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biomedical technology and device research laboratories

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Collabody™ is a unique fusion protein design platform which utilizes a short triplex-forming collagen-like peptide (about 40 amino acids in length) as a scaffold protein binder for fusing with antibody fragments, hormones, cytokines, lymphokines, growth factors, lectins, enzymes, soluble receptor fragments and chemo agents.

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Vandana Sharma
14bph099

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MedScape Website: Trusted website for health care professionals on individual immunosuppressants agents listed with their details on dosing, uses, interactions, adverse effects, pharmacology etc. 

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MedScape Website: Trusted website for health care professionals on individual immunosuppressants agents listed with their details on dosing, uses, interactions, adverse effects, pharmacology etc. 

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Immunosuppressants | Drug, OTCs & Herbals | Medscape Reference

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Immunosuppressants: Dosing, Uses, Side Effects, Interactions, Patient Handouts, Pricing and more from Medscape Reference

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Immunosuppressant drugs may interact with other medicines. When this happens, the effects of one or both drugs may change or the risk of side effects may be greater. Other drugs may also have an adverse effect on immunosuppressant therapy. This is particularly important for patients taking cyclosporin or tacrolimus. For example, some drugs can cause the blood levels to rise, while others can cause the blood levels to fall and it is important to avoid such contraindicated combinations. Other examples are:

The effects of azathioprine may be greater in people who take allopurinol, a medicine used to treat gout.

A number of drugs, including female hormones (estrogens), male hormones (androgens), the antifungal drug ketoconazole (Nizoral), the ulcer drug cimetidine (Tagamet) and the erythromycins (used to treat infections), may increase the effects of cyclosporine.

When sirolimus is taken at the same time as cyclosporin, the blood levels of sirolimus may be increased to a level where there are severe side effects. Although these two drugs are usually used together, the sirolimus should be taken four hours after the dose of cyclosporin.

Tacrolimus is eliminated through the kidneys. When the drug is used with other drugs that may harm the kidneys, such as cyclosporin, the antibiotics gentamicin and amikacin, or the antifungal drug amphotericin B, blood levels of tacrolimus may be increased. Careful kidney monitoring is essential when tacrolimus is given with any drug that might cause kidney damage.

The risk of cancer or infection may be greater when immunosuppressant drugs are combined with certain other drugs which also lower the body's ability to fight disease and infection. These drugs include corticosteroids such as prednisone; the anticancer drugs chlorambucil (Leukeran), cyclophosphamide (Cytoxan) and mercaptopurine (Purinethol); and the monoclonal antibody muromonab-CD3 (Orthoclone), which also is used to prevent transplanted organ rejection.

Not every drug that may interact with immunosuppressant drugs is listed here. Anyone who takes immunosuppressant drugs should let the physician know all other medicines he or she is taking and should ask whether the possible interactions can interfere with treatment.

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Indications for Renal Transplant

Any condition that leads to end-stage renal (kidney) disease:

·         Diabetes

·         Glomerulonephritis

·         Pyelonephritis

·         Polycystic kidney disease

·         Obstructive uropathy

·         Congenital urinary tract abnormalities

·         Alport's disease

·         Hypertensive nephrosclerosis

·         Reflux nephropathy

·         Interstitial nephritis

·         IgA nephropathy

·         Goodpasture's syndrome

·         Hemolytic uremic syndrome

·         Chemical nephrotoxicity

·         Renal artery emboli

·         Sickle cell nephropathy

Indications for Pancreatic Transplant

·         Type I diabetes with advanced nephropathy in an adult

Contraindications for Transplantation

·         Malignancy within the past two years

·         Lack of adequate social or family support

·         Significant non-compliance with medical regimen

·         Central vascular disease (aortoiliac)

·         Significant coronary artery disease Severe malnutrition/cachexia

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selective inhibitors of cytokine production and function

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selective inhibitors of cytokine production and function

