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Hydroxyzine was discovered in 1956 by Union Chimique Belge and it was approved for sale by Pfizer in the United States later that year. Hydroxyzine is also commonly known as Atarax and Vistaril. It can be taken as an oral capsule, oral suspension, or injectable product. This drug is known as a first-generation antihistamine of diphenylmethane and piperazine classes. In fact, hydroxyzine acts via its major main metabolite, cetirizine, available by oxidation of the primary alcohol to a carboxylic acid. As far as indications go, Hydroxyzine is a symptomatic relief of anxiety and tension associated with psychoneuroses, and as an adjunct in organic disease states in which anxiety is manifested. Also, it's indicated in the treatment of histamine-mediated pruritus and pruritis due to allergic conditions such as chronic urticaria. I learned that the target for Hydroxyzine is anxiety without serotonin reuptake inhibition and without effect of GABA. The mechanism of action for Hydroxyzine is an H1 histamine receptor that is responsible for mediating hypersensitivity and allergic reactions. It's an inverse agonist so rather than blocking activity at a receptor, they actively dampen its activity. The histamine receptor is responsible for symptoms such as pruritus, rhinorrhea, and watery eyes. There are also more side effects including chest pain (discomfort and tightness), irregular or slow heart rate, hives (itching and skin rash), difficulty swallowing, fast heartbeat,  puffiness or swelling of the eyelids or around the eyes, face, lips, or tongue, and trouble breathing. With this drug, alcohol and grapefruit products must be avoided! The functional groups for Hydroxyzine include an N-alkylpiperazine which is a piperzine and nitrogen atoms that are substituted by 2-(2-hydroxyethoxy) ethyl and (4-chlorophenyl)(phenyl) which are methyl groups. As far as heterocycles, there is 1 piperazine ring. The role of Hydroxyzine is to help control anxiety and tension caused by nervous and emotional conditions. It also helps in producing sleep before surgery and relieves symptoms due to the amino acid histamine. Aside from the facts we had to enter into padlet, I learned some fun facts about Hydroxyzine that I didn't know before starting this project. I learned that when you take Hydroxyzine with another medication, Hydroxyzine's effect can be diminished as well as how long it works for. There are some medications that may affect Hydroxyzine which include Alzheimer's disease medication, anticholinergics, antipsychotics, nervous system depressants, pain relievers, and medications that induce drowsiness. Overall, this was a cool drug to learn about especially because I experience high volumes of anxiety so I know there is an option out there if needed.

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I was assigned the drug Losartan for this semester of BMS’s padlet activity. Through this semester long activity, I was able to learn so much about this drug and how it affects the human body. Since hypertension is a very prominent disease in the United States, this drug plays a huge part in trying to get patient’s hypertension under control. Losartan was discovered in 1986 by DuPont scientists. It went on the market in 1995 under the name Cozaar, and became a generic drug in 2009. Losartan is used to treat hypertension in adults. The structure of Losartan contains the following functional group: primary alcohol, benzene ring, and halogenated compound. It also contains imidazole and tetrazole heterocycles. Losartan was a first in class angiotensin 2 antagonist. This drug helped pave the way for many hypertension drugs that are now used every day all over the country. Losartan, like many other hypertension drugs, is an angiotensin 2 competitive antagonist. Losartan blocks the vasoconstrictor and aldosterone secreting effects of angiotensin 2. Losartan can also be used to protect kidney function in patients with diabetes who have protein loss. Finally, it can also be used to lower the risk of stroke in people who suffer from high blood pressure and a heart problem called left ventricular hypertrophy. Bioavailability is the most important factor when determining if a drug is successful or not. Losartan passes all of Lipinski’s rules which makes it available as an oral drug. Losartan’s bioavailability is around 33 percent and about 14 percent is actually converted to an active metabolite. Losartan is a prodrug that gets metabolized by CYP3A4 and CYP2C9 into EXP3174 which is the active compound. Losartan comes in three different strengths: 25mg, 50 mg, and 100mg. The usual starting dose for adults is 25mg by mouth once a day. Losartan only comes in tablet form but can be crushed and mixed with water to make an oral solution for patients that struggle taking tablets. The ratio of this mixture must be 1:1. A person should not take losartan is they are pregnant or are planning to get pregnant. Losartan can cause harm or death to the fetus. Overall, losartan was a groundbreaking drug for treating people with hypertension. It is not used as much today compared to the second-class drugs that we now have because of how influential losartan was. It has been replaced by drugs such as irbesartan.

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For this semester of BMS and the ALE component part of the course, I was assigned Tiotropium as my drug. Throughout the process of completing these ALEs, I have loved learning about this drug and what all it entails. Tiotropium, brand name being Spiriva, is an anticholinergic, long-acting agent that works by competitively and reversibly inhibiting the action of acetylcholine. This blocking action occurs at muscarinic (M3) receptors in the bronchial smooth muscle that, in turn, causes bronchodilation. It also acts on M1 and M2 receptors. It dissociates slowly from M1 and M3, while dissociating fast from M2 receptors. Since it is an anticholinergic agent, it provides long term blocking of neural bronchoconstriction in airways, providing only bronchodilation. Tiotropium is indicated for the use in Chronic Obstructive Pulmonary Disease (COPD) and asthma in both children and adults. Due to its role in competitive inhibition, it is a competitive antagonist on the muscarinic receptors. Tiotropium was first discovered and developed by Boehringer Ingelheim in 1989. It was then FDA approved in January of 2004 and has since been one of the best products sold for COPD. In fact, it is the only long-acting anticholinergic agent that is available for use. It started out as an inhalation powder that was given through a dry-powder inhaler. It then became available as an inhalation spray. Due to it being a long-acting agent, it is a much more effective treatment that maintains the appropriate response the longer you use it. As of today, the only dosage form of Tiotropium available is oral inhalation. Common side effects of Tiotropium include acting on the GI tract, neurologic effects, renal, and respiratory effects. Constipation and xerostomia occur in the GI tract, a headache could occur, UTIs can be a common factor within the renal system, and for respiratory, bronchitis, a cough, pharyngitis, sinusitis, and an upper respiratory infection could occur. More of the serious side effects include bowel obstruction, a hypersensitivity reaction, an angle-closure glaucoma can occur, urinary retention, and paradoxical bronchospasm could possibly happen. Like I said, these are the more serious side effects and are highly unlikely to occur, but keep watch on anything that occurs that is abnormal and call your doctor immediately if the effects get worse. There is currently no black box warning for Tiotropium and the only contraindication that is associated with this drug is hypersensitivity, which is if you are allergic to any component within the drug. There are no drug-food interactions and some of the major drug-drug interactions include pramlintide, potassium citrate, methacholine, and scopolamine. As for educating a patient on this drug, I would instruct them to take a missed dose as soon as they think about it, but if it is the next day, skip it and get back on track with your next one. You want to store Tiotropium in a dry environment, room temperature, not in the bathroom, don’t freeze it, and throw the inhaler away three months after first using it or if the inhaler locks. Throughout this semester, it has been fun getting to learn about a new drug that I had never heard of before. I was not familiar with any of the information I found through looking up Tiotropium and what its indication was, its effects on the body, its role against targets or the mechanism of action. By doing this activity, I really look forward to learning more about all the other drugs that are out there and diving deep into knowing all the details that each one entails.

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Oseltamivir (Tamiflu) is a prescription drug that was discovered and patented in 1996 by Gilead Sciences. Tamiflu, as indicated in its name, is used to treat the seasonal inFLUenza A and B. It comes in an oral suspension form and a capsule form. Both of these forms should be stored at 25 degrees Celsius or 77 degrees Fahrenheit. It can also be mechanically vented into patients via naso or -orogastric tubes. If you have an altered kidney function, hemodialysis, peritoneal dialysis, CRRT, and PIRRT, there are dosage adjustments to be made. In 1999,  the US Food and Drug Administration approved it for sale. Oseltamivir's mechanism of action works by inhibiting the neuraminidase that the influenza virus uses to spread its progeny. Essentially, it is a neuraminidase inhibitor prodrug. The actual structure of Oseltamivir contains a pyrazole, indole, imidazole, thiazole, pyridine, and a quinaxoline. It contains many side effects which make it not the best option anymore for treating influenza. These side effects include diarrhea, nausea, vomiting, headache, confusion, behavioral changes, trouble speaking, tremors, seizures, sensing things that are not there, and Stevens-Johnson Syndrome. This is a limited list of all the side effects but it makes you wonder if there is a better option. Also, oseltamivir's byproducts can cross the placenta. This being said, however, does not harm the baby. Many studies show that oral use of oseltamivir has no effect on the mother or the child. For oseltamivir's pharmacokinetics, it breaks down into its active metabolite called oseltamivir carboxylate. It is orally available with a bioavailability of 75 percent. The half life of oseltamivir is one to three hours whereas its active metabolite is six to ten hours. After oseltamivir is degraded down and used by our bodies, it is excreted mostly in our urine (99%). After learning all about oseltamivir, I wondered if this class was the best at what it does. From my research, however, oseltamivir is a first-line drug in treating the influenza and chemoprophylaxis. This does not mean it does not have better substitutes though. For example, Xofluza is an alternative one can take for the flu. If you are not very young or pregnant, this would be the preferred drug due to its smaller chance of side effects. In some small studies, Xofluza actually proved to help people with influenza in a shorter timespan than Tamiflu did. I thoroughly enjoyed learning about the history of oseltamivir. I found it to be very interesting since it was one of the first breakthroughs for the influenza at its time. Not to mention, the flu season is coming up. This research gave me my go-to drug for if I ever caught the flu.

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Montelukast, under the trade name of Singulair, was discovered by Merck and gained FDA approved  on February 20, 1998. During the drug development process, Merck ran two parallel experiments with one targeting 5-lipooxygenase and the other targeting the leukotriene D4 receptor. Along the course of 10 years, there were many lead compounds that failed. 6 compounds made it to clinical trials, and ultimately, Singulair was the winner. It is currently indicated for the prophylaxis of asthma (including exercise-induced asthma) as well as perennial and seasonal allergic rhinitis. Montelukast produces its therapeutic effects by acting as a leukotriene receptor antagonist. It selectively antagonists cysteinyl leukotriene type-1 receptors found in the respiratory tract. Leukotriene type-1 receptors are responsible for airway edema resulting from contraction, and Singulair actively blocks this smooth muscle contraction to allow free airflow. Although not FDA approved, montelukast may also be used for atopic dermatitis and obstructive sleep apnea. The only contraindication associated with Singulair is hypersensitivity. A precaution that should be taken into consideration before taking montelukast is concomitant use with aspirin or NSAIDs in aspirin sensitive patients. The most common side effects that patients experience while taking Singulair are gastrointestinal problems (abdominal pain and diarrhea), headache, otitis, nasal discharge, cough, and fever. Some serious side effects that may occur include eosinophilic granulomatosis with polyangiitis, disorientation, hallucinations, irritability, anxiety/depression, and aggressive behavior. There is a black box warning associated with montelukast for serious neuropsychiatric events. If patients do experience these neuropsychiatric events such as suicidal thinking and/or behavior, the medication should be discontinued immediately and the prescriber should be contacted. Currently in the US, Singulair is available in 3 oral dosage forms: packet, tablet, and chewable tablet. The distinguishing factor between the 3 dosage forms is that the chewable tablet contains phenylalanine. This medication can be taken with or without food, and the medication should be taken regularly even the patient is not experiencing any symptoms. In the event of a missed dose, the patient should skip the dose and take it at the next instructed time.  There are no recommended dosage adjustments for renal failure, hepatic insufficiency, or geriatric patients. There are 3 significant drug interactions associated with Montelukast. Gemfibrozil may increase serum concentration of montelukast. Lumacaftor and Ivacaftor may decrease the serum concentration of montelukast. Co-administration of montelukast and Loxapine may increase the risk of toxic effects associated with Loxapine. I have frequently dispensed this drug during my time as a pharmacy technician, and I have enjoyed gaining a better understanding of montelukast this semester!

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Duloxetine was approved for patient use in 2004, although it was discovered in 1993 by Eli Lilly. Another commonly known name for Duloxetine is Cymbalta. It is a very useful drug when treating the symptoms of major depression disorder, anxiety, fibromyalgia, and is commonly used to treat diabetic neuropathy. This drug contains the functional groups of naphthalene, ether, and secondary amine; it also contains a thiophene heterocycle in its structure. Duloxetine is an inhibitor of serotonin and norepinephrine reuptake and is a less active inhibitor of dopamine. Which is also commonly referred to as an SNRI inhibitor. Some common side effects that can become apparent with cymbalta are: dizziness, dry mouth, nausea, constipation, and difficulties sleeping. There are other more serious side effects such as: excessive swelling or bleeding, intense itching, yellow tinted eyes, and loss of appetite. If experiencing these signs, the patient should immediately call their prescribing physician. It might take patients 4-8 weeks to see changes in their everyday life. The role of duloxetine interaction with the target is it is an corticotropin releasing hormone receptor-1 antagonist. This receptor is responsible for responses in a behavioral aspect. When accidentally skipping a dose of this medication, you can either take it as soon as you remember, or if it is closer to the time of the next dose, wait and take it like normal. Drugs that should be avoided when taking Duloxetine are: MOAIs (monoamine oxidase inhibitors) such as Parnate and Nardil. Another contraindication of Duloxetine is having a hypersensitivity to Duloxetine. This can result in renal impairment and hepatic impairment. The warnings and precautions while taking this drug include CNS depression, Hyperglycemia, orthostatic hypotension. This drug can also increase alcohol intoxication. Duloxetine is usually taken by mouth and is usually prescribed as 20 mg, 30 mg, 40 mg, or 60 mg once or twice daily. You can take this medication with or without food. It is important not to crush or chew the capsule and to take it whole. Duloxetine is often metabolized in the liver by CYP2D6 and CYP1A2. The half life of this drug is 9.2-19.1 hours. The time that duloxetine reaches its peak effect is within 5-6 hours after taking the drug by mouth. Around 70% of Duloxetine is excreted in the urine and around 20% is excreted in the feces. If the patient is a smoker, Duloxetine’s bioavailability is decreased to around 33%. I have enjoyed being able to learn more about this drug and how it affects the body!

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Propranolol was discovered by Sir James Black and was approved by the FDA for use in 1964. Sir Black first came upon pronethalol as a precursor to propranolol, but propranolol became preferred because it showed a higher potency and less side effects than its predecessor pronethalol. Hemangeol is the brand name for propranolol, and its pharmacologic category is antihypertensive beta-blocker. It is indicated for use in numerous situations such as hypertension, atrial fibrillation/flutter, migraine prevention, ventricular arrhythmias, supraventricular tachycardia, myocardial infarction, antipsychotic-induced akathisia, chronic stable angina, essential tremor, performance anxiety disorder, pheochromocytoma, postural orthostatic tachycardia syndrome, thyroid storm, thyrotoxicosis, lithium-induced moderate to severe tremor, and variceal hemorrhage prophylaxis. As a nonselective beta-adrenergic blocker, it blocks both beta-1 and beta-2 receptors. This leads to a decrease in heart rate which also decreases blood pressure. Propranolol is specifically an antagonist to the beta adrenergic receptors which means it blocks the receptors ability to turn on. The majority of propranolol is metabolized by both CYP2D6 and CYP1A2. The functional groups found in the propranolol structure are alkane, ether, naphthalene, secondary alcohol, secondary amine, and there are no heterocycles. Propranolol is also orally bioavailable, about 25% reaches systemic circulation, or can be administered by IV which has a pH of 2.8 to 3.5. It has 6 rotatable bonds, 3 hydrogen bond acceptors, 2 hydrogen bond donors, a molecular weight of 259 g/mol, and a LogP of 3.12. Contraindications include hypersensitivity to propranolol or beta blockers, as well as uncompensated heart failure, cardiogenic shock, severe sinus bradycardia, sick sinus syndrome, heart block greater than first-degree, and bronchial asthma. Pregnant women should not use propranolol to treat migraine headaches, and mothers that are breastfeeding should also take caution while using propranolol because it has been shown to be present in breast milk and decrease an infant's heart rate as well. Common side effects of propranolol include feeling dizzy, sleepy, tired, or weak, upset stomach or throwing up, stomach pain or cramps, diarrhea or constipation, trouble sleeping, and strange or odd dreams. More serious adverse effects include bradyarrhythmias, bronchospasm, CNS effects, potentiation/masking of hypoglycemia, and withdrawal. Immediate release tablets should be taken on an empty stomach, but extended release tablets can be taken with or without food. After taking propranolol, the drug’s absorption is rapid and complete. It may take a few days to weeks after starting therapy to see changes in blood pressure and decrease hypertension.

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Ergocalciferol, also known as Vitamin D2, was first described in 1936. It is typically seen as a green capsule in oral form of dosing. It is used to treat and prevent Vitamin D deficiencies. It can also be used to treat hypoparathyroidism, rickets, and low blood calcium. It can be administered orally as a tablet or injected into muscle. It is available as an over the counter medication in the United States. It is currently in the top 50 most commonly prescribed medications in the United States. It is also on the World Health Organization’s list of essential medicines. Ergocalciferol utilizes UV light to break a steroid bond photochemically. Alone, Ergocalciferol is inactive, but through hydroxylations in the liver then the kidney is activated. Ergocalciferol and its metabolites have lower binding affinity to vitamin D-binding protein. Ergocalciferol can be sourced from multiple origins including Vitamin D is found in egg yolks, fatty fish, fortified milk, fortified cereal, and infant formulas. It is also found in the wild in fungus, lichens, and plantae are some of the main sources for vitamin D2. Mushrooms grown in sunlight are found to have higher levels of vitamin D2 due to the UV exposure. Ergocalciferol is also known as Viosterol. Be careful when taking calciferol not to confuse it with calcifediol or calcitriol as they sound similar. Similarly, Ergocalciferol sounds like alfacalcidol or cholecalciferol which are different drugs. Initially, 20 to 25 mcg PO once daily. May increase dose to a maximum of 50 mcg PO once daily to maintain a serum vitamin D concentration of at least 30 ng/mL. Some of the most common side effects found in taking Ergocalciferol are feeling tired, difficulty thinking clearly, loss of appetite, nausea, vomiting, constipation, increased thirst, increased urination, or weight loss, drowsiness, muscle aches and stiffness. The half life is around 2-3 weeks and onset is 10-24 hours. There are no indicated dosage adjustments for renal impairment or hepatic impairment in pediatric patients. Overall this was an interesting drug to learn about this semester. We have mentioned it in class multiple times and I knew questions regarding vitamin D2 being ergocalciferol. I would not have known that without this being my assigned drug for the semester. No person I personally know is prescribed this medication for deficiencies in vitamin D2. I have enjoyed furthering my knowledge in this drug and seeing how it is used and benefits the public.

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Trazodone is a prescription drug that was discovered in Italy in the 1960s by Angelini Research Institute, but it was not approved by the FDA for use until December 24, 1981. Early on, trazodone was not used often because it had many side effects, but it was later found to be beneficial when given in smaller doses. Trazodone is the generic name of the drug, and brand names include Desyrel, Desyrel Dividose, and Oleptro. Although, the brand name Oleptro has been discontinued in the United States for more than a year. Trazodone is primarily indicated to treat unipolar major depressive disorder (MDD), however, a non-FDA approved use for trazodone is insomnia. Trazodone is a Serotonin Reuptake Inhibitor/Antagonist antidepressant drug. These types of drugs work by blocking the reabsorption of serotonin neurotransmitters, causing more available serotonin in the brain to be transmitted. The targets of this action are 5-HT-2A/2C serotonin receptors, sodium-dependent serotonin transporters, and histamine H1 receptors. Trazodone is in a class of antidepressants known as triazolopyridine, due to its structure which consists of a triazole ring connected to a pyridine ring. Concerning the pharmacokinetics of trazodone, its oral bioavailability is 65 percent and its absorption is affected by food. The volume distribution of trazodone is 0.47 to 0.84 liters per kilogram and its protein binding percentage is 89 percent to 95 percent. The metabolism of trazodone occurs extensively through CYP3A4, and its active metabolite is m-chlorophenylpiperazine (mCPP). The total clearance of trazodone is 5.3 liters per hour. The elimination half life of the immediate release tablets is 7 hours, and the elimination half life of the extended release tablets is 10 hours. Trazodone has a Black Box Warning for the risk of increased suicidal thoughts and behaviors, especially in young adults and adolescents, and it is not approved to be used in pediatric populations. Trazodone’s only available dosage form is oral, and it is available in immediate release tablets and extended release tablets. Each of these should be taken differently. The immediate release tablets should be taken with food, while the extended release tablets should be taken on an empty stomach due to the absorption of each type of tablet.  Trazodone has several side effects, but the most common adverse reactions that can occur due to trazodone consist of nausea and vomiting, xerostomia, dizziness, drowsiness, fatigue, headache, nervousness, and blurred vision. Overall, learning about trazodone has been interesting, and it will be extremely beneficial to me in the future because it is such a commonly used drug.

