It is taken orally or intravenously for rheumatoid arthritis, psoriasis, Crohn's disease, nephrotic syndrome, eczema, and in organ transplants to prevent rejection.

[16] Common side effects include high blood pressure, headache, kidney problems, increased hair growth, and vomiting.

[15] It does this by forming a complex with cyclophilin to block the phosphatase activity of calcineurin, which in turn decreases the production of inflammatory cytokines by T-lymphocytes.

The increase in blood pressure can cause cardiovascular events; it is thus recommended that the lowest effective dose for people requiring long-term treatment be used.

[33] Ciclosporin's main effect is to lower the activity of T-cells; it does so by inhibiting calcineurin in the calcineurin–phosphatase pathway and preventing the mitochondrial permeability transition pore from opening.

[18] Ciclosporin, by preventing the dephosphorylation of NF-AT, leads to reduced effector T-cell function;[34][35][36][37] it does not affect cytostatic activity.

[42] Ciclosporin blocks the calcineurin-mediated dephosphorylation of synaptopodin, a regulator of Rho GTPases in podocytes, thereby preserving the phosphorylation-dependent synaptopodin-14-3-3 beta interaction.

Altogether, the antiproteinuric effect of Ciclosporin results, at least in part, from the maintenance of synaptopodin protein abundance in podocytes, which, in turn, is sufficient to maintain the integrity of the glomerular filtration barrier and to safeguard against proteinuria.

[55] In 1970, new strains of fungi were isolated from soil samples taken from Norway and from Wisconsin in the US by employees of Sandoz (now Novartis) in Basel, Switzerland.

[56] The immunosuppressive effect of the natural product ciclosporin was discovered on 31 January 1972[57] in a screening test on immune suppression designed and implemented by Hartmann F. Stähelin at Sandoz.

Calne and colleagues at the University of Cambridge,[61] and in liver transplants performed by Thomas Starzl at the Children's Hospital of Pittsburgh.

[63][64][65][66] Thomas Starzl's 1992 memoir explains through the eyes of a transplant surgeon that ciclosporin was an epoch-making drug for solid organ allotransplantation.

[67] Put simply, the biggest limits of applying such transplantation more widely were not cost or surgical skill (as formidable as those are) but rather the problem of allograft rejection and the scarcity of donor organs.

[69] Ciclosporin exhibits very poor solubility in water, and, as a consequence, suspension and emulsion forms of the medication have been developed for oral administration and for injection.

Ciclosporin was originally brought to market by Sandoz (now Novartis), under the brand name Sandimmune, which is available as soft gelatin capsules, an oral solution, and a formulation for intravenous administration.

[71][72] Generic ciclosporin preparations have been marketed under various brand names, including Cicloral (by Sandoz/Hexal), Gengraf (by Abbott) and Deximune (by Dexcel Pharma).

Since 2002, a topical emulsion of ciclosporin for treating inflammation caused by keratoconjunctivitis sicca (dry eye syndrome) has been marketed under the brand name Restasis.

[78] 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.

Ciclosporin's neuroprotective properties were first discovered in the early 1990s when two researchers (Eskil Elmér and Hiroyuki Uchino) were conducting experiments in cell transplantation.

[79] This same process of mitochondrial destruction through the opening of the MPT pore is implicated in making traumatic brain injuries much worse.

Inappropriate opening of the mitochondrial permeability transition pore (MPTP) manifests in ischemia[35] (blood flow restriction to tissue) and reperfusion injury[35] (damage occurring after ischemia when blood flow returns to tissue), after myocardial infarction[36] (heart attack) and when mutations in mitochondrial DNA polymerase occur.

Cyclosporin A binds to cyclophilin D to block the opening of MPTP, and thus decreases the release of protein cytochrome C, which can cause programmed cell death.