SML0770
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
产品名称
P5091, ≥98% (HPLC)
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
assay
≥98% (HPLC)
form
powder
color
light yellow to dark yellow
solubility
DMSO: 10 mg/mL, clear
storage temp.
2-8°C
Quality Level
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 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.
signalword
Danger
hcodes
Hazard Classifications
Acute Tox. 3 Oral - Aquatic Chronic 4
存储类别
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
12th International Detonation Symposium. null
13th ACS Winter Fluorine Conference, paper No. 8 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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