Z-VDVAD-FMK

Z-VDVAD-FMK is a special inhibitor of caspase-2. Z-VDVAD-FMK produces a reduction in Lovastatin-induced apoptosis[1][3][3].

Research Areas >> Cancer

Signaling Pathways >> Apoptosis >> Caspase

Caspase-2

"Cotreatment of cells with the caspase inhibitors Ac-DEVD-CHO, Z-VDVAD-FMK (100μM), Z-IETD-fmk, and Z-LEHD-fmk alone or in combination, or overexpression of CrmA, prevents many morphological features of apoptosis but not loss of mitochondrial membrane potential (DCm), phospatidilserine exposure, and cell death[1]. Z-VDVAD-FMK (2 μM) greatly inhibits the Rho-kinase activity in HMEC-1 cells stimulated by Thrombin and displays no effect on control cells[2].  Z-VDVAD-FMK (zVDVAD-fmk) produces a reduction in Lovastatin-induced apoptosis. Z-VDVAD-FMK (100 μM) significantly reduces Lovastatin-induced loss of DNA by 19.1±8.3%[3]." Cell Viability Assay[1] Cell Line: The human T-cell leukemia Jurkat (Clone E6.1, ATCC TIB-152) Concentration: 100 μM Incubation Time: 22 hours Result: Prevented Doxorubicin (1 μM)-induced nuclear apoptosis, but not cell death.

[1]. S Gamen, et al. Doxorubicin treatment activates a Z-VAD-sensitive caspase, which causes deltapsim loss, caspase-9 activity, and apoptosis in Jurkat cells. Exp Cell Res. 2000 Jul 10;258(1):223-35.

[2]. Cédric Sapet, et al. Thrombin-induced endothelial microparticle generation: identification of a novel pathway involving ROCK-II activation by caspase-2. Blood. 2006 Sep 15;108(6):1868-76.

[3]. Simon W Rabkin, et al. Lovastatin-induced cardiac toxicity involves both oncotic and apoptotic cell death with the apoptotic component blunted by both caspase-2 and caspase-3 inhibitors. Toxicol Appl Pharmacol. 2003 Dec 15;193(3):346-55.