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THERAPEUTIC USES :-                                             Immunosuppressant drugs are used to make the body less likely to reject a transplanted organ, such as a liver, heart, or kidney. These drugs are called anti-rejection drugs. Other immunosuppressant drugs are often used to treat autoimmune disorders such as lupus,                       psoriasis,                                                                                    rheumatoid.                                                                         arthritis.                                                      Immunosuppressant drugs are used to treat autoimmune diseases. With an autoimmune disease, the immune system attacks the body’s own tissue. Because immunosuppressant drugs weaken the immune system, they suppress this reaction. This helps reduce the impact of the autoimmune disease on the body.Autoimmune diseases treated with immunosuppressant drugs include:    psoriasis.                                                                               lupus.                                                                           Rheumatoid arthritis.                                                        Crohn’s disease.                                                multiplesclerosis.                                                                 Organ transplant                                                                 Almost everyone who receives an organ transplant must take immunosuppressant drugs. This is because our immune system sees a transplanted organ as a foreign mass. As a result, our immune system attacks the organ as it would attack any foreign cell. This can cause severe damage and lead to needing the organ removed.   Immunosuppressant drugs weaken your immune system to reduce your body’s reaction to the foreign organ. The drugs allow the transplanted organ to remain healthy and free from damage.There are several different types of immunosuppressant drugs.                           Many people who receive immunosuppressant drugs are prescribed medications from more than one of these categories.                          

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THERAPEUTIC USES :-                                             Immunosuppressant drugs are used to make the body less likely to reject a transplanted organ, such as a liver, heart, or kidney. These drugs are called anti-rejection drugs. Other immunosuppressant drugs are often used to treat autoimmune disorders such as lupus,                       psoriasis,                                                                                    rheumatoid.                                                                         arthritis.                                                      Immunosuppressant drugs are used to treat autoimmune diseases. With an autoimmune disease, the immune system attacks the body’s own tissue. Because immunosuppressant drugs weaken the immune system, they suppress this reaction. This helps reduce the impact of the autoimmune disease on the body.Autoimmune diseases treated with immunosuppressant drugs include:    psoriasis.                                                                               lupus.                                                                           Rheumatoid arthritis.                                                        Crohn’s disease.                                                multiplesclerosis.                                                                 Organ transplant                                                                 Almost everyone who receives an organ transplant must take immunosuppressant drugs. This is because our immune system sees a transplanted organ as a foreign mass. As a result, our immune system attacks the organ as it would attack any foreign cell. This can cause severe damage and lead to needing the organ removed.   Immunosuppressant drugs weaken your immune system to reduce your body’s reaction to the foreign organ. The drugs allow the transplanted organ to remain healthy and free from damage.There are several different types of immunosuppressant drugs.                           Many people who receive immunosuppressant drugs are prescribed medications from more than one of these categories.                          

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Corticosteroids
prednisone (Deltasone, Orasone)
budesonide (Entocort EC)
prednisolone (Millipred)
https://youtu.be/DU2YoRINYzw
Calcineurin inhibitors
cyclosporine (Neoral, Sandimmune, SangCya)
tacrolimus (Astagraf XL, Envarsus XR, Prograf)
https://youtu.be/FMeLObw6CmI
mTOR inhibitors
sirolimus (Rapamune)
everolimus (Afinitor, Zortress)
https://youtu.be/lfxJDzb9sww
IMDH inhibitors
azathioprine (Azasan, Imuran)
abatacept (Orencia)
anakinra (Kineret)
certolizumab (Cimzia)
etanercept (Enbrel)
infliximab (Remicade)
ixekizumab (Taltz)
natalizumab (Tysabri)
rituximab (Rituxan)
vedolizumab (Entyvio)
Monoclonal antibodies
basiliximab (Simulect)
daclizumab (Zinbryta)
muromonab

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Immunosuppressants in Organ Transplant: 

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Immunosuppressants in Organ Transplant: 