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Clopidogrel is a very interesting drug. It was first introduced to the market in 1987 as a racemic mixture of hemisulfate salt. It wasn’t until ten years later that the drug we know today as Clopidogrel was developed. There was a drug that existed before Clopidogrel, ticlopidine that was essentially the original version. Both drugs irreversibly block the ADP P2Y12 receptor and are both indicated in reducing the atherothrombotic events found in patients with cardiovascular diseases. However, the main difference that made Clopidogrel more effective than its counterpart is the more advantageous side effect profile. Ticlopidine showed to induce more severe neutropenia in comparison to Clopidogrel and is also second-in line for failure when paired with aspirin. Clopidogrel can also be indicated for other cardiovascular diseases: prophylaxis for myocardial infarction; percutaneous coronary intervention for thrombosis; prophylaxis for unstable angina; and peripheral arterial occlusive disease for thrombosis. Clopidogrel’s mechanism of action is as an inhibitor of CYP2Y12 adenosine diphosphate platelet receptors. It is also a prodrug so it must be enzymatically metabolized by CYP450 enzymes in order to transition to its active metabolite. This active metabolite will then irreversibly inhibit the binding of ADP to platelet P2Y12 receptor and the subsequent ADP-mediated activation of glycoprotein GPIIb/IIIa complex. This reduces the pooling and collection of platelets at bleeding sites internal or external.  There are also some contraindications to be aware of before one should take this medication. One of the primary ones being the possibility of current or developing hypersensitivity to Clopidogrel. IN this case, patients can undergo anaphylaxis due to exposure to the formulation. Another contraindication would be pathological bleeding, typically leading to peptic ulcers or intracranial hemorrhaging. This is because of the lack of coagulation within the blood. Adverse effects can result from taking this medication. Some different categories to consider would be Gastrointestinal, hepatic, neurologic, and ophthalmic. The first category, gastrointestinal, one would have to be aware of possible gastrointestinal hemorrhaging as well as colitis if taken concomitantly with aspirin. With hepatic, one would have to consider possible liver failure, hepatotoxicity, and hepatitis. With neurologic, one would have to consider the possibility of an epidural hematoma, intracranial hemorrhage and with ophthalmic, one would have to consider the possibility of an intraocular hemorrhage. For all these possible side effects, Clopidogrel has a wealth of good to offer. It can be used for prevention of ischemic events in at risk patients as well as providing a significant help in patients at risk of myocardial infarction.

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My assigned drug is Valganciclovir. Valganciclovir is the prodrug of Ganciclovir, and also an antiviral drug used to treat cytomegalovirus retinitis in autoimmune deficiency diagnosed people. Valganciclovir is a prodrug because it is inactive before metabolism and active after metabolism. Another name for Valganciclovir is Valganciclovir hydrochloride or Valcyte. This drug is most commonly an oral drug taken by mouth. To determine the dose of Valganciclovir for a patient, a physician would take and read the patient's creatinine clearance levels. This drug is found under the brand Valcyte or Genentech, and it was first FDA approved on February 29, 2001. Valganciclovir is also known to be on the World Health Organization’s List of Essential Medicines. In 2017, a generic version of Valganciclovir was approved for the market and the use of people. The functional groups contained in the Valganciclovir structure include ether, primary alcohol, and carbamate, and the heterocycle contained in Valganciclovir structure is a purine more specifically guanine. Valganciclovir targets deoxyribonucleic acid or DNA and is an enzyme inhibitor that inhibits the binding of deoxyguanosine triphosphate to DNA polymerase resulting in inhibition of viral DNA synthesis. This leads to the mechanism of action of Valganciclovier which is rapidly converted to ganciclovir in the body. Ganciclovir is phosphorylated to a substrate which competitively inhibits the binding of deoxyguanosine triphosphate to DNA polymerase resulting in inhibition of viral DNA synthesis. The black boxed warnings of Valganciclovir include hematologic toxicology, fertility impairment, fetal toxicity, mutagenesis, and carcinogenesis. As these black box warnings are serious, the less serious side effects include but are not limited to hypertension, headache, insomnia, diarrhea, nausea, vomiting, abdominal pain, anemia, thrombocytopenia, neutropenia, graft rejection, tremor, retinal detachment, increased serum creatinine, and fever. As a future pharmacist, I will educate the patient on information that is relevant to this drug. Valganciclovir should be taken with food. Valganciclovir should be taken with a lot of non caffeinated drinks. Valganciclovir should not be broken on your skin, eyes, nose, or mouth as it will cause pain or irritation. I will also make aware to the patient that if he/she does miss a dose of Valganciclovir, to go ahead and take it unless it is too close to the next dose. If it is too close to the next dose, I will tell the patient to skip the missed dose and continue with the next dose. In addition, I will tell the patient to store Valganciclovir at room temperature, however, not the bathroom because the bathroom stores a lot of moisture.

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Quetiapine was developed in 1985 by scientists at AstraZeneca (formally Zeneca) Pharmaceuticals. It was later approved for medical use in the United States by the US Food and Drug Administration on September 26, 1997. Quetiapine is also sold under the brand name, Seroquel. Quetiapine's pharmacologic category is antimanic agent, a second-generation antipsychotic. Quetiapine has a U.S. Boxed Warning of increased risk of suicidal thoughts and behavior and increased mortality in elderly patients with dementia-related psychosis. The indication of the drug is bipolar disorder, major depressive disorder, and treatment of schizophrenia. It is primarily used to treat schizophrenia bipolar disorder or depression. The drug targets 5- hydroxytryptamine receptors, dopamine receptors, histamine receptors, and monomine transport subfamily (GPCRs). Quetiapine is a dibenzothiazepine atypical antipsychotic. It has been proposed that this drug's antipsychotic activity is mediated through a combination of dopamine type 2 (D2) and serotonin type 2 (5-HT2) antagonism. It is an antagonist at multiple neurotransmitter receptors in the brain. Quetiapine is primarily metabolized by CYP3A4 to its inactive sulfoxide metabolite.Quetiapine belongs to a group of medicines known as atypical antipsychotics. Atypical means that quetiapine is less likely than older antipsychotics to cause movement-related side effects, and may be more effective in the treatment of symptoms such as lack of motivation and social withdrawal. Quetiapine is normally dosed in an oral form such as a tablet. However, it is offered through a nasogastric/enteral tube. Immediate-release tablets can be administered either with or without food. Administer extended-release tablets without food or following a light meal (less than 300 calories). Swallow extended-release tablets whole, do not crush or chew.

It is a long-term treatment for episodes of mania and disorders and is usually prescribed for at least six months. Quetiapine is stored at room temperature. All drugs cause side effects. Some common side effects that are resulted from taking quetiapine are feeling fatigued, headache, constipation, dry mouth, a gain of appetite, weight gain, upset stomach, stomach pain, back pain, stuffy nose, and feeling nervous and excitable. Some serious effects include depression, high blood sugar, infection like fevers, chills, or sore throat, low thyroid levels, neuroleptic malignant syndrome, seizures, and trouble passing urine. Quetiapine may cause hyperprolactinemia, which may decrease reproductive function in both males and females.  I have attached the drug’s structural group above. Their functional group is alcohol, phenol, and amine. It contains the heterocycle, piperazine. Throughout this semester, I have enjoyed learning about this drug and how it negatively and positively affects the body.

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My assigned drug was Acyclovir. Acyclovir has two brand names which are Sitavig and Zovirax. This drug’s purpose is to treat infections caused by the herpes virus. These infections include shingles, genital herpes, and chickenpox, which are very common in the United States of America. Although Acyclovir can relieve some of the terrible, painful symptoms caused by the herpes virus, it can not cure you from the virus itself. Acyclovir is a prodrug which means it is inactive and does nothing for you until it is metabolized by your body. During metabolism of it, it is phosphorylated by an enzyme called thymidine kinase. This process converts Acyclovir into Acyclovir triphosphate which is capable of entering viral DNA therefore inhibiting its functions. When a patient is prescribed Acyclovir, their dosage is determined by their body weight in order to try to avoid toxicity effects. Acyclovir is usually taken orally with or without food and should be taken at the same time everyday until the prescription is out. Patients with renal failure should be extremely cautious when taking this drug. Prescribers also have the option to prescribe an injection for the treatment of HSV and herpes. Patients should store their Acyclovir prescription in a room temperature location and make sure to keep away from any areas prone to high moisture. There are a couple of contraindications and adverse effects to be cautious of when taking this drug. If a patient has known hypersensitivity to acyclovir, valacyclovir, or any component of the formulation, they should not take this medication. Acyclovir IV is also an irritant, so medical personnel and others should be advised to avoid extravasation. For the treatment of varicella in children, acyclovir should be administered within twenty four hours of the rash developing. This is sometimes difficult because parents don’t always think about varicella being the cause of a rash. In older adults it is less time sensitive. The drug just still be administered as quickly as possible, but they have a bigger window of about seventy two hours. For female patients that are pregnant or breastfeeding, acyclovir can be taken but should be monitored. This drug can cross the placental barrier and is found in breast milk, but is not harmful usually. Adverse effects caused by taking Acyclovir include decreased hemoglobin, decreased neutrophil count, skin rash, diarrhea, headache, increased bilirubin, hypotension and a few others that are not as common. If a patient experiences any of these symptoms or any other side effects they should report them to their doctor immediately.

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Lamotrigine is a drug that was founded by the pharmaceutical drug industry company, GlaxoSmithKline, which is  indicated for bipolar disorder, Lennox-Gastaut syndrome, partial seizures, and tonic clonic seizures that was approved by the Food Drug Administration (FDA) in 1994.  Lamotrigine was just recently in 2010 allowed to be an adjunct for epilepsy. Lamotrigine is most commonly called lamictal. Lamotrigine is an anti seizure agent. There is not a definite known mechanism of action of Lamotrigine. However, research over the last three decades has shown that Lamotrigine is a triazine derivative that inhibits the release of glutamate and voltage sensitive sodium-channels that essentially stabilizes the neuronal membrane. Lamotrigine has a weak inhibitory effect on the protein 5-HT3 receptor. Lamotrigine follows a first order kinetic with a half-life of 29 hours. Lamotrigine is absorbed by the first pass metabolism continuously throughout the gastrointestinal tract and is metabolized by glucuronidation. The major metabolite of Lamotrigine is an inactive 2-N glucuronide conjugate. The clearance of Lamotrigine is affected by the co administration of drugs that induce or inhibit glucuronidation. There is a U.S. Black Box Warning for this drug from causing serious skin rashes such as Steven Johnson’s Syndrome which is caused by the extended release and not the immediate release version. These cases of serious skin rashes occur within the first 8 weeks of the initial start of the drug. There are some less serious side effects such as dizziness, stomach pain, nausea, heartburn, insomnia, and pain in the throat. Some more serious side effects include aspectic meningitis liver failure, and suicidal behavior/tendencies. When patients are pulled off of the medicine it has to be gradual, since there can be an increase in seizure activity and withdrawal symptoms. In those with diagnosed bipolar disorder, there has to be a 50% reduction that must last two weeks. If the therapy has been discontinued for longer than 5 half lives, the dose must be restarted at the initial dosing, not the dose they are currently on.  This medication has many safety issues such as the sound-alike/look-alike and high alert. The drug name lamictal can be confused with labetalol, lamisil, and lomotil. This is a high alert medication, it has an increased risk of causing significant patient self harm when used in error. I have learned from researching this medication over the semester, that this medication has to be distributed and taken very carefully.

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My assigned drug for this semester was Pantoprazole. Pantoprazole was first discovered by a small group of scale up chemists in 1985. The drug discovery program of this drug started in 1980, then producing pantoprazole in 1985.This medication is used to reduce the amount of stomach acid your body makes. It also helps prevent erosive esophagitis or “heartburn”, which is inflammation that damages the tube running from the throat to the stomach. Pantoprazole treats symptoms of gastroesophageal reflux disease, a condition where the acid in the stomach washes back up into the esophagus.This medication may also be used to treat Zollinger-Ellison syndrome, a condition where the stomach produces too much acid. Pantoprazole is available in three different forms which include an oral tablet, an oral liquid suspension, and an intravenous (IV) form that's injected into your vein by a healthcare professional. The tablet form of pantoprazole comes in two different strengths of 20 mg and 40 mg. The oral tablet is available in both generic and brand name drug. The brand name of pantoprazole is called protonix. Alternative forms of the oral tablet include lansoprazole esomeprazole, omeprazole, rabeprazole, and dexlansoprazole. Pantoprazole is a proton pump inhibitor that surpasses gastric acid secretion by inhibiting the parietal cell H+/K+ ATP pump. Proton pumps are the enzymes in the lining of your stomach that help make it easy for acid to digest your food. Pantoprazole prevents proton pumps from working properly, which then reduces the amount of acid the stomach is able to make. The metabolism of pantoprazole occurs in the liver by cytochrome P450. The functional groups present in the structure of pantoprazole include ethers, amines, and sulfoxides. Pantoprazole also consists of heterocyles such as imidazole, pyridine, and indole. Some common side effects of pantoprazole include headaches, diarrhea, stomach pain, nausea, vomiting, dizziness, and joint pain. The more serious side effects of pantoprazole include low magnesium levels which could lead to symptoms such as seizures, tremors, or abnormal fast heart rate. Other serious side effects caused by pantoprazole include nervousness, bone fractures, Cutaneous lupus erythematous, Systemic lupus erythematous, and Vitamin B12 deficiency. Pantoprazole may interact with medications such as HIV drugs, Anticoagulants or cancer drugs. Some of these drugs may include ampicillin, atazanavir, erlotinib, levoketoconazole, nelfinavir, pazopanib, rilpivirine, and certain azole antifungals. Overall, I have really enjoyed learning about pantoprazole this semester and how it effects the body.

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My assigned drug was Omeprazole. Omeprazole has the brand name Prilosec. The main active ingredient in Omeprazole is a substituted benzimidazole.
The indications of Omeprazole is to treat too much acid in the stomach usually associated with acid reflux disorders and also healing and maintenance of erosive esophagitis and symptomatic gastroesophageal reflux diseases, called GERD, and peptic ulcer disease. Omeprazole contains several functional groups, these include amines, ethers, phosphates and oxides. The two herocycles in Omeprazole are Indole and Pyridine. Omeperzole targets CYP2C19 and is a proton pump inhibitor. It works by blocking gastric acid secretion by irreversibly binding to and inhibiting the hydrogen -potassium ATPase pump that resides on the luminal surface of the parietal cell membrane. Omeprazole's mechanism of action works by suppression stomach acid at the secretory surface of gastric paternal cells. Because this enzyme system is regarded as the acid (proton, or H⁺) pump within the gastric mucosa, omeprazole inhibits the final step of acid production. Omeprazole's binding affinity is 97% and has a bioavailabitly of 30 to 40%. It is mainly exerted in the renal tubules and has a total body clearance of 500-600 mL/min.
The half-life of Omeprazole is 30 minutes to one hour.

Omeprazole is safe for patients over 1 year of age.
The standard adult dose is 20-40 mg daily and is usually prescribed for a duration of at least 8 weeks. The standard pediatric dose is 5 mg once daily.
Administration of Omeprazole is orally and is to be administered 30 minutes prior to the first meal of the day.
It is available as an oral tablet, oral capsule, and oral powder and is delayed release.

Contraindiacations include use of any rilpivirine-containing products. Hypersensitivity to substituted benzimidazoles can lead to anaphylaxis and acute interstitial nephritis. Concomitant use includes avoiding use of Omeprazole with Clopidogrel, St. John's wort, or rifampin.

Avoid use of Omeprazole for longer than 8 weeks if you have Beers Critera due to risk of Clostridium difficile infection and bone loss and fractures. Vitamin B12 efficiency may occur with prolonged use such as 1 to 2 years. Hypomagnesemia has been reported in patients who have used for longer than 3 months.

Fetal risk cannot be ruled out regarding if it is safe to take while pregnant, and infant risk cannot be ruled out regarding if it is safe to take while lactating.
Omeprazole has adverse effects that include, rash, abdominal pain, constipation, diarrhea, flatulence, nausea, vomitting, dizziness, headache, upper respiratory infection, and fever.
Omeprazole does not have any Black Box Warnings according to MicroMedex.
Overdose is  rare and only mild toxicity has been reported.
Omeprazole should be stored in a cool, dark place.

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My assigned drug this semester was Levothyroxine. The brand names for Levothyroxine are Synthroid, Levoxyl, and Tirosint. This particular drug is used to treat an underactive thyroid gland. This is also known to be called hypothyroidism. The target interaction of Levothyroxine is the agonist of the alpha and beta thyroid hormone receptors. Levothyroxine also has other indications such as myxedema coma and thyroid stimulating hormone suppression  therapy. Myxedema coma is a severe hypothyroidism attack leading to decreased mental status, hypothermia, and other symptoms related to slowing of function in multiple organs. Thyroid stimulating hormone suppression therapy uses the administration of Levothyroxine (LT4) in order to reduce serum TSH levels below the normal range, maintaining normal levels of serum free T4 (FT4) and free T3 (FT3). Levothyroxine was discovered in the early 20th century. Thyroxine was first isolated in pure form in 1914, at the Mayo Clinic by Edward Calvin Kendall from extracts of hog thyroid glands. The hormone was synthesized in 1927 by British chemists Charles Robert Harington and George Barger. Natural thyroid preparations , which contain both thyroxine (T4) and triiodothyronine (T3), were the first pharmacologic treatments available.

Moreover, Levothyroxine has a unique mechanism of action. According to Fresenius Kabi, “Thyroid hormones exert their physiologic actions through control of DNA transcription and protein synthesis. Triiodothyronine (T3) and levothyroxine (T4) diffuse into the cell nucleus and bind to thyroid receptor proteins attached to DNA. This hormone nuclear receptor complex activates gene transcription and synthesis of messenger RNA and cytoplasmic proteins. The physiological actions of thyroid hormones are produced predominantly by T3, the majority of which (approximately 80%) is derived from T4 by deiodination in peripheral tissues” [1].

Although Levothyroxine works well in what it is intended to do, it does come with side effects just like any drug. These side effects include: weight gain or loss, headache, vomiting, diarrhea, changes in appetite, fever, changes in menstrual cycle, sensitivity to heat, hair loss, joint pain and leg cramps. Overall, Levothyroxine was a great drug to learn about this semester. I am glad the Dr. Le gave us the opportunity to tackle and understand at least one of the many drugs we will have to know about. I look forward to learning more.

[1] Product Information: Levothyroxine sodium intravenous injection, levothyroxine sodium intravenous injection. Fresenius Kabi USA LLC (per FDA), Lake Zurich, IL, 2019.

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Furosemide was discovered in 1959 by a scientist named Karl Sturm and his team.  This prescription drug was released to the public market in 1964 after being approved by the Food and Drug Administration (FDA). Furosemide, which is also known as Furocot and Lasix, is prescribed for the reason of fluid retention and swelling that is caused by congestive heart failure, liver disease, kidney disease, or other medical conditions. Furosemide contains amines, amine salts, carboxylic acids, carboxylic salts, alkyl halides, sulfonamides, and sulfamoyl functional groups and also has a heterocycle that is an oxole.  The indications for Furosemide are edema associated with congestive heart failure, cirrhosis of the liver, renal disease, and nephrotic syndrome commonly found in adults and pediatric patients alike.  Furosemide works by targeting the genes SLC12A1, CA2, and GPR35.  This ultimately leads into Furosemide inhibiting the luminal Na-K-Cl cotransporter.  Furosemide’s mechanism of action consists of promoting diuresis by blocking tubular reabsorption of sodium and chloride in the proximal and distal tubules, as well as in the thick ascending loop of Henle.  Furosemide may cause some slight side effects such as: peeing more than usual, feeling thirsty, dry mouth, headaches and migraines, feeling confused or dizzy, or the feeling of being sick.  Furosemide can potentially be an inappropriate medication for people older than 65 years old because it could cause syndrome of inappropriate antidiuretic hormone secretion.  Therefore older adults should keep an eye on their sodium concentrations when starting Furosemide.  If the prescribed patient has any hypersensitivities toward Furosemide or any of its components then they should stop immediately and contact their doctor.  The side effects of Furosemide are hyperuricemia, which may cause gout but is rare, having a sulfonamide allergy, which could be very severe, and it could cause an increase in free thyroid hormones, which decreases total thyroid hormone levels.  Patients should avoid Furosemide if they have or have had any of these: adrenal insufficiency, bariatric surgery, cirrhosis, or diabetes.  Tablet dosage forms come in 20mg, 40mg, and 80mg.  Furosemide takes anywhere from 30 to 60 minutes to take action in the body.  Symptomatic improvement usually starts within 15 to 20 minutes.  Peak effect for oral is 1 to 2 hours.  Furosemides' effect on the body usually lasts around 6 to 8 hours.  Furosemide primarily binds to the protein albumin at a percentage of 91% to 99%.  It has an oral bioavailability of 47% to 64%.  The half-life of Furosemide is 30 minutes to 2 hours, and in end-stage kidney disease, 9 hours.

