Tacrolimus (also referred to as FK506) is a macrolide antibiotic identified as a product of the actinobacterium Streptomyces tsukubaensis in Japan in 1984. Studies demonstrated that tacrolimus is 10‑100 times more active than cyclosporine at inhibiting several immune responses.

The main mechanism through which tacrolimus exerts its immunosuppressive effect is believed to be via the inhibition of T cell activation and proliferation.

Tacrolimus is highly lipophilic, and absorption is incomplete and variable. Following absorption, tacrolimus is highly bound to proteins and erythrocytes, with 99 % of the drug within the plasma being bound to albumin or α‑1‑glycoprotein

The bioavailability and metabolism of tacrolimus are predominantly influenced by the activity of the cytochrome P450 isozymes CYP3A4 and CYP3A5, as well as the efflux pump p‑glycoprotein, which show significant inter- and intra‑individual variability in expression and function.

Tacrolimus displays a high degree of inter- and intra‑patient variability, as well as potentially severe side effects from doses that are either too low or too high. Inadequate tacrolimus concentrations might result in rejection of the transplanted organ. High levels may lead to severe adverse effects.

Principle adverse effects associated with tacrolimus include nephrotoxicity, neurotoxicity, gastrointestinal disturbances, diabetogenesis, hypertension and malignant complications.