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Probe drugs that can be safely administered to humans may be used in vivo to estimate enzyme activity (i.e., phenotyping). For example, midazolam is predominantly metabolized by CYP3A4/5 to 1′-hydroxymidazolam (18), which justifies its use as an in vivo index of CYP3A4/5 activity. Other in vivo probe substrates include caffeine (CYP1A2), coumarin (CYP2A6), bupropion (CYP2B6), tolbutamide (CYP2C9), omeprazole (CYP2C19), dextromethrophan (CYP2D6), and chlorzoxazone (CYP2E1). The phenotyping process typically involves oral or intravenous administration of the probe drug (usually in a small dose) followed by collection of blood and/or urine samples to determine some measure of the enzyme's functional activity, for example, rate of metabolite(s) formation.

In Vitro Functional Assay of Cytochrome P450 Enzymes-Application to Immunosuppressants

Several in vitro systems are available to examine xenobiotic metabolism and identify metabolic pathways as shown in Table 2. Human tissues, including freshly prepared hepatocytes, cryopreserved hepatocytes, and freshly isolated liver slices, provide cellular integrity with respect to enzyme architecture and contain the full complement of drug metabolizing enzymes. Subcellular fractions (microsomes, cytosols, S9) and recombinant CYP enzymes can be used in combination with tissues after adding appropriate cofactors.

Identification of the metabolic pathway may be achieved by incubating the drug with hepatocytes or liver slices, followed by analysis of the incubation medium by HPLC-MS/MS (19). Incubation of the drug with human liver microsomes with and without nicotinamide adenine dinucleotide phosphate is used to confirm that the formed metabolite(s) is/are phase I metabolite(s) produced by CYP enzymes.

In vitro assays serve as a screening mechanism to rule out the importance of a metabolic pathway and the drug-drug interaction that occur through this pathway so that subsequent in vivo studies may not be necessary. For example, in vitro studies show that ciclosporin (CsA) at concentration of 20 μM inhibits the activities of CYP2C19 and CYP2D6 by 30% and CYP3A4 by 70% (20). Accordingly, corresponding in vivo inhibition-based studies of CsA and concomitant medications eliminated by these pathways are needed. On the other hand, in vitro studies show that tacrolimus (TAC) has no effect on CYP1A2, CYP2E1, CYP2C9, CYP2D6, and CYP3A4 at concentrations below 1.0 μM (20), and thus, further in vivo inhibition studies are not warranted.

In vitro characterization of a specific CYP enzyme(s) involved in the metabolic pathway can be achieved by at least two of the following methods.

Use of Specific Chemical Inhibitors

A valuable attribute of chemical inhibitors is their commercial availability. However, most chemical inhibitors are not absolutely specific for an individual CYP enzyme. Although not all-inclusive, the chemical inhibitors listed in Table 1 can be used to identify individual CYP enzymes responsible for a drug's metabolism, and to determine the relative contribution of an individual CYP enzyme.

For example, ketoconazole inhibits mycophenolic acid (MPA) demethylation by 50% in primary hepatocytes; however, quinidine, sulfaphenazole, and ticlopidine inhibitory activity was less than 15% (19). These results indicate the significant involvement of CYP3A4/5 in the phase I metabolism of MPA. Triacetyl oleandomycin and gestodene (specific CYP3A4/5 inhibitors) inhibit liver metabolism of tacrolimus (TAC) and sirolimus (SRL) by more than 80% in human and rat hepatic microsomes (21). CYP1A2 may also metabolize TAC based upon the partial inhibition of TAC metabolism by α-naphthoflavone in hepatic microsomes from human, rabbits, and rats (22).

Use of Specific Antibodies

The inhibitory effect of an antibody should be tested at sufficiently low and high concentrations to establish a titration curve. For example, CYP3A4 antibodies have been shown to inhibit metabolism of CsA and TAC by greater than 80% in vitro (23, 24). Partial inhibition of TAC metabolism is observed also after incubation with CYP1A2 antibodies, which indicates the involvement of this CYP enzyme, in addition to CYP3A4/5 in TAC metabolism (22).

