterus to allow a fertilized egg to implant. Estrogens can also occur in skin, bone, liver, adrenal glands, and the brain.

# data[].attributes.body
Indication:

Spironolactone is a medication prescribed to patients for treatment of low potassium levels, high blood pressure, and heart failure. Spironolactone can be taken with other medications, or it can be taken by itself. The class of drugs spironolactone is classified in are called aldosterone antagonists. Spironolactone is indicated for the management in patients with congestive heart failure, cirrhosis of the liver, primary hyperaldosteronism, hypertension, severe heart failure, hypokalemia, and nephrotic syndrome. The drug is used to treat anyone with one or more of the conditions listed above. Spironolactone also has another name called Aldactone. Spironolactone is insoluble in water but soluble in alcohol. The drug is used for short-term and long-term treatment of primary hyperaldosteronism in patients. Aldactone comes in twenty-five, fifty, or one hundred milligrams tablets.¹

Target Interaction:

Aldactone competitively inhibits receptors located in the distal convoluted tubule. The specific receptors the drug inhibits are mineralocorticoid receptors. Inhibiting these receptors helps promote water and sodium excretion while keeping the same amount of potassium.²

Mechanism of Action:

Spironolactone is an aldosterone antagonist which acts mainly through binding competitively through receptors on the aldosterone-dependent sodium-potassium exchange site located in the distal convoluted renal tubule. Spironolactone causes more water and sodium to be removed but retains the same amount of potassium. During this mechanism, aldactone is an antihypertensive drug and a diuretic. Aldactone can be taken with other diuretic drugs or by itself. The other diuretic agents it can be taken with act in a closer manner with the renal tubule.¹

History of Discovery and Development:

Spironolactone was initially created for the retention of potassium and excretion of water and sodium. Other pharmacodynamic properties of the drug were discovered later, which broadened its use, such as treatment for heart failure and hypertension. Aldactone was created in 1957, but it was not placed on the market until 1959. The drug was approved by the FDA in 1960.²

Side Effects:

Spironolactone has multiple side effects. Some of the side effects are more serious compared to others. A few side effects are slow heart rate, slurred speech, vomiting, discomfort in lower limbs, headache, increased urination, confusion, and slurred speech. If you experience any of the symptoms listed above, the best course of action is to receive medical help immediately. A few of the most common side effects are nausea, dizziness, breast tenderness, vomiting, breast swelling, headache, and diarrhea. Anyone that is taking aldactone needs to inform their doctor if they experience any side effects that do not go away or are bothersome.¹

Citations:

1. Aldactone (spironolactone): Uses, dosage, side effects, interactions, warning. RxList. https://www.rxlist.com/aldactone-drug.htm#description. Published July 30, 2020. Accessed November 28, 2021.

2. Spironolactone. Uses, Interactions, Mechanism of Action | DrugBank Online. https://go.drugbank.com/drugs/DB00421. Published June 13, 2005. Accessed November 28, 2021.

# data[].attributes.body
Lorazepam, or Ativan as its known by its brand name,  is a benzodiazepine that is taken orally and used for indications such as insomnia, epilepsy, and anxiety. This drug was developed by D. J. Richards in 1977 with Wyeth Pharmaceuticals with the brand names Ativan and Temesta.  The advantage to using Lorazepam over other benzodiazepines is that it is fast acting and it more rapidly metabolized.  Since it leaves a persons system more quickly, it reduces the risk of toxicity and side effects.  Lorazepam contains the functional groups chloro, hydroxyl, amide, and imide. Lorazepam is metabolized by the CYP450 enzymes in the liver.

Lorazepam is also considered a schedule IV drug.  It is monitored to decrease the risk for addiction, but the likely hood of dependence is low.  Lorazepam can have negative interactions in people with diseases such as liver and renal disease, drug dependance, and alcohol intoxication.  Some adverse effects of lorazepam include CNS depression, anterograde depression, and withdrawal syndrome.  The most common side effect is drowsiness and being in a sedated state.  Alcohol is the main negative interaction associated with lorazepam, because lorazepam enhances the CNS depressing effect of alcohol.  I would advise against drinking any alcohol while taking lorazepam.  Lorazepam should also not be taken with other opioids, oxycodone, or zolpidem.  The US boxed warning alerts the following, “ risks from concomitant use with opioids; abuse, misses, and addiction; dependence, withdrawal reactions.” Like other benzodiazepines, the GABAa is the target for lorazepam.  Lorazepam binds to a cleft between the subunits of alpha1 and gamma2 on GABA.  This action causes a conformational change in the receptor.  Lorazepam does not activate GABAa directly, but it is a positive allosteric modulator of the effects of GABA.  Lorazepam works by binding to the receptors on post synaptic GABA-A ligand-gated chloride channel neuron within the CNS.  They allow lower concentrations of the neurotransmitter to open Cl- channels, and this action increases Cl going into the cell.

# data[].attributes.body
The molecular weight of Ergocalciferol is 396.6 grams/mol. Ergocalciferol is Vitamin D2, this is a fat-soluble vitamin that helps the body take in key nutrients like calcium and phosphorous. Having the correct amount of these two elements are vital for building and maintaining strong bones. This vitamin is prescribed to help treat and prevent bone disorders such as rickets and osteomalacia. This vitamin is also used in the treatment of hypoparathyroidism. Hypoparathyroidism is a condition where the body doesn’t produce sufficient amounts of the parathyroid hormone. The parathyroid hormone is responsible in the role of regulating calcium levels in your blood. If the parathyroid hormone is not regulating calcium correctly then ergocalciferol is the drug that will make sure the body absorbs the correct amount of calcium. There are no heterocycles found in this drug. Ergocalciferol contains one functional group which is a hydroxy group. Ergocalciferol is absorbed in the intestine and transported to the liver. This vitamin requires the presence of bile for absorption to take place. The target group for this vitamin is the vitamin D receptor. This VDR (voltage dependent calcium channel) is also known as the calciferol receptor. Ergocalciferol acts as an agonist and also an inducer. It is an agonist for the vitamin D3 receptor. As an agonist it initiates a response when bonded to a receptor. As an inducer for the voltage-dependent calcium channel it will enhance/induce a specific response. Ergocalciferol should not be taken if the patient has had an allergic reaction to vitamin D. Precaution should also be taken if the patient has high levels of calcium in their body or any condition that makes it difficult for the body to absorb nutrients from food. Too much vitamin D could possibly harm an unborn child. Therefore a pregnant woman’s dose may need to be reduced during pregnancy. Ergocalciferol can pass into the breast milk and may cause side effects in the baby. If the patient misses a dose then take it as soon as you can unless it is almost time for the next dose. Never take two doses at one time. Taking other medication may make it more difficult for your body to absorb vitamin D. If the patient is taking other medications they should take them either two hours before or two hours after taking ergocalciferol.

# data[].attributes.body
Ian McVeay

Glimepiride

Glimepiride is a long-acting sulfonylurea with hypoglycemic activity. It is more potent and has a longer duration of action when compared to other sulfonylurea compounds. Glimepiride is used alongside diet and exercise programs to help control high blood sugar in people that suffer from type 2 diabetes. Glimepiride works by stimulating the secretion of insulin granules from pancreatic islet beta cells by blocking ATP-sensitive potassium channels and causing depolarization of beta cells. It is also thought that extra pancreatic effects may play a role in the activity of this drug as well, and this is supported in trials showing administration of glimepiride can lead to an increase in the sensitivity of peripheral tissues to insulin. Glimepiride is metabolized by the CYP2C9 to produce M1. M1 then goes further metabolization by several other enzymes to produce M2. M1 possesses about a third of the activity of glimepiride in animal models, but it is not clear if this is clinically relevant in humans. Some of the more common side effects of glimepiride include low blood sugar (hypoglycemia), headache, nausea, dizziness, weakness, and unexplained weight gain. Glimepiride also has drug interactions with quinolone antibiotics, ACE inhibitors, and other drugs that affect blood sugar. Since glimepiride is a substrate of CYP2C9, inhibitors or inducers of this enzyme also have to be taken into account when looking for drug interactions. It is also recommended to not drink alcohol while taking this drug, as it can raise or lower your blood sugar levels. Glimepiride is a third-generation sulfonylurea and was introduced in the United States in 1995. Compared to other sulfonylureas on the market, glimepiride was associated with lower risk of hypoglycemia and less weight gain. It also is considered safer in patients with cardiovascular diseases due to its lack of effects on ischemic preconditioning. The starting dose of glimepiride is 1 mg and the maximum recommended dose is 8 mg. Glimepiride is often taken with food and people often take this medication once a day with their breakfast. Taking glimepiride on an empty stomach can cause your blood sugar to reach levels that are too low. There has not been enough research and studies to show if glimepiride can be safely taken with pregnant patients, so it usually recommended that pregnant patients do not take this medication. However, in some special circumstances where the benefits of the medication outweigh the risk of effects on the unborn baby this medication is used.

