Boc-D-FMK is a cell-permeable broad-spectrum caspase inhibitor that fully inhibits the pro-apoptotic effect of tumor necrosis factor-α (TNFα) with the half maximal inhibition concentration IC50 value of 39 μM [1].
Boc-D-FMK has been found to reduce the activation of nuclear factor kappa light chain enhancer of activated B cells (NF-kB), suppress the phosphorylation of subunit nuclear factor kappa light polypeptide gene enhancer in B cells inhibitor α (IkBα) and inhibits TNF-induced expression of intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) [2].
Moreover, Boc-D-FMK has also effectively attenuated the hepatocyte apoptosis in bile duct-ligated rats potentially improving the survival rates [3].
References:
[1] Cowburn AS, White JF, Deighton J, Walmsley SR, Chilvers ER. z-VAD-fmk augmentation of TNF alpha-stimulated neutrophil apoptosis is compound specific and does not involve the generation of reactive oxygen species. Blood. 2005 Apr 1;105(7):2970-2. Epub 2004 Nov 30.
[2] Wu X, Guo R, Chen P, Wang Q, Cunningham PN. TNF induces caspase-dependent inflammation in renal endothelial cells through a Rho- and myosin light chain kinase-dependent mechanism. Am J Physiol Renal Physiol. 2009 Aug;297(2):F316-26. doi: 10.1152/ajprenal.00089.2009. Epub 2009 May 6.
[3] Sheen-Chen SM, Hung KS, Eng HL. Effect of Boc-D-Fmk on hepatocyte apoptosis after bile duct ligation in rat and survival rate after endotoxin challenge. J Gastroenterol Hepatol. 2008 Aug;23(8 Pt 1):1276-9. doi: 10.1111/j.1440-1746.2008.05368.x. Epub 2008 Mar 27.
