Cyclosporine is a calcineurin phosphatase pathway inhibitor, used as an immunosuppressant drug to prevent rejection in organ transplantation.

Cyclosporine induces phenotypic changes, including invasiveness of non-transformed cells, by a cell-autonomous mechanism. Cyclosporine treatment of adenocarcinoma cells results in striking morphological alterations, including membrane ruffling and numerous pseudopodial protrusions, increased cell motility, and anchorage-independent (invasive) growth. [1] Cyclosporine (cyclosporin A, CsA) has potent immunosuppressive properties, reflecting its ability to block the transcription of cytokine genes in activated T cells. Cyclosporine through formation of a complex with cyclophilin inhibits the phosphatase activity of calcineurin, which regulates nuclear translocation and subsequent activation of NFAT transcription factors. Cyclosporine also blocks the activation of JNK and p38 signaling pathways triggered by antigen recognition, making CsA a highly specific inhibitor of T cell activation. [2] Cyclosporine-mediated inhibition of the biliary excretion of MPAG by the Mrp2 transporter is the mechanism responsible for the interaction between Cyclosporine and mycophenolate mofetil (MMF). [3] Cyclosporine inhibits biochemical and morphological differentiation of skeletal muscle cells while having a minimal effect on proliferation. [4]

Cyclosporine enhances tumour growth in immunodeficient SCID-beige mice. [1] Cyclosporine inhibits muscle regeneration after induced trauma in mice. [4] Cyclosporine peaks at 1 hour in blood, spleen, and kidney, with higher concentrations in spleen and kidney than in blood. [5]