# data[].attributes.headline
Bethany Thomas: Sertraline Hydrochloride 

# data[].attributes.subject
Bethany Thomas: Sertraline Hydrochloride 

# data[].attributes.body
Sertraline is a drug commonly used to combat anxiety, panic, and depression, which is very common within today’s society. Sertraline is an anti-depressant that comes from the class of SSRIs, which are selective serotonin reuptake inhibitors. Sertraline specifically affects the chemicals in the brain which are directly linked to depression, anxiety, panic, obsessive-compulsive disorder, post-traumatic stress disorder, and premenstrual dysphoric disorder. Sertraline selectively inhibits the reuptake of serotonin at the presynaptic neuronal membrane. This increases serotonergic activity. By doing this, synaptic concentration of serotonin in the central nervous system increases, therefore leading to multiple functional changes. Sertraline’s bioavailability has been estimated to be above 44%. The area under the curve in healthy volunteers after a 100mg dose of sertraline was 456 μg × h/mL in one study. The effects of food on the bioavailability of the sertraline tablet and oral concentrate were studied in subjects given a single dose with and without food. Sertraline is heavily metabolized in the liver, which is one of its major metabolites. It undergoes N-demethylation to form N-desmethylsertraline, which is much less potent in its pharmacological activity than sertraline. In addition to N-demethylation, sertraline metabolism involves N-hydroxylation, oxidative deamination, and finally, glucuronidation. The metabolism of sertraline is mainly catalyzed by CYP3A4 and CYP2B6, with some activity accounted for by CYP2C19 and CYP2D6. Sertraline dates back to the 1970s, involving chemist Reinhard Sarges. Sertraline was then approved by the Food and Drug Administration in 1991, becoming available in the United Kingdom a year before. Although sertraline was approved by the FDA, Paul Leber, the director of the FDA Division of Neuropharmacological Drug Products, said that it was a tough decision because the treatment effect on patients with depression was minimal. In 2002, sertraline was finally approved for adults ages 18 years and older. Sertraline is the same drug under the brand name Zoloft. Sertraline usually is prescribed in tablet form or a liquid concentration. It is usually taken once daily in the morning or in the evening. Most of the time, it takes sertraline some time in order to fully feel its effects, so patients should not abruptly stop taking this medication. Some common side effects associated with sertraline include nauseua, diarrhea, constipation, vomitting, difficulty falling asleep or staying asleep, dry mouth, heartburn, and loss of appetite. Other side effects can be more serious, including seizures, abnormal bleeding or bruising, hallucinations, rashes, hives, swelling, and difficulty breathing.

# data[].attributes.body
Billy Gray
Rivaroxaban

I have learned so much about the drug Rivaroxaban. The brand name for Rivaroxaban is Xarelto. Rivaroxaban was patented in 2007 and approved for medical use in the United States in 2011. In the United States, it will not be available as a generic medication until 2024. It is on the World Health Organization's List of Essential Medicines. In 2019, it was the 91st most commonly prescribed medication in the United States, with more than 8 million prescriptions. Rivaroxaban is a Non-Vitamin K Antagonist Oral Anticoagulant (NOAC). Rivaroxaban is a blood thinner that is used to treat and reduce strokes, blood clots in patients with atrial fibrillation, deep vein thrombosis, and pulmonary embolism. Rivaroxaban is indicated for patients with Atrial fibrillation, nonvalvular by obtaining to Prevent stroke and systemic embolism in patients with nonvalvular atrial fibrillation. Rivaroxaban is indicated for patients with coronary artery disease (stable) or peripheral artery disease and the goal is to Reduce the risk of major cardiovascular (CV) events (CV death, myocardial infarction, and stroke) in patients with coronary artery disease (chronic) or peripheral artery disease. Rivaroxaban is indicated for the use of patients with Indefinite anticoagulation (reduced intensity dosing against venous thromboembolism recurrence) and the goal of rivaroxaban drug is to Reduce the risk of recurrence of deep vein thrombosis (DVT) and pulmonary embolism (PE) in patients at continued risk of DVT and PE following greater than or equal to 6 months of initial full therapeutic anticoagulant treatment for deep vein thrombosis and/or pulmonary embolism. Rivaroxaban is also indicated for patients with Venous thromboembolism prophylaxis in acutely ill medical patients.
Bleeding is the most common side effect of rivaroxaban. Rivaroxaban can be stored at room temperature. Rivaroxaban is an oral factor Xa inhibitor that selectively blocks the active site of factor Xa and does not require a cofactor such as Anti-thrombin III for activity. Rivaroxaban inhibits free factor Xa and prothrombinase activity; inhibition of factor Xa decreases the generation of thrombin. Rivaroxaban has no direct effect on platelet aggregation, but indirectly inhibits platelet aggregation induced by thrombin. The heterocycles that are in the drug, Rivaroxaban, are Thiazole and Oxazole. The functional groups that are in the compound drug, Rivaroxaban, are Thioether, Amide, Aromatic amine, and Ether. Rivaroxaban is Absorption dependent upon site of drug release. The AUC of rivaroxaban was decreased by 29% and Cmax reduced by 56% when released in proximal small intestine, it is reduced further when released in distal small intestine or ascending colon. Sixty-six percent of Rivaroxaban is excreted in the Urine (66% primarily via active tubular secretion [~36% as unchanged drug; 30% as inactive metabolites]). Twenty-eight percent of Rivaroxaban is excreted through the feces (28% [7% as unchanged drug; 21% as inactive metabolites]). Elderly patients tend to exhibit higher plasma concentrations of rivaroxaban than younger patients, with mean AUC values being 50 percent higher, mainly because of reduced (apparent) total body and renal clearance.

# data[].attributes.body
Fenofibrate

Fenofibrate is used with a low-fat diet, exercise, and sometimes with other medications to reduce the amounts of fatty substances such as cholesterol and triglycerides in the blood and to increase the amount of HDL in the blood. It has a molecular weight of 360.8. Fenofibrate is not known to have any heterocycles, but does include functional groups such as an ester, ketone, and phenyl group.  It is available in an oral tablet and oral capsule. The brand names of Fenofibrate are Fenoglide, Tricor, and Triglide.

Common side effects of fenofibrate include: stomach pain, back pain, headache, and runny or stuffy nose. Infrequent side effects of fenofibrate include: gallstones and liver problems. Fenofibrate may interact with blood thinners, cyclosporine, or other cholesterol-lowering medicines. Fenofibrate is also not recommended for use during pregnancy because of the possible risk during breastfeeding.

Fenofibrate can cause serious liver damage. This can occur within the first few weeks of treatment or after several months of treatment. It can require a liver transplant and may be life threatening. Symptoms of liver damage include dark urine, an upset stomach or stomach pain, muscle pain, feeling tired, or yellowing of your skin or eyes.

Fenofibrate can cause severe allergic reactions. These can include anaphylaxis and angioedema (swelling), and can be life threatening. Some reactions can occur days or weeks after starting this drug. Among the possible reactions are Stevens-Johnson syndrome, toxic epidermal necrolysis, and drug reaction with eosinophilia and systemic symptoms

Fenofibrate was first synthesized in 1974, as a derivative of clofibrate, and was initially offered in France. It was initially known as procetofen, and was later renamed fenofibrate' to comply with World Health Organization International Nonproprietary Name guidelines.The development of Fenofibrate was discovered by Groupe Fournier SA, before it was acquired by Solvay Pharmaceutical in 2005.  This reformulation was controversial, seen as an attempt to stifle competition from generic equivalents, and was the subject of antitrust litigation by Teva.

Fenofibrate decreases low-density lipoproteins and total cholesterol levels, reduces triglyceride levels, and increases the levels of high-density lipoproteins. It is most effectively absorbed as a micronized preparation. The lipid modifying effects are mainly mediated via the activation of the peroxisome proliferator-activated receptors (PPARs). Fenofibrate activates PPAR, which regulates several genes involved in lipid metabolism.

Fenofibrate is a peroxisome proliferator receptor alpha activator used to lower LDL-C, total-C, triglycerides, and Apo B, while increasing HDL-C in hypercholesterolemia, dyslipidemia, and hypertriglyceridemia.

# data[].attributes.body
Ondansetron is a drug mainly used to treat nausea that can occur after undergoing surgery or receiving cancer treatment. Ondansetron was developed by GlaxoSmithKline (GSK) in London, England in the mid-1980s, and it was approved for use in the United States by the FDA in 1991. Ondansetron is sold under the brand name Zofran, is administered orally or by IV or IM injection, and has an oral bioavailability of roughly 60%. The drug has an elimination half-life of just under 6 hours and is cleared through the kidneys. Some side effects include diarrhea, constipation, drowsiness, headache, and itchiness, as well anaphylaxis in more rare and severe cases. The drug works by antagonizing the Serotonin-3 receptor to prevent nausea post-surgery or treatment. This drug thus acts as an enzyme inhibitor since it slows the action of this receptor. As of 2019, this drug is the 60th most prescribed drug in the United States, with more than 11 million prescriptions filled for it. The drug has a molecular weight of 329.8 g/mol, contains two heterocycles (pyrrole and imidazole), and contains amine and ketone functional groups. The log p of this drug could not be found, but this drug contains 4 hydrogen bond acceptors and zero hydrogen bond donors, which makes the drug orally bioavailable as it meets Lipinski’s criteria. The tablet is usually an oral dissolving tablet that will dissolve in seconds when placed on the tongue. For adults and children older than 12, the dose is 8 mg to be taken 30 minutes before treatment for cancer begins. From there, the dose is taken again after 8 hours, and then the 8 mg dose is repeated every 12 hours for the next 1-2 days. For children 4 to 11 years old, the dose is halved (4 mg) and then taken again 4 and 8 hours after the initial dose. The dose is then repeated every 8 hours for the next 1-2 days. The drug is rarely used for children younger than 4, so the dosing information available is sparse. For more sever cases of nausea, the initial dose can be tripled for adults and children over the age of 12 (as a result the dose would be 24 mg.) For treatment of nausea after surgery, the medication can be given to adults as a 16 mg tablet an hour before anesthesia is administered. Any uses other than described is at the discretion of the doctor.