Use of Recombinant Enzymes

Metabolism of a drug by only one human CYP enzyme makes the interpretation of the results relatively straightforward. Involvement of more than one enzyme makes the measurement of enzyme activity less informative on the relative importance of each individual pathway. These techniques can be helpful to determine the relative importance of each of the enzymes in the overall metabolite formations. Using this approach it was shown that TAC is metabolized primarily by CYP3A4 (4).

Use of Correlative Analyses

This approach relies on statistical analyses to establish a correlation between the formation rate of an individual metabolite and activities determined for each CYP enzyme in a set of microsomes prepared from individual donor livers. For example, metabolism of TAC and SRL in human liver microsomes shows a significant correlation with CYP3A4 activity as estimated by nifedipine oxidation (21).

Other Proposed Methods

Other helpful methods may include immunoblotting using specific antibodies, measurement of mRNA levels using specific nucleic acid probes (15), and receptor gene assays for receptors mediating induction of P450 enzymes (24).

Drug-Drug Interactions With Immunosuppressive Agents-Role of Cytochrome P450 Enzymes

Calcineurin Inhibitors

Hepatic and enteric CYP3A enzyme systems are key determinants for metabolism, oral bioavailability, and elimination of calcineurin inhibitors (25). Accordingly, drugs and chemicals affecting expression and activity of this enzyme can profoundly impact the blood concentrations of these immunosuppressive agents.

Cyclosporine

Cyclosporine (CsA) is extensively metabolized in the liver by CYP3A, and to a lesser extent in the intestine (5). Only 0.1% is excreted unchanged in the urine (5). Dose adjustment is necessary in the presence of liver dysfunction, but not generally required for dialysis or renal failure patients (6). Although the cyclic peptide structure of CsA is resistant to metabolism, the side chains are extensively metabolized with more than 25 metabolites being identified in human urine, bile, blood, and feces (23). Compared with the parent drugs, CsA metabolites have less biological activity and toxicity.

CsA interacts with a wide variety of commonly used drugs and natural products that requires close attention. Any substance that affects the activity of CYP3A isozymes can potentially impact the blood concentration of CsA (23). Using nifedipine oxidation and testosterone 6β-hydroxylation as markers of CYP3A activity, CsA was found to inhibit hepatic CYP3A activity by more than 30% at a concentration of 2 μM (20, 26). In the same study, CsA exerted no significant effect on ethoxyresorufin-O-deethylase activity (CYP1A2), or hydroxylation of chlorzoxazone (CYP2E1), tolbutamide (CYP2C9), or debrisoquine (CYP2D6).

Inhibitors of the CYP3A enzyme system (reviewed in Refs. [3, 20, 25, 27]) will reduce metabolism of CsA and increase its blood concentration, resulting in potential for toxicity. For examples, the use of ketoconazole for 1-year results in more than 50% reduction of the cost of CsA therapy (28). Erythromycin causes a twofold increase in CsA AUC by increasing CsA absorption rather than inhibiting its metabolism (3). HIV protease inhibitors are both substrates and inhibitors for CYP3A4 system. Concomitant oral administration of CsA and indinavir results in significant increase in CsA AUC 0-∞ and T max (27). Grapefruit and its juice inhibit CYP3A activity. Studies show 16% to 200% increase in CsA AUC with grapefruit juice (3). Its use should be avoided by patients taking CsA.

On the other hand, substances that induce CYP3A activity (reviewed in Refs. [3, 4, 29]) can increase CsA metabolism and elimination and decrease its blood concentration, resulting in subtherapeutic concentration and potential risk of rejection (6). For example, rifampin, a potent inducer for CYP3A4, causes more than 10-fold increase in CYP3A4- mediated erythromycin-N-demethylation and eightfold increase in CYP3A4 mRNA content in both human hepatocytes and enterocytes (24). Standard oral doses of the anticonvulsants, phenobarbital, phenytoin, and carbamazepine reduce CsA bioavailability by more than 50% (3).

