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The backbone of modern immunosuppressant regimens after kidney transplantation is Calcineurin Channel Inhibitor (CNI) drugs including tacrolimus and cyclosporine A. Its mechanism is binding to immunophilins, forming complexes, binding to calcineurin, and leading to inhibition of T cell activation. Since CNI drugs are eliminated by cytochrome P450 system, especially the CYP3A subfamily, exploring their interaction exhibits great importance. It is known that CYP3A4 and CYP3A5 are involved in tacrolimus metabolism while CYP3A5 alone plays a major role in cyclosporine A metabolism. The polymorphism of CYP3A4 and CYP3A5 genes results in different CNI drugs dose requirements in transplant recipients. Pharmacogenetic approaches to figure out donors’ and recipients’ CYP3A4 and CYP3A5 genotypes may give us better understanding of pharmacodynamics of CNI drugs. Additionally, monitoring CNI blood concentration can reflect its pharmacokinetics. Combination of pharmacodynamics and pharmacokinetics may be used as a guide in clinical practice to administer CNI drugs in optimal dose, to avoid acute rejection or adverse effects of CNI drugs such as nephrotoxicity.

Calcineurin Inhibitor - A Necessary Evil: Pharmacogenetical Approach to a Promising Future