# data[].attributes.body
Hydrochlorothiazide is used to treat high blood pressure mainly. It is also used to treat peripheral and pulmonary edema due to chronic heart failure. This drug is often used in combination with others in drug therapy regimens. It is in a class of drug called diuretics (also called water pills), that work by causing kidneys to get rid of unnecessary water and salt from the body through induced urination. This medication is a tablet and is usually taken once or twice a day. Severe side effects include: frequent urination, diarrhea, loss of appetite, headache, and hair loss. Hydrochlorothiazide exerts its action by acting at site-3(central dilating segment of early distal tubule). It binds to Na+Cl- symporter and inhibits Na+Cl- symport at the luminal membrane. It decreases Ca2+ excretion and increases Mg2+excretion. The antihypertensive actions of the drug may be attributable to depletion of sodium and subsequent reduction in plasma volume and a decrease in peripheral resistance. Decrease in peripheral resistance is due to either the loss of sodium from the arteriolar wall or a direct action on the vascular bed. When treating adults with hypertension, the recommended dosage is 25mg once daily or in divided doses. Increased to 50mg if required; depending up on the patient`s response.

In children with hypertension, the recommended dose would be a 1mg/kg single daily dose.

To treat adults with edema, the recommended dosage is to start with 25 to 50mg. Increased the dose until desired response is obtained. The maximum dose for anyone to take is 200mg/day while the maintenance dosage is around 25 to 100mg daily or on alternate days. In children it is 1mg/kg single daily dose or 1 to 3mg/kg/day in two divided doses. Thiazide diuretics like hydrochlorothiazide (HCTZ) were derived from sulfonamides in the late 1950’s by chemists who were looking for a non-mercurial, orally active compound that would increase salt and water excretion by the kidneys safely for treatment of hypertension and edema. Two companies, Merck and Ciba, state they discovered the medication which became commercially available in 1959. In 2019, it was the eleventh most commonly prescribed medication in the United States, with more than 38 million prescriptions. Hydrochlorothiazide is available as a generic drug under a large number of brand names, including Apo-Hydro, Aquazide, BPZide, Dichlotride, Esidrex, Hydrochlorot, Hydrodiuril, HydroSaluric, Hypothiazid, Microzide, Oretic and many other names.

# data[].attributes.body
Amlodipine is a long acting calcium channel antagonist that selectively inhibits the calcium ion influx across the cell membranes. It targets L-type calcium channels in muscle cells and N-type calcium channels in the central nervous system. It is used to treat hypertension, chest pain and other conditions that are caused by coronary artery disease. Amlodipine has a molecular weight of 408.9 g/mol and it also contains two heterocycles, they are chlorophenyl and dihydropyridine. It is also composed of the functional groups: chlorophenyl, dihydropyridine, dicarboxylate, methyl, ethyl, and aminoethoxy methyl. Amlodipine is considered to be a peripheral arterial vasodilator that exerts its action directly on vascular smooth muscle, this leads to a reduction in peripheral vascular resistance, ultimately causing ones blood pressure to decrease. With it being a dihydropyridine calcium antagonist, causes it to inhibit the influx of calcium ions in vascular smooth muscle and cardiac muscle. Amlodipine selectively blocks the influx of calcium ions across cell membranes. A stronger effect is seen on vascular smooth muscle cells than with cardiac muscle cells and the direct actions of amlodipine on vascular smooth muscle result in a decrease in blood pressure. Amlodipine was approved in 1987 by the FDA and is one of the most used antihypertensive drugs and belongs to a group of drugs known as dihydropyridine calcium channel blockers. It is one of the most used and popular antihypertensive drugs because of the single daily dosing option. There are several brand names of amlodipine: Amlobenz, Azor, Caduet, Consensi, Dafiro, Exforge, Exforge Hct, Katerzia, Lotrel, Norvasc, Prestalia, Tribenzor, Twynsta, and Viacoram. Amlodipine comes as a tablet or in a suspension liquid and is usually taken one time per day. When administered, amlodipine should not be taken with grapefruit products and natural licorice. This drug can be taken with or without food because it is absorbed the same. Patients should avoid taking amlodipine with nitroglycerin, simvastatin, or any other heart or blood pressure medications. Common side effects that one may experience when taking amlodipine are, dizziness, drowsiness, a feeling of tiredness, stomach pain, nausea, and flushing. Serious but not common side effects of amlodipine are pounding heartbeats, fluttering in the chest, worsening chest pain, swelling in the feet or ankles, severe drowsiness, and feeling light-headed or like you may pass out. Amlodipine is currently not approved for anyone under the age of six years old and one should talk to their doctor about any allergies to amlodipine or any other medications before taking it.

# data[].attributes.body
Carvedilol is a nonselective beta- and alpha 1-adrenoceptor antagonist that reduces the blood pressure and heart rate in patients with heart failure by decreasing sympathetic tone. Carvedilol is the first drug of its kind to be approved for the treatment of all forms of congestive heart failure (mild, moderate, severe) and is now the standard of care for this disease. This drug was patented in 1978 and approved for medical use in the United States in 1995. Carvedilol works by blocking the action of certain natural substances in your body, such as epinephrine, on the heart and blood vessels. This effect lowers your heart rate, blood pressure, and strain on your heart. Carvedilol inhibits exercise-induced tachycardia through its inhibition of beta adrenoceptors. Carvedilol's action on alpha-1 adrenergic receptors relaxes smooth muscle in vasculature, leading to reduced peripheral vascular resistance and an overall reduction in blood pressure. At higher doses, calcium channel blocking and antioxidant activity can also be seen. The antioxidant activity of carvedilol prevents oxidation of low-density lipoprotein and its uptake into coronary circulation. Carvedilol targets Beta-1 adrenergic receptor, Alpha-1A adrenergic receptor, NADH dehydrogenase [ubiquinone] 1 subunit C2, Beta-2 adrenergic receptor, Vascular endothelial growth factor A, Natriuretic peptides B, Gap junction alpha-1 protein, Potassium voltage-gated channel subfamily H member 2, Vascular cell adhesion protein 1, Alpha-1D adrenergic receptor, Alpha-1B adrenergic receptor, Alpha-2C adrenergic receptor, Alpha-2B adrenergic receptor, Alpha-2A, adrenergic receptor, E-selectin, Hypoxia-inducible factor 1-alpha, Inward rectifier potassium channel 4, Inward rectifier potassium channel 2, and Alpha-1 adrenergic receptors. Carvedilol has a molecular weight of 406.474 g/mol. This drug also contains functional groups known as alcohol, ether, amines, and a heterocycle known as pyrrolidine. Some side effects of Carvedilol include extreme thirst, frequent urination, extreme hunger, weakness, blurred vision, tiredness, weakness, lightheadedness, dizziness, headache, diarrhea, nausea, vomiting, vision changes, joint pain, difficulty falling asleep or staying asleep, cough, dry eyes, numbness, burning or tingling in the arms or legs, fainting, shortness of breath, weight gain, swelling of the arms, hands, feet, ankles, or lower legs, chest pain, slow or irregular heartbeat, rash, hives, itching, difficulty breathing and swallowing. If a patient were to experience any unusual problems while taking this medication, it is advised that the patient should contact their doctor and tell them of these symptoms. When taking this medication, if the patient were to miss a dose, then they should take the missed dose as soon as they remember it. However, if it is almost time for the next dose, then it is advised to skip the missed dose and continue the regular dosing schedule. A person should never take a double dose to make up for a missed one.

# data[].attributes.body
Fluticasone propionate was patented in 1980. It is accessible as a generic drug. Fluticasone was the 15th most often prescribed drug in the United States in 2017, with over 32 million prescriptions written. Fluticasone propionate is a glucocorticoid that is synthesized. For diverse inflammatory indications, these medicines are offered as inhalers, nasal sprays, and topical therapies. Fluticasone propionate was licensed for the first time in 1990. Fluticasone propionate stimulates glucocorticoid receptors in the body and suppresses pulmonary eosinophilia in rats. Fluticasone propionate as a topical formulation has also been linked to skin vasoconstriction. Fluticasone propionate affects the function of many cell types and inflammatory mediators via an unclear mechanism. Cytochrome P450 3A4 removes fluticasone propionate from hepatic metabolism. Fluticasone propionate is hydrolyzed at the FIVE-S-fluoromethyl carbothioate group, resulting in the formation of an inactive metabolite.