In general, concomitant administration of CsA and these drugs requires close monitoring of blood concentrations of both CsA and other drug(s) to avoid potential drug-drug interactions. Because CYP3A4 is the major CYP enzyme involved in CsA metabolism, coadministration of rifampin with CsA results in increasing CsA systemic elimination and reduction in its bioavailability by 70% (3).

Given the contribution of the CYP3A system in its metabolism and possibly in the interpatient variability in its pharmacokinetics (PK), several studies have extensively examined the genetic polymorphism in the CYP3A system as a determinant of interpatient variability in CsA PK (30-34). Although readily identifiable in the CYP3A4 system, genetic polymorphism is not readily translated into phenotypic relevance to metabolism of CsA (and tacrolimus; see later) (34). Genotypic variations in CYP3A5 system have been shown to correlate significantly with CYP3A protein expression and activity (17, 30, 31). Eng et al. (31) showed a significant correlation between CsA dose requirement and CYP3A5 linked genotype, where patients with *1 *1*1*1 linked genotype require significantly higher doses of CsA to achieve the target trough level compared with patients with *1 *3*1*3 or *3 *3*3*3 linked genotypes. Several other studies demonstrate high association between CYP3A5 polymorphism and CsA dose requirement in heart and renal transplant patients (32). Such studies indicate that routine CYP3A5 phenotyping may have an important clinical role in individualization and optimization of CsA dosing of allograft recipients. Because CsA is both a substrate and inhibitor for the intestinal pGp, pharmacogenetics of this transporter could also contribute to the marked interpatient variability in CsA (32, 35, 36). Nevertheless, other studies reported that haplotypes of pGp and CYP3A5*1 genotype have a minor influence on the pharmacokinetics of ciclosporin and are unlikely to be of value in developing a pharmacogenetic strategy based on achieving target blood concentrations (35, 37).

Tacrolimus

Tacrolimus (TAC) is extensively metabolized in the liver by CYP3A system with less than 1% of the administered dose excreted unchanged in the urine. Demethylation to 13-O-demethyltacrolimus by CYP3A4 is quantitatively the most important metabolic route (22). Several independent clinical studies recently demonstrated significant associations between blood concentrations of TAC and/or maintenance dose in transplant patients and the CYP3A5 concentration. Carriers of CYP3A5*1 alleles (CYP3A5 high expressers) require higher doses of TAC than do homozygous carriers of the CYP3A5*3 allele (CYP3A5 "low expressers") (35, 38). At present, the potential of CYP3A5 genotyping in tacrolimus therapies is unclear (39).

Of importance is the reported impact of the polymorphism during the early posttransplant period. CYP3A5 high expressers had lower mean TAC concentrations during the first week after renal transplantation, and rejection occurred earlier in these patients (33). Based upon these results, it has been proposed that a CYP3A5 genotype-based adjusted initial dosing regimen for TAC has the potential to improve transplant survival (30). Additional components of the CYP system may be involved in the metabolism of TAC based on the fact that only partial inhibition is achieved by anti-CYP3A4 antibodies (40). In vitro studies demonstrate significant correlation between TAC metabolism and CYP2E1- mediated chlorzoxazone hydroxylation and CYP2A6-mediated 7-ethoxycoumarin demethylation (4).

Sirolimus

In vitro metabolic studies using human liver microsomes with SRL yields two major metabolites, 41-O-demethyl-SRL and hydroxy-SRL, that have less than 10% of the immunosuppressive activity of the parent drug (40). Formation of these metabolites correlates with CYP3A4 activity as estimated by nifedipine oxidation and inhibition with triacetyl oleandomycin or anti-CYP3A4 antibodies (4). Contribution of other CYP enzymes (e.g. CYP2E1, CYP2A6, CYP2D6) in SRL metabolism has not been confirmed yet.

