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There is one exact (name or code) match for cyclosporine

 
Cyclosporins are cyclic polypeptide macrolides that were originally derived from the soil fungus Tolypocladium inflatum. Cyclosporine (also known as cyclosporine A) was discovered by Sandoz and developed for the tretment of immune disorders. The drug was approved by FDA for such diseases as Rheumatoid Arthritis, Psoriasis (Neoral), Keratoconjunctivitis sicca (Restasis) and prevention of transplant rejections (Neoral and Sandimmune). Cyclosporine’s primary immunosuppressive mechanism of action is inhibition of T-lymphocyte function. Upon administration cyclosporine binds to cyclophilin A and thus inhibits calcineurin, leading to immune system suppression.

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Cyclosporins are cyclic polypeptide macrolides that were originally derived from the soil fungus Tolypocladium inflatum. Cyclosporine (also known as cyclosporine A) was discovered by Sandoz and developed for the tretment of immune disorders. The drug was approved by FDA for such diseases as Rheumatoid Arthritis, Psoriasis (Neoral), Keratoconjunctivitis sicca (Restasis) and prevention of transplant rejections (Neoral and Sandimmune). Cyclosporine’s primary immunosuppressive mechanism of action is inhibition of T-lymphocyte function. Upon administration cyclosporine binds to cyclophilin A and thus inhibits calcineurin, leading to immune system suppression.
2S,4R ketoconazole or levoketoconazole is the 2S,4R enantiomer of ketoconazole, purified from racemic ketoconazole. Both enantiomers exerts antifungal activity. Ketoconazole activates AhR in gene reporter cell line and dose-dependently induces CYP1A1 mRNA and CYP1A1 protein in HepG2 cells, with enantiospecific pattern, i.e. 2R,4S ketoconazole was much more active as compared to 2S,4R ketoconazole. Levoketoconazole was shown to be a more potent inhibitor than the 2R,4S enantiomer of several enzymes in the steroidogenic pathway (CYP11B1, CYP17 and CYP21). Levoketoconazole was tested for the treatment of endogenous Cushing’s syndrome (Phase III) and type 2 diabetes mellitus (Phase II).
Status:
Investigational
Source:
INN:geclosporin [INN]
Source URL:

Class (Stereo):
CHEMICAL (ABSOLUTE)

Geclosporin (Cyclosporine) is an immunosuppressive agent, that is used to prevent rejection of a transplanted organ by the body. Geclosporin is isolated from a fungus, Beauveria nivea, and was first discovered in 1970. By suppressing the immune system, this drug prevents white blood cells from rejecting the transplanted organ. Geclosporin primarily does this by suppressing T cells and T cell cytokine production, but also acts in other ways, for example by inhibiting growth and activation of B cells and antigen presenting cells, and by reducing antibody production. Geclosporin is usually combined with other compounds, and has been studied as potential treatment for a large range of disorders. It is used for the treatment of several other conditions, such as severe recalcitrant plaque psoriasis, severe active rheumatoid artritis, and to prevent rejection of donor cells as a result of bone marrow transplantation. Relapse after discontinuation of this compound is to be expected, and therefore, patients should receive maintenance therapy at the lowest effective dosage. The most common adverse events are hypertrichosis, gingival hyperplasia, and neurological and gastrointestinal effects. Renal dysfunction is also possible, but irreversible damage is rare.
Status:
Investigational
Source:
INN:enisoprost
Source URL:

Class (Stereo):
CHEMICAL (MIXED)

Enisoprost is a prostaglandin E1 analog. Enisoprost exerts immunosuppressive activity and gastric antisecretory effect. Enisoprost was being studied for the treatment of peptic ulcer and transplant rejection. Enisoprost development has been discontinued.
Status:
Other

Class (Stereo):
CHEMICAL (ABSOLUTE)


Conditions:

The ciclosporin analogue ciclosporin H is a potent and selective inhibitor of mediator release from basophils induced by activation of the formyl peptide receptor, and therefore has potential as an anti-inflammatory agent. It acts by interfering with agonist binding to formylmethionylleucylphenylalanine (FMLP) receptors. Unlike ciclosporin [ciclosporin A], ciclosporin H has Dmethyl valine (rather than the Lisomer) at position 11, has an extremely low affinity for cyclophilin, and is devoid of immunosuppressive activity. Ciclosporin H was undergoing preclinical investigation with researchers at the University of Naples Federico II in Italy as an antiinflammatory agent. However, no recent development has been reported.
Status:
Other

Class (Stereo):
CHEMICAL (ABSOLUTE)

Status:
Other

Class (Stereo):
CHEMICAL (ACHIRAL)