While they reduce systemic (blood) absorption, the nasal spray and oral inhaler formulations have less corticosteroid adverse effects than the tablet version when used appropriately. Even with proper dosage, systemic absorption is not insignificant. Using the spray or inhaler at greater than recommended dosages or in conjunction with other corticosteroids increases the risk of significant, systemic corticosteroid-induced adverse effects. These adverse effects include a weaker immune system, a higher risk of systemic infections, osteoporosis, and increased intraocular pressure. Nasal irritation (burning, stinging, bleeding), headache, upset stomach (nausea, vomiting), and diarrhea are common adverse effects. Infection (evidenced by fever, sore throat, and cough, for example), vision issues, severe swelling, hoarse voice, and trouble breathing or swallowing, upper respiratory tract infection, throat irritation, thrush, cough, and headache are all rare adverse effects. Bruising, swelling of the face/neck, sadness, weariness, and shortness of breath are all rare adverse effects.

The usage of fluticasone propionate in certain populations has not been well researched. Fluticasone propionate is neither carcinogenic, mutagenic, or clastogenic, and it has not been shown in animal tests to impair fertility. Fluticasone propionate has been demonstrated to have teratogenic effects in rats when administered subcutaneously, but not when administered orally. In general, there have been no reports of fluticasone side effects in pregnancy. Fluticasone propionate in human milk may decrease growth, interfere with endogenous corticosteroid synthesis, or have other consequences. Adrenal suppression occurred in pediatric patients who received fluticasone propionate ointment. Geriatric individuals receiving fluticasone propionate showed no difference in safety or efficacy when compared to other patient groups, albeit older patients may be more susceptible to side effects. There is no variation in fluticasone propionate clearance between genders or races. Because of the elimination process, patients with hepatic impairment should be continuously watched.

# data[].attributes.body
Esomeprazole is a common drug used by patients suffering from acid reflux related issues. Esomeprazole was patented in 1993 and received approval from the FDA in 2001. Esomeprazole was created from another proton pump inhibitor, omeprazole, by the separation of enantiomers. Esomeprazole is the S-isomer of omeprazole, and it is known to have a better therapeutic effect than omeprazole. It was introduced to the market by AstraZeneca, and the brand name of the drug is Nexium. Esomeprazole magnesium, better known as Nexium, is available over the counter. The molecular weight of esomeprazole is 345.4 grams/mole. The esomeprazole structure includes the heterocycles imidazole and pyridine as well as the functional groups ether, sulfoxide, and primary amine. It is used to treat acid reflux disorders such as gastroesophageal reflux disease, short term treatment of erosive esophagitis, and maintenance of erosive esophagitis healing. It can also be used in combination with antibiotics to treat duodenal ulcers. Esomeprazole is a proton pump inhibitor that works by irreversibly binding to the H+/K+ ATPase of the proton pump in the gastric parietal cell. Since the proton pump of the gastric parietal cell is the last pathway for secretion of hydrochloric acid, inhibiting the proton pump decreases the secretion of hydrochloric acid into the stomach and alters gastric pH to be less acidic. This mechanism of action is what helps relieve the symptoms of acid reflux and heal the esophagus. This drug is eliminated from the body through hepatic metabolism by the enzymes CYP3A4 and CYP2C19, but mostly CYP2C19. About 80% of the drug is excreted through urine and 20% through feces as inactive metabolites, and less than 1% of the drug is still active when excreted. Esomeprazole is a delayed release capsule that should be taken an hour before eating. It is available in 20 mg capsules or 40 mg capsules, and the dosing varies according to the illness being treated and the age of the patient. This drug is also available as an intravenous injection, but it is more commonly known for being a capsule. Esomeprazole is meant to be used for short term treatment. Some of the common adverse events associated with esomeprazole include diarrhea, abdominal pain, flatulence, gastritis, nausea, and headaches.  Esomeprazole being taken with diazepam or other drugs that are metabolized by CYP2C19 will decrease that drug’s clearance, but those are the only known drug-drug interactions.

# data[].attributes.body
Sumatriptan is a serotonin-receptor 1B and 1D agonist (triptan) indicated for the acute treatment of migraine with or without aura. Sumatriptan is not indicated for long-term migraine prophylaxis or for the management of hemiplegic or basilar migraine. Sumatriptan tablets are indicated for the acute treatment of migraine with or without aura in adults and pediatric patients 12 years of age and older. Therefore you should only use it if you have a clear and accurate diagnosis of migraine headache. Additionally, this medication is not used for the prevention of migraine attacks but to help manage the attacks. Sumatriptan is a sulfonamide triptan with vasoconstrictor activity. Sumatriptan selectively binds to and activates serotonin 5-HT1D receptors in the central nervous system (CNS), thereby constricting cerebral blood vessels. Sumatriptan may also relieve vascular headaches by decreasing the release of vasoactive neuropeptides from perivascular trigeminal axons in the dura mater during a migraine, by reducing extravasation of plasma proteins, and by decreasing the release of other mediators of inflammation from the trigeminal nerve. With taking Sumatriptan be sure to inform the patients taking this combination of the possible increased risk and monitor for the emergence of serotonin syndrome particularly during treatment initiation and dose adjustment. Sumatriptan stimulates presynaptic 5-HT1D receptors, an action that inhibits both dural vasodilation and inflammation. It directly inhibits trigeminal nuclei cell nociceptive neurotransmission via 5-HT1B/D receptor agonism within the trigeminocervical complex of the brainstem and upper spinal cord. The development of the triptans were determined by the membership of the American Headache Society to be the most important breakthrough in headache medicine in the last 50 years. The prototypical triptan, sumatriptan, first became available in Europe in 1991 and revolutionized the treatment of this debilitating condition that affects millions of people throughout the world. As the first highly effective and well-tolerated drug for the acute treatment of migraine, it was hailed as a medical breakthrough. The discovery of sumatriptan confirmed, once and for all, that migraine truly is an organic disease and not just the figment of imagination of “neurotic” patients. Indeed, in the early days of sumatriptan's availability, it was hailed as diagnostic for whether or not a patient's headache was migrainous in origin. In conclusion all drugs may cause side effects, however, many people do not have any side effects or either only have minor side effects. While taking sumatriptan anyone is susceptible to effects like flushing, fatigue, vomiting, seizures, abnormal heartbeat, etc. Therefore, if any of these symptoms happen or do not go away, patients should seek medical help.

# data[].attributes.body
Molecular weight: 136.11
Drug Class: Antigout Agents/Gout Suppressants
The plasma half-life is 1-2 hours

Indication

Labeled

Allopurinol is a medication used to lower uric acid levels. Due to the medications ability to lower uric acid levels, it has an indication for primary and secondary gout. This could include an acute gouty attack, tophi, uric acid lithiasis and nephropathy. Allopurinol is indicated in all patients who suffer from recurring bouts of the symptoms associated with high uric acid levels. Patients 40 and younger with extremely high serum acid levels are indicated for allopurinol use. Patients with recurrent calcium stones are another indication for allopurinol use. The last indication is for the prevention of tumor lysis syndrome in patients with cancer.

Off-Labeled

One off-label use identified in the literature was in the prevention of recurrent uric acid stones in patients with nephrolithiasis.

Target Interaction

Allopurinol is a xanthine oxidase inhibitor. Allopurinol inhibits xanthine oxidase, the enzyme responsible for breaking down purines into uric acid. The medication is specific to xanthine oxidase and does not interfere with the making of other vital purines. Allopurinol stops the reaction that occurs to form uric acid. The end result is that decreasing the production of uric acid leads to a decrease in the symptoms.

The Mechanism of Action (MoA)

Allopurinol is similar to the structure of hypoxanthine. Hypoxanthine is a natural occurring purine in the body. When the medication is taken, it is then metabolized in the liver to oxypurinol, the enzyme that stops the production of xanthine oxidase. As stated above, hypoxanthine converts into xanthine and then turns into uric acid. This shows that the inhibition of the enzyme leads to the effects of allopurinol. There are decreased amounts of uric acid in the urine and the serum so it decreases the occurrence of gout symptoms. Although there becomes an increase in hypoxanthine and xanthine, the solubility decreases so it is more easily excreted by the kidneys. This helps the kidneys by not being exposed to high levels of uric acid and decreases the risk of crystalluria. In summary, the mechanism of action of allopurinol is a xanthine oxidase inhibitor.

Side Effects/Adverse Reactions

There are side effects or adverse reactions with allopurinol use. The most common side effect is a skin rash. This occurs in less than 3% but it can be severe so it needs to be advised to the patient. Allopurinol is commonly associated with Stevens-Johnson syndrome, a potentially fatal diagnosis. There are also possible endocrine and metabolic side effects. Nausea, vomiting, diarrhea, drowsiness and renal failure syndrome are listed as rare, less than 1%, but possible side effects/adverse reactions with allopurinol use.

