Something you never heard about Cyclosporin A
Cyclosporin A is an immunosuppressive drug. Since 1983 is used as prophylaxis in patients after transplantation what increases the post-transplantation survival rate and improves patient’s quality of life. Although the drug was discovered in 1970 and used to treat psoriasis in 1973, it is more commonly associated with transplantology.
Cyclosporin A(CAS NO:59865-13-3) inhibits humoral and cellular components of inflammatory response. That is why it is also used not only in the treatment of chronic inflammatory and autoimmune diseases such as rheumatoid arthritis or psoriasis, but also in severe atopic eczema which is resistant to other treatment.
Prophylaxis of organ rejection in kidney, liver, and heart allogeneic transplants in conjunction with adrenal corticosteroid therapy; Sandimmune may be used in the treatment of chronic rejection in patients previously treated with other immunosuppressive agents; increase tear production in patients whose tear production is presumed to be suppressed because of ocular inflammation associated with keratoconjunctivitis sicca .
Treatment of severe, active RA where disease is not adequately responsive to methotrexate; treatment of adult, nonimmunocompromised patients with severe, recalcitrant, plaque psoriasis who have failed to respond to a least one systemic therapy or in patients for whom other systemic therapies are contraindicated, or cannot be tolerated.
Cyclosporin A(CAS NO:59865-13-3) and FK506 (tacrolimus) are potent immunosuppressive drugs widely used in reducing the incidence and severity of allograft rejection after organ transplantation. Owing to their capacity to antagonize calcineurin activity and hence calcium-dependent T-cell activation, both drugs were thought to have identical cellular and molecular effects, despite differences in their structure.
This notion was challenged by both clinical and experimental evidence clearly showing that Cyclosporin A and FK506 immunosuppressive effects are not identical, and that FK506 affects Cyclosporin A-sensitive and Cyclosporin A-insensitive T-cell activation pathways. Here we discuss recent findings, including our own, which highlight differences in efficacy and mechanisms between Cyclosporin A and FK506.
Treatment may be associated with a number of potentially serious adverse drug reactions. They can include gingival hyperplasia, convulsions, peptic ulcers, pancreatitis, fever, vomiting, diarrhea, confusion, hypercholesterolemia, dyspnea, numbness and tingling particularly of the lips, pruritus, high blood pressure, potassium retention possibly leading to hyperkalemia, kidney and liver dysfunction (nephrotoxicity and hepatotoxicity), burning sensations at finger tips and an increased vulnerability to opportunistic fungal and viral infections.
In short, it is nephrotoxic, neurotoxic, causes hypertension (due to renal vasoconstriction and increased sodium reabsorption), increases the risk of squamous cell carcinoma and infections. It also causes gingival hypertrophy and hirsutism which is not seen with tacrolimus (another calcineurin inhibitor).
An alternate form of the drug, cyclosporin G has been found to be much less nephrotoxic than the standard cyclosporin A. Cyclosporin G (molecular mass 1217) differs from cyclosporin A in the amino acid 2 position, where an L-norvaline replaces the α-aminobutyric acid.
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