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Merck
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Key Documents

SML0770

Sigma-Aldrich

P5091

≥98% (HPLC)

Sinônimo(s):

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

Fórmula empírica (Notação de Hill):
C12H7Cl2NO3S2
Número CAS:
Peso molecular:
348.22
Código UNSPSC:
12352200
NACRES:
NA.77

Ensaio

≥98% (HPLC)

forma

powder

cor

light yellow to dark yellow

solubilidade

DMSO: 10 mg/mL, clear

temperatura de armazenamento

2-8°C

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

chave InChI

LKZLGMAAKNEGCH-UHFFFAOYSA-N

Aplicação

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)

Ações bioquímicas/fisiológicas

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.

Pictogramas

Skull and crossbones

Palavra indicadora

Danger

Frases de perigo

Classificações de perigo

Acute Tox. 3 Oral - Aquatic Chronic 4

Código de classe de armazenamento

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

Classe de risco de água (WGK)

WGK 3

Ponto de fulgor (°F)

Not applicable

Ponto de fulgor (°C)

Not applicable


Certificados de análise (COA)

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12th International Detonation Symposium. null
11th Int. Conf. Adv. Prostagl. Leukot. Res. 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
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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