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Drug: Finasteride

Finasteride, also known as Propecia or Proscar, is a 5 alpha-reductase inhibitor. Blocking 5 alpha reductase prevents the conversion of testosterone to dihydrotestosterone thus reducing the levels of dihydrotestosterone. Dihydrotestosterone contributes to the growth of the prostate and also causes hair follicle damage leading to hair loss or alopecia. Finasteride can help shrink the prostate and help manage the symptoms of Benign Prostatic Hyperplasia (BPH) or, alternatively, male pattern baldness. Dihydrotestosterone is a much more potent androgen than testosterone. When it comes to dosing, the BPH dose is larger than that for hair loss, 5mg to 1mg. The most commonly reported adverse effect is sexual dysfunction or impedance. It can potentially lower blood pressure as well, usually, this is because it is used in combination with alpha-blockers but there is some potential for the lowering of blood pressure just from finasteride as well. There are risks associated with this drug for young women of childbearing age if they are exposed while possibly handling this drug for patients. Finasteride is teratogenic, classified under category X. This means that studies in animals or humans have demonstrated fetal abnormalities or there is positive evidence of human fetal risk based on adverse reaction data from investigational or marketing experience, and the risks involved in the use of the drug in pregnant women clearly outweigh potential benefits. Something that is important to inform patients of when first giving them finasteride is that it takes the drug a long time to work. It can take months for the drug to take effect irrespective of what the drug is being taken for, either BPH or hair loss. More specifically, for BPH, to see a shrinkage of the prostate the wait will probably be anywhere from 6 to 12 months. In the case of BPH patients who have severe symptoms, an alpha blocker, like tamsulosin, is given in combination with finasteride. Then again with hair loss, there is a long wait of 3 to 6 months before any possible benefits can be seen by the patient. There are a few drug interactions that must be considered when taking finasteride. Anticholinergics can oppose beneficial effects in the management of BPH. Anticholinergics block urine flow which can lead to worsening symptoms like urinary retention. Another class of medications that work against finasteride is decongestants that use alpha agonist activity. They also can restrict urine flow and exacerbate symptoms of BPH.

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My assigned drug was Valacyclovir. The brand name of the Valacyclovir is Valtrex. Valacyclovir (valacyclovir), also known as Valtrex, is an antiviral drug that has been used to manage and treat various herpes infections for more than 2 decades. Valacyclovir was patented in 1987 and came into medical use in 1995. Valacyclovir is the L-valine ester of acyclovir. It is a member of the purine (guanine) nucleoside analog drug class. This class of drugs forms an important part of hepatitis, HIV, and cytomegalovirus drug regimens. One major use of valacyclovir is the treatment of genital herpes episodes or outbreaks. It is caused by infection with the herpes simplex virus (HSV). Infection with this virus is lifelong with periodic episodes of reactivation. The indication of Valacyclovir is a nucleoside analog DNA polymerase inhibitor indicated for Label: Adults, Cold Sores (Herpes Labialis), and Genital Herpes, Treatment of genital herpes lesions in immunocompetent patients (initial or recurrent episode), Suppression of genital herpes lesions in immunocompetent or HIV-infected patients, Reduction of viral transmission, Herpes Zoster. The mechanism of action Valacyclovir is the L-valine ester of acyclovir. It is classified as a nucleoside analog DNA polymerase enzyme inhibitor. Acyclovir is a purine (guanine) nucleoside analog is a metabolite that heavily contributes to the pharmacological actions of valacyclovir. In fact, most of valacyclovir's activity is attributed to acyclovir 1. Valacyclovir is rapidly and almost completely converted in man to acyclovir and valine, likely by the enzyme valacyclovir hydrolase. Acyclovir is a selective inhibitor of the herpes viruses, possessing in vitro activity against herpes simplex viruses (HSV) type 1 and type 2, varicella zoster virus (VZV), cytomegalovirus (CMV), Epstein-Barr Virus (EBV), as well as human herpesvirus 6 (HHV-6). Acyclovir has been shown to inhibit herpes virus DNA synthesis after it has been phosphorylated to the active triphosphate form 10. The first stage of drug phosphorylation for acyclovir requires activation by a virus-specific enzyme. In the case of HSV, VZV and EBV this enzyme is the viral thymidine kinase (TK), which is only found in virus-infected cells. The process of phosphorylation is completed (conversion from mono- to triphosphate) by cellular kinases. Acyclovir triphosphate competitively inhibits the virus DNA polymerase and incorporation of this agent results in DNA chain termination, stopping virus DNA synthesis and blocking virus replication 10. The inhibitory capabilities of acyclovir are highly selective due to the drug's strong affinity for thymidine kinase. Target of the drug is thymidine kinase and DNA polymerase catalytic subunit. Side effects is Headache, Nausea, Vomiting, Loss of strength and energy, abdominal pain, menstrual pain.

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The name of my assigned drug is levetiracetam, and I have learned a lot over the course of the semester about this fascinating anti-seizure medication. The indication of levetiracetam is partial onset seizures. The target interaction is likely one of the following: voltage-dependent N-type calcium channels, GABA-ergic inhibitory transmission, reduction in slow-potassium channels, or synaptic proteins that modulate neurotransmitter release. The exact binding site could be SV2A, a synaptic vesicle protein. The exact mechanism of action of levetiracetam is unknown. Levetiracetam was discovered in 1992 by Alma Gower at UCB, a multinational pharmacy company, while screening audiogenic seizure susceptible mice. Audiogenic meaning the mice had seizures that were caused by sounds. This research found Brivaracetam, which was then selected as one the first clinically effective antiepileptic drugs. Brivaracetam is basically levetiracetam, but without a propane group (3 carbons). Levetiracetam was found to have a specificity to binding to an important molecular target that showed antiseizure/anticonvulsant activity. The audiogenic seizure susceptible mice were found to not have SV2A, a deletion in their genome, leading to more seizures, and less life expectancy for these mice. The S-enantiomer of levetiracetam is 150 fold more potent than the R-enantiomer of levetiracetam. The side effects of levetiracetam are numerous but I will list the some most common: Increase of blood pressure, Vomiting, Infection, Behavioral problems, drowsiness, fatigue, headache, irritability (all from nervous system), Asthenia, and Nasopharyngitis. Asthenia is abnormal physical weakness and a lack of energy. Levetiracetam is available as IV, oral solutions, and tablet dosage forms. The tablet comes in five-hundred and seven-hundred and fifty milligram doses. Levetiracetam is contraindicated in patients that have hypersensitivity to levetiracetam. Levetiracetam has no black box warning. Some of the common names for levetiracetam are Keppra, Spritam, and Roweepra. Levetiracetam should be administered without thought to meals. For administration of the oral solution, the patient should not use a household spoon to measure the dose. If the patient is taking the tablet form, the tablet should be taken whole. The patient should be older than twelve to be prescribed levetiracetam. The usual dose for tablet is five-hundred milligrams twice daily. Levetiracetam should be stored around room temperature at twenty-five degrees Celsius. Levetiracetam is often used in combination with other drugs to prevent seizures. When patients cease using levetiracetam, they are usually slowly withdrawn from levetiracetam to prevent withdrawal related seizures. The most important information for patient counseling on the medication guide is likely that levetiracetam causes suicidal thinking in one out of five-hundred patients. If the patient is suicidal or having bad thoughts they should call their healthcare provider.

sources:
1. Rogawski MA. Brivaracetam: a rational drug discovery success story. Br J Pharmacol. 2008 Aug;154(8):1555-7. doi: 10.1038/bjp.2008.221. Epub 2008 Jun 16. PMID: 18552880; PMCID: PMC2518467.
2.
Levetiracetam's Lexicomp page:
https://online.lexi.com/lco/action/doc/retrieve/docid/patch_f/7162?cesid=0stBr8NCriS&searchUrl=%2Flco%2Faction%2Fsearch%3Fq%3Dlevetiracetam%26t%3Dname%26acs%3Dfalse%26acq%3Dlevetiracetam#
3. Levetiracetam's DailyMed page
https://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=c508a392-0603-477d-8a45-3ec550371111

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Assigned Drug: Spironolactone
After the discovery of aldosterone, scientists recognized that it greatly contributes to disease by causing edema. Therefore, they began to research compounds that would antagonize aldosterone to prevent edema among diseases like heart failure or hypertension. This research led to the discovery of the drug Spironolactone. Spironolactone, also called Aldactone or CaroSpir, was first discovered by Cella and Tweit in 1957 to act as a steroidal aldosterone blocker, and it was later introduced for use in 1959 in the class of potassium-sparing diuretics. It was first reported to be administered parenterally but later reported that the compound improves antagonist activity if administered orally. It is categorized pharmacologically as an antihypertensive, potassium-sparing diuretic and behaves as a mineralocorticoid/aldosterone receptor antagonist. It is primarily indicated for hypertension, but it can be used to treat an abundance of health issues such as heart failure, primary hyperaldosteronism, fluid buildup, and ascites due to cirrhosis. It is a renal competitive aldosterone antagonist that competes for the aldosterone-dependent sodium-potassium exchange site in the distal tubule cells to inhibit the effect of aldosterone. This agonist activity of spironolactone will decrease potassium and hydrogen excretion and increase sodium chloride and water secretion. The effectiveness of spironolactone depends on the level of aldosterone circulating, in which the more circulating aldosterone, the more effective the drug is as a diuretic agent. Spironolactone’s most common significant adverse reactions include gynecomastia and hyperkalemia. Although significant, these two adverse reactions are usually reversible following discontinuation of therapy. Other common adverse reactions include diarrhea, nausea, vomiting, somnolence, disordered menstruation, and erectile dysfunction. Some contraindications occur with this drug such as hyperkalemia, Addison disease, and concomitant use with eplerenone. The warnings and precautions that are potential concerns related to the adverse effects that could come with taking this drug are tumorigenic characteristics and fluid/electrolyte imbalances. This drug can be administered orally or as a suspension but is most commonly administered in its tablet form. If taken as a suspension or orally, administer with or without food, but consistently with respect to food. If administered as a suspension, shake well before administering the dose. The suspension is not therapeutically equivalent to tablets; the suspension has a higher concentration compared to tablets. Administration with food increased the drug’s bioavailability, so one should make sure to avoid excessive potassium intake. It is commonly taken in combination with a potassium-wasting diuretic to help reduce potassium loss. A fun fact about this drug is that as of 2020, it was the 51st most commonly prescribed drug in the United States.

Sources links:
https://www.acs.org/content/acs/en/molecule-of-the-week/archive/s/spironolactone.html

https://www.acs.org/content/acs/en/molecule-of-the-week/archive/s/spironolactone/

Micromedex & Lexicomp

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I was assigned the drug Tramadol. Tramadol is a prodrug that gets converted to the primary active drug O-desmethyl tramadol. This targets the μ-opiate receptors with the intention of producing pain relief. The structure of tramadol includes a benzene ring with oxygen extended from its meta position. This oxygen is bound by a hydrogen through the process of N-demethylation and then further metabolization by O-demethylation into an oxybenzone. It is now in the first metabolite structure, which is the active metabolite O-desmethyl tramadol. While tramadol is not as active as its metabolite, it does have a small amount of affinity, but is extremely ineffective compared to O-desmethyl tramadol. Tramadol is a synthetic codeine analogue and can be addictive like codeine and morphine as it is a narcotic for severe pain.

I was able to learn the mechanism of action of this drug. The μ-opiate receptors are binded by the drug tramadol and its active metabolite O-desmethyl tramadol. The central nervous system would cause an inhibition of an ascending pain pathway which only alters the perception of pain. This in turn will also alter the response to pain, as the pain won’t seem or feel severe to the patient. Norepinephrine and serotonin will be inhibited, allowing them to stay outside of cells and within the body. This aids in pain relief, as norepinephrine which is part of the rest and digest system or parasympathetic portion of the central nervous system, and serotonin play a role in the intrinsic control of pain and the response or mood related to pain respectively. By targeting these two neurotransmitters and hormones alike, the body is able to relieve the patient of pain, and deliver a physical and emotional/mental response as the patient will be able to think better and feel better due to the feeling of decreased pain.

It is classified as a non-controlled analgesic. Aside from tramadol being indicated for chronic pain, it has an off-label use for premature 🤬 or orgasms. Normal side effects include feeling dizzy, sleepy, tired, or weak. Constipation, diarrhea, throwing up, dry mouth, headache, itching, trouble sleeping, flushing, sweating a lot, or an upset stomach are possible. There are other side effects that are more dangerous and a doctor or physician should be consulted. As I have been able to learn about this drug and its properties, I have been able to form a deeper understanding of how it affects the body and its host. Although it may not be the best option as it is an addictive drug, it is very effective in what it does.

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My assigned drug is Metformin. Metformin is a first-line therapeutic indicated to treat Type 2 Diabetes Mellitus along with diet and exercise. Metformin is an asymmetrical biguanide composed of primary and tertiary amine functional groups. It has no heterocycles in its structure. Drug targets include the mitochondrial complex 1 and glucagon-like peptide 1 (GLP-1). The exact mechanism of action of metformin is unknown. What is known is that metformin decreases the production of glucose in the liver, decreases the absorption of glucose in the intestine, and increases the uptake of peripheral glucose to improve insulin sensitivity. Major side effects include lactic acidosis (which can lead to death), gastrointestinal effects (including diarrhea, nausea, vomiting, flatulence, and abdominal pain), and vitamin B12 deficiency (which can lead to anemia and neuropathy). Other possible side effects include chest discomfort, flushing, palpitations, hypoglycemia, chills, dizziness, headaches, muscle pain, trouble breathing, flu-like symptoms, and upper respiratory tract infections.

Metformin is a chemically-synthesized compound with a structure resembling that of isoamylene guanidine, which originates from the plant Galega officinalis. It was first described in scientific literature in 1922 as a product of a synthesis reaction. In 1929, its blood sugar-lowering effects were discovered by two scientists testing it in rabbits. It was found to be the most potent of all biguanide analogs. However, it would not be tested on again until the 1950s when a Filipino physician used it to treat influenza. A French diabetologist then studied its properties and became the first person to try it on humans for the treatment of diabetes. He coined the name “Glucophage” and published his results in 1957. Metformin would go on to be first available in the UK in 1958 and FDA-approved in 1994. It is now available in several countries and is believed to be the world’s most widely prescribed antidiabetic medication. It is on the World Health Organization’s List of Essential Medicines.

Sources: Clinical Pharmacology, Lexicomp, Wikipedia

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During this semester, I have learned about the drug diazepam (Valium, Valtoco) through literature searches and in-class lectures. Diazepam is a benzodiazepine, a class of drugs frequently used to treat anxiety and seizures. The structure of a benzodiazepine can be identified through the fused ring system of a benzene and a diazepine. Diazepam specifically has chlorine, methyl, and ketone as functional groups. Diazepam was derived from the drug chlordiazepoxide (Librium), both of which were discovered by the scientist Leo Sternbach. Originally, the research focused on benzheptoxdiazines as potential tranquilizers, but it was found serendipitously that benzodiazepines were more effective for the treatment of anxiety.

Diazepam acts as a positive allosteric modulator on the GABA(A) receptor, which is a ligand-gated ion channel. GABA works as an inhibitory transmitter, so by upregulating it, diazepam leads to hyperpolarization and consequently muscle relaxation and anti-anxiety effects. However, like other depressants, diazepam can be habit-forming and dangerous when used with other depressants. As such, diazepam is a Schedule IV controlled substance and has Black Box Warnings of “risk of contaminant use with opioids,” “abuse, misuse, and addiction,” and “dependence and withdrawal reactions” (Lexicomp).

As for the metabolism of diazepam, its active metabolite is nordiazepam or N-desmethyldiazepam. The metabolism of diazepam to nordiazepam is mediated by the CYP2C19 and CYP3A4. Nordiazepam is then metabolized by CYP3A4 to oxazepam, which is then eliminated through glucuronidation. When metabolized by the CYP3A4 and CYP3A5 enzymes, diazepam can also become temazepam, a drug used for insomnia. Diazepam can cross the placenta, so pregnant women should not take this drug as it can harm the fetus and in some cases cause “floppy infant syndrome.”

Apart from anxiety and seizures, diazepam has many other indications, both FDA-approved and off-label. FDA-approved uses include hydroxychloroquine/chloroquine toxicity, muscle spasms, and substance withdrawal. Off-label indications include intoxication from cocaine and meth, neuroleptic malignant syndrome, serotonin syndrome, and acute episodes of vertigo. Given the nature of the drug, diazepam can have side effects like drowsiness and muscle weakness, but it can also have more serious side effects. If used with opioids, it can lead to sedation, coma, and death. Other serious side effects include shortness of breath, confusion, hallucinations, memory loss, passing out, change in eyesight, slurred speech, loss of appetite, and increased risk of suicidal thoughts. Finally, diazepam has many dosage routes such as intramuscular, intravenous, oral, intranasal, and rectal. Learning about diazepam this semester has been useful, especially since so many people take this drug and other benzodiazepines like it.

Sources: Lexicomp, MicroMedex, Drug Bank, Dr. Roy and Dr. Ashpole's lectures, Wikipedia

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This semester , my assigned top 200 drug was Docusate. Alphons O. Jaeger and Coleman R. Caryl, first patented Docusate in 1937. Originally Docusate was used as a detergent under the name Aerosol OT. Docusate use changed in 1957 when David Dickinson and James Wilson found the drug helpful in treating constipation. Docusate is a laxative, specifically a stool softener. The indication for treatment includes constipation, associated with dry, hard stool, and opioid-induced constipation, mostly found in the small intestine. These indications are treated through Docusate's fascinating mechanisms of action. Docusate is an Anionic surfactant. It lowers the surface tension at the oil-water interface of the feces. This decrease in surface tension allows an increase of water and liquids into the stool, which softens the stool. With a softened stool, bowel movement and excretion become much easier for the patient, relieving them of constipation. The structure of Docusate, like its mechanism of action, is relatively simple but gets the job done. Docusate structure includes two esters and one sulfone bond connected by four carbon atoms. The single-bond oxygen in each ester is connected to a hexane group, and the second carbon of the attached hexane contains an ethane group. Docusate also contains sodium which is attached to the sulfone by an ionic bond. This structure and mechanism of action have led Docusate to be prescribed over three million times in America, which ranks 163rd among prescriptions. Patients prescribed docusate might experience common side effects such as Abdominal cramps, nausea, diarrhea, and bloating; some patients even experience a bitter taste. Side effects can also be more severe and cause rectal irritation and signs of allergic reaction in the rectum, including rash, hives, and blisters. These allergic reaction symptoms have also been seen in the throat and face. While researching side effects, I found a fascinating topic of laxative addiction and misuse. Laxative misuse is often associated with body dysmorphia, eating disorders, and weight loss. Laxatives such as Docusate create a sense of weight loss due to increased bowel movement. This false sense of weight loss leads many people to misuse and become addicted to laxatives. I found it very interesting, considering there are no addictive properties associated with most laxatives, including Docusate. My research on Docusate has given me excellent knowledge of one of the most common prescriptions filled in America. This project has also given me the tools and experience to research medications with great detail. Overall, I found this research extremely interesting and gained skills I will use throughout my pharmacy career.

