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Merck
CN
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文件

573126

Sigma-Aldrich

STAT3 Inhibitor XI, STX-0119

The STAT3 Inhibitor XI, STX-0119 controls the biological activity of STAT3. This small molecule/inhibitor is primarily used for Phosphorylation & Dephosphorylation applications.

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别名:
STAT3 Inhibitor XI, STX-0119, N-(5-(Furan-2-yl)-1,3,4-oxadiazol-2-yl)-2-phenylquinoline-4-carboxamide
经验公式(希尔记法):
C22H14N4O3
分子量:
382.37
MDL编号:
UNSPSC代码:
12352200
NACRES:
NA.77

质量水平

检测方案

≥90% (HPLC)

形式

solid

制造商/商品名称

Calbiochem®

储存条件

OK to freeze
protect from light

颜色

gray to off-white

溶解性

DMSO: soluble

运输

ambient

储存温度

2-8°C

SMILES字符串

O=C(NC1=NN=C(C2=CC=CO2)O1)C3=CC(C4=CC=CC=C4)=NC5=C3C=CC=C5

一般描述

A cell-permeable oxadiazolyl-quinolinecarboxamide that is shown to selectively suppress STAT3, but not STAT1, STAT5a, or STAT5b, DNA binding activity and prevent IL-6-stimulated STAT3 dimerization in HEK293 cells (by 99% at 100 µM), as well as inhibit the expression of STAT3 target genes both in cultures in vitro (effective conc. 50 µM) and in SCC3-derived tumors in mice in vivo (160 mg/kg/day; p.o.).
A cell-permeable oxadiazolyl-quinolinecarboxamide that is shown to selectively suppress STAT3, but not STAT1, STAT5a, or STAT5b, DNA binding activity in nuclear extract from IL-6-stimulated MDA-MB-468 cells (by 74% at 50 µM) and prevent IL-6-stimulated STAT3 dimerization in HEK293 cells (by 50% and 99%, respectively, at 74 and 100 µM), as well as inhibit the expression of STAT3 target genes, c-myc, cyclin D1, and survivin, both in cultures in vitro (effective conc. 50 µM) and in SCC3-derived tumors in mice in vivo (160 mg/kg/day; p.o.).

包装

Packaged under inert gas

警告

Toxicity: Standard Handling (A)

其他说明

Ashizawa, T., et al. 2011. Int. J. Oncol.38, 1245,
Matsuno, K., et al. 2010. ACS Med. Chem. Lett.1, 371.

法律信息

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

WGK

WGK 2

闪点(°F)

Not applicable

闪点(°C)

Not applicable


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Guoming Hu et al.
Cancer immunology research, 8(10), 1273-1286 (2020-08-28)
The tumor microenvironment induces immunosuppression via recruiting and expanding suppressive immune cells such as regulatory T cells (Treg) to promote cancer progression. In this study, we documented that tumor-infiltrating CD73+ γδTregs were the predominant Tregs in human breast cancer and

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