The immunosuppressive effect of ciclosporin 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. Stähelin, M.D. The success of ciclosporin in preventing organ rejection was shown in kidney transplants by Calne and colleagues at the University of Cambridge,^[5] 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.^[6] Ciclosporin was subsequently approved for use in 1983.

Apart from in transplant medicine, ciclosporin 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 ciclosporin 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.^[7] This drug is also used as a treatment of posterior or intermediate uveitis with noninfective etiology.

Ciclosporin 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.^[8] 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 is a drug currently used to experimentally treat cardiac hypertrophy