The History of Discovery and Development

Allopurinol dates back to research in the 1940s and was first approved for use in the United States in 1966. Allopurinol was first synthesized when trying to find a treatment for leukemia. It was not successful in the treatment of leukemia, but researchers took that work and started testing it as a treatment for gout. It gained FDA approval and became a drug of choice in the treatment of primary and secondary gout in 1966.

# data[].attributes.body
Losartan potassium is a nonpeptide angiotensin II receptor blocker that is used for the treatment of hypertension. It is administered orally. Its molecular weight is 461 daltons and logP is 5.37. Along with being an antihypertensive, it is also indicated to treat proteinuric chronic kidney disease in patients with type 2 diabetes. Off-label uses include heart failure with reduced ejection fraction, marfan syndrome with aortic aneurysm, post-transplant erythrocytosis, proteinuric chronic kidney disease in nondiabetics, and more. Potential risk factors include hypotension, hyperkalemia, and renal function deterioration. Potential adverse effects include diarrhea, muscle cramps, insomnia, nasal congestion, persistent cough, and dizziness. This drug should not be taken during pregnancy and should be discontinued immediately upon detection of pregnancy due to the boxed warning for fetal toxicity. Its mechanism of action is an angiotensin II receptor antagonist. Angiotensin II acts as a vasoconstrictor and secretes aldosterone, so losartan blocks these effects. It is a reversible antagonist at both the AT1 and AT2 receptors, but has a significantly greater affinity for AT2. It is selective and competitive and displays slow dissociation kinetics. Losartan has a significant first pass metabolic effect and is primarily metabolized by CYP2C9 and CYP3A4. The metabolite that is produced is significantly more potent than Losartan itself. Losartan was discovered by DuPont pharmaceuticals in March 1986 and was one of the first drugs to be discovered by this company. It was also the first angiotensin II receptor blocker to be discovered. The initial approaches to discovering a compound that would block angiotensin II included peptide synthesis. The researchers at DuPont used a fragment-based design and tested relatively small analogues of fragments of angiotensin II. However, this approach ended up being unsuccessful as binding activity was relatively low and the molecules were considered inactive. This is likely due to the fact that the fragments that were being used consisted of one or two amino acids, but it was determined that a successful peptide would need to be between six to eight amino acids in length, which was considered too large to create analogues. A nonpeptide antagonist of angiotensin II was discovered in a patent search and was assigned to Takeda Chemical Industries. The researchers at DuPont synthesized this compound to verify the effects. The test was considered unsuccessful. Despite relatively weak potency, the researchers decided to test it in rats. The pharmacologist noted that although the effects were weak, the compound had a high degree of selectivity. Efforts then shifted to lead optimization to discover a compound with a higher potency and oral bioavailability. Once optimized, Losartan was shown to be 1000 times more potent than the original lead. It was FDA approved in April 1995.

# data[].attributes.body
Oxybutynin is used to treat and control overactive bladders and its muscles. Individuals must be six years and older to use. Younger patients typically use the drug to treat night time urination. This drug is shown to be linked to a neurological condition, such as having dreams of urinating. It is sold under the brand name Ditropan. This drug has been on the market since 1975.  It helps eliminate the  uncontrollable and frequent use of urination. However, it is not a cure for this condition.

It is available orally as a syrup or tablet, as a transdermal gel, and a transdermal patch. It is targeted to relax the bladder by inhibiting the postganglionic muscarinic receptors types 1,2, and 3, which expands the bladder’s capacity to hold more content. Oxybutynin is a muscarinic antagonist that blocks calcium channels. This blocks the actions of the acetylcholine on the smooth muscle and the influx of calcium into the cell membrane. As a result, the muscle of the bladder is relaxed. Some side effects of Oxybutynin include dry mouth, dizziness, constipation, and urinary tract infections. Some potential cautions that oxybutynin can cause include renal impairment or memory loss. This drug is not recommended for patients with glaucoma or individuals that have problems urinating. Since its purpose is to decrease the excretion of fluid, it will be harmful for individuals who already can’t urinate normally. Furthermore with its ability to decrease the excretion of fluid, it increases the risk for heat stroke.

Oxybutynin tablets are to be taken with a glass of water, with or without food , the same time each day. Because some of the tablets can’t be metabolized by the body, it is normal to see pieces of it in stool. It is recommended that individuals taking this medication not drink alcohol due to increased side effects. It has an absorption rate of one hour, and half life elimination rate of  two to five hours. Oxybutynin transdermal patches (Oxytrol)  for men have to be prescribed, but women are able to purchase the patches over the counter. This medication is also available as a gel. The gel has to be applied to either the stomach, shoulder, upper arms, or thighs. The area then has to be covered with cloth so that it will not spread to other areas or individuals. Patients must wait at least an hour before they perform any physical activity that may cause them to sweat or have wet skin such as bathing or exercising.

# data[].attributes.body
Insulin aspart is a rapid acting insulin therapy used to treat type 1 and type 2 diabetes. It is used to stabilize blood sugar levels. The pancreas naturally secretes insulin allowing food to be broken down into usable sources of energy. Patients with diabetes have too much sugar in their blood with too little insulin causing them to need extra insulin to help break down glucose. Type 1 diabetes is an autoimmune disorder that causes the body to destroy insulin producing cells and type 2 diabetes is typically lifestyle related that develops over time.  Insulin aspart acts as an insulin replacement to help manage sugar levels. Insulin aspart differs from human insulin in the structure having a substitution of proline to aspartic acid. This substitution allows for higher rates of absorption. Since it is a rapid acting insulin, it is supposed to mimic insulin spikes after meals. It targets the insulin receptor making it an agonist. The binding to insulin receptors results in the activity of glucose transports that stimulate metabolism and catabolism. Adverse reactions are typically the result of incorrect dosing. If the patient is given too much insulin, they could have hypoglycemia. Hypoglycemia means that blood sugar is too low. Without treatment, hypoglycemia could lead to seizures, loss of consciousness, and possible death. On the opposite end of the spectrum, if a patient is not given enough insulin, their blood sugar levels will remain uncontrolled and too high—also known as hyperglycemia. Hyperglycemia is not as rapid as hypoglycemia. If the patient has already been diagnosed with diabetes, their symptoms will remain. These symptoms could eventually result in more serious issues such as cardiovascular disease, nerve damage, and kidney damage. Other adverse effects can be dermatologically related to the injection site. Insulin was discovered about one hundred years ago when looking at reducing blood glucose in diabetic dogs. Insulin continued to develop into different varieties of treatment. Insulin aspart was developed in 2000 when looking faster onset of action.

# data[].attributes.body
Levothyroxine is a drug that acts as a substitute for the thyroid-stimulating hormone (TSH) in order to stimulate the thyroid gland. It is a prescription drug that treats hypothyroidism by binding to receptors on the thyroid to create a cascade of events that affect metabolism. Symptoms of hypothyroidism include fatigue, constipation, weight gain, dry skin, and increased sensitivity to cold. Also known as L-thyroxine, it is a synthetic form of the thyroid hormone thyroxine (T₄). It is an oral medication that should not be taken with food as this can decrease the absorption of the drug in the gut. It can also be given intravenously or as a suppository if the patient cannot take oral medication. Levothyroxine can also cause several side effects including, but not limited to, weight gain or loss, vomiting, diarrhea, fever, and changes in appetite. It can also cause hyperthyroidism, and so the patient usually requires his or her thyroid-stimulating hormone levels to be monitored for several weeks after beginning treatment. It does not contain any heterocycles, but it does include two arene rings. For its mechanism of action, levothyroxine enters the cell and binds to receptors found in the cell nucleus. It then directly affects DNA transcription to increase the body’s metabolism by increasing gluconeogenesis, protein synthesis, and other functions. It also can affect the actions of other drugs. It may increase the effects of blood thinners, such as warfarin, and may require a lower dosage of such drugs. In diabetic patients, it may lead to the patient needing either an increase or decrease in their insulin dosage. The intravenous administration of epinephrine may also increase the chances of a heart attack for patients taking levothyroxine. It may also decrease the action of beta-blockers and lead to an increase in dosage requirements for these medications in patients. Levothyroxine binds to several receptors on the thyroid in order to regulate metabolism. Thyroxine was first extracted in its pure form in 1914 by Edward Calvin Kendall at the Mayo Clinic from hog thyroid glands. Levothyroxine was then synthetically created by Charles Robert Harington and George Barger in 1927. Since then, levothyroxine has been one of the most prescribed drugs, becoming the most prescribed drug in 2016 and is currently the second most prescribed drug in the present day. Levothyroxine, since its creation, has been one of the most helpful drugs and has assisted patients with problematic metabolisms for many years.

