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Merck
모든 사진(1)

주요 문서

SML0770

Sigma-Aldrich

P5091

≥98% (HPLC)

동의어(들):

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

실험식(Hill 표기법):
C12H7Cl2NO3S2
CAS Number:
Molecular Weight:
348.22
UNSPSC 코드:
12352200
NACRES:
NA.77

분석

≥98% (HPLC)

양식

powder

색상

light yellow to dark yellow

solubility

DMSO: 10 mg/mL, clear

저장 온도

2-8°C

SMILES string

[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

관련 카테고리

애플리케이션

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)

생화학적/생리학적 작용

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 is a cell permeable, potent and specific inhibitor of deubiquitylating enzyme USP7.
P5091 plays an important role in ovarian cancer, as it can prevent the growth of cells and can promote necrosis and apoptosis.

픽토그램

Skull and crossbones

신호어

Danger

유해 및 위험 성명서

Hazard Classifications

Acute Tox. 3 Oral - Aquatic Chronic 4

Storage Class Code

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

WGK

WGK 3

Flash Point (°F)

Not applicable

Flash Point (°C)

Not applicable


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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
Pablo Palazón-Riquelme et al.
EMBO reports, 19(10) (2018-09-13)
The assembly and activation of the inflammasomes are tightly regulated by post-translational modifications, including ubiquitin. Deubiquitinases (DUBs) counteract the addition of ubiquitin and are essential regulators of immune signalling pathways, including those acting on the inflammasome. How DUBs control the

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