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My assigned drug is Loratadine. Temporary relief of sinus and nasal congestion, runny nose, sneezing, itching of nose or throat and itchy, watery eyes due to common cold, hay fever (allergic rhinitis), or other upper respiratory allergies or sinusitis. Loratadine exerts it's effect by targeting H1 histamine receptors. Loratadine binds to H1 histamine receptors found on the surface of epithelial cells, endothelial cells, eosinophils, neutrophils, airway cells, and vascular smooth muscle cells among others. This drug uses the monoamine oxidase inhibitors. It may enhance the hypertensive effect of alpha/beta agonists. While linezolid is expected to interact via this mechanism, management recommendations differ from other monoamine oxidase inhibitors. A chemist named Magatti had his eureka moment in the lab, 17 years would pass before loratadine became available as prescription Claritin in the United States. It quickly went on to become one of the most used drugs in the world -- and is now included on the World Health Organization's list of essential medicines. Schering-Plough developed loratadine as part of a quest for a potential blockbuster drug: a nonsedating antihistamine. By the time Schering submitted the drug to the U.S. Food and Drug Administration (FDA) for approval, the agency had already approved a competitor's nonsedating antihistamine, terfenadine (trade name Seldane), and, therefore, put loratadine on a lower priority. However, terfenadine had to be removed from the U.S. market by the manufacturer in late 1997 after reports of serious ventricular arrhythmias among those taking the drug. Loratadine was approved by the FDA in 1993. The drug continued to be available only by prescription in the U.S. until it went off patent in 2002. It was then subsequently approved for over-the-counter sales. Once it became an unpatented over-the-counter drug, the price dropped significantly. Side effects include: headache, dry mouth, nosebleed, sore throat, mouth sores, difficulty falling asleep or staying asleep, nervousness, or weakness. Some additional warnings for pediatric patients do extend this list: Safety and efficacy for the use of cough and cold products in pediatric patients <4 years of age is limited; the AAP warns against the use of these products for respiratory illnesses in young children. Serious adverse effects including death have been reported (in some cases, high blood concentrations of pseudoephedrine were found). Many of these products contain multiple active ingredients, increasing the risk of accidental overdose when used with other products. The FDA does not recommend OTC uses for these products in pediatric patients <2 years of age and recommends to use with caution in pediatric patients ≥2 years of age. Health care providers are reminded to ask caregivers about the use of OTC cough and cold products in order to avoid exposure to multiple medications containing the same ingredient

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Diltiazem is an antagonist and calcium channel blocker that is commonly indicated for the treatment of hypertension as well as to manage chronic stable angina. It is sold under the brand names of Cardizem, Cartia, Dilacor, Diltia, Diltzac, Matziam, Taztia, and Tiazac. It is also indicated for angina pectoris, nonsustained ventricular tachycardia, ventricular premature beats, and supraventricular tachycardia. It is available in an oral capsule form that is most commonly taken but can also be administered intravenously. It was synthesized in 1971, approved by the FDA in 1982, and primarily works by targeting cardiac and vascular smooth muscle by inhibiting calcium influx during depolarization. Diltiazem can also be used to manage atrial fibrillation and atrial flutter due to it being a potent vasodilator and has off-label indications for conditions such as migraines and pulmonary hypertension. Its mechanism of action involves preventing calcium ions from the entering the slow channels (L-type calcium channels) or certain voltage-sensitive areas of myocardial and vascular smooth muscle. It relaxes the smooth muscle in the walls of the arteries, allowing them to open and allowing blood to flow more easily to increase oxygen delivery as well. In SHR experimental models, renal hypertensive, and DOCA/saline rats, antihypertensive action of diltiazem was shown as well as diuretic effects. This led to the discovery of the drug, as chronic administration of diltiazem to SHR showed significant lowering of blood pressure without a change in body fluid. Some side effects that are seen taken with this condition are conduction abnormalities, cutaneous hypersensitivity reactions, headaches, fatigue, and dizziness; it should be used with caution in patients with hepatic impairment. Diltiazem's development was significant and vital to serving as a template for future drug discovery by use of ligand-based virtual screening to discover new chemotypes such as verapamil and lacidipine that block L-type calcium channels. It is a CYP3A4 inhibitor, and concomitant use of inhibitors with diltiazem may lead to an increase in serum concentration. It is available in immediate-release and extended-release formulations. In its structure, it has the functional groups tertiary amines, benzene, thioether, aldehyde, and a ketone, and does not contain any heterocycles. It is a well-tolerated and effective medication that can be taken for long-term use; however, it has been shown that extensive use can lead to worsening of congestive heart failure. Overall, the benefits of diltiazem as primarily a blood pressure reducer has made it an important drug in management of many cardiac disorders as well.

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Throughout this semester, I was assigned to research about the drug Clonidine. While doing research, I have been able to learn about the different characteristics that make up the drug. Clonidine was discovered in 1966 by Stähle. It was first used as a hypertension treatment under the trade name of Catapres. It is now FDA approved and indicated for hypertension, treatment of attention deficit hyperactivity disorder in children, management of tics commonly found with Tourette syndrome, adjunct therapy for severing cancer-related pain, and as an adjunct in neonatal opioid withdrawal syndrome. Additionally, Clonidine has multiple off-label uses, such as managing withdrawal symptoms from opioids, benzodiazepines, and alcohol and treating anxiety, insomnia, and post-traumatic stress disorder (PTSD). Clonidine comes in various dosing forms including tablets, extended-release tablets, patches, and epidurals. Clonidine works by targeting the alpha 2-adrenergic site. It stimulates alpha-2 adrenoceptors in the brain stem, thus activating an inhibitory neuron, resulting in reduced sympathetic outflow from the CNS, producing the desired effects. It has an antagonist effect in the posterior hypothalamus and medulla. Researchers are unsure of the mechanism of action in regards to treating attention deficit hyperactivity disorder in children. Various ideas have been proposed but the exact action of the drug is unknown. Clonidine has a drug interaction with digoxin, diltiazem, verapamil, and beta blockers like metoprolol or propranolol. These drugs should not be taken together. If a patient is taking any of those drugs currently it is important that they notify their doctor immediately. There are various side effects that can come along with taking clonidine. It has a black box warning for epidural clonidine. Epidural clonidine is not recommended for obstetrical, postpartum, or perioperative pain management. The risk of hemodynamic instability, especially hypotension and bradycardia, from epidural clonidine may be unacceptable in these patients. All clonidine products tend to have side effects of dry mouth, constipation, feeling dizzy, sleepy, tired, or weak, headache, and upset stomach. The extended-release tablets tend to have side effects of trouble sleeping, bad dreams, decreased appetite, stomach pain, and feeling irritable. The skin patch can have side effects of skin irritation. The epidural formulation has side effects of sweating a lot, throwing up, and ringing in the ears. It is important when taking this medication to monitor side effects to make sure that therapy is effective. Clonidine can be taken at any time of the day, with or without food. It is stored at room temperature. If a dose is missed, take it as soon as remembered or if close to the next dose continue with normal regimen and do not double dose.

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The image above is the prescription drug, alprazolam. This is the drug I was assigned for the duration of this BMS semester. I have enjoyed learning all about this drug throughout this time, and look forward to applying this knowledge to my future rotations and jobs.

The drug alprazolam, more commonly known as its trade name, Xanax, is used to treat anxiety disorders and panic disorders. It is one of the most commonly prescribed medications in the US, falling at number 23 of top 200 drugs prescribed. It is in a class of medications known as benzodiazepines. It is a schedule IV drug. This means that it is a substance that has a low potential for abuse relative to other scheduled drugs, like schedule III, II, or I drugs. On the other hand, those who take alprazolam should not take a larger dose than prescribed, should not take it more often, and should not take it for a longer time than what the doctor says. Alprazolam also has serious harmful effects if it is used recreationally. It is commonly used amongst teenagers, and they build up a tolerance to it quickly, which causes the teens to take more pills to feel the same effect. Alprazolam works to enhance the GABA neurotransmitter at the GABA-A receptor. This produces a sedative, hypnotic, anxiolytic, anticonvulsant, and muscle relaxing effect. GABA is the main inhibitory neurotransmitter in the central nervous system, and its main function is to reduce neuronal excitability. When GABA is bound to the GABA-A receptors, the neuron opens a channel to let negative chloride ions pass through. These chloride ions make the neuron less reactive to excitatory neurotransmitters like serotonin or norepinephrine. Serious side effects can include shortness of breath, seizures, skin rashes, yellowing of skin or eyes, confusion, problems with speech, or problems with coordination or balance. Its less serious side effects can include drowsiness, light-headedness, headache, dizziness, irritability, dry mouth, talkativeness, difficulty concentrating, increased salivation, changes in sex drive or ability, changes in appetite, weight changes, difficulty urinating, joint pain, nausea, or constipation.

The first benzodiazepine, Librium, was discovered in 1955 from chemist Leo Sternbach. It was modified to be more effective, producing the common drug diazepam, or Valium. More research was done with benzodiazepines, which was how the discovery of alprazolam came about. J.B. Hester, who worked with Pfizer, was given the patent for alprazolam in Germany in 1970. It was FDA approved on October 16, 1981.

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This semester in BMS, I was assigned the drug Fenofibrate. Throughout this semester's activity, I was able to learn all about Fenofibrate. Fenofibrate, the most commonly used medication in the fibrate class, was invented by Fournier Laboratories in the 1980’s, but was first synthesized as a derivative of clofibrate in 1974. The drug’s primary indication is hypertriglyceridemia, which is when you have too many triglycerides (fats) in your blood. This ultimately raises your risk of atherosclerosis and related heart diseases. Fenofibrate is used to lower triglycerides, lower bad cholesterol (LDL) and raise good cholesterol (HDL). Even though the drug’s primary indication is hypertriglyceridemia, it can also be used for hypercholesterolemia or mixed dyslipidemia. Fenofibrate’s brand names include: Antara, Fenoglide, Fibricor, Lipofen, Tricor, Triglide [DSC], and Trilipix. The mechanism of action according to Lexicomp is fenofibric acid, an agonist for the nuclear transcription factor peroxisome proliferator-activated receptor-alpha (PPAR-alpha), downregulates apoprotein C-III (an inhibitor of lipoprotein lipase) and upregulates the synthesis of apolipoprotein A-I, fatty acid transport protein, and lipoprotein lipase resulting in an increase in VLDL catabolism, fatty acid oxidation, and elimination of triglyceride-rich particles; as a result of a decrease in VLDL levels, total plasma triglycerides are reduced by 30% to 60%; modest increase in HDL occurs in some hypertriglyceridemic patients. Side effects include headache, back pain, and abdominal pain. Tell your doctor right away if you have bloating, sudden and severe stomach pain, chills, diarrhea, fast heartbeat, fever, indigestion, loss of appetite, nausea, pains in stomach, side, or abdomen, possibly radiating to the back, or vomiting. This medicine may also increase your risk of having gallstones. Fenofibrate comes as a capsule, a delayed-release (long-acting) capsule, and a tablet to take by mouth in either 67 mg, 134 mg, or 200 mg. It is usually taken once a day. Some fenofibrate products (Fenoglide, Lipofen, and Lofibra) should be taken with a meal. Other brands (Antara, Fibricor, Tricor, Triglide, and Trilipix) may be taken with or without food. Depending which product is given will depend on how to counsel the patient. This drug should be used with a low-fat diet, and exercise. It should also be known that the patient should not take this medicine if they have a history of hypersensitivity to fenofibrate or fenofibric acid or any component of the formulation, liver disease, gallbladder disease, severe kidney disease, or if they are breast-feeding a baby. Fenofibrate can cause the breakdown of muscle tissue, which can lead to kidney failure.

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The drug I was assigned to for this semester’s padlet activity was alfuzosin. From the above image, it can be seen that alfuzosin does contain a chiral center. The functional groups contained within alfuzosin includes a secondary and tertiary amine as well as an ether functional group. Alfuzosin is a racemate as its two enantiomer forms (R- and S-) are seen in a 1:1 mixture. Sanofi-Synthelabo first submitted a new drug application for alfuzosin in December of 2000 based on the results of their three-part, phase III clinical trial. All three parts of the trials were double blind and placebo controlled taking place in different locations across the country. On June 16th, 2003, Sanofi-Synthelabo’s New Drug Application for UroXatral was approved by the U.S. Food and Drug Administration. It was approved for the symptomatic treatment of benign prostatic hyperplasia (BPH). UroXatral is the most common brand name for the drug; however, another brand name that can be seen is Xatral. Although its primary indication is for the symptomatic treatment of benign prostatic hyperplasia, it is often used off-label for the treatment of ureteral stones. Benign Prostatic Hyperplasia is a disorder resulting from an enlarged prostate. The condition is marked with frequent urinary tract infections, bladder stones, and reduced kidney function. In regards to the pharmacokinetics of the drug, Alfuzosin is an alpha blocker. To elaborate on this, it as an antagonist of the alpha-1 receptors located in the lower urinary tract. Alfuzosin works as a blockage at the Alpha-1 receptors. When these receptors are blocked, it causes a relaxation of the smooth muscles along the neck of the bladder and prostate. This reduces the amount of pressure placed on the urethra by benign prostatic hyperplasia and improves the quality of urine flow. Alfuzosin is available in a 10 mg extended release tablet. Patients should be instructed to take the tablet immediately following a meal at the same time each day. Peak effects are seen around 8 hours after in take. Some common side effects the patient should be warned of includes tiredness, headache, runny/stuffy nose, pain, stomach pain, heartburn, constipation, nausea, or a decrease in sexual abilities. The doctor should be alerted immediately if severe dizziness, passing out, chest pain, or an erection lasting longer than 4 hours occurs. The patient’s International Prostate Symptom Score should be analyzed at the start of treatment and again 4-12 weeks later to ensure medication is having the desired effect.

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The drug that was assigned to me this semester was 🤬 also known as Sildenafil. In 1989 British scientists began developing a drug called Sildenafil Citrate that would be very useful in treating high blood pressure and angina. In the early 1990’s several trials were being completed with very little hope of it ever being used to treat high blood pressure and angina. However, quite a few male volunteers that were involved in the clinical trials reported increased erections many days after taking a single dose. Fast forward to 1996, Pfizer is able to patent the “Miracle Drug” in the United States. It was not until 1998 that the United States Food and Drug Administration chose to approve the use of 🤬 to treat erectile dysfunction in men. It took over ten years to get this product to market, and in the first few weeks pharmacists across America dispensed more than forty thousand little blue tablets.

The mechanism of action for 🤬 includes a key enzyme phosphodiesterase 5 enzyme inhibitor that is involved in the regulation of cGMP specific signaling pathways in normal physiological processes such as smooth muscle contraction and relaxation. For this reason, inhibition of the enzyme can alter those pathophysiological conditions associated with a lowering cGMP level in tissues. In patients with erectile dysfunction, sildenafil citrate enhances the effect of nitric oxide by inhibiting PDE5 in the corpus cavernosum. When sexual stimulation causes the local release of nitric oxide, inhibition of PDE5 by sildenafil citrate causes increased levels of cGMP resulting in smooth muscle relaxation and inflow of blood to the corpus cavernosum.

This drug does not come without some very serious and some not so serious side effects. The most common of these serious side effects is cardiovascular morbidity, myocardial infarction, sickle cell anemia with vaso occlusive crisis, ophthalmic non-arteritic ischemic optic neuropathy, retinal hemorrhage, Otic decreased hearing, sudden onset, and sudden hearing loss. Reproductive prolonged erection of the 🤬.

This drug should always be taken as prescribed by your primary care physician. You should take it approximately thirty to forty five minutes before you plan on having sexual intercourse for maximum effect. Never use more than what has been prescribed by your doctor. This drug is intended to be used on an as needed bases. However, you are never to exceed two doses in a single day because this could lead to serious side effects or death in the patient.

If you experience any side effects or think you are experiencing a side effect. Do not wait, contact your doctor Immediately or go to the nearest emergency room.

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The drug I was assigned for this semester was atenolol, otherwise known as its trade name, Tenormin. I enjoyed the ALE activity this semester because I have been able to learn a lot of about atenolol. This drug was founded by Mylan in 1961 and was patented in 1969. Atenolol was first approved for medical use in 1975. This drug is a second-generation beta-1 selective adrenergic blocker and was developed to treat high blood pressure. This drug is significant because it treats a disease that affects many patients worldwide, and the drug itself and those in its class are widely used. There was a manufacturing defect which caused potentially toxic doses of atenolol 50 mg tablets in 2010. This resulted in a recall of the drug; however, it has since been lifted. Atenolol is indicated for angina, hypertension, and myocardial infarctions. The off label uses for the drug are atrial fibrillation, Marfan syndrome with aortic aneurism, migraine prevention, supraventricular tachycardia, thyrotoxicosis, and ventricular arrythmias/ventricular premature beats. The target of the drug is the beta-1 adrenergic receptor. The drug acts by competitively blocking the beta-1 receptors. This brings forth the blocking of beta-1 stimulation. Atenolol is a Beta-1 selective drug, therefore it has little to no effect on the beta-2 adrenergic receptors. This drug most commonly leads to bradyarrhythmia, cold extremities, hypotension, dizziness, depression, shortness of breath, and fatigue. The more serious side effects associated with atenolol are heart failure, myocardial infarction, ventricular arrythmias, thyrotoxicosis, anaphylaxis, systemic lupus erythematosus, pulmonary embolism, and withdrawal symptoms. This drug contains a black box warning that states those who take this should not end drug therapy immediately, but they should taper their doses. There are severe cases of angina, myocardial infarction, and ventricular arrythmias that have arisen due to immediate termination of drug without dose tapering. Patients who are terminating therapy should be monitored to ensure safety. The patient should keep their activity levels low; if severe symptoms continue to arise then the patient should begin the treatment with atenolol again. When stopping the therapy of atenolol, coronary artery disease is trying to be prevented, so the therapy should not end immediately, even if the only indication the patient has is for hypertension. This drug should be taken as prescribed. If a dose is missed a patient should take the drug as soon as they remember, or if it is close to the next dose, take it then.

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During this semester's Padlet activity, I was assigned the drug Fluticasone. Research has taught me various of information about my drug. In the corticosteroids drug class, Fluticasone was patented in 1980 and approved for medical use in 1990. It is used as a powder or aerosol inhalation for the prophylaxis of asthma and for management of seasonal and perennial of chronic rhino sinusitis. In other words, it's used for the treatment and prevention of seasonal allergies. Fluticasone is a highly selective agonist at the glucocorticoid receptor producing anti-inflammatory and vasoconstriction effects. It is broken down by CYP3A4, therefore, has been shown to interact with strong CYP3A4 inhibitors. Some side effects may include headache, nausea, vomiting, cough, stinging, and sneezing. For patients with mucous crusting, rinsing with saline nasal spray before fluticasone administration can remove mucous crusting and improve nasal coating. If nasal obstruction is so severe that sprays cannot penetrate, the patient should consider concomitant use of an intranasal decongestant for up to 5 days. For patients with allergic rhinitis, Fluticasone may be used as monotherapy or as part of an appropriate combination regimen. Scheduled administration is more efficacious and generally recommended. However, for mild or episodic symptoms, it may be administered as needed. For patients with chronic rhinosinusitis, a one-to-three-month course of nasal corticosteroids is part of a multimodal approach to initial treatment of chronic rhinosinusitis. Patients with refractory symptoms or significant blockage by polyps may require systemic therapies or surgical intervention (Fokkens 2020; Hamilos 2021). The intranasal administration route is used in the nostril only. It is important to not spray it in the eyes or mouth. The bottle should be shaken gently before each use. Make sure that the nose is clear by blowing it to clear the nostrils. After ensuring the nostrils are clear, the applicator should be inserted into the nostril, keeping the bottle upright and head tilted downward, close off the other nostril and press the pump to release spray while breathing in through the nose. It should be stored at room temperature (39 degrees F to 86 degrees F). When used for self-medication (over the counter), do not use in children less than four years of age for the treatment of asthma, or with current injury or surgery to the nose that is not fully healed. Prolonged use of this type of drug class may increase the incidence of secondary infection, mask acute infection, prolong or exacerbate viral infections, or limit response to vaccines.

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The drug I was assigned this semester was paroxetine.  Paroxetine, also known as Brisdelle or Paxil, was discovered in 1975 by a Danish company named Ferrosan, who transferred to what is now known as GlaxoSmithKline in 1980. It is indicated for many mental disorders including body dysmorphic disorder, generalized anxiety disorder, major depressive disorder, obsessive compulsive disorder, panic disorder, posttraumatic stress disorder, premature 🤬, premenstrual dysphoric disorder, social anxiety disorder, and vasomotor symptoms of menopause. The drug was approved by the FDA in 1992. There has been many issues since the FDA approval in 1992. To start, in 1998, Apotex Corporation filed an abbreviated new drug application for a generic version of paroxetine, so GSK filed a lawsuit against them.  Apotex won the lawsuit due to the fact that the variant converted to the final product eventually. But this is only the beginning. Paroxetine is an SSRI, so it’s goal is to block the serotonin reuptake transporter in the presynaptic terminal and thus increase the concentration of serotonin in the postsynaptic terminal.  The side effects include activation of mania or hypomania, bleeding risk, fragility fractures, hypotranemia, ocular effects, serotonin, syndrome, sexual dysfunction, withdrawal syndrome, and suicidal thinking and behavior. There is a black boxed warning for Paroxetine because some antidepressants can cause an increased risk of suicidal thoughts in behavior in pediatric patients and young adults. It is also not an approved drug for pediatric patients. Around 5,000 people have filed a lawsuit against Paxil due to the birth defects it caused, poor withdrawal symptoms, and increased thoughts of suicide. The first case was in 2009 because a child was born with heart malformations due to his mother taking Paxil for her anxiety while she was pregnant. The son, who was three years old, received 2.5 million dollars from the drug manufacturer. By 2010, GSK (GlaxoSmithKline) had around 800 birth defect settlements, which cost the company around 1.14 billion dollars, with an average of 1.2 million to each family with affected children.  In 2012, GSK was involved in the largest pharmaceutical settlement in history, paying 3 billion dollars for their failure to report safety information about this medication. Due to the long list of side effects in patients, experts suggest starting with a low dose and gradually increasing if working properly. Due to the withdrawal symptoms seen in patients, it is recommended to taper the dose over 2-4 weeks to minimize these symptoms.