# data[].attributes.body
Pantoprazole Sodium

Pantoprazole Sodium, sold under the brand name Protonix, is a proton pump inhibitor used for acid reflux, erosive esophagitis, and Zollinger-Ellison syndrome. Some off label uses for the drug include duodenal ulcer disease and some GI tract infections. When it comes to dosing the most common range of dosing is from 80 mg/day to 160 mg/day in adults with 240mg/day being the maximum dose for adults. However, for children and adolescents the FDA has approved up to 40 mg/day to be taken but in certain cases up to 80 mg/day is acceptable. Adults, adolescents, and children can take the medication in both an oral and IV dose. As a proton pump inhibitor, pantoprazole binds to the H+/K+-ATPase pump and reduces its function, which is essential for the secretion of stomach acid. Some functional groups and heterocycles in the structure of pantoprazole that contribute to the overall function of the drug include Pyridine and Imidazole heterocycle groups as well as sulfonic acid and ether functional groups. When it comes to side effects of the drug the most common ones include abdominal pain, diarrhea, flatulence, and headache. Some less common but potentially serious adverse effects include Stevens-Johnson syndrome, thrombocytopenia, and epidermal necrolysis. When counseling patients about the medication it is important to not only discuss the potential side effects but that the medication can be taken both with or without food but is best taken before meals to reduce the acid production caused by the intake of food. Furthermore, it is important to check to see if the patient is taking methotrexate or clopidogrel as those medication result in drug-drug interactions. Competitive inhibition occurs when pantoprazole is taken with the prodrug clopidogrel resulting in reduced effectiveness. As for methotrexate, pantoprazole blocks the secretion of methotrexate resulting in increased levels and potentially toxic effects. When it comes to the metabolism of pantoprazole the medication is primarily metabolized via first pass metabolism in the liver by the CYP2C19 enzyme. Additionally, pantoprazole has a relatively short half-life with a renal half-life of 1 hour in normal metabolizing patients and 10 hours in CYP2C19 deficient patients. Lastly, there is some data to suggest that pantoprazole is a competitive inhibitor of the CYP2C9 and CYP3A4 enzymes. That being said, these inhibitions do not result in any notable drug-drug interactions and no change of dosage is needed as a result of concurrent pantoprazole usage.

# data[].attributes.body
Buspirone Hydrochloride chemical formula is C21H32ClN5O2. The molecular weight is 422.0 g/mol which means that buspirone hydrochloride is a small molecule. Buspirone Hydrochloride contains functional groups of amides and butane, and it has heterocycles of imide, pyrimidine, and piperazine. Buspirone Hydrochloride is first synthesized by a team from Mead Johnson in 1968, and it was not patented until 1980. It was approved by the FDA in 1986 for the use of general anxiety disorder. It was first developed as an antipsychotic with a target on the D2 receptor. However, it was found ineffective for the treatment of psychosis, so then it was used as an anxiolytic. As mentioned, Buspirone Hydrochloride is indicated for short-term treatment of general anxiety disorders and relieves symptoms of anxiety with or without accompanying symptoms of depression. The drug affects the chemicals in the brain that might be unbalanced in patients with anxiety. It changes the certain numbers of natural substances in the brain. Moreover, the dosage of buspirone hydrochloride is individualized to each patient, and food will increase the bioavailability of buspirone hydrochloride. It is said that for patients that take buspirone hydrochloride, the initial effects take about a week to two weeks to kick in, and full clinical effect should kick in around 4 to 6 weeks. Therefore, for a patient who is in an urgent need or rapid effect, buspirone hydrochloride would not be the best option. Buspirone Hydrochloride comes in tablet form. There are 5 different dosages of tablets, including 5mg, 7.5mg, 10mg, 15mg, 30mg. The target is that Buspirone acts as an agonist of the serotonin 5-HT1A receptor with a high-affinity antagonist of the dopamine D2 receptor with a weak affinity agonist of the serotonin 5-HT1A receptor. The mechanism of action is extremely complex, but the main neuropharmacological effects are mediated by 5-HT1A receptors. There are many side effects when it comes to taking buspirone hydrochloride. Some of the common side effects include dizziness, nausea, diarrhea, headache, excitement, confusion, and etc. There are serious side effects that patients should be aware of which include rash, hives, itching, swelling to face, eyes, mouth, throat, tongue and lips, blurred vision and etc. If these side effects persist, the patient should contact their primary physician or pharmacist. However, there are benefits to taking buspirone hydrochloride which leads to patients living clear thinking, relaxing, worrying less life. It leads to more control symptoms like troubled sleeping, sweating, and pounding heartbeat. Buspirone Hydrochloride can be very beneficial for patients with generalized anxiety disorder.

# data[].attributes.body
Clopidogrel bisulfate, also known as Plavix, is an oral prodrug that acts as an antiplatelet agent. It is a small molecule that was approved by the FDA to inhibit the blood from clotting and leading to serious medical conditions. The common conditions that this drug treats are strokes, heart attacks, blood clots, and blood circulation problems. This drug significantly helps patients by reducing the likelihood of them having a stroke or a heart attack. Clopidogrel was approved by the FDA in 1997 for its effectiveness in treating acute coronary syndrome in adults. It was manufactured by Bristol-Myers Squibb. As stated earlier, the brand name for Clopidogrel is Plavix. Plavix was patented in 1982. This patent expired in 2012, which made room for other manufacturers to begin making generic versions of the same medication. Clopidogrel bisulfate works by binding to the P2RY12 receptor. It acts as an antagonist to block the normal processes of platelet aggregation. By binding to this receptor, clopidogrel works to inhibit ADP from creating platelets. Clopidogrel is metabolized by carboxylesterase into its active metabolite. This active form is responsible for the antiplatelet effects in patients. There are a range of side effects that patients experience while taking Clopidogrel. The mild side effects include headaches, dizziness, nausea, and stomach pain. The more severe side effects of this medication are hives, swelling of the throat, tongue, eyes, etc., bloody vomit, and shortness of breath. Because of its chemical formula, there are a number of drugs that counteract with Clopidogrel. Esomeprazole and Omeprazole should not be used in combination with Clopidogrel because they are both proton pump inhibitors and they will decrease the amount of Clopidogrel that is in the patient’s body, which will ultimately decrease the effectiveness of the drug. Opioids, such as Morphine, will also diminish the effectiveness of Clopidogrel. Other drugs, such as Amodiaquine, will increase the concentration of Clopidogrel in the body, which yields to overexposure and the patient could be at risk of fatal toxicity. Just like any other medication, Clopidogrel can be toxic if taken at a too high dose. There are symptoms that indicate toxicity from Clopidogrel; these symptoms include vomiting, gastrointestinal hemorrhaging, and prostration. Fortunately, overdoses and toxicity can be reversed by platelet transfusions. Along with certain drug interactions, grapefruit juice should be avoided while taking Clopidogrel because it significantly reduces its efficacy in the body. Other than that, Clopidogrel is a very cost-effective and therapeutic drug for many people who are at risk of a heart attack or stroke.

# data[].attributes.body
Omeprazole is a proton pump inhibitor, also referred to as Prilosec. The drug is prescribed typically on a once-daily basis and reaches a plateau after four to five days. The delayed release capsules of omeprazole contain an enteric coating of granule formated omeprazole; this is due to the fact that omeprazole is acid-labile, meaning absorption of omeprazole happens to begin after the granules have exited the gut. Delayed release capsules are associated with a higher bioavailability of the drug. It is a small molecule drug, and the chemical formula of omeprazole is : C17H19N3O3S. The average weight of omeprazole is 345.416. It is used to treat frequent heartburn, gastroesophageal reflux disease, peptic ulcer disease, esophagus damage, active benign gastric ulcers, maintenance of healing of erosive esophagitis, and active duodenal ulcers. It is available over the counter and with a prescription, too. It is even approved for veterinary usage. Omeprazole is metabolized in the liver. The enzyme responsible for the metabolism of omeprazole is cytochrome p450, and it is also dependent on cytochrome p2c19 and cytochrome p3a4. It works by decreasing the amount of acid made in the stomach. It inhibits the parietal cell H+/K- ATP pump to suppress gastric basal and stimulated acid secretion. This is done by binding of the proton pump inhibitors to the cysteine residues, and it is done by disulfide bridges on the alpha subunit of the H+/K- ATPase pump. This process inhibits the gastric acid secretion in the patient for about thirty-six hours. Omeprazole is absorbed rapidly. The maximum effect of the drug omeprazole is achieved around after two hours after administration, but the actual range can be anywhere from half an hour to three and one half hours following administration of the drug. The half life of omeprazole is estimated to be around one half hour to one hour in healthy patients that are taking the delayed release capsules, and if they are hepatically impaired, the half life is about three hours. The drug is eliminated, or excreted in urine, at an approximate concentration of seventy seven percent, and is eliminated in the form of six metabolites. The remainder is excreted in feces.  Studies indicate that omeprazole can lead to increased variations and amounts of gut bacteria. Patients taking omeprazole may have a higher risk of diarrhea due to this. Another study indicates that omeprazole has an impact on heart health, specifically it may increase cardiovascular risks by seventy percent.

