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Merck
CN

506126

Sigma-Aldrich

p38 MAP Kinase Inhibitor

The p38 MAP Kinase Inhibitor, also referenced under CAS 219138-24-6, controls the biological activity of p38 MAP Kinase. This small molecule/inhibitor is primarily used for Phosphorylation & Dephosphorylation applications.

别名:

p38 MAP Kinase Inhibitor, 2-(4-Chlorophenyl)-4-(4-fluorophenyl)-5-pyridin-4-yl-1,2-dihydropyrazol-3-one

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关于此项目

经验公式(希尔记法):
C20H13ClFN3O
化学文摘社编号:
分子量:
365.79
UNSPSC代码:
12352200
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质量水平

方案

≥95% (HPLC)

表单

solid

效能

35 nM IC50

制造商/商品名称

Calbiochem®

储存条件

OK to freeze
protect from light

颜色

pale yellow

溶解性

DMSO: 25 mg/mL

运输

ambient

储存温度

−20°C

InChI

1S/C20H13ClFN3O/c21-15-3-7-17(8-4-15)25-20(26)18(13-1-5-16(22)6-2-13)19(24-25)14-9-11-23-12-10-14/h1-12,24H

InChI key

DZFBYHUKZSRPHU-UHFFFAOYSA-N

一般描述

A potent p38 MAP kinase inhibitor (IC50 = 35 nM).

生化/生理作用

Cell permeable: no
Product does not compete with ATP.
Reversible: no

包装

Packaged under inert gas

其他说明

de Laszlo, S.E., et al. 1998. Bioorg. Med. Chem. Lett. 8, 2689.

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

11 - Combustible Solids

WGK

WGK 1


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S E de Laszlo et al.
Bioorganic & medicinal chemistry letters, 8(19), 2689-2694 (1999-01-05)
Investigation of furans, pyrroles and pyrazolones identified 3-pyridyl-2,5-diaryl-pyrroles as potent, orally bioavailable inhibitors of p38 kinase. 3-(4-pyridyl-2-(4-fluoro-phenyl)-5-(4-methylsulfinylphenyl)-pyrrol e (L-167307) reduces secondary paw swelling in the rat adjuvant arthritis model: ID50 = 7.4 mg/kg/b.i.d.
Guoqi Zhang et al.
Cancer research, 68(6), 1691-1696 (2008-03-15)
One of the physiologic consequences of excessive UV radiation (UVR) exposure is apoptosis. This critical response serves to eliminate genetically injured cells and arises, in part, from activation of DNA damage and p53 signaling. Other contributory pathways, however, likely exist
Charles B Trelford et al.
Frontiers in cell and developmental biology, 9, 712124-712124 (2021-11-12)
The mechanism(s) in which transforming growth factor beta 1 (TGFβ) modulates autophagy in cancer remain unclear. Here, we characterized the TGFβ signaling pathways that induce autophagy in non-small cell lung cancer cells, using cells lines stably expressing GFP-LC3-RFP-LC3ΔG constructs that

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