A recent study by Le et al. (41) reported that sirolimus metabolic activity and oral clearance are significantly decreased in patients who are homozygous for the CYP3A5*3 single-nucleotide polymorphism and suggested that the determination of this polymorphism could be useful for a priori dose adjustment of sirolimus, given the long half-life of this drug.

As with CsA and TAC, substances that affect the activity of CYP3A system or pGp can potentially affect the bioavailability and therapeutic effect of SRL (42). Using regiospecific and stereospecific hydroxylation of testosterone on the 6β positions in rat hepatic microsomes as a marker of CYP3A activity, SRL was shown to inhibit the activity of CYP3A by 38% (26). Concomitant administration of both CsA and SRL resulted in 55% decrease in the catalytic activity of CYP3A and 41% increase in steady state concentration of CsA, resulting in severe histologic damage in the kidney (26).

Concomitant oral administration of CsA and SRL significantly increases bioavailability of CsA by twofold to threefold, increases SRL bioavailability by 2- to 11-fold (3, 43), and increases SRL concentration in the kidney by 17-fold (44). Separation of the oral doses of CsA and SRL by 4 hr minimizes the interaction, resulting in 45% increase in AUC, 49% increase in trough concentration, and 72% increase in maximum concentration of SRL without any significant changes in CsA pharmacokinetic parameters (45, 46).

Mycophenolate Mofetil

Mycophenolate mofetil (MMF) is an ester prodrug of mycophenolic acid (MPA) (47). A new MMF metabolite is reported to be a product of CYP enzyme system because it was produced by incubation of MPA with hepatic microsomes in the presence of nicotinamide adenine dinucleotide phosphate, and its formation was prevented by the general CYP inhibitor 1-aminobenzotriazole (48). A better knowledge of this metabolite might help understanding MPA toxicity and drug interactions (47). This metabolite was identified by Picard et al. (19) as 6-O-desmethyl MPA and is produced by CYP3A4/5 and probably CYP2C8. An in vitro study shows that TAC metabolism was inhibited after incubation with only a high MPA concentration (0.5 mmol/L) (19). Although CsA is also a substrate for CYP3A4/5 system, there was no apparent effect on its metabolism by MPA at any concentration (19). Collectively, MPA at its therapeutic concentration is not considered a competitor for CYP3A isozymes.

CONCLUSION

There is a complex bidirectional relationship between cytochrome P450 enzymes and immunosuppressive drugs. The activity of most CYP isoforms involved in drug metabolism can be tested in vitro by a variety of methods, including isolated perfused organs, tissue slices, tissue cultures, microsomal fractions, and cloned enzymes. Each method has its advantages and disadvantages. Cyclosporine and tacrolimus inhibit hepatic CYP3A activity by more than 30% whereas sirolimus inhibits CYP3A by 38%. Concomitant administration of both ciclosporin and sirolimus leads to 55% decrease in CYP3A activity. Mycophenolic acid derivatives do not have appreciable affect on CYP activity. Understanding the biology of CYP enzymes help to predict putative potential drug interactions and, therefore, appropriate in vitro functional assays of CYP activity is a primary step for further evaluation of drug-drug interaction.

REFERENCES

Keywords:
Cytochrome P450 enzymes; Immunosuppressive drugs; Drug interactions

© 2008 Lippincott Williams & Wilkins, Inc.

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eview summarizes current in vitro functional assays of CYP activity to assist in understanding the bidirectional relationship between immunosuppressants and CYP enzyme system. To achieve our goal we describe the constituents of CYP system followed by discussing their role in the common immunosuppressive drug-drug interactions.

