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The Medical uses of Cyclosporin A Cyclosporin A, guidechem,59865-13-3

The immunosuppressive effect of Cyclosporin A was discovered on 31 January 1972 by employees of Sandoz (now Novartis) in Basel, Switzerland, in a screening test on immune suppression designed and implemented by Hartmann F. Sthelin, M.D. The success of this medicne in preventing organ rejection was shown in kidney transplants by Calne and colleagues at the University of Cambridge, and in liver transplants performed by Dr. Thomas Starzl at the University of Pittsburgh Hospital. The first patient, on 9 March 1980, was a 28-year-old woman. It was subsequently approved for use in 1983. Since then, it has been used to prevent and treat graft-versus-host reactions in bone-marrow transplantation and to prevent rejection of kidney, heart, and liver transplants. In addition to transplants, Cyclosporin A(CAS NO:59865-13-3) is also used in psoriasis, severe atopic dermatitis, pyoderma gangrenosum, chronic autoimmune urticaria, and, infrequently, in rheumatoid arthritis and related diseases, although it is only used in severe cases. It is commonly prescribed in the US as an ophthalmic emulsion for the treatment of dry eyes.It has been investigated for use in many other autoimmune disorders, and is sometimes prescribed in veterinary cases, particularly in extreme cases of immune-mediated hemolytic anemia. Inhaled Cyclosporin A(CAS NO:59865-13-3) has been investigated to treat asthma and is being studied as a preventive therapy for chronic rejection of the lungs. Ciclosporin has also been used to help treat patients with acute severe ulcerative colitis that do not respond to treatment with steroids. This drug is also used as a treatment of posterior or intermediate uveitis with noninfective etiology. Cyclosporin A is a drug currently used to experimentally treat cardiac hypertrophy (an increase in cell volume). It has been investigated as a possible neuroprotective agent in conditions such as traumatic brain injury, and has been shown in animal experiments to reduce brain damage associated with injury.Ciclosporin blocks the formation of the mitochondrial permeability transition pore, which has been found to cause much of the damage associated with head injury and neurodegenerative diseases. Its neuroprotective properties were first discovered in the early 1990s when two researchers were conducting experiments in cell transplantation. An unintended finding was that CsA was strongly neuroprotective when it crossed the blood brain barrier. This same process of mitochondrial destruction through the opening of the MPT pore is implicated in making traumatic brain injuries much worse. It is currently in a phase II/III (adaptive) clinical study in Europe to determine its ability to ameliorate neuronal cellular damage in traumatic brain injury. This multi-center study is being organized by NeuroVive Pharma and the European Brain Injury Consortium using

NeuroVive's formulation of cyclosporine called NeuroSTAT. Cyclosporin A is a powerful immunosuppressive agent whose lack of myelotoxicity makes it unique among nonsteroidal drugs currently given for immunosuppression. It has been used with initial success in recipients of kidney, liver, bone marrow and pancreas transplants, and it may also have clinical application in the treatment of autoimmune disorders. In regard to its use in transplant recipients, there are many remaining questions about its mechanism of action, the optimum dose, whether Cyclosporin A should be used alone or with other immunosuppressants, whether it can suppress chronic rejection and what its long-term side effects may be. These questions can only be answered by further careful laboratory investigation and controlled clinical trials. Until then, Cyclosporin A should only be administered in centres experienced in its use. Want to learn more information about Cyclosporin A, you can access the guidechem.com. Guidechem.com is just a place for you to look for some chemicals.