# data[].attributes.body
Stacy Truong
Acetaminophen

MW: 151.16 g/mol
Functional groups: Phenol (a benzene ring with a hydroxyl group) and amide
Heterocycles: None
I learned the following information about this medication:
-The name depends on the location: Acetaminophen in the United States and Japan or Paracetamol in Europe and most of the rest of the world.
-In the late 19th century, acetaminophen was accidentally discovered after the wrong chemical, acetanilide, was administered to a patient, who had intestinal parasites. The patient still had the parasites, but their fever was reduced. As a result, it became a focus of research, which later led to a widely used painkiller. How that happened: when Harmon Northrop Morse synthesized acetaminophen, it can not be used for a while; however, in 1893, the substance was found in the urine of patients who had consumed phenacetin. The new compound was then isolated and concentrated into a pure white, crystalline form. Originally, these fever-reducing compounds were found in Cinchona tree bark dating back to Medieval times, but the source became harder to find after it was commonly harvested. This also later led to the development of various agents such as acetanilide (1886), phenacetin (1887), and acetaminophen (1873).
-The mechanism of action is still in debate. The theory is that it acts on the central nervous system by enzyme inhibiting the synthesis of prostaglandins (COX pathways; cyclic fatty acids; plays a role in the development of inflammation, pain, and fever). The targets are Prostaglandin E synthase 3, Prostaglandin G/H synthase 2, Prostaglandin G/H synthase 1, and Transient receptor potential cation channel subfamily V member 1.
-The roles are reducing the activity of COX with a different mechanism (not binding to the active site of COX-1 or 2 enzymes).
As a result, it is able to relieve mild to moderate pain from headaches, muscle aches, menstrual periods, colds and sore throats, toothaches, backaches, and reactions to vaccinations (shots), and to reduce fever.
-The precautions are to discuss with a doctor or a pharmacist before taking acetaminophen. The patient needs to make sure to disclose information about allergies and medical history (potentially involving liver disease/regular or abuse use of alcohol or diabetes/phenylketonuria (PKU)/other conditions requiring them to limit or avoid products of liquid, chewable/dissolving/effervescent tablets, and powders).
-The side effects include nausea, stomach pain, loss of appetite, itching, rash, headache, dark urine, clay-colored stools, or jaundice (yellowing of skin or eyes) If symptoms of rare serious allergic reactions occur such as rash, itching/swelling (especially of the face/tongue/throat), severe dizziness, or trouble breathing then the individual must receive medical help immediately.

# data[].attributes.body
Insulin Glargine is used alongside other medications for both type 1 and type 2 diabetes. Insulin Glargine is long acting and is a manmade version of human insulin which helps move sugar from the liver to other parts of the body. It also prevents the liver from making more sugar. The side effects of this medication include rapid weight gain, swelling in feet or ankles, shortness of breath, low blood sugar, itching, rash, and a thickening or hollowing of the skin around the injection site. The mechanism of action of insulin glargine is it targets specific membrane-bound receptors that regulate the metabolism of carbohydrates, proteins, and fats. Specifically it targets the liver, skeletal muscle, and adipose tissue and causes the uptake of glucose into these tissues and organs to be converted into energy. Hepatic glucose production, lipolysis, and proteolysis is inhibited, while protein synthesis is enhanced. Insulin also activates sodium-potassium ATPases which promotes intracellular movement of potassium ions. All this together helps bring blood sugar levels down to prevent ketoacidosis and decrease the risk of heart attack, stroke, and diabetic neuropathy.

In the insulin receptor, insulin glargine is an agonist, and in the insuline-like growth factor 1 receptor, it is an activator. Before insulin was discovered, getting diabetes was essentially a death sentence with most people not making it past two years of diagnosis. In the early 1920s after several failed experiments with trying to figure out the exact cause, four scientists named Banting, Best, Macleod, and Collip discovered that extracting insulin from a dog’s pancreas and giving it to individuals with diabetes mellitus successfully lowered blood sugar levels. Once they were able to fully purify their insulin product, they were able to get a patent and successfully treat diabetes. Until the 1980s, insulin had to be extracted from human cadaver pancreases. However in the 1980s, scientist discovered how to make semi-synthetic insulin that was easily made and could be readily available. Once recombinant DNA technology was made in the late 1980s, scientists began producing mostly biosynthetic insulin which was a major step towards creating the insulin of today. All attempts to give insulin in forms other than injection have failed due to the insulin being destroyed before it can be effective in the body. Scientists were able to give diabetic patients a way to live; however, insulin was only short acting and had to be taken multiple times per day. Finally in 2000, the technology to make insulin glargine was developed, and insulin glargine became the first long-acting form of insulin approved for use in 2000.

# data[].attributes.body
MW: 230.093 g/mole
Heterocycle: Imidazole
Functional groups: aromatic hydrocarbon, secondary amine

Indication

Clonidine’s main indication is for hypertension, or high blood pressure. Combination therapy is common with this drug in hypertension. However, Clonidine can have many other uses. Extended-release tablets of Clonidine can be used alone or in combination with other drugs to treat attention deficit hyperactivity disorder in children through affecting the areas in the brain that play a part in attention span. This drug can also be used for severe menstrual cramps and other pain conditions, Tourette’s syndrome, menopausal symptoms such as hot flashes, and as a smoking-cessation aid. It can also be used as a mild sedative for various anxiety, stress, and sleep disorders.

Target and Mechanism of Action

Clonidine is an alpha-adrenergic agonist, meaning it binds to and stimulates alpha adrenergic receptors in the brain. This binding reduces the amount of norepinephrine released to the sympathetic nervous system. The reduction of this hormone results in a decreased heart rate, relaxed blood vessels, and decreased peripheral vascular resistance. Thus, a decrease in blood pressure is achieved. The mechanism of action is also why clonidine can be used for anxiety and sleep disorders due to the decreased stimulation of the sympathetic nervous system. The same mechanism of action also achieves successful therapeutic effect in attention deficit hyperactivity disorder.

Side effects

Dry mouth, constipation, headache, dizziness, weakness, and upset stomach are among the most common side effects of this drug. Hypotension can occur due to the drug’s mechanism of action to lower blood pressure. Clonidine also has risks for skin irritations along with other symptoms of an allergic reaction, such as rashes, hives, itchiness, wheezing, tightness in the chest or throat, and swelling of the mouth, face, tongue, or throat. Clonidine should not be discontinued abruptly, or serious sudden acute hypertension can occur. Therefore, clonidine therapy is tapered down when being discontinued.

History

Clonidine was first introduced in 1966. In the early 1960s, Boehringer Ingelheim, a pharmaceutical company, originally planned to synthesize an adrenergic compound for nasal congestion. And although this effect was achieved during discovery, its other effects proved to be much more significant. After drug administration to a secretary, she experienced hypotension, bradycardia, dryness of the mouth, and even fell asleep for 24 hours. After the discovery of these effects, the drug was then pursued as an antihypertensive rather than a nasal decongestant and was soon introduced to the clinical scene.

# data[].attributes.body
My assigned drug was lisinopril. Lisinopril is also known as Qbrelis, Prinivil, and Zestril.  This drug is an angiotensin converting enzyme inhibitor or ACEI for short. Lisinopril has a molecular weight of 405.488 g/mol. This is a drug that contains no heterocycles. The structure includes the functional groups amid, carboxylic acid, and amino groups. It is used to treat hypertension, heart failure, and myocardial infarction.  Lisinopril works by inhibiting angiotensin converting enzymes and the renin angiotensin aldosterone system. This inhibition prevents angiotensin I from converting into angiotensin II, a vasoconstrictor. This inhibition also leads to increased serum renin activity. Lisinopril is an ACE inhibitor that blocks angiotensin I from converting to angiotensin II. Angiotensin is a substance that constricts arteries preventing the even flow of blood out of the heart to our tissues and organs in the body. When angiotensin is unable to work due to the ACE inhibitors, blood vessels relax and blood flows normally through the arteries. Lisinopril discovery goes back to the discovery of ACE inhibitors in the 1960s.  Discovery came from snake venom. It was discovered that a substance in the snake venom inhibits the activity of ACE. The problem originally was that the  substance was not orally active so while there were beneficial effects, the drug could not be taken.  There was then a search for synthetic ACE inhibitors that could be taken orally.  When those were found that further led to the discovery of ACE inhibiting drugs such as lisinopril. Lisinopril was patented in 1978 and was not approved for medical use in the United States until nine years later in 1987. The drug was derived from captopril and enalapril but is structurally modified to to be a long lasting drug.  Lisinopril was created at Merck by scientists who altered the blocks of the active form of enalapril.  These scientists found that the long lasting effects came from the addition of an amino acid and lysine to one end of the drug. The name of the drug, lisinopril, comes from “lysine”. Lisinopril has a wide therapeutic range with recommended doses ranging from 10 to 80 milligrams. The recommended dose depends on the medical condition it is treating as well as the individual who is taking the drug. Lisinopril is not recommended for those who are pregnant or have ever had angioedema. Lisinopril is known to cause a wide array of side effects.