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Immunosuppression had concomitant risks of opportunistic infections and secondary tumors. Therefore, the ultimate goal of research on organ transplantation and autoimmune diseases is to induce and maintain immunologic tolerance, the active state of antigen- specific no responsiveness. Tolerance if attainable would represent a true cure for conditions without the side effects of the various immunosuppressive therapies. The calcineurin inhibitors prevent tolerance induction is some but not all preclinical models. In these same models systems, sirolimus does not prevent tolerance and may even promote tolerance induction. Several other promising approaches are being evaluated in clinical trials.

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BY: 14BPH099,100,102,103,104

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Introduction:  The Immune System and Immunosuppressants

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Introduction:  The Immune System and Immunosuppressants

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The Immune system enables the body to recognize a foreign agent as nonself, which is something other than a person's own substances (self). The immune system takes a specific action for neutralizing, killing, and eliminating that agent. The action involves nonspecific resistance as well. On occasion, the immune system activity may lead to tissue damage as seen in allergic disorders and other states of hypersensitivity.

The immune system's activity is based on its ability to distinguish characteristic proteins or protein-linked components associated with alien substances. Once this distinction has been made, certain lymphocytes are provoked to produce antibodies directed against the foreign matter, while other lymphocytes are sensitized to the invading agent and react with it directly. Thus, there are two major branches of the immune system: antibody-mediated immunity (also known as humoral immunity) and cell-mediated immunity.
1. Prevent the rejection of transplanted organs and tissues (e.g., bone marrow, heart, kidney, liver)

2. Treat autoimmune diseases or diseases that are most likely of autoimmune origin (e.g., rheumatoid arthritis, multiple sclerosis, myasthenia gravis, systemic lupus erythematosus, sarcoidosis, focal segmental glomerulosclerosis, Crohn’s disease, Behcet’s Disease, pemphigus, and ulcerative colitis)

3. Treat some other non-autoimmune inflammatory diseases (e.g., long term allergic asthma control)

4. Treat some other non-autoimmune inflammatory diseases (e.g., long term allergic asthma control)

1. Induction drugs: Powerful antirejection medicine used at the time of transplant

2. Maintenance drugs: Antirejection medications used for the long term.

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What do I need to be aware of while taking this kind of medicine?

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What do I need to be aware of while taking this kind of medicine?

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Immunosuppressant medicines can increase your susceptibility to infections because your suppressed immune system is less able than normal to fight off bacteria, viruses and other foreign substances.

For this reason, you should consult your doctor immediately if you develop a sore throat, fever, any infections, including skin infections, or begin to feel generally unwell.

If you are having long-term or intensive immunosuppressive treatment you may be at increased risk of developing lymphomas and other cancers, particularly skin cancer.

To reduce the risk of skin cancer you should minimise your exposure to strong sunlight and UV light by wearing protective clothing and using a sunscreen with a high protection factor.

Sun beds and UV light treatment such as PUVA should also be avoided.

Females should ensure they have had a cervical smear before starting these medicines.

You should not eat grapefruit or drink grapefruit juice in the hour before taking a dose of ciclosporin as this can interfere with the medicine.

Ciclosporin can occasionally increase potassium levels in your bloodstream. For this reason you should avoid consuming excessive amounts of foods that have high potassium content, for example dried fruit, bananas, tomatoes and 'low sodium' salt, while you are taking the medicine.

You should also avoid potassium supplements.

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1)  http://www.healthline.com/health/immunosuppressant-drugs#uses2

2)
https://en.wikipedia.org/wiki/Immunosuppressive_drug

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in this video we will look at: - mechanism of action of MTX - MTX administration - ADRs

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A quick look at: - why we need immunosuppression - mechanism of action of glucocorticoids - effects of glucocorticoids in inflammation - uses of glucocorticoids - ADRs

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https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3264940/

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Cellcept   Side Effects, Uses, Dosage, Overdose, Pregnancy, Alcohol   RxWiki

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Representation of Immunosuppressant's mechanism.