IMMUNOSUPPRESSANT

IMMUNOSUPPRESSANT

·         Immunosuppressant are drugs that inhibit cellular or humoral or both types of immune responses.

·         These drugs have met a high degree of success in organ transplant and autoimmune diseases.

Cytokine

·         Cytokines are soluble, antigen-nonspecific signaling proteins that bind to cell surface receptors on a variety of cells.

·         Cytokine includes interleukins (ILs), interferons (IFNs), tumor necrosis factors (TNFs), transforming growth factors, and colony-stimulating factors.

·         IL-2, a growth factor that stimulates the proliferation of antigen-primed (helper) T cells, which subsequently produce more IL-2, IFN-γ, and TNF-α.

Cytokine

Action

IL-1

·         Enhances the activity of (natural killer) NK cells.

·         Attracts neutrophils and macrophages.

IL-2

·         Induces proliferation of antigen-primed T cells.

·         Enhances the activity of NK cells.

IFN-γ

·         Enhances the activity of macrophages and NK cells.

·         Increases expression of (major histocompatibility complex) MHC molecules.

·         Enhances the production of IgG2a.

TNF-α

·         Cytotoxic eff­ect on tumor cells.

·         Induces cytokine secretion in the inflammatory response.

 Classification

1. Calcineurin inhibitors (Specific T-cell inhibitors)

·         Cyclosporine (Ciclosporin), Tacrolimus

2. m-TOR inhibitors

·         Sirolimus, Everolimus

3. Anti-proliferative drugs (Cytotoxic drugs)

·         Azathioprine, Methotrexate, Cyclophosphamide, Chlorambucil, Mycophenolate mofetil (MMF)

4. Glucocorticoids

·         Prednisolone and others

5. Biological agents

            (a) TNFα inhibitors: Etanercept, Infliximab, Adalimumab

            (b) IL-1 receptor antagonist: Anakinra

            (c) IL-2 receptor antagonists: Daclizumab, (anti CD-25 antibodies) Basiliximab

            (d) Anti CD-3 antibody: Muromonab CD3

            (e) Polyclonal antibodies: Antithymocyte antibody (ATG), Rho (D) immune globulin.

Calcineurin inhibitors (Specific T-cell inhibitors)

Cyclosporine (Ciclosporin)

·         Cyclosporine is a lipophilic cyclic polypeptide extracted from the soil fungus Beauveria nivea.

Mechanism of action

·         Self and foreign antigen interact between macrophage antigen presenting cell (APC) and T-helper cell in the immune response.

·         Normally, after activation through T-cell receptor, calcineurin dephosphorylates a ‘nuclear factor of activated T-cells’ (NFAT) which translocates to the nucleus and triggers transcription of cytokine genes resulting in production of IL-2 and other cytokines.

·         IL-2 diffuses out and acts on IL-2 receptor to stimulate T-cell proliferation and other processes, carrying forward the immune response.

·         Cyclosporine binds to an intracellular protein ‘Cyclophilin’ and this complex inhibits Ca2+-Calmodulin (Ca2+-CAM) activated phosphatase ‘Calcineurin’.

·         Tacrolimus also inhibits calcineurin, but after binding to a different protein FKBP (FK binding protein).

Therapeutic uses

·         Cyclosporine is used to prevent rejection of kidney, liver, and cardiac allogeneic transplants.

Pharmacokinetics

·         Given orally or i.v.

·         Oral absorption is variable due to metabolism by a cytochrome P450 (CYP3A4) iso-enzyme in the gastrointestinal (GI) tract and efflux by P-glycoprotein (P-gp).

·         About 50% of the drug is bound to erythrocytes.

·         Metabolized by liver.

·         Excretion through biliary route into the feces.

Adverse effects

·         Nephrotoxicity is the most common.

·         Hepatotoxicity.

·         Hypertension

·         Hyperlipidemia

·         Hyperkalemia

·         Tremor

·         Hirsutism

·         Glucose intolerance, and gum hyperplasia.

Tacrolimus

·         It is isolated from the soil fungus Streptomyces tsukubaensis.

Mechanism of action

·         Tacrolimus exerts its immunosuppressive effects in the same manner as cyclosporine, except that it binds to a different immunophilin, FKBP-12 (FK-binding protein), and the complex then binds to calcineurin.

Therapeutic uses

·         Preventing heart, liver, pancreas, and kidney rejections (along with glucocorticoids).

Pharmacokinetics

·         Administer orally or i.v. but, as with cyclosporine oral absorption of tacrolimus is incomplete and variable

·         Tacrolimus is subject to gut metabolism by CYP3A4/5 isoenzymes and is a substrate for P-gp.

·         Absorption is decreased if the drug is taken with high-fat or high-carbohydrate meals.

·         Drugs and metabolites are primarily eliminated in the feces.

Adverse effect

·         Nephrotoxicity and neurotoxicity

·         Alopecia

·         Cardiovascular toxicities, such as hypertension and hyperlipidemia (lower incident).

·         Other toxicities are same as cyclosporine except Hirsutism.

m-TOR inhibitors

Sirolimus (rapamycin)

·         It is obtained from fermentations of the soil mold Streptomyces hygroscopicus.

Mechanism of action

·         Binds to FK-binding protein as tacrolimus.

·         Sirolimus binds to m-TOR (a serine/threonine kinase), interfering with signal 3.

·         Binding of sirolimus to m-TOR blocks the progression of activated T cells from the G1 to the S phase of the cell cycle.

·         Sirolimus does not lower IL-2 production but, rather, inhibits the cellular response to IL-2.

Therapeutic uses

·         Renal transplantation

·         In combination with cyclosporine and corticosteroids – lower doses and also lower toxicity.

·         The combination of sirolimus and cyclosporine is synergistic because sirolimus works later in the immune activation cascade.

Pharmacokinetics

·         Available as oral solution and tablet.

·         Readily absorbed.

·         Decrease the absorption with high fat meals.

·         Half-life 57-62.

·         Metabolized by the CYP3A4 iso-enzyme.

·         Sirolimus also increases the concentrations of cyclosporine, and careful blood level monitoring of both agents must be done to avoid harmful drug toxicities.

Adverse effect

·         Hyperlipidemia (common).

·         Headache, nausea and diarrhea.

·         Leukopenia, and thrombocytopenia.

Everolimus

·         Another m-TOR inhibitor, is approved for use in renal transplantation. It is also indicated for second-line treatment in patients with advanced renal cell carcinoma.

Mechanism of action

·         It inhibits activation of T cells by forming a complex with FKBP-12 and subsequently blocking m-TOR.

Therapeutic uses

·         Used to prevent rejection in kidney transplant recipients in combination with basiliximab, cyclosporine, and corticosteroids.

Pharmacokinetics

·         Rapidly absorbed, but absorption is decreased with high-fat meals.

·         Short half-life, requires twice daily dosing.

·         Everolimus increases drug concentrations of cyclosporine, thereby enhancing the nephrotoxic effects of cyclosporine, and is, therefore, recommended to be used with reduced doses of cyclosporine.

Adverse effects

·         Similar to sirolimus.

·         An additional adverse effect noted with Everolimus is angioedema.

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