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Metoprolol is a beta-1 adrenergic receptor blocker used in succinate and tartrate derivatives depending on the desired release formulation. This drug has little to no effect against the beta-2 adrenergic receptors in bronchial and vascular smooth muscle, making this a very “selective” drug. Metoprolol was first made in 1969, patented in 1970, and then approved by the United States for medical use in 1978. This drug is now available in generic formulations and was the 6th most prescribed drug in the U.S. during 2020. With above 27 million prescriptions filled yearly, it is safe to say this is one of the more important drugs on the market to date.

The labeled indications for this drug are heart failure, angina, myocardial infarction (heart attack), and hypertension. Off-Label indications include things like Atrial fibrillation/flutter, Migraine prevention, Thyrotoxicosis, and Ventricular arrhythmias. There hasn’t been a ton of studies focusing on these off-label indications; however, migraine prevention has shown promising results from the limited number of studies surrounding this indication and metoprolol. Its target interactions are like mentioned above, but I will go over them again in a bit more detail. Metoprolol interacts with Beta-1 adrenergic receptor as an antagonist, but not Beta-2. It’s a bit more unknown as to whether it interacts with the Beta-adrenergic receptor. Metoprolol does not bind to proteins extremely well. Therefore, only 11% of an administered dose is bound to the receptor site. The rest is bound to an albumin serum.

The mechanism of action of metoprolol is rather simple. When it blocks the Beta-1 receptor in cardiac cells, a decrease in cardiac output occurs by the production of negative chronotropic and inotropic effects. This happens without any activity in the membrane or intrinsic sympathomimetics. As far as the metabolism goes, metoprolol goes through a first-pass hepatic wave that covers around 50% of the dose. This is mainly covered by CYP2D6 and a smaller portion by CYP3A4.

Metoprolol has a black box warning for ischemic heart disease related to cessation of therapy. These patients have experienced things such as episodes of angina pectoris and myocardial infarction. They can be very deadly and require a gradual reduction in dosage over a period of 1 to 2 weeks with careful monitoring to discontinue therapy. The most common side effects outside of the black box warning are dizziness, tiredness, and weakness. Some of the more uncommon effects that are a bit rarer are things like: depression/low Mood, bradycardia/arrhythmias, extreme dizziness/passing out, chest pain, shortness of breath, weight gain, and arm/leg swelling. While these effects are rare, if they occur while on metoprolol; you need to tell your doctor or get medical attention right away.

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Simvastatin is derived from lovastatin and was the second statin drug to be used clinically. It was first approved for marketing in Sweden in 1988 and then became approved worldwide. The brand name for Simvastatin in the United States is FloLipid or Zocor, and it is classified as an antilipemic agent and an HMG-CoA reductase inhibitor. Simvastatin is used for hypercholesterolemia or high cholesterol levels. This drug helps treat hypercholesterolemia by lowering LDL levels, which is the “bad” cholesterol, and increasing HDL, or the “good” cholesterol, levels. This means that simvastatin can be useful for the prevention of cardiovascular, or heart, disease. This drug helps treat hypercholesterolemia by acting as an HMG-CoA, or 3-hydroxy-3-methylglutaryl-coenzyme A, reductase competitive antagonist. HMG-CoA reductase, when functioning normally, catalyzes the rate limiting step in cholesterol biosynthesis. Inhibiting this enzyme leads to a decreased level of high sensitivity C-reactive protein, or hsCRP, and increases endothelial function. This drug also reduces inflammation at the site of coronary plaque, inhibits platelet aggregation and has anticoagulant, or anti- clotting, effects.

When taking Simvastatin, it is important to also make lifestyle changes, including diet and exercise changes. Since it is also considered a moderate intensity statin, simvastatin should only be used if LDL levels need to be lowered by less than 50%. Simvastatin comes in both 20 mg and 40 mg tablets, with 20 mg a day being the average starting dose. After one to three months of therapy, it is important to assess the patient’s response. If the patient has not shown substantial improvement then the dosage can be raised to 40 mg a day. After the dose adjustment, the patient’s response to therapy can be monitored every three to twelve months. If the patient still does not show improvement with the 40 mg dose, then the patient can be switched to a high intensity statin.

Taking Simvastatin can also lead to adverse events or different side effects. The most common side effects are headaches, stomach pain, upset stomach, constipation and signs of a common cold. There are also some more serious side effects, that if experienced by a patient they should report back to their prescribing physician. These more serious side effects include a heartbeat that does not feel normal, inability to pass urine or a change in how much urine is passed, abnormal muscle pain, tenderness or weakness, and liver problems like dark urine, feeling tired, not hungry or an upset stomach or stomach pain.

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My assigned drug this semester was Topiramate, which is considered an anti-epileptic drug. Topiramate was initially approved by the FDA in 1996 and 2004, topiramate was approved for the prevention of migraine in adults. Since 2012, the extended-release formulation has been approved in combination with phentermine for chronic weight management therapy in adults. This drug can be taken anytime and with or without meals. The functional groups this drug is made of are ethers, oxides, and sulfur containing compounds. This drug is used to treat epilepsy, but it is mainly indicated for patients who are 2 years and older suffering from seizures. It is also indicated for migraine treatment in people who are 12 years or older. Topiramate is classified as an anticonvulsant, which works by decreasing the abnormal excitement in the brain. This drug targets voltage-dependent sodium channels, Gamma aminobutyric acid (GABA) receptors, and glutamate receptors. One way the drug works is through the combination of potential mechanisms. The first one is blocking neuronal voltage dependent sodium channels, which enhances GABA(A) activity and antagonizes AMPA/kainite glutamate receptors, which weakly inhibits carbonic anhydrase. This reduces the excitability of cortical neurons and suppresses neural discharges in the Maximal Electroshock model, an animal model of generalized clonic seizures. This drug may also enhance the action of GABA, which is a neurotransmitter that acts as a natural 'nerve calming' agent. Topiramate also decreases the action of glutamate, which is a neurotransmitter that normally has a 'nerve exciting' effect.

Like every other drug on the market, this drug can also cause side effects. These side effects may vary in severity due to what a patient is taking them for. The most common side effects that may occur are blurred vision, burning, prickling, confusion, dizziness, double vision, drowsiness, eye redness or pain, increased eye pressure, memory problems, nervousness, speech or language problems, and usual tiredness or weakness. Other side effects that may occur are diarrhea, constipation, throwing up, upset stomach, joint pain, and common cold symptoms. These side effects don’t generally show up all the time when taking this medication, however, if they were to show up the best way to go about it is to reach out to the physician or pharmacist. One thing to look for when taking Topiramate is your alcohol intake. Alcohol can affect the efficacy of the medication and may increase the side effects and make them more intense.

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Ondansetron, otherwise known as Zofran, was invented in England by a company known as GlaxoSmithKline (GSK). The drug was patented in 1987 and approved by the FDA in January 1991. It is indicated to treat nausea and vomiting caused by cancer therapy and surgical operation. While Zofran has been frequently prescribed for morning sickness in pregnant women, this is an off-label or non-FDA-approved use. In fact, GSK has never requested approval for Ondansetron treatment in pregnant women. It is also important to note that Ondansetron is not effective for motion-sickness induced nausea. Ondansetron is currently available in various forms: tablet, disintegrating tablet, oral solution, and injection. The onset of action occurs anywhere from thirty minutes to an hour after taking the medication and it stays in the individual’s system for about eight hours. It should be stored at room temperature and away from heat, moisture, and direct sunlight. As far as the chemical structure of Ondansetron, it consists of imine, tertiary amine, ketone, and arene functional groups. It also contains an imidazole heterocycle. Ondansetron is an antagonist that works on the 5-hydroxytryptamine-3 (5-HT3) receptor by blocking serotonin, which is responsible for triggering nausea and vomiting. One interesting thing I learned while researching Ondansetron, is that it is not recommended for individuals who are CYP2D6 ultrarapid metabolizers. Ondansetron is also contraindicated with the concomitant use of apomorphine. Common side effects of Ondansetron occur in different systems throughout the body including gastrointestinal, neurologic, and respiratory. These adverse effects consist of constipation, diarrhea, headache, hypoxia, fatigue, and malaise. More serious side effects involve the cardiovascular system and include electrocardiogram abnormalities, prolonged QT interval, and torsades de pointes. Serotonin syndrome may also occur as a result of building up high levels of serotonin. According to Micromedex, fetal and infant risk while taking Ondansetron cannot be ruled out. However, the FDA classifies Ondansetron as a “Pregnancy Category B” medication due to the lack of studies to determine the effects of Ondansetron on pregnant women and their offspring. Therefore, there is currently no official black box warning for Ondansetron. As a future pharmacist, I am thankful for the opportunity this semester-long project has given me to learn drug information that will be valuable to me in the future. I hope to use not only the knowledge I have gained about Ondansetron but also the information I have learned from my classmates’ research to educate patients!

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My assigned drug for this semester was Citalopram. I had not heard of this drug before this semester, so I was able to learn a lot about it through research and the weekly ALE assignments. Citalopram is a selective serotonin reuptake inhibitor, and is therefore primarily indicated to treat depression including major depressive disorder. When taken as an antidepressant, the antidepressant effects can take from one week to up to four weeks to occur. While this drug is mainly used to treat depression, it is also used in the treatment of other diagnoses such as anxiety disorder, obsessive-compulsive disorder, panic disorder, and post traumatic stress disorder. Some of the common brand names of this drug include Celexa, Cipramil, and others. Citalopram was first synthesized in 1972 by Klaus Bogeso, who was working with the pharmaceutical company Lundbeck in Denmark. It was approved for medical use in the United States in the year 1998, and is available as a generic medication. Citalopram is taken orally in the tablet form, and is generally taken in one dose. It is safe to take this drug with or without food, and is well tolerated in the therapeutic dose range. Citalopram is metabolized mostly by the enzyme CYP2C19 in the liver, but can also be metabolized by CYP3A4 and CYP2D6. I learned that the half life of this drug is approximately 35 hours and that the elimination process of this drug takes longer in elderly patients who experience kidney or liver failure. This is a very commonly prescribed drug, so it is important to be aware of the many side effects or adverse events that can come with Citalopram. Some of the most common side effects with this drug are nausea, trouble sleeping, sexual problems, shakiness, feeling tired, and sweating. While these are more minor side effects, Citalopram can also cause some more serious side effects. Serious side effects include an increased risk of suicide in those under the age of 25, serotonin syndrome, glaucoma, and QT prolongation. Citalopram contains a black boxed warning that indicates the drug may increase suicidal thinking and behavior in people under 24. Citalopram can also have negative interactions with other drugs such as St John’s wort, tryptophan, or 5-HTP because this combination could potential lead to serotonin syndrome. Overdose of this drug can cause vomiting, disturbances in hearth rhythm, and nausea, but is unlikely to cause death if Citalopram is the sole agent.

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My assigned drug for the semester was Glipizide. Glipizide is just the generic name. The brand names are Glucotrol and Glucotrol XL. Glipizide was developed in 1984. The FDA approved Glipizide in 1994. It is also a sulfonylurea drug. Glipizide is prescribed for Type 2 Diabetes. Glipizide is an orally administered drug. The extended release pill should be taken with the first meal of the day. The immediate release pill should be taken thirty minutes before meals. It has the intended purpose to lower blood sugar levels. Glipizide is to be administered alongside a diet and exercise plan. Some prescribers will add Metformin onto the plan as well. This happens after three to six months of taking Glipizide and A1c levels still are not being met. No more than 40mg of Glipizide should be taken per day. If 40mg is not working for the patient, a different medication therapy needs to be implemented. Pancreatic beta cells are the target of Glipizide. This is the site where insulin is released. Glipizide sparks a release of insulin from the pancreas. Therefore, the amount of glucose that is put out by the liver is decreased. Also, an increase in insulin sensitivity is observed in peripheral target sites. Insulin is secreted from the pancreatic beta cells because Glipizide opens up voltage-gated calcium channels. This is a result from a partial block on the potassium channels. This means that there is a longer period before cellular repolarization happens. The functional groups within the structure of Glipizide include Benzene, Amide, Sulfonylurea, and cyclohexane. Glipizide also contains the pyrazine heterocycle. It is recommended to avoid drinking alcohol when taking Glipizide until you know how the medicine affects you. Operating machinery and driving should also be avoided while taking Glipizide until you know how the medicine affects you. Glipizide lowers blood sugar levels, so that could lead to hypoglycemic events. Hypoglycemia is when blood sugar is too low. This can lead to blurred vision, headaches, dizziness, blacking out, and fainting. However, the risk of long-lasting hypoglycemia is small because of the short half-life and duration. The duration is roughly 12-24 hours and only takes about thirty minutes for initial onset effects. Glipizide has the fastest onset and absorption than any other sulfonylureas in its class. Glipizide is excreted in the urine, primarily. Abdominal pain, constipation, diarrhea, nausea, vomiting, and skin rash are some of the common side effects seen from patients taking Glipizide.

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For this semester of BMS I was assigned Oxycodone as my drug of the semester. It was very strange having to study oxycodone for me because I am actually allergic to it, I am allergic to all opioids and Oxycodone is a opioid. Oxycodone also goes by Oxaydo, OxyContin, Roxicodone, Roxybond, and Xtampza ER. Oxycodone was founded in Germany in 1916 by Martin Freund and Edmund Speyer at the University of Frankfurt, it is a semisynthetic opioid analgesic derived from thebaine. The first FDA approved product with oxycodone in it is Percodan, and it was approved on April 12, 1950. With Purdue Pharma taking over the drug with OxyContin in 1996. Oxycodone is used for pain management and it targets opiate receptors. Oxycodone works by binding to opioid receptors in the central nervous system, which inhibits the ascending pain pathways.  Oxycodone is metabolized by CYP 3A4 and 3A5 to turn it into noroxycondone and the CYP 2D6 metabolizes it into noroxymorphone. Both of those are active metabolites that can later be conjugated before elimination. The immediate release oxycodone has a half-life of 3.2 hours with the extended release has a 4.5-hour half-life. Oxycodone has multiple black box warnings including: addiction, misuse, and abuse; opioid analgesic risk evaluation and mitigation strategy; life-threatening respiratory depression; accidental ingestion; neonatal opioid withdrawal; cytochrome P450 3A4 interaction; Risks from concomitant use with benzodiazepines or other CNS depressants; and risk of medication errors (oral solution). Common side effects of oxycodone are constipation, feeling or being sick, stomach discomfort, feeling tired, feeling dizzy, confusion, headaches, and itchiness or rash. Serious side effects include muscle stiffness and feeling tired, dizzy, and having low energy which combined point to hypotension. This drug should not be taken while you are pregnant and not recommended if you are breast feeding. Drug abuse of pain killers is very common, oxycodone is no different. Recently they started putting naloxone in oxycodone preventing it from working if it is crushed. They did this to stop people from crushing it to get a fast high. Oxycodone also has a structure similar to heroin it is only 3 oxygens off, both have similar effects on the central nervous system. Oxycodone is a restricted drug due to its addicting properties with it being a schedule II in the United States and a schedule I or Class A everywhere else.

Sources Used: Lexicomp, Drug Bank, Wikipedia, NHS, and Rightstep.com

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The drug that I was assigned for this semester’s ALEs and capstone project was atorvastatin. Over the course of the semester, I have learned so much about this drug and all of its key components through padlet. The brand name of atorvastatin is Lipitor and the structure (which is pictured above) contains a pyrrole and several functional groups which include carboxylic acid, aromatic amine, and ketone. The primary indication is hyperlipidemia and its mechanism of action is that inhibits 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase. This specific target 3-hydroxy-3-methylglutaryl, is a rate limiting enzyme in cholesterol synthesis. The role of this drug in an interaction would be that it is an enzyme inhibitor as it inhibits the enzyme reductase. Fasting lipid profile levels should be checking every 4 to 12 weeks after the patient has started taking this drug. It is recommended when taking this drug, to take it with or without food and to take it the same time every day. It is suggested to keep this drug at room temperature for storage purposes. If a patient were to miss their schedule dose, it is recommended to go on to the next dose and to not take more than one dose at a single time. As for its potential side effects, patients who take this drug can experience diarrhea, nausea, sore throat, joint pain, have trouble sleeping, and a stuffy nose. There are also many other side effects that the patient should be aware of which include urinary tract infections, memory loss, and feelings of confusion and it is recommended to contact the doctor if these side effects are happening. So these are the main components of the drug atorvastatin (Lipitor) but there is an interesting history behind the discovery of this drug. Atorvastatin was synthesized initially in 1985 and it would not get its brand name Lipitor until 1996 about eleven years later. In 1996, Lipitor was officially approved under the FDA after it went through the four key clinical trials under the Parke-Davis company. As of recently, Lipitor has actually come into scrutiny by the FDA after it was discovered that taking this drug has major effects that link with type 2 diabetes and some serious liver, kidney, and muscle damage. Throughout this whole semester, learning about atorvastatin and the history of its discovery and development has been a great educative experience. This drug is commonly used in the world today and it is great that I know almost everything about Lipitor.

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I was assigned the drug Estradiol for the ALE padlet assignments this semester. Edward Doisy and Alfred Butenandt are credited with the discovery of oestradiol in 1929. They simultaneously purified and crystallized oestrone, which ultimately led Doisy to the discovery of oestriol and oestradiol. The investigators recognized that oestrogens must be synthesized from androgens, and they labeled the process aromatization. Their focus on aromatase enzyme was extensive, finding the mechanism of action as well as the structure. After this discovery, they focused on validating the effects of the drug on males and females. Ultimately, their discovery led to the production of oral contraceptives, menopausal treatments, breast cancer treatments and many more therapies. Estradiol is currently FDA approved to treat metastatic breast cancer, post-menopausal osteoporosis, advanced prostate cancer, hypoestrogenism, vasomotor symptoms associated with menopause and vulvar and vaginal atrophy associated with menopause. This medication contains a benzene ring, phenolic hydroxyl group at the 3 position, and an additional hydroxyl group on the 17B position. Estradiol targets estrogen receptors and is labeled as an agonist. The mechanism of action of Estradiol reduces the release of gonadotropin-releasing hormones and luteinizing hormone-releasing hormones from the hypothalamus, and reduces gonadotropin release from the pituitary. It is absorbed by the GI tract, skin, and mucous membrane. Some of the available formulations of this drug are gels, injectable solutions, tablets, transdermal patches and topical emulsions, which are all available in varying strengths. Some common names associated with Estradiol are Alora, Climara, Delestrogen, Depo-Estradiol, Divigel, Estrace and there are many more. When taking this medication, patients should be aware of potential side effects they may experience. Some of these common side effects include anxiety, bloating, angioedema, headache, weight changes. More severe side effects of taking this medication include an increased risk of endometrial cancer, cardiovascular risks (stroke and deep vein thrombosis), and risk for breast cancer. If the patients experience any unusual growths in their breasts, unusual vaginal bleeding, dizziness or faintness, severe headaches, changes in vision or pain in their legs, they should contact their health provider. Overall, I have learned a lot about Estradiol and I plan to use this knowledge when I educate patients on their medications. This activity has helped me to remember the concepts taught in class and apply them to an actual medication. By doing this, it can also help me dive into the detailed process of drug development and medication structure analysis.

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For the fall semester, I was assigned Omalizumab for the BMS padlet activities. Throughout the semester, I have learned several key components of this drug through weekly activities and extended research. Omalizumab’s brand name is Xolair, and its’ primary indications are moderate-to-severe asthma, chronic idiopathic urticaria, and nasal polyps. Xolair was initially approved by the FDA in 2003 for moderate-to-severe asthma. Around 460,000 patients have been treated in the US for asthma with Xolair since its approval in 2003. It was then approved for chronic idiopathic urticaria in 2014, followed by approval for allergic asthma in 2016, and most recently, it was approved for nasal polyps in adults in 2020. Omalizumab is normally self-administered by subcutaneous injection in the abdomen region. Its storage guidelines including storing the original prefilled syringe in a refrigerator at 2 degrees to 8 degrees Celsius and protected from sunlight. It should not be kept outside of a refrigerator for more than 2 days. For asthma and nasal polyps, Omalizumab is an Immunoglobulin G (IgG) monoclonal antibody that inhibits binding to the high-affinity Immunoglobulin E (IgE) receptor, which is on basophils and mast cells. Once the bound IgE levels are decreased, there is limited activation of mediators in the allergic response. Patients with allergic asthma showed a decrease in corticosteroid usage and asthma exacerbations during long-term therapy treatment. In treatment of chronic spontaneous urticaria, Xolair binds to Immunoglobulin E and lowers the free Immunoglobulin E levels. In result, the activity on IgE receptors decreases on cells which causes an improvement of chronic spontaneous urticaria symptoms for unknown reasons. The response to therapy for Omalizumab ranges from 12 to 16 weeks and its bioavailability within the body is around 62%. Omalizumab’s half-life is around 24 days for chronic spontaneous urticaria and 26 days for asthma patients. Dosage levels for asthma and nasal polyps are heavily dependent on the patients’ body weight and free/total IgE serum levels. As the patient’s body weight or serum levels change throughout the treatment plan, dosing measurement and frequency should be adjusted. When the dosing for chronic spontaneous urticaria is considered, it is not in any way dependent on body weight or IgE serum levels and is administered at 150 or 300 mg only over a 4-week span. The most common adverse reactions include injection site reactions and headache. Other less common adverse reactions include anxiety, dizziness, toothache, urinary tract infection, upper abdominal pain, and alopecia. Omalizumab has a black boxed warning for Anaphylaxis, which can be presented as bronchospasms, hypotension, or angioedema of the throat or tongue. Patients rarely have reactions of anaphylaxis but should be considered seriously when they do occur. Omalizumab is most often given when inhaled corticosteroids or nasal corticosteroids are ineffective in treating asthma or nasal polyps.

