Cyclosporine

Cyclosporine binds cyclophilin and inhibits calcineurin-dependent signaling. Its established pharmacology is broad systemic immunosuppression, especially through T-cell pathways; it is not a selective mast-cell stabilizer.

Two published case reports describe cyclosporine exposure in people with advanced systemic mastocytosis. Both reports combined it with a corticosteroid, and the patients had aggressive clonal disease rather than MCAS. One paper also paired the case with an experiment in cultured human umbilical-cord-derived mast cells. These reports establish use in mast cell disease, not an attributable cyclosporine effect or a result that transfers to MCAS.

A separate laboratory study exposed isolated human lung mast cells and blood basophils to cyclosporine before IgE-mediated activation and examined histamine release and calcineurin activity. That supplies a direct human-cell mechanism outside the body. Two randomized studies instead examined chronic idiopathic urticaria with background antihistamine therapy; their population and endpoints are recorded separately as adjacent-condition evidence.

Formulation identity matters. The current US label states that modified cyclosporine has greater bioavailability than non-modified Sandimmune and that the formulations are not bioequivalent or interchangeable without medical supervision. The label’s approved indications and intensive monitoring framework do not include MCAS or chronic urticaria.