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Merck
CN

218761

Sigma-Aldrich

Caspase-9 Inhibitor I - Calbiochem

Caspase-9 Inhibitor I, CAS 210345-04-3, is a potent, cell-permeable, and irreversible inhibitor of caspase-9.

别名:

Caspase-9 Inhibitor I - Calbiochem, Z-LE(OMe)HD(OMe)-FMK

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关于此项目

经验公式（希尔记法）:
C32H43FN6O10
分子量:
690.72
UNSPSC代码:
12352200

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质量水平

100

表单

solid

制造商/商品名称

Calbiochem®

储存条件

OK to freeze
desiccated

颜色

white to light brown

溶解性

DMSO: 10 mg/mL

运输

ambient

储存温度

−20°C

一般描述

This product has been discontinued.



A potent, cell-permeable, and irreversible inhibitor of caspase-9. May also inhibit caspase-4 and caspase-5. When using with purified native or recombinant enzyme, pretreatment with an esterase is required. A 5 mM (250 µg/72 µl) solution of Z-LEHD-FMK (Cat. No. 218841) in DMSO is also available.

A potent, cell-permeable, and irreversible inhibitor of caspase-9.

生化/生理作用

Cell permeable: yes
Primary Target
caspase-4, caspase-5, caspase-9
Product does not compete with ATP.
Reversible: no

外形

Supplied as a trifluoroacetate salt.

制备说明

Following reconstitution aliquot and freeze (-20°C). Stock solutions are stable for up to 3 months at -20°C.

分析说明

single spot by TLC

其他说明

Fadeel, B., et al. 1999. Leukemia 13, 719.
Thornberry, N.A., and Lazebnik, Y. 1998. Science 281, 1312.
Z-Leu-Glu(OMe)-His-Asp(OMe)-CH₂F*

法律信息

CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany

免责声明

Toxicity: Standard Handling (A)

储存分类代码

10-13 - German Storage Class 10 to 13

法规信息

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Frank A Schildberg et al.
Cell and tissue research, 320(1), 91-98 (2005-02-17)
The possible protection provided by enhancement of the cAMP signal in the process of lipopolysaccharide (LPS)-induced endothelial cell death has been addressed, with special emphasis on the endoplasmic initiation of caspase-12-mediated apoptosis. Human umbilical vein endothelial cells were challenged with
W D Thomas et al.
Journal of immunology (Baltimore, Md. : 1950), 165(10), 5612-5620 (2000-11-09)
Past studies have shown that TNF-related apoptosis-inducing ligand (TRAIL) induced apoptosis in a high proportion of cultured melanoma by caspase-dependent mechanisms. In the present studies we have examined whether TRAIL-induced apoptosis of melanoma was mediated by direct activation of effector

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