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Throughout this semester, I was tasked with familiarizing myself with the drug naproxen, known by its brand names Aleve, Anaprox, and Naprosyn, among others. It is a non-selective cyclooxygenase-1 and cyclooxygenase-2 (COX-1 and COX-2) inhibitor primarily indicated for treating inflammation, pain (including menstrual pain), and fever. An off-label indication for the drug is to treat acute migraines. Due to its functions, naproxen falls under the nonsteroidal anti-inflammatory drug (NSAID) pharmacological category. Its structure includes a naphthalene ring, a carboxylic acid, and an aromatic ether. It was patented under Syntex Laboratories, and it became FDA-approved in March of 1976. Originally, it was a prescription-only drug, but lower strength formulations of the drug were approved to be sold over-the-counter since 1994.

As previously stated, naproxen inhibits the COX-1 and COX-2 enzymes which are involved in the process of creating prostaglandins from arachidonic acid, effectively reducing an important component in inflammation. The reversible inhibition of these enzymes by naproxen leads to a decrease in the inflammatory response. As with other NSAIDs, it has a Black Box Warning for increased risk of serious cardiovascular thrombotic events as well as increased risk of GI bleeding and ulceration. Because of the increased risk of thrombotic events, naproxen is contraindicated in patients undergoing a coronary artery bypass graft. Aside from these Black Box Warnings, naproxen also has a range of side effects, both minor and severe. Some of its more common and minor side effects include abdominal pain, indigestion, constipation, drowsiness, nausea, dizziness, headache, ringing in the ears, rash, itchy skin, edema, heartburn and difficulty breathing. Serious side effects include cardiovascular events such as myocardial infarctions and strokes, bleeding events, kidney injury, and hepatotoxicity. It has been found that naproxen both crosses the placenta and is present in breastmilk, so considerations must be made for pregnant or breastfeeding patients. It is not recommended for pregnant patients to use naproxen or NSAIDs in general after the second trimester. Additionally, some studies correlate their usage with an elevated chance of miscarriage by affecting implantation of the embryo in the uterus.

Naproxen is currently available in two forms: naproxen sodium and naproxen base. As such, they have different dosing. The time it takes to reach the peak of the drug absorption curve for naproxen sodium is 1-2 hours compared to 2-4 hours with naproxen base. Therefore, it is recommended to use naproxen sodium for acute migraines and other acute pains. Naproxen is metabolized primarily in the liver and excreted primarily in the urine. Concerning pharmacogenomics, CYP2C9 is involved in the metabolism of naproxen; however, there is currently no alternative dosing of naproxen based on CYP2C9 metabolizer status.

Sources used: Lexicomp, Micromedex, Drug Bank, Wikipedia.

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I was assigned the drug Potassium Chloride this semester for the ALE component of BMS. Potassium chloride is an extremely important drug, but it seems so vague compared to other drugs we have learned about. Doing the padlet activities let me learn a lot about potassium chloride and how it works. Potassium chloride is a metal halide salt composed of potassium and chloride and is noted as KCl. Potassium is a mineral that is found naturally in many foods, but potassium chloride came into use as a commercial fertilizer first in 1861 and was later used medically in the 1950s. Slow-K was a 1950s development where the drug was formulated to enter the bloodstream at delayed intervals. It was originally prescribed to the British military forces to balance their diets while serving in Korea. It is now listed as an essential medicine on WHO’s List of Essential Medicines. Potassium chloride’s structure is a potassium ion attached to a chloride ion. The structure consists of a halogenated ion functional group and has no heterocycles. Potassium chloride is indicated for the treatment of hypokalemia (low potassium levels). Potassium levels can be low if you have an adrenal gland disorder, a long bout of diarrhea or vomiting, chronic laxative abuse, taking diuretics, low magnesium levels, or can result from taking other medications and medical conditions. It can also be used to treat diabetic ketoacidosis and is used for parenteral nutrition. When taking these electrolyte supplements, they target the other potassium chloride solute carriers and group with them in the body to replenish the potassium already found in your body. Potassium is extremely important for heart function because it is the major cation of the intracellular fluid. This means that it is essential for the conduction of nerve impulses in the heart, brain and skeletal muscle; as well as the contraction of cardiac, skeletal, and smooth muscle. Too much potassium can stop the heart which is used in some surgeries so that the procedure can be carried out on the heart. Common side effects of potassium chloride include diarrhea, gas, nausea, and vomiting. When potassium chloride is injected too quickly, heart problems may result. When taken orally, severe side effects can include abdominal pain, peptic ulcers, or gastrointestinal bleeding. Potassium chloride should not be taken if you already have high levels of potassium in your bloodstream. Overall, potassium chloride was a really interesting drug to learn about.

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My assigned drug for this semester was sitagliptin. Through literature research, I have learned several facts about this drug. Sitagliptin’s creation was due to a DPP-4 inhibitor program started at Merck in 1999. This program was the result of the development of glucagon-like peptide 1 (GLP-1). Instead of GLP-1 therapy, researchers wanted to use an alternate route, thus DPP-4 inhibitors. Sitagliptin, or Januvia, known commercially, has been approved since late 2006 and has been on market since 2007. Sitagliptin’s indication is type II diabetes mellitus. Diabetes type II occurs when the body does not create enough insulin to monitor blood glucose levels. Insulin is a natural hormone that the body creates to regulate cellular glucose uptake. Sitagliptin works by inhibiting the enzyme, dipeptidyl peptidase 4 (DDP-4). DDP-4 slows the production of hormones that decreases blood glucose levels, while insulin synthesis is increased. Hepatic glucose synthesis is lowered as a result of decreased glucagon secretion. Incretin hormones are secreted by the gut throughout the day under physiologically normal conditions, and their levels rise in response to meals. The DPP-4 enzyme quickly deactivates incretin hormones.

While this drug is effective, it is recommended by doctors for patients to use adjuncts with diet and exercise. Patients will take the drug orally without regard to meals. Also, sitagliptin is sometimes used in combination therapy such as metformin which makes the common brand name: Janumet. Side effects of my assigned drug include headache, signs of a common cold, and nose or throat irritations. The following are adverse reactions that are not so common: arthralgia, severe cutaneous adverse reactions, heart failure, anaphylaxis, and acute pancreatitis. Patients that have undergone bariatric surgery or renal impairment should use it with caution. Additionally, for people with type II diabetes who want to get pregnant, dipeptidyl peptidase 4 (DPP-4) inhibitors are not advised. Individuals who risk becoming pregnant with treatment should utilize reliable contraception.

The hemoglobin A1C test, HbA1c, should be used by patients with type II diabetes. It will help them monitor their levels. The HbA1c is a great indicator to assess whether Sitagliptin is effective at reducing hyperglycemia. Patients who maintain a stable level of control and are fulfilling their treatment objectives should be monitored two to three times a year. Patients whose treatment goals have not been attained or whose medication has changed should be monitored every three months. The literature on Sitagliptin was truly interesting and I have learned a great deal about its history of discovery and development.

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Benztropine was developed by USL Pharma and approved by the FDA in 1996. It was developed by combining a tropane ring from cocaine and a diphenyl ether from the dialkylpiperazines to better improve dopamine reuptake and decrease serotonin and norepinephrine inhibition. The diphenyl ether is a proved dopamine uptake inhibitor. Through development, researchers improved its action by adding a chlorine substituent to the para position of one of the phenyl rings.

It is indicated for the reduction of Parkinson symptoms, drug-induced extrapyramidal symptoms, and dystonic reactions. It has been used off-label to treat chronic sialorrhea and intractable hiccups. It helps patients regain control of their movements by acting as an anticholinergic and antihistamine agent. Benztropine targets acetylcholine and histamine receptors. The drug blocks muscarinic receptors by competing with acetylcholine in the central nervous system and smooth muscles. By blocking these receptors, the drug helps reduce the spastic movements.

Benztropine is long-lasting and can be administered less frequently. It can be administered orally, intravenously, and through intramuscular routes. Orally, it is available in 0.5 mg, 1 mg, and 2 mg tablets. Starting doses begin at 0.5 mg and can be increased in 0.5 intervals up to 6 mg as needed. Benztropine can be taken with or without food. Oral administration is the preferred method of treatment for initial and acute symptoms of Parkinson’s disease. The drug is available for 1 mg per mL injection for intramuscular and intravenous administration. The intravenous administration is the preferred treatment for drug-induced extrapyramidal symptoms and can be used when oral and IM cannot be administered.

Benztropine is contraindicated in patients under the age of three and breastfeeding women. The drug can be more potent in the geriatric population due to their sensitivity to anticholinergic agents, so the geriatric population should be started at the lowest dose. The most common side effects include tachycardia, confusion, depression, disorientation, skin rash, constipation, nausea, dysuria, and blurred vision. However, they can range from mild to severe. Mild effects include fever, rash, general weakness, and insomnia. The most severe reactions include toxic megacolon, paralytic ileus, and ocular hypertension.

It is important to monitor the patients’ responses to benztropine because certain populations can be more sensitive. However, it has been in use for fifty years and has not been associated with any major toxicity events. The most concerning consideration is overdose which can be detected used an ECG and blood glucose concentrations. Overall, benztropine has proved to be an effective agent to improve the quality of life for patients suffering with Parkinson’s disease and other movement disorders.

References:

Benztropine. Login. (n.d.). Retrieved November 27, 2022, from https://online.lexi.com/lco/action/doc/retrieve/docid/patch_f/6439?cesid=4W0r7LEa1dz&searchUrl=%2Flco%2Faction%2Fsearch%3Fq%3Dbenztropine%26t%3Dname%26acs%3Dfalse%26acq%3Dbenztropine#

U.S. National Library of Medicine. (n.d.). Benztropine. National Center for Biotechnology Information. PubChem Compound Database. Retrieved November 27, 2022, from https://pubchem.ncbi.nlm.nih.gov/compound/BENZTROPINE

U.S. National Library of Medicine. (n.d.). Home - books - NCBI. National Center for Biotechnology Information. Retrieved November 27, 2022, from https://www.ncbi.nlm.nih.gov/books

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Dabigatran (brand name: Pradaxa) is a specific, reversible, and direct thrombin Inhibitor used to prevent stroke and systemic embolism in patients with nonvalvular atrial fibrillation. The discovery of this drug was important because it offered a safe and convenient alternative to warfarin. It can inhibit both free and fibrin-bound thrombin by preventing thrombin-mediated effects, including cleavage of fibrinogen to fibrin monomers, activation of factors V, VIII, XI, and XIII, and inhibition of thrombin-induced platelet aggregation. As an orally available prodrug, it achieves its peak concentration 1-2 hours after ingestion and has a half-life of 12-14 hours. The drug is not metabolized by cytochrome P450 isoenzymes and does not interact with food (1).

X-ray crystal structure of the bovine thrombin complex formed with the peptide-like benzamidine-based inhibitor NAPAP revealed the conformation of an enzyme-bound thrombin inhibitor and its interactions with the residues of the active site cleft. This data was the cornerstone for designing a new class of inhibitors for α-thrombin. Dabigatran was identified as a lead compound because of its favorable selectivity profile and strong in vitro and in vivo activity, exhibiting long anticoagulation duration in rats after i.v. Administration and toleration at high doses (2). The drug itself was not orally active due to its polarity, so it was later converted into an orally active prodrug, dabigatran etexilate, by adding ethyl ester and hexyloxycarbonyl carbamide hydrophobic side chains(3).

The usual dose for adults is 150mg twice daily orally with water. It comes in 75mg or 150mg capsules. The capsules should not be broken or chewed. This action can lead to a 75 increase in absorption and potentially severe adverse reactions. These side effects include Gastrointestinal (such as dyspepsia with possible abdominal discomfort/pain, GI hemorrhage, GERD), Hematologic (such as bleeding, anemia, hematoma), Hepatic (increase in ALT), and renal (hematuria). Patients with hepatic and renal impairments should use the drug with caution. The use of the drug is not recommended in patients with valvular heart disease. Due to the increased risk of bleeding, the use of this drug alongside other antithrombotic agents is not recommended. Moreover, P-glycoprotein (P-gp) inducers/inhibitors may reduce dabigatran bioavailability and should be avoided. This drug should also be used with extreme caution when it is administered in an elderly population, and other treatment options should be considered in this group (4). It’s regarded as a drug with risk factor C in pregnancy, with some implications in animal studies. Still, the data is insufficient to assess the safety of direct thrombin inhibitors during pregnancy, and excretion in breast milk is also unknown (5).

References

1.        Eisert WG, Hauel N, Stangier J, Wienen W, Clemens A, van Ryn J. Dabigatran: An Oral Novel Potent Reversible Nonpeptide Inhibitor of Thrombin. Arterioscler Thromb Vasc Biol [Internet]. 2010 Oct 1 [cited 2022 Nov 25];30(10):1885–9. Available from: https://www.ahajournals.org/doi/abs/10.1161/ATVBAHA.110.203604

2.        van Ryn J, Goss A, Hauel N, Wienen W, Priepke H, Nar H, et al. The Discovery of Dabigatran Etexilate. Front Pharmacol [Internet]. 2013 [cited 2022 Nov 25];4. Available from: /pmc/articles/PMC3569592/

3.        Hauel NH, Nar H, Priepke H, Ries U, Stassen JM, Wienen W. Structure-based design of novel potent nonpeptide thrombin inhibitors. J Med Chem [Internet]. 2002 Apr 25 [cited 2022 Nov 25];45(9):1757–66. Available from: https://pubs.acs.org/doi/abs/10.1021/jm0109513

4.        Dabigatran Uses, Side Effects & Warnings - Drugs.com [Internet]. [cited 2022 Nov 25]. Available from: https://www.drugs.com/mtm/dabigatran.html

5.         Guyatt GH, Akl EA, Crowther M, Gutterman DD, Schünemann HJ. Executive summary: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest [Internet]. 2012 [cited 2022 Nov 25];141(2 Suppl):7S-47S. Available from: https://pubmed.ncbi.nlm.nih.gov/22315257/

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For this semester, I was assigned the drug Venlafaxine which has the brand name of Effexor. This drug is really interesting as it was the first serotonin and norepinephrine reuptake inhibitor to be placed on the market. It is said to be as just effective as its tricyclic antidepressants with less side effects. With the growing prevalence of mental disorders such as depression, this drug is actually very important. Venlafaxine is FDA approved for the treatment of generalized anxiety disorder, panic disorder, social phobia, and major depressive disorder which is what it majorly used for. It also has some non-FDA uses as well such as attention deficit hyperactivity disorder, obsessive compulsive disorder, migraines, bipolar disorders, and even flushing due to menopause. It was approved by the FDA in 1993 as an oral medication. Venlafaxine works by inhibiting neuronal uptake of serotonin, dopamine, and norepinephrine. It is very potent toward the reuptake of serotonin and norepinephrine, but it is only mildly potent toward the reuptake of dopamine. At low doses, venlafaxine works as a selective serotonin reuptake inhibitor while at high doses it acts as a serotonin and norepinephrine reuptake inhibitor. By inhibiting the re-uptake of these neurotransmitters, it allows for increased levels of serotonin and norepinephrine which leads to an increase in energy, happier feelings, and a calming sensation. Venlafaxine is metabolized through first-pass metabolism by CYP2D6. CYP2D6 transforms venlafaxine into its active metabolite, O-desmethylvenlafaxine. Other metabolites include N-desmethylvenlafaxine and N,O-didesmethylvenlafaxine which are not as active as the previous mentioned metabolite. Due to metabolism through CYP2D6, strong CYP2D6 inhibitors and inducers should be avoided in order to prevent efficacy and toxicity issues that could arise.  If a strong CYP2D6 inhibitor was administer with venlafaxine, it could prevent a majority of the drug from being converted to its active metabolite which would greatly reduce the effectiveness of the medication. If a strong CYP2D6 inducer was used with venlafaxine, it could lead to toxic side effects as there would be a greater number of the active metabolite, O-desmethylvenlafaxine, in the body.

This medication comes with a black box warning for a risk of suicidal thoughts and behavior.  One thing I found really interesting while researching venlafaxine is that all antidepressants are required to have a black-box warning for suicidal thoughts and behavior. Another interesting thing about this medication is that patients do not need to be taking off venlafaxine abruptly as it can cause withdrawal like syndromes. Their dosage should be reduced at a consistent rate until it is safe to say they can stop using the medication.

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Ramipril inhibits the RAAS system by binding to and inhibiting ACE thereby preventing the conversion of angiotensin I to angiotensin II. As plasma levels of angiotensin II fall, less activation of the G-protein coupled receptors angiotensin receptor I (AT1R) and angiotensin receptor II (AT2R) occurs. AT1R mediates vasoconstriction, inflammation, fibrosis, and oxidative stress through a variety of signaling pathways. These include Gq coupling to the inositol triphosphate pathway, activation of phospholipases C, A2, and D which contribute to eicosanoid production, activation of Ca2+-dependent and MAP kinases, Gi and G12/13, and eventual activation of the Jak/STAT pathway leading to cell growth and production of extracellular matrix components. AT1R activation also leads to increased activity of membrane-bound NADH/NADPH oxidase which contributes to production of reactive oxygen species. Decreased activation of this receptor mediates the renoprotective, antihypertensive, and cardioprotective effects of ramipril by reducing inflammation and vasoconstriction. AT2R acts in opposition to the effects of AT1R by activating phosphotyrosine phosphatases which inhibit MAP kinases, inhibiting Ca2+ channel opening, and stimulating cGMP and nitric oxide production leading to vasodilation. These counteracting effects are shared by the Mas receptor which is activated by Ang (1-7), a subtype of angiotensin produced by plasma esterases from AngI or by ACE2 from AngII produced through a secondary pathway by tonin and cathepsin G. Ang (1-7) also activates AT2R although the bulk of its effect is mediated by MasR. ACE is also responsible for the breakdown of bradykinin. The resulting buildup of bradykinin due to ACE inhibition is thought to mediate the characteristic dry-cough as a side effect of ACE inhibitor medications. Ramipril is used for the management of mild to severe hypertension. It may be used to reduce cardiovascular mortality following myocardial infarction in hemodynamically stable individuals who develop clinical signs of congestive heart failure within a few days following myocardial infarction. Label To reduce the rate of death, myocardial infarction and stroke in individuals at high risk of cardiovascular events. May be used to slow the progression of renal disease in individuals with hypertension, diabetes mellitus and microalubinuria or overt nephropathy. Following oral administration, about 60% of the dose is eliminated in the urine as unchanged ramipril (<2%) and its metabolites. About 40% of the dose is found in the feces, representing both unabsorbed drug and drugs and metabolites eliminated via biliary excretion. The urinary excretion of ramipril may be reduced in patients with impaired renal function. Hepatic metabolism accounts for 75% of total ramipril metabolism. 25% of hepatic metabolism produces the active metabolite ramiprilat via liver esterase enzymes. 100% of renal metabolism converts ramipril to ramiprilat. Other metabolites, diketopiperazine ester, the diketopiperazine acid, and the glucuronides of ramipril and ramiprilat, are inactive. These common side effects of ramipril happen in more than 1 in 100 people. There are things you can do to help cope with them: a dry, tickly cough that does not get better, feeling dizzy or lightheaded, headaches, diarrhea, vomiting, a mild skin rash, and blurred vision. Ramipril was patented in 1981 and approved for medical use in 1989. It is available as a generic medication.In 2020, it was the 196th most commonly prescribed medication in the United States, with more than 2 million prescriptions.

