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Merck
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SML0770

Sigma-Aldrich

P5091

≥98% (HPLC)

Sinónimos:

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 (notación de Hill):
C12H7Cl2NO3S2
Número de CAS:
882257-11-6
Peso molecular:
348.22
UNSPSC Code:
12352200
NACRES:
NA.77

assay

≥98% (HPLC)

form

powder

color

light yellow to dark yellow

solubility

DMSO: 10 mg/mL, clear

storage temp.

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

InChI key

LKZLGMAAKNEGCH-UHFFFAOYSA-N

Application

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)

Biochem/physiol Actions

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.

pictograms

Skull and crossbones
GHS06

signalword

Danger

hcodes

H301,H413

Hazard Classifications

Acute Tox. 3 Oral - Aquatic Chronic 4

Storage Class

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

wgk_germany

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

Certificados de análisis (COA)

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13th ACS Winter Fluorine Conference, paper No. 8 null
12th International Detonation Symposium. null
13th ACS Winter Fluorine Conference, paper No. 8 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
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