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Merck
CN
所有图片(1)

主要文件

SML0770

Sigma-Aldrich

P5091

≥98% (HPLC)

别名:

1-[5-[(2,3-Dichlorophenyl)thio]-4-nitro-2-thienyl]-ethanone; 1-[5-(2,3-dichlorophenyl)sulfanyl-4-nitro-2-thienyl]ethanone

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About This Item

经验公式(希尔记法):
C12H7Cl2NO3S2
分子量:
348.22
UNSPSC代码:
12352200
NACRES:
NA.77

质量水平

方案

≥98% (HPLC)

表单

powder

颜色

light yellow to dark yellow

溶解性

DMSO: 10 mg/mL, clear

储存温度

2-8°C

SMILES字符串

[s]1c(c(cc1C(=O)C)[N+](=O)[O-])Sc2c(c(ccc2)Cl)Cl

InChI

1S/C12H7Cl2NO3S2/c1-6(16)10-5-8(15(17)18)12(20-10)19-9-4-2-3-7(13)11(9)14/h2-5H,1H3

InChI key

LKZLGMAAKNEGCH-UHFFFAOYSA-N

应用

P5091 has been used:
  • as a ubiquitin specific peptidase 47 (USP47) inhibitor in 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay to evaluate the cellular viability of MCF-10A cells
  • as a USP7 inhibitor to study the regulatory role for USP7 on inflammasome activation
  • as USP7 inhibitor in drug susceptibility assays to study its effect on bone marrow−resident tumor cells (BMRTCs)/ circulating tumor cells (CTCs)

生化/生理作用

P5091 is a cell permeable, potent and specific inhibitor of deubiquitylating enzyme USP7 (Ubiquitin-Specific Protease-7) that induces HDM2 polyubiquitylation and accelerates degradation of HDM2. P5091 induces apoptosis in MM cells resistant to conventional and bortezomib therapies. P5091 inhibits tumor growth and prolongs survival in animal models of cancer.
P5091 plays an important role in ovarian cancer, as it can prevent the growth of cells and can promote necrosis and apoptosis.

象形图

Skull and crossbones

警示用语:

Danger

危险声明

危险分类

Acute Tox. 3 Oral - Aquatic Chronic 4

储存分类代码

6.1C - Combustible acute toxic Cat.3 / toxic compounds or compounds which causing chronic effects

WGK

WGK 3

闪点(°F)

Not applicable

闪点(°C)

Not applicable


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12th International Detonation Symposium. null
13th ACS Winter Fluorine Conference, paper No. 8 null
11th Int. Conf. Adv. Prostagl. Leukot. Res. null
13th ACS Winter Fluorine Conference, paper No. 8 null
Sandhini Saha et al.
Cell death & disease, 13(6), 563-563 (2022-06-23)
Nutrient surplus and consequent free fatty acid accumulation in the liver cause hepatosteatosis. The exposure of free fatty acids to cultured hepatocyte and hepatocellular carcinoma cell lines induces cellular stress, organelle adaptation, and subsequent cell death. Despite many studies, the

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