Tacrolimus (FK506),104987-11-3,IC-0206384

Tacrolimus (FK506), a macrolide antibiotic with potent immunosuppressive effects was isolated from Streptomyces tsukubaensis and has been previously used to prevent allograft and for treatment of autoimmune disorders in humans[1-3].
Tacrolimus(FK506) (0-2 μM;24 h)reduces synthesis of type I collagen protein without affecting expression of collagen mRNAs in Human lung fibroblasts (HLFs)[8]. T cell proliferation in response to ligation of the T cell receptor is inhibited by tacrolimus(FK506) [4]. Ttacrolimus(FK506) (concentration gradient;48 h)inhibited oral squamous cell carcinoma (OSCC) progression in vitro [9].
Tacrolimus (FK506) was given intramuscularly at the dose of 0.5 and 1.0 mg/kg for three days before burn injury. Thermal trauma to the skin caused a statistically significant increase in MPO activity and MDA content in remote organs. Tacrolimus (FK506) was effective in reducing lipid peroxidation and neutrophil infiltration especially at 24 h postinjury in lung, liver and kidney[5]. Tacrolimus (FK506) has the ability to down-regulate free radical levels in severe ischemia-reperfusion liver, and tachlimus has also been shown to be an effective inhibitor of cytokine response[6]. A study on pulmonary fibrosis in mice suggested that FK506 can be a potent antifibrotic agent [7]. Tacrolimus (FK506) treatment inhibited activation of HSCs or reduced their number in the liver. In vivo, administration of Tacrolimus (FK506) at a dose of 4 mg/kg(i.p.; 4 weeks) completely prevented development of alcohol/carbon tetrachloride induced liver fibrosis in rats[8].