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Merck
CN
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主要文件

368050

Sigma-Aldrich

颗粒酶B抑制剂I

≥95% (HPLC), solid, Granzyme B inhibitor, Calbiochem®

别名:

颗粒酶B抑制剂I, Z-AAD-CMK

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About This Item

经验公式(希尔记法):
C19H24ClN3O7
分子量:
441.86
UNSPSC代码:
12352200
NACRES:
NA.77

产品名称

颗粒酶B抑制剂I, The Granzyme B Inhibitor I controls the biological activity of Granzyme B. This small molecule/inhibitor is primarily used for Cancer applications.

质量水平

方案

≥95% (HPLC)

表单

solid

制造商/商品名称

Calbiochem®

储存条件

OK to freeze
desiccated

颜色

off-white

溶解性

DMSO: 5 mg/mL

运输

ambient

储存温度

−20°C

一般描述

人和鼠丝氨酸蛋白酶颗粒酶B的弱抑制剂。还通过片段化蛋白2(一种与颗粒酶B同源的大鼠淋巴细胞颗粒蛋白酶)抑制淋巴细胞中与凋亡相关的DNA片段化(ID50=300 nM)。
人和鼠颗粒酶B的弱抑制剂。还通过片段化蛋白2(一种与颗粒酶B同源的大鼠淋巴细胞颗粒蛋白酶)抑制淋巴细胞中与凋亡相关的DNA片段化(ID50=300 nM)。

生化/生理作用

主要靶标
颗粒酶B
产物不与ATP竞争。
可逆:否
细胞可渗透性:是
靶标IC50:300 nM,针对片段化蛋白2引起的淋巴细胞凋亡相关DNA片段化

警告

毒性:标准处理(A)

序列

Z-Ala-Ala-Asp-CH₂Cl

重悬

复溶后,等分并冷冻保存(-20°C)。储备溶液在-20°C下可稳定保存至多3个月。

其他说明

Gong, B., et al. 1999.Cell Growth Different.10, 491.
Shi, L., et al. 1992.J. Exp.Med. 176, 1521.
Odake, S., et al. 1991.Biochemistry30, 2217.

法律信息

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

储存分类代码

11 - Combustible Solids

WGK

WGK 1

闪点(°F)

Not applicable

闪点(°C)

Not applicable


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Ganta Vijay Chaitanya et al.
Brain pathology (Zurich, Switzerland), 21(1), 16-30 (2010-09-10)
Infiltration of leukocytes into post-ischemic cerebrum is a well-described phenomenon in stroke injury. Because CD-8(+) T-lymphocytes secrete cytotoxic proteases, including granzyme-b (Gra-b) that exacerbates post-ischemic brain damage, we investigated roles of Gra-b in human stroke. To study the role of
Yan Su et al.
Cell discovery, 8(1), 35-35 (2022-04-20)
Penetration of immune cells into tumor cells was believed to be immune-suppressive via cell-in-cell (CIC) mediated death of the internalized immune cells. We unexpectedly found that CIC formation largely led to the death of the host tumor cells, but not
Ning-Ning Ji et al.
Frontiers in neurology, 10, 1306-1306 (2020-01-11)
Hippocampal neuronal apoptosis is a devastating consequence of cardiac arrest (CA) and subsequent cardiopulmonary resuscitation (CPR). In this study, we assessed the contribution of cytotoxic T lymphocyte (CTL)-derived toxic mediator granzyme B (Gra-b) to the hippocampal neuronal apoptosis following CA/CPR

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