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For this semester of BMS and the ALE component, I was assigned the drug, Denosumab. On June 1, the FDA approved a new osteoporosis treatment. The drug denosumab, under the trade name, Prolia, was discovered using an early application of genomic technology. Denosumab is approved for the treatment of postmenopausal women with osteoporosis who are at high risk of fractures. The drug, which is administered as an injection every six months, significantly reduces the risk of hip, spine, and neck fractures. The new medication is the result of genomic research. Scientists at Immunex, a business later acquired by Amgen, identified a new gene fifteen years ago that specifies a protein called osteoprotregerin that stimulates the osteoclast cells, which are responsible for bone deterioration. They used the then-new rapid genomic-based gene identification techniques to make the discovery. An antibody that blocks osteoprotegerin's action was created by scientists. Osteoclasts are prevented from destroying bone by the antibody (the medication denosumab), which binds to a protein known as RANK Ligand. Osteoclasts, which break down bone, must form, survive, and function in order to produce RANK Ligand. There were many tests conducted before denosumab was approved. Three years of treatment were given to more than 7,800 women who had finished menopause. The drug-treated women reportedly experienced a 40% decrease in hip fractures and a nearly 70% decrease in vertebral fractures. Significant increases in spine, hip, and neck bone density were seen in women receiving treatment. Denosumab offers a new way to treat osteoporosis. Denosumab can cause side effects, just like any other medication. There may be an increased risk of skin rashes and some infections, such as endocarditis and cellulitis. Similar to bisphosphonates, denosumab may slow the healing of broken bones and hinder bone remodeling, a physiological process by which our bodies change the shape of our bones in response to stress. However, overall, in the treated group, the advantages greatly outweighed the disadvantages. Amgen is currently conducting additional long-term studies to evaluate the medication's long-term safety. Ten years will be spent monitoring the drug's four thousand female users. New medicines based on genomic research are now starting to reach those in need after nearly 20 years of research. I have been a pharmacy technician for two years and I never heard of this drug, so it was interesting to learn about it especially since I am interested in specializing in women’s health when I start my pharmacy career.

Narayanan P. (2013). Denosumab: A comprehensive review. South Asian journal of cancer, 2(4), 272–277. https://doi.org/10.4103/2278-330X.119895

Lexicomp, Micromedex, Drug Bank

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Over the course of this semester, I was assigned the drug escitalopram. The drug Escitalopram, also known as Lexapro, was developed in the summer time of 1997. Escitalopram was developed and invented by Lundbeck and Forest Laboratories in the United States. Forest Laboratories from New York specializes in the  central nervous system. Following its creation of Celexa, they soon discovered this drug, which is Lexapro or escitalopram. Following this, its new drug application was submitted to the FDA in March of 2001. It then later became approved for the market for sales in March of 2009 by the FDA. This drug was discovered from the drug Celexa, also known as Citalopram. This specific medication falls into the category of being a selective serotonin reuptake inhibitor. SSRI. It is indicated and approved to treat major depressive disorder and generalized depressive disorder. This medication also treats social anxiety disorder, panic disorder and obsessive compulsive disorder. Escitalopram is the S-stereoisomer of citalopram, Celexa. It targets serotonin, also known as the 5-HT receptor. The mechanism of action is presumed to be connected to the potentiation of the serotonergic activity of the central nervous system resulting from the inhibition of the CNS neuronal reuptake of 5-HT. It acts by increasing the intrasynaptic level of the neurotransmitter serotonin by blocking the reuptake. This helps  to  balance the amount of serotonin in the brain which results in relieving depression symptoms, thoughts and actions. When compared to other SSRIs, this drug has the highest affinity for the human serotonin transporter. Therefore it has a higher chance of controlling depressive moods. When taking this drug, there are a variety of side effects ranging from mild to very severe. While starting Lexapro, there are some side effects that are considered normal. These include dry mouth, headache and nausea, but should go away within the first two weeks while your body adjusts to the medication. There are other lingering side effects. The most common side effects include feeling dizzy, fatigue, upset stomach, diarrhea and/or constipation, dry mouth and many others. These side effects are not present in everyone who takes this medication, but serves as a general list of those that could potentially occur. More severe side effects include neurological disorders, seizures, lack of mood control and much more complicated things that could disrupt other body systems. If experiencing these side effects become noticeable or unbearable, it is best to end the medication and contact your healthcare provider as soon as possible to avoid further complications.

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My assigned drug for the semester was Amphetamine. This drug is used for the treatment of attention-deficit/hyperactivity disorder and narcolepsy for adults and for some children as young as 6 years old. Amphetamine is commonly found in many drugs and is used for its stimulatory effects. It is sold under the brand names Adzenys, Dyanavel, and Eveko, and Adderall. Additionally, derivatives of amphetamine are also used as a stimulant and for the same indications; some of these drugs include Concerta, Dexedrine, Focalin, Metadate, Methylin, Ritalin. Amphetamine works by stimulating the release of catecholamines, mainly norepinephrine and dopamine, from presynaptic neurons. This is what creates the stimulatory effects on the central nervous system, and initiates somewhat of a “fight or flight” response. Amphetamine has also been noted to block the re-uptake of catecholamines by competitive inhibition as a secondary mechanism of action. A wide range of side effects are associated with amphetamine; some of the most common include: weight loss, decreased appetite, nausea, abdominal pain, headache, dizziness, insomnia, mood swings, anxiety, agitation, myocardial infarction, sudden cardiac death, cerebrovascular events, and psychotic disorder. Amphetamine is a schedule II controlled substance, so a prescription is necessary to be able to receive any drugs containing amphetamine.

Amphetamine was originally discovered as a racemic mixture in 1910 by Barger and Dale, but was not utilized as a drug until 1927 when chemist G. A. Alles discovered its ability to induce insomnia. The first drug containing the discovered amphetamine racemic mixture was called Benzedrine, and it was released to the market in 1935 as a treatment for narcolepsy and for mild depression. Additionally in 1937, the use of amphetamines to treat attention deficit/hyperactive disorders in people and children as young as 6 years old was discovered by Charles Bradley. By the late 1940’s, two amphetamine-containing drugs, Benzedrine and Dexedrine were on the market. After widespread and unrestricted use of amphetamines throughout the 1940’s and 50’s, its ability to elevate mood, increase attention, and promote weight loss were revealed through extensive use and study in the military and general population. However, the dangers of amphetamines became largely known, and included severe dependence problems, dangerous heart rate elevation, and stimulant induced psychosis. In 1959, the FDA mandated that amphetamine drugs were for prescription only. However, that did not deter the usage of these drugs, because they were seen as the drug of choice for a wide range of  mental and physical issues. The amphetamine epidemic continued from the 1950’s all the way until 1970 when the Controlled Substance Act was passed. In 1971, amphetamines were issued as a schedule II controlled substance due to their now well known abuse potential, and they still remain on the market for prescription only.

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During the entirety of this semester in BMS and the weekly ALE assignments required of this course, I was assigned the drug Rosuvastatin which I was directed to research. Throughout the semester, I have learned so much about this drug. The brand names for Rosuvastatin are Crestor for tablets and Ezallor for the capsule. Rosuvastatin should be taken around the same time every day and if missed should be taken as soon as possible unless close to the next scheduled dose. Rosuvastatin is a statin drug and similar to other statin drugs it helps reduce the amount of cholesterol in the body. Rosuvastatin primary indication or purpose is to treat familial hypercholesterolemia as well as cardiovascular disease. Its primary target is 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA). Something unique about Rosuvastatin in comparison to other statin drugs, however, is that it contains a sulfonyl functional group. Rosuvastatin was discovered by Shionogi during his drug research after running a series of pyrimidine substituted 3,5-dihydroxy-6-heptenoates containing a sulphonyl moiety through the process of synthesis and screening [1 & 2]. Rosuvastatin was patented in 1991 and was approved by the Food and Drug Administration (FDA) in February 2010. This medication is a selective inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA). “HMG-CoA is the rate-limiting enzyme in cholesterol synthesis. The lipid-modifying effects result from its capacity to upregulate hepatic LDL receptors enhancing uptake and catabolism of LDL as well as its activity of inhibiting hepatic synthesis of VLDL contributing to the reduction of VLDL and LDL particles [3].” The functional groups and heterocycle components that make up Rosuvastatin include a carboxylic acid, sulfonamide, alkene, halogenated benzene ring, two secondary alcohols, and a pyrimidine. This medication in its oral form as either a capsule or tablet should be stored at a controlled temperature around 20 to 25 degrees C and should be kept away from moisture. Some of the common side effects of Rosuvastatin are abdominal pain, nausea, Asthenia, headaches, myalgia, and muscle pains. Some of the more serious adverse effects include the following: Pancreatitis, liver issues, diabetes, Rhabdomyolysis, autoimmune necrotizing myopathy, Acute renal failure, Hematuria, and proteinuria [3]. I have really enjoyed learning about this drug and how it positively impacts those suffering from hypercholesterolemia or cardiovascular disease. I guaranty that I will recognize this drug if I ever dispense it to patients in a pharmaceutical setting.  I look forward to learning more about other medications and committing them to my ever-growing medication knowledge bank.

References:

Wikipedia contributors.

1.     "Rosuvastatin." Wikipedia, The Free Encyclopedia. Wikipedia, The Free Encyclopedia, 23 Nov. 2022. Web. 27 Nov. 2022.

2.     Quirk, Jeremy, et al. “Rosuvastatin Calcium.” Nature News, Nature Publishing Group, https://www.nature.com/articles/nrd1205.

3.  https://www.micromedexsolutions.com/micromedex2/librarian/CS/CD85B9/ND_PR/evidencexpert/ND_P/evidencexpert/DUPLICATIONSHIELDSYNC/E813DF/ND_PG/evidencexpert/ND_B/evidencexpert/ND_AppProduct/evidencexpert/ND_T/evidencexpert/PFActionId/evidencexpert.DoIntegratedSearch?SearchTerm=Rosuvastatin&UserSearchTerm=Rosuvastatin&SearchFilter=filterNone&navitem=searchALL#

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Over the course of this semester, I was assigned to research the drug Diclofenac. Diclofenac was a product of rational drug design based on the structures of non-steroidal anti-inflammatory drugs such as phenylbutazone, indomethacin, and mefenamic acid. Scientists Alfred Sallmann and Rudolf Pfister sought to synthesize a nonsteroidal anti-inflammatory drug with both high activity and tolerability. Diclofenac was developed by the scientists and introduced by a former Swiss pharmaceutical known as Ciba-Geigy in 1973. In July of 1988, Diclofenac was approved by the FDA and was placed on the market in the United States as an enteric-coated tablet under the trade name, Voltaren. In 2007, 1% Diclofenac gel was approved by the FDA and became available in the United States as a topical form of the prescription drug. Diclofenac has come a long way in over the last five decades. This drug is now available as both a generic and brand name medication, sold under multiple trade names, and taken in a variety of dosage forms such as delayed-release and extended-release tablets, capsules, powders, creams, or gels. In 2020, the FDA declared that diclofenac sodium 1% gel could now be purchased as an over-the-counter medication. Diclofenac is a benzene-acetic acid derivative with analgesic, anti-inflammatory, and antipyretic properties. It is classified as a non-steroidal anti-inflammatory drug. Diclofenac is indicated to provide anti-inflammatory and analgesic effects to relieve symptoms of osteoarthritis, rheumatoid arthritis, and ankylosing spondylitis. It has also been used off-label to provide temporary relief to patients suffering from gout, migraine attacks, and myalgia. Although its mechanism of action is not completely understood, we are aware that it acts as an inhibitor of cyclooxygenase-1 and -2, also known as COX-1 and COX-2, which are the enzymes responsible for the production of prostaglandins. This mechanism is what allows the drug to reduce inflammation. Voltaren gel is indicated for reducing inflammation and providing relief of localized osteoarthritis joint pain, particularly in the knees and hands. Diclofenac shouldn’t be used in patients who have known hypersensitivity to Diclofenac or other components of the drug, history of asthma or allergic-type reactions after taking aspirin or other NSAIDs or have undergone a Coronary Artery Bypass Graft (CABG) Surgery. Patients taking this medication may experience side effects such as nausea and vomiting, high blood pressure, abdominal pain, or pain in extremities. The FDA also issued a black box warning stating that it increases the risk of serious cardiovascular and gastrointestinal events.

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Throughout this semester of BMS, I have been assigned methylphenidate as my drug. More commonly known by the brand name, Ritalin, methylphenidate was first synthesized in 1944 by Leandro Panizzon. This drug was not reported to have stimulating effects until 1954 and was not used as a treatment for ADHD in the United States until the 1960s. When the drug was first synthesized, it was a mixture of two racemates with 80% erythro and 20% threo. The threo racemate was found to be the stimulating one, so it was isolated. Now the modern formulations for methylphenidate contain threo in a racemic mixture of 50-50 between d and l isomers.

Methylphenidate is a stimulant that is indicated for the treatment of ADHD (especially in children) and Narcolepsy. It can be taken through a variety of different ways including oral capsule, tablet, solution, and transdermal patch. It works by targeting three different receptors, those being the Sodium-dependent dopamine transporter, 5-hydroxytryptamine receptor, and Sodium-dependent noradrenaline transporter. While its exact mechanism is unclear, methylphenidate has been shown to act as a norepinephrine and dopamine reuptake inhibitor (NDRI), thereby increasing the presence of these neurotransmitters in the extraneuronal space and prolonging their action. It also appears to stimulate the cerebral cortex and subcortical structures which is similar to what amphetamines do. Because of the ways that methylphenidate interacts with the central nervous system, it has a black box warning for abuse and dependence. It is recommended that this drug not be given to those that have a history with alcohol dependence and other drug dependencies. Methylphenidate is also contraindicated for hypersensitivity in patients and should not be taken if the patient has a history of bipolar disorder, cardiovascular disorder, seizure disorder, or tourette syndrome. The common side effects associated with this drug are gastrointestinal and nervous system based. Specifically, there is decreased appetite, nausea, and xerostomia in the GI and headache (including migraine and tension headaches), insomnia (including initial insomnia), and irritability in the nervous system. The serious side effects that can occur are cardiovascular events such as acute myocardial infarctions, sudden cardiac death, stroke, increased heart rate, and increased blood pressure. The patients are also at risk for growth suppression in pediatric, priapism, and psychiatric/behavioral effects such as psychosis and mania symptoms. It was very interesting to learn about this drug over the course of the semester, and it didn’t feel like it was a large amount of information because of how it was broken up into smaller assignments.

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Bupropion, or also known by the brand name Wellbutrin, was discovered in 1969 by Nariman Mehta of Burroughs Wellcome (now GlaxoSmithKline). The patent for the drug was granted in 1974 and was later approved by the Food and Drug Administration as an antidepressant in December of 1985. After its initial approval, instances of seizures began to occur due to high dose regimens. This resulted in the drugs withdrawal in 1986 and then was reintroduced in 1989. The FDA later approved an alcohol-resistant formulation of the drug in 1993 under the name of Wellbutrin SR. This new formulation was recommended to be taken two times a day rather than the three times a day with the immediate release formulation. The primary indications for Bupropion are major depressive disorder, seasonal affective disorder, bipolar disorder and attention-deficit/ hyper-activity disorder. Another formulation of Bupropion was introduced in 1997 under the name Zyban which is indicated for smoking cessation. Bupropion is administered orally through tablets that range in formulations. Some of these formulations include slow release, extended release and immediate release. These formulations come as either Hydrobromide salts or Hydrochloride salts. 150 milligrams of Bupropion Hydrochloride are equivalent to 174 milligrams of Bupropion Hydrobromide. Bupropion Hydrobromide is also known by the brand name Aplenzin. The ideal recommended storage of Bupropion is 15 degrees Celsius to 30 degrees Celsius (59 degrees Fahrenheit to 86 degrees Fahrenheit). Store where it is protected from light and moisture.  Bupropion is a norepinephrine/dopamine-reuptake inhibitor (NDRI) that exerts its pharmacological effects by weakly inhibiting the enzymes involved in the uptake of the neurotransmitters norepinephrine and dopamine from the synaptic cleft, therefore prolonging their duration of action within the neuronal synapse and the downstream effects of these neurotransmitters. It acts by inhibiting Sodium-dependent dopamine transporters and Sodium-dependent noradrenaline transporters. Side effects range variably depending on the patient. Some of the more common side effects being dizziness or headache, constipation, diarrhea, stomach pain, loss of appetite, shakiness, gas, dry mouth, trouble sleeping, muscle or joint pain, nose or throat irritation, sweating a lot and change in weight. In 2009, tests were run to determine the relation between Wellbutrin and its generic versions. The results concluded that the generic Budeprion increased the chances of side effects and produced a lower efficacy than its name brand counterpart. Some of these side effects being irritation, hostility and worsened depressive/suicidal behaviors. In 2013, the Food and Drug Administration conducted additional test and proved that generic products from four separate companies lacked in bioequivalence compared to Wellbutrin, concluding the lack of efficacy.

Sources: Lexicomp, Micromedex and Wikipedia

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Enoxaparin is sold under the brand name Lovenox. It belongs to Heparins drug class and acts as an anti-coagulant. The medical use of enoxaparin was authorized in 1993, however it was originally produced in 1981. It is listed as one of the Essential Medicines by the World Health Organization. There are numerous other brand names and generic versions of enoxaparin on the market. Heparin is used to make enoxaparin. It is a low molecular weight heparin (LMWH) that received its initial medical approval in 1993. Enoxaprin with Molecular weight of 4000 to 5000 Daltons has 15 hydrogen bond donors and 38 hydrogen bond acceptors.

FDA approved enoxaparin for Deep vein thrombosis (DVT), Non-ST-elevation myocardial infarction (NSTEMI), ST-elevation myocardial infarction (STEMI), pulmonary embolism (PE), and for venous thromboembolism treatment (VTE). It can be administered in sub-cutaneous (SC) and intravenous (IV) routes.

Enoxaparin is an indirect anticoagulant that binds to and amplifies antithrombin III (a serine protease inhibitor), forming a complex that permanently inactivates factor Xa. The relative degree to which thrombin (factor-IIa) and factor-Xa are inhibited varies between unfractionated heparin and enoxaparin. Antithrombin and thrombin cannot be bound by smaller heparin fragments. LMWH have stronger efficacy against factor-Xa and lessen the amount to which thrombin is inhibited because of their shorter chain length and lower molecular weight.

Its peak effect can be seen after four hours of administration. Desulfation and depolymerization in the liver break it down into lower molecular weight fragments with decreased physiologic action. Enoxaparin is predominantly excreted in the urine and has first-order kinetics. It has an elimination half-life of 3 to 4.5 hours after a single dose.

Because LMWH formulations can be injected subcutaneously (sc), they can be given to both inpatients and outpatients without the requirement for laboratory monitoring, which is one of its benefits. For the prophylaxis of venous thromboembolism 40 mg SC is recommended once daily. Enoxaparin’s adverse impact profile is comparable to that of heparin. Because the antidote is less effective, bleeding consequences can be serious and even fatal. Some of the adverse effects include bleeding, Heparin-induced thrombocytopenia, Hypoaldosteronism, Gastrointestinal bleeding, Rectal sheath hematoma, Osteoporosis and Hepatotoxicity. It is contraindicated in patients with hypersensitivity to enoxaparin, gastrointestinal bleeding, and hypersensitivity to benzyl alcohol in neonates. FDA provided a boxed warning stating that patients anticoagulated with low molecular weight heparins (LMWH), such as enoxaparin, who get neuraxial anaesthesia or undergo spinal puncture are more likely to develop epidural and spinal hematomas.

References:

[1]: https://www.ncbi.nlm.nih.gov/books/NBK539865/

[2]: Lieberman, Jay R., and Jennifer A. Bell. "Venous thromboembolic prophylaxis after total hip and knee arthroplasty." JBJS 103.16 (2021): 1556-1564.

[3]: National Center for Biotechnology Information. "PubChem Compound Summary for CID 772, Enoxaparin" PubChem, https://pubchem.ncbi.nlm.nih.gov/compound/Enoxaparin.

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Esomeprazole is a drug known to treat gastrointestinal disorders, such as tending to an erosive esophagitis from overuse of NSAIDs, symptomatic gastroesophageal reflux disease (GERD), Zollinger-Ellison Syndrome, and peptic ulcers. This drug treats these disorders by inhibiting proton pumps, specifically H+/K+ ATPase pumps, through irreversible binding mechanisms. To bind to the H+/K+ ATPase pumps, esomeprazole is converted to an active, achiral sulfenamide. This active form of the drug is able to bind to these pumps in an irreversible fashion through the formation of one or more covalent disulfide bonds. By inhibiting these proton pumps, the stomach’s parietal cells are hindered from secreting hydrochloric acid. The mechanism of esomeprazole is important for the reduction of gastric pH due to the chronological significance of the H+/K+ ATPase pump being the last step in producing a stomach’s pH. Therefore, this results in a reduction of the stomach’s pH levels.

