Z-VDVAD-FMK 是一种特异性的 caspase-2 抑制剂。Z-VDVAD-FMK 可减少 Lovastatin 诱导的细胞凋亡 (apoptosis)。

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

Solid

Caspase-2

Cotreatment of cells with the caspase inhibitors Ac-DEVD-CHO, Z-VDVAD-FMK (100 μM), 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.
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. 
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%. has not independently confirmed the accuracy of these methods. They are for reference only.

Room temperature in continental US; may vary elsewhere.

Sealed storage, away from moisturePowder -80°C 2 years；-20°C 1 year

{Cbz}-V{Asp(OMe)}-VA-{Asp(OMe)}-CH2F

[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.