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Ac-DEVD-CMK
本产品不向个人销售,仅用作科学研究,不用于任何人体实验及非科研性质的动物实验。
Ac-DEVD-CMK图片
CAS NO:285570-60-7
规格:98%
分子量:551
包装与价格:
包装价格(元)
1mg电议
5mg电议

产品介绍
cell-permeable, and irreversible inhibitor of caspase
CAS:285570-60-7
分子式:C21H31ClN4O11
分子量:551
纯度:98%
存储:Store at -20°C

Background:

Ac-DEVD-CMK is a cell-permeable and irreversible caspase-3 inhibitor [1][2][3].


Apoptosis is a process of programmed cell death that occurs in multicellular organisms. Caspase are a family of protease enzymes playing essential roles in programmed cell death (including apoptosis, pyroptosis and necroptosis) and inflammation. Caspase activation is a major event in apoptosis. Caspase-3 cleaves and activates caspases 6 and 7, and is processed and activated by caspases 8, 9, and 10 [1][2][3].


Ac-DEVD-CMK (Ac-Asp-Glu-Val-Asp-CH2Cl) is a cell-permeable, irreversible and specific caspase-3 inhibitor. In coronary occlusion/reperfusion rat isolated hearts, Ac-DEVD-CMK reduced infarct size (the percentage of infarction 27.8+3.3% vs control 38.5+2.6%), suggesting that caspase inhibition during early reperfusion protected myocardium against lethal reperfusion injury [1]. In BL41 cells, Ac-DEVD-CMK partially inhibited Mn2+-induced apoptosis and PARP cleavage, and partially blocked B cell death by 37% even at 100 μM [2]. Ac-DEVD-CMK significantly blocked neurotoxicity at 24 hr after 1 hr of SIN-1 exposure and also protected against neurotoxicity at 24 hr after 90 min of zinc (75 μM) exposure. Ac-DEVD-CMK completely blocked SIN-1-induced activation of caspase-3 [3].


参考文献:
[1].  Mocanu MM, Baxter GF, Yellon DM. Caspase inhibition and limitation of myocardial infarct size: protection against lethal reperfusion injury. Br J Pharmacol. 2000 May;130(2):197-200.
[2].  Schrantz N, Blanchard DA, Mitenne F, et al. Manganese induces apoptosis of human B cells: caspase-dependent cell death blocked by bcl-2. Cell Death Differ. 1999 May;6(5):445-53.
[3].  Zhang Y, Wang H, Li J, et al. Peroxynitrite-induced neuronal apoptosis is mediated by intracellular zinc release and 12-lipoxygenase activation. J Neurosci. 2004 Nov 24;24(47):10616-27.