Esomeprazole’s structure may not look chiral, but the sulfur atom at the center of the molecule acts as a chiral atom. This sulfur atom allows esomeprazole and its original racemic structure, omeprazole, to have different isomers and preferred enantiomers for enhanced treatment. Esomeprazole is similar to Omeprazole; however, esomeprazole is present solely as the (S)-isomer of the racemic omeprazole to optimize treatment of gastric pH regulation.

The journey of discovering, developing, and marketing this acid reflux treatment began on February 2, 2001 for pediatric patients experiencing acid reflux issues. Esomeprazole was marketed under the brand name, Nexium, and sponsored by the company, AstraZeneca. According to the FDA files regarding this drug approval, there were four studies done regarding the pharmacokinetic and pharmacodynamic implications of this drug. Initially, they conducted a multi-dose study in pediatric patients experiencing GERD in the 1-11 year old range. Following that initial study, they conducted a multicentered, randomized, double-blind, parallel-group, dose-response study in patients of the same age group as the previous. This FDA document also included an in vivo study on healthy adults and a subjective study on pediatric patients less than two years old. After performing these various studies, they collectively found that depending on the patient's body weight, as body weight increases, the area under the curve, a measurement of effectiveness of the drug, increases. After approval of esomeprazole, patients were able to tolerate the drug better than omeprazole due to its reduced first-pass metabolism and plasma clearance rate. In turn, this makes esomeprazole have less side effects than comparative treatments. However, patients may still experience diarrhea, headache, and stomach pain.

Sources: FDA, PubChem

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Carvedilol, trade name Coreg, is used in the treatment and prevention of mild to severe chronic heart failure. It is an antihypertension medication that is used to treat high blood pressure, left ventricular dysfunction, and congestive heart failure. Carvedilol is both a non-selective β-adrenergic receptor antagonist (β1, β2) and an α-adrenergic receptor antagonist (α1). Carvedilol roughly has a 25-35% bioavailability. Carvedilol is normally considered a second line medication to ace-inhibitors or in addition to diuretics, ACE inhibitors, and digitalis, to increase survival and, also, to reduce the risk of hospitalization. Carvedilol is a tablet available in immediate release and in extended release. It is normally taken by mouth twice a day. The starting dose for patients who start carvedilol is  3.125mg twice a day for 2 weeks. If it is well tolerated patients can have their dose increase to 6.25, 12.5    and 25mg twice daily. There are many side effects associated with carvedilol. They include hyperglycemia, 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. Carvedilol was patented in 1978 and approved for medical use in the United States in 1995. It is considered a third-generation beta-blocker. Carvedilol has many drug interactions. CYP2D6 Inhibitors and poor metabolizers such as (such as quinidine, fluoxetine, paroxetine, and propafenone. Carvedilol is the first beta blocker approved for treatment of all forms of congestive heart failure. Carvedilol is one of the longest studied drugs. There were long difficult stages of scientific, medical, business, and regulatory issues that came with the discovery of the drug. The discovery and development of carvedilol encountered an adverse regulatory climate, skepticism by the cardiology community and hesitance by the company, and in the early 1990s, the fate of the drug was uncertain. Nonetheless, in the largest heart failure study conducted up until that point, carvedilol produced marked reductions in morbidity and mortality, and has given new hope to patients afflicted with congestive heart failure. The story behind carvedilol contains important observations and lessons for scientists, regulators and physicians.

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For this semester of BMS, my assigned ALE drug was lorazepam. I have learned so much about this drug throughout the semester from the drug literature. Lorazepam has the brand names Ativan, Lorazepam Intensol, and Loreev XR. The drug is pharmacologically classified as an antiseizure agent and a benzodiazepine and is indicated for anxiety, premedicated procedural anxiety, and status epilepticus. It also has off-label indications for antipsychotic-induced akathisia, alcohol withdrawal syndrome, catatonia, chemotherapy-induced nausea and vomiting, intoxication, sedation for mechanically-ventilated patients in the ICU, neuroleptic malignant syndrom, opioid withdrawal, seratonin syndrome, and vertigo. Lorazepam binds to benzodiazepine receptors stereospecifically on the postsynaptic GABA neuron and enhances its inhibitory effects. It increases the membrane permeability on the GABA neuron to chloride ions, allowing more chloride ions to enter. The increase in chloride ions causes hyperpolarization of the postsynaptic neuron, resulting in stabilization. It binds to GABA-A receptors in the limbic system and several other sites within the central nervous system. Lorazepam has a US Boxed Warning alert for a risk of respiratory depression, coma and death when used with other opioids, a risk of overdose and death with abuse, missuse, and addiction, and a risk for clinically significant dependence and addiction. Contraindications for this drug include a hypersensitivity to lorazepam or any other benzodiazepines, acute narrow-angle glaucoma, and additional contraindications for parenteral administration include hypersensitivity to polyethylene glycol, propylene glycol, or benzyl alcohol, sleep apnea, intra-arterial injection, and severe respiratory insufficiency. Adverse effects, or side effects, of lorazepam can include hazardous sleep-related activities such as sleep-driving, cooking and eating food, and making phone calls while sleeping, depression, hepatic impairment, renal impairment, anterograde amnesia, CNS effects, neurodevelopmental effects in children, paradoxical reactions, propylene glycol toxicity, withdrawal syndrome, and respiratory disease. There are concurrent drug therapy issues with lorazepam and opioids, and lorazepam and flumazenil because flumanezil can cause withdrawal in patients recieving long-term benzodiazepine therapy. The FDA approval date of lorazepam was July 25, 1980. The IV form of lorazepam should be stored in a refrigerator and protected from light. The parenteral admixture should be prepared in D5W, LR, or NS at room temperature for 24 hours. The oral concentrate should be stored in the refrigerator and protected from light. The oral ER capsule and oral IR tablet should be stored at room temperature. Lorazepam is classified by the Institute for Safe Medication Practices as a high alert medication due to its heightened risk of causing significant harm to patients when used in error.

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Enalapril, brand name Vasotec or Epaned, is a dicarboxylic acid monoester and angiotensin-converting enzyme inhibitor that has antihypertensive properties for adults and children at least one month old. It is a prodrug that is converted to its more active metabolite enalaprilat via de-esterification in the liver. The active form competitively binds and inhibits angiotensin-converting enzyme to block the conversion of angiotensin I to angiotensin II to cause vasodilation. Because of the reduction in angiotensin II, there is also a decrease in angiotensin II-induced aldosterone output by the adrenal cortex. This results in an increased sodium excretion and increased water outflow. This work is done through the renin-angiotensin-aldosterone system which is a signaling system that regulated blood pressure and fluid homeostasis. Enalapril inhibits ACE which suppresses RAAS. Enalapril is orally active and is used to treat hypertension, congestive heart failure, diabetic kidney disease, and post-myocardial infarction. Some of the most common side effects are dizziness, tiredness, cough, and light-headedness. Other side effects include irregular heartbeats, little to no urination, jaundice, numbness, cold and flu symptoms, and high potassium levels, which can cause nausea, weakness, tingling, chest pain, irregular heartbeats, and loss of movement. When taking this drug, foods with high potassium should be avoided, it can cause elevated blood potassium levels. There are also eight disease interactions which include angioedema, bone marrow suppression, CHF, hemodialysis, hyperkalemia, hypotension, liver disease, and renal dysfunction. When it entered the market, it was a "first-line" antihypertensive and was the only US approved ACE inhibitor, at the time, that could be given to most patients once a day. Once enalapril, under the brand name of Vasotec, was approved in December of 1984, it, along with captopril, was the only approved ACE inhibitor in the US. It was classified as a 1B agent which means it is a new molecule with therapeutic gain compared to others like it. This allowed for enalapril to be used to treat "hypertension of all degrees of severity". The patent expired in 2000 and generics were seen on the market. In 2013, it was approved as a liquid form for children and adults, under the brand name of Epaned. The next year, it was granted FDA approval for two new indications, symptomatic heart failure and asymptomatic left ventricular dysfunction and in a new dosage form as a powder for oral solutions. It is a small molecule that is also approved for use in animals.

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Lyrica, known generically as pregabalin, has made a world of difference in patients with neuropathic pain. Pregabalin has been used by over 9 million people in the United States, and many more worldwide. Pregabalin was first discovered by Professor Richard Silverman and his colleague Ryszard Andruszkiewicz in 1987 at Northwestern University. The National Institutes of Health gave these two professors a $680,000 grant to develop this drug. Pregabalin was approved by the FDA December 30, 2004 and was first introduced to the market in 2005 as Lyrica by Pfizer. When first approved at the end of 2004, pregabalin’s only FDA approved indication was neuropathic pain. In June of 2007, pregabalin was FDA approved for the treatment of fibromyalgia and became the first FDA approved drug to treat fibromyalgia. In 2012, pregabalin became FDA approved for the treatment of neuropathic pain related to spinal cord injury, and in 2017 the first extended-release form of pregabalin was FDA approved for the treatment of neuropathic pain.

Currently, the FDA approved indications for pregabalin include neuropathic pain associated with diabetic peripheral neuropathy, neuropathic pain associated with spinal cord injury, postherpetic neuralgia, seizures, and fibromyalgia. Other non-FDA approved indications include cancer-associated neuropathy, chronic refractory cough, generalized anxiety disorder, social anxiety disorder, neuropathic pain in critically ill patients, pruritus, restless leg syndrome, and vasomotor symptoms associated with menopause.

Pregabalin is a GABA analog that targets voltage gated calcium channels. Pregabalin was converted to a lipophilic molecule of GABA to increase absorption and diffusion across biological membranes. Pregabalin binds to the alpha(2)-delta subunit of voltage gated calcium channels, specifically in central nervous system tissues. Pregabalin antagonizes these calcium channels and reduces the release of calcium. The complete mechanism of action is not completely understood, but its antagonism of voltage gated calcium channels is believed to play a major role in the inhibition of neuropathic pain and seizures. It is also believed that pregabalin interacts with descending serotonergic and noradrenergic pathways in the brain stem, which modulates pain transmission in the spinal cord. This mechanism is also related to the inhibition of neuropathic pain related to spinal cord injury.

Because the mechanism of pregabalin is not fully understood, it has some off target effects that cause side effects. Some common adverse reactions associated with pregabalin include central nervous system depression, respiratory depression, delayed hypersensitivity reactions, peripheral edema, suicidal tendencies, weight gain, and visual disturbances. Some less common side effects include dizziness, drowsiness, fatigue, chest pain, contact dermatitis, decreased libido, abdominal pain, and erectile dysfunction.

Pregabalin does not currently have any contraindications besides hypersensitivity, but it does come with a few warnings. Because pregabalin can cause symptoms of withdrawal when treatment is discontinued, prescribers should use caution when prescribing pregabalin to patients with previous substance abuse disorders. Pregabalin may also result in angioedema and should be used with caution in patients with previous history of angioedema. Patients with renal impairment should also use caution when taking pregabalin, and dosing adjustments may be required for safety.

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This semester, I was assigned the drug Albuterol to research and learn more about. Personally, I was very interested in doing this assignment throughout the semester due to the fact that both my brother and I take this medication via an inhaler and nebulizer. Albuterol, also known as salbutamol, is a racemic mixture that was formed in 1972 primarily by L.H.C Lunts. Albuterol was created by researchers at Allen and Hanburys and was the first selective Beta 2 adrenergic agonist developed. This drug contains a phenolic hydroxyl group and a secondary amine group. It also has one stereocenter, meaning there are two diastereomers. Of the two enantiomers, it is clear that R-albuterol is much more effective than S-albuterol and is responsible for creating the needed bronchodilation in order for the most optimal outcome to take place. There was a high demand for the formation of a new Beta agonist due to the major side effects from previous medications lacking selectivity of Beta 2. By May of 1981, the drug found itself being FDA-approved. Albuterol is considered to be a breakthrough therapy that allows for relief of airway obstruction by producing short-acting effects pertaining to bronchodilation. This drug is indicated for those with asthma, bronchospasms due to anaphylaxis, chronic obstructive pulmonary disease or hyperkalemia. It works by relaxing the smooth muscle of the bronchial by acting as an agonist on the Beta 2 receptors. Significant adverse effects to keep in mind when taking this medication include but are not limited to cardiovascular effects, CNS effects or paradoxical bronchospasm. It is still used today as a rescue therapy for many diagnosed with asthmatics. Albuterol is metabolized in the liver, where seventy percent of the dose is excreted in the urine within twenty four hours. The remaining drug and metabolites are excreted within seventy two hours of exposure. There is limited information available on the metabolites available for albuterol but there have been a total of twelve identified. The main metabolism types that have been seen are oxidation, reduction, glucuronidation and sulfation pathways; therefore, indicating that there are both phase I and phase II reactions taking place. When taking this medication, if there is a missed dose take it as soon as you remember or if it is close to the next dose skip it and take the next one as indicated. Albuterol is best stored in a room temperature, dry place protected from light and out of reach from children and pets.

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Through the course of the semester, this assignment has granted me the grand opportunity to gain a deeper understanding and appreciation of the drug allopurinol. I recall seeing this medication a few times in the pharmacy and being curious about what it was for, but never investigating its use. Fortunately, this project has enlightened me and brought clarity to my curiosity.

As a result of internet exploration, I have learned that allopurinol is indicated to treat several conditions. Gout is one of the primary indications, but it is also used to treat nephrolithiasis, recurrent calcium or uric acid stones, and tumor lysis syndrome¹. It comes in tablet and intravenous forms sold under the brand names Aloprim and Zyloprim respectively. When allopurinol enters the body, it targets the xanthine dehydrogenase. It then metabolizes into oxypurinol and inhibits xanthine oxidase. Doing this halts the production of uric acid and hopefully brings relief to the patient who is taking it. It is recommended that this drug be taken after meals, and both the intravenous and tablet preparation can be stored at room temperature.

Allopurinol is not indicated for anyone who has hypersensitivities to it. There are also a few side effects to be aware of when taking it as prescribed. The most common side effects are maculopapular eruption, and pruritus (which occurs less than 1%). The more serious effects to look for include the following: rash, Stevens-Johnson syndrome, toxic epidermal necrolysis; agranulocytosis, aplastic anemia, eosinophil count raised, myelosuppression, thrombocytopenia; granulomatous hepatitis, hepatic necrosis, hepatotoxicity; hypersensitivity reaction; renal failure². Many of the serious adverse effects also occur at less than 1%, but it is highly recommended that the patient reaches out to their doctor if they are experiencing any of these reactions.

Perhaps the most intriguing thing about this drug is that its discovery came from the search for the next anticancer medication. Back in 1956, Roland K. Robins at New Mexico Highlands University reported his finding of this relatively novel drug. While searching for antineoplastics, Robins thought that pyrazolo [3,4-d] pyrimidine would exhibit biological activity. As a result, he wound up piecing together allopurinol³. In Switzerland, P. Schmidt and J. Druey at CIBA reported the same discovery³. In the years following, scientists discovered and demonstrated the medicinal benefits of allopurinol, and in 1966 the Food and Drug Administration announced its approval of this drug as a medication³.

In short, I hope to remember allopurinol and its indications easily because this project has allowed me to spend extra time becoming more familiar with it.

References

1.     Allopurinol (Lexi-Drugs) [Internet]. Lexicomp. [cited 2022 Nov 27]. Available from: https://online.lexi.com/lco/action/doc/retrieve/docid/patch_f/6303?cesid=4rXqm8VFFl4&searchUrl=%2Flco%2Faction%2Fsearch%3Fq%3Dallopurinol%26t%3Dname%26acs%3Dtrue%26acq%3Dallo#

2.     Micromedex products: Allopurinol [Internet]. IBM Micromedex. [cited 2022 Nov 27]. Available from: https://www.micromedexsolutions.com/micromedex2/librarian/CS/F4DC74/ND_PR/evidencexpert/ND_P/evidencexpert/DUPLICATIONSHIELDSYNC/582C80/ND_PG/evidencexpert/ND_B/evidencexpert/ND_AppProduct/evidencexpert/ND_T/evidencexpert/PFActionId/evidencexpert.DoIntegratedSearch?fromInterSaltBase=true&false=null&SearchTerm=Allopurinol&UserMdxSearchTerm=%24userMdxSearchTerm&=null

3.     Allopurinol [Internet]. American Chemical Society. [cited 2022 Nov 27]. Available from: https://www.acs.org/content/acs/en/molecule-of-the-week/archive/a/allopurinol.html

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Pravastatin is a competitive 3-hydroxy-3-methylglutaryl coenzyme-A (HMG Co-A) reductase inhibitor that treats homozygous and heterozygous familial hypercholesterolemia, hyperlipidemia, and dyslipidemia. Additionally, this drug can be used in patients with coronary artery disease to prevent various cardiovascular events. Pravastatin is an orally administered tablet taken once daily with or without food and is available in four different doses. It was patented and FDA-approved for medical use in 1980 and 1991, respectively, and has the trade name Pravachol. Pravastatin was first developed by Sankyo Co. Ltd. in Japan, but the first approved drug product was developed by Bristol Myers Squibb in the United States. It is one of seven drugs categorized as a statin which helps to lower the cholesterol in the body. Additionally, it was the first statin to be administered as an active form instead of a prodrug. Like other statin drugs, pravastatin is most effective when used as an adjunctive therapy with diet and exercise. This drug has been determined safe and efficacious for many patients including adults, geriatrics, and children who are over seven years old. It is not recommended for use in infants or pregnant women. Due to the ability of crossing the placenta and physiological changes throughout pregnancy, pravastatin is contraindicated in treating pregnant women and nonstatin therapies are recommended instead for treatment. Pravastatin’s target is HMG Co-A Reductase, which is the rate-limiting enzyme used in synthesizing cholesterol in the body. The inhibition of this enzyme increases the metabolism of hepatic low-density lipoprotein and is then excreted from the body. By competitively inhibiting this enzyme, the drug can reduce LDL cholesterol and the total amount of cholesterol in the body. Pravastatin experiences the first-pass effect in the liver once administered, however, only a small amount of the drug is affected by the metabolism in the liver. This drug is mostly metabolized in the stomach while also in the kidneys. The active drug is metabolized into inactive metabolites which have no further action on the body. After metabolism, pravastatin and its metabolites are mostly excreted from the body through feces but also through the urine. The side effects of pravastatin vary between each patient, however, some common symptoms to be aware of are dizziness, headache, nausea or vomiting, and upper respiratory infection. Some serious adverse events may occur, such as chest pain, edema, muscle pain and weakness. If any of these events occur, the patient should seek medical care and dosing adjustments may take place to continue treatment safely and effectively if necessary. It has similar side effects to the other statin drugs but tends to have fewer interactions and complications in comparison to them. Pravastatin is a common form of treatment for many patients and is recognized as an essential medicine by the World Health Organization. I look forward to further my knowledge about this drug throughout pharmacy school.
Sources: Lexicomp, NIH, PubMed

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My assigned drug for this semester was Gabapentin. Gabapentin was first discovered in the 1970s by Satzinger and Hartenstein and was developed at Parke-Davis pharmaceutical company. Gabapentin was then approved by the FDA in the 90s. Originally, gabapentin was used as a muscle relaxer, but later was found the be an anti-convulsant. Currently, this medication is used to treat seizures and postherpetic neuralgia after shingles. This medication is also used for alcoholism, bi-polar disorder, and many other things, however it is not FDA approved for these uses. Gabapentin has a long list of adverse effects, a few being Cardiomyopathy, Abdominal pain, Peripheral edema, Nausea, and Vomiting. Gabapentin should not be used with ORLISTAT, as this medication can decreases the anticonvulsant effects of gabapentin. Drugs such as LEVOCETIRIZINE, REMIMAZOLAM, and ROPEGINTERFERON-ALFA-2B-NJFT, should also not be taken at the same time as a CNS depressant like gabapentin. Gabapentin should not be taken with another CNS depressant as this could result in respiratory depression.  The mechanism of action for gabapentin is unknown, it does not bind to GABA receptors, it is possible that gabapentin prevents thrombospondin from binding to alpha 2 delta-1. While Gralise and Neurontin of both brands of gabapentin that are administered orally, the different brands of the drug can be taken different ways. For example, when taking Gralise, you should swallow the tablet whole with a meal, don’t crush it or chew it. However, when taking Neurontin, you can take it without regard to food and you can split the capsule and mix it with food or a drink. This can be useful for individuals who may not be able to swallow a pill. Another brand of gabapentin is Horizant, which can also be used to treat restless leg syndrome. I was surprised to learn that gabapentin could also be administered topically. I was surprised to learn about the topical form of gabapentin, Neuraptine, which is also used to treat seizures as well as pain from shingles. Overall, I have really enjoyed getting to learn about this drug along with all the other medications we have researched of the course of this class, I did not know about gabapentin before this class started, but after researching it I have learned about not only this drug but other anticonvulsant drugs. Reading through other people’s posts on our padlet exercise has also familiarized me with many drugs that I originally didn’t know much about.