Z-VDVAD-FMK

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Z-VDVAD-FMK 

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

Z-VDVAD-FMK Chemical Structure

CAS No. : 210344-92-6

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生物活性

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

IC50 & Target[1]

Caspase-2

 

体外研究
(In Vitro)

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[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].

上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.

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.

分子量

695.73

Formula

C32H46FN5O11
CAS 号

210344-92-6
Sequence Shortening

{Cbz}-V{Asp(OMe)}-VA-{Asp(OMe)}-CH2F
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献

  • [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.

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