# data[].attributes.body
My assigned drug was Divalproex Sodium. Its molecular weight is 310.4 grams per mole, and it includes a valproic acid heterocycle. The brand names for this drug in the United States include Depakote, Depakote ER, Depakote DR, and Depakote Sprinkles. Divalproex Sodium is an anticonvulsant that treats certain types of seizures caused by epilepsy. It also treats migraine headaches and the manic phase of bipolar disorder. The dosage form of this drug is tablets, and it comes in three different strengths of 125mg, 250mg, and 500mg. Divalproex Sodium should be taken orally and should never be chewed or crushed. Depending on what issue the drug is treating will determine the dosage taken. For example, the starting dose for manic patients is 750mg daily while those who suffer from migraines should start out taking 250mg twice daily. In most cases though, Divalproex Sodium is dosed according to body weight. Some of the warnings and precautions include hepatoxicity, pancreatitis, suicidal behavior or ideation, thrombocytopenia, hyperammonemia and hyperammonemic encephalopathy, hyperthermia, multi-organ hypersensitivity reaction, and somnolence in elderly patients. Stevens-Johnson syndrome is also associated with taking Divalproex Sodium. Though this condition is rare, it is a very serious disorder that leads to a painful rash and blistering. While taking this drug can cause fetal harm, pregnant women are not advised completely against taking this medication if it is essential to the treatment of her medical condition. Women who are planning to become pregnant should be counseled on the risks and benefits of continuing Divalproex Sodium during pregnancy, and other options should be considered. There is evidence that suggests adding folic acid supplements to a daily regimen before pregnancy and during the first trimester could decrease the adverse effect of congenital neural tube defects in the fetus. In the GI tract, this drug dissociates to the valproate ion. Although the mechanism of action is unknown, it is suspected to then bind to and inhibit GABA transaminase. Its anticonvulsant properties are seemed to be exercised by increasing the brain concentration of GABA and prohibiting enzymes that catabolize or block reuptake of GABA into nerve endings and glial cells while also increasing sodium channel inhibition. Recently, studies have shown that valproic acid has shown to be an HDAC inhibitor, particularly an HDAC1 inhibitor. Histone deacetylase inhibition can potentially upregulate the expression of certain genes responsible for regulating antitumor action and apoptosis. These findings could potentially give Divalproex another usage.

# data[].attributes.body
Rosuvastatin is an HMG-CoA reductase inhibitor used to lower lipid levels and reduce the risk of cardiovascular disease including myocardial infarction and stroke.

Indication of Rosuvastatin is a statin medication used as a lipid-lowering agent. The FDA-approved indications are homozygous familial hypercholesterolemia, hyperlipidemia, mixed dyslipidemia, primary dysbetalipoproteinemia, hypertriglyceridemia, and prevention of cardiovascular disease.

Target interaction of the drug acts primarily in the liver, where decreased hepatic cholesterol concentrations stimulate the upregulation of hepatic low-density lipoprotein (LDL) receptors which increase hepatic uptake of LDL. Rosuvastatin also inhibits hepatic synthesis of very-low-density lipoprotein (VLDL). The overall effect is a decrease in plasma LDL and VLDL.

Mechanism of action of the statin medication. It is a competitive inhibitor of the enzyme HMG-CoA (3-hydroxy-3-methylglutaryl coenzyme A) reductase, which catalyzes the conversion of HMG-CoA to mevalonate, an early rate-limiting step in cholesterol biosynthesis.

History of the statin. Rosuvastatin was patented in 1991 and approved for medical use in the United States in 2003. It is available as a generic medication In 2019, it was the 21st most commonly prescribed medication in the United States, with more than 27 million prescriptions.

Side effects of the drug may include myalgia, constipation, asthenia, abdominal pain, and nausea. Other possible side effects include myotoxicity (myopathy, myositis, rhabdomyolysis) and hepatotoxicity. To avoid toxicity in Asian patients, lower doses should be considered. Pharmacokinetic studies show an approximately two-fold increase in peak plasma concentration and AUC in Asian patients. Cases of myopathy and rhabdomyolysis with acute renal failure secondary to myoglobinuria have been reported with HMG-CoA reductase inhibitors, including rosuvastatin. These risks can occur at any dose level but are increased at the highest dose (40 mg). Rosuvastatin should be prescribed with caution in patients with predisposing factors for myopathy (e.g., age ≥ 65 years, inadequately treated hypothyroidism, renal impairment).

Rosuvastatin is also a unique member of the class of statins due to its high hydrophilicity which increases hepatic uptake at the site of action, low bioavailability, and minimal metabolism via the Cytochrome P450 system. This last point results in less risk of drug-drug interactions compared to atorvastatin, lovastatin, and simvastatin, which are all extensively metabolized by Cytochrome P450 (CYP) 3A4, an enzyme involved in the metabolism of many commonly used drugs. Drugs such as ciclosporin, gemfibrozil, and some antiretrovirals are more likely to interact with this statin through antagonism of OATP1B1 organic anion transporter protein 1B1-mediated hepatic uptake of rosuvastatin.

# data[].attributes.body
This drug is typically used to prevent osteoporosis in menopausal women. It can also be used in combination with cholecalciferol to increase bone mass in men with osteoporosis. Osteoporosis causes bones to become weak and brittle, and as osteoporosis progresses it can permanently alter or threaten one’s life. Alendronate Sodium is a drug that helps prevent osteoporosis and it can often be used in conjunction with cholecalciferol for better effects.This drug was developed in 1970 while searching for inhibitors of calcification. They eventually discovered It is a potent inhibitor of bone reabsorption and obtained a patent in order to use it for osteoporosis. The drug alendronate sodium belongs to a class of drugs called biphosphonates. It is often recommended that you do not take this drug at bedtime or in the morning because it might not be fully absorbed, which would make the drug less efficacious. Alendronate targets a bone mineral called hydroxyapatite. This drug can also be used in conjunction with hormone replacement therapy for post menopausal women. This inhibits bone reabsorption.Bone reabsorption relates alendronic acid which is taken into osteoclasts by endocytosis. The endocytosed vesicles are acidified and alendrotnic acid is released into the cytosol of osteoclasts where apoptosis. Inhibition of osteoclasts results in decreased bone reabsorption. Though there are not many side affects 3% of patients taking alendronate sodium report having abdominal pain, acid regurgitation, constipation, diarrhea, dyspepsia, musculoskeletal pain, and nausea.  You should take this medication as least 30 minutes before consuming any food, and you should avoid lying down for 30 minute after taking it. It can also be administered as a weekly dose or daily dose which is nice in order to get better patient compliance. This drug can cause renal impairment and should not be taken if the patient has a previous history of renal impairment or complications. Severe side effects can include esophageal complications. This drug is not indicated for children because studies show that it was not effective. It is only orally administered and usually does not have another form of administration. Overall, it selectively inhibits osteoclast-mediated bone reabsorption in a dose dependent manner, and it increases bone mineral density. It is inactive when in the bone matrix, and it requires continuous administration.

# data[].attributes.body
Alprazolam, more commonly known as Xanax, is used to alleviate anxiety and panic attacks in patients. It is classified as a benzodiazepine, which means it acts on the central nervous system. More specifically, Alprazolam binds γ-aminobutyric acid (GABA) type-A receptors (GABAARs) to enhance their inhibitory effect on neurotransmission, especially in the brain. The goal of alprazolam is to increase the frequency of chloride channel influx, which hyperpolarizes the GABA receptor, resulting in increased inhibitory postsynaptic potential and a relaxing effect for the patient.

According to goodtherapy.org, Dr. Leo Sternbach is credited with the discovery of benzodiazepines. Alprazolam was first released by Upjohn Laboratories (which is now a part of Pfizer) in 1981, as the first approved drug for panic attacks. It’s name grew in popularity for the treatment of other conditions similar to panic attacks. Now, this medication is one of the most prescribed benzodiazepines in America.

This medication is very beneficial when used appropriately. Oftentimes, however, this medication is susceptible to abuse. Some people inappropriately use this medication for recreational use as opposed to their intended use. Alprazolam has a history of causing dependency in patients that misuse the medication. It can also potentially cause patients to have withdrawal symptoms, which is why the medication dosage is slowly decreased over time rather than immediately stopped.

This benzodiazepine is approved for use in patients with anxiety and panic attack disorders. While it is a great choice to help combat these intense feelings of panic, it does come with some potential side effects to the patient. One of the most frequently noted side effects of this medication is drowsiness. More than 41% of people that take this medication experience some form of drowsiness as a side effect. Another significant effect of the medication is imparied coordination, greater than 40-50% of patients experience this. Other effects that occur to 30-50% of patients are symptoms like increased appetite, fatigue, irritability, memory impairment and decreased salivation. Although these symptoms seem like a lot when read to a patient, oftentimes they are not very severe. If these symptoms become life threatening or feel as if they are too much to handle, the patient should stop taking the medication and notify their health care provider.

Alprazolam is a miracle worker for many patients that are facing the feelings of anxiety. It also appeals to any patient suffering from panic disorders. After years of research, this miracle drug hit the market and helped to alleviate many of these feelings that patients have. In fact, this medication was prescribed to nearly 21 million people in the year 2018. This shows how drastically the medication changes patients’ lives.