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ChemicalBook--->CAS DataBase List--->392721-37-8

392721-37-8

392721-37-8 Structure

392721-37-8 Structure
IdentificationBack Directory
[Name]

N-[4-chloro-3-(trifluoromethyl)phenyl]-3-oxobutanamide
[CAS]

392721-37-8
[Synonyms]

Fasentin
Fasentin NEW
Fasentin >=98% (HPLC)
Fasentin - CAS 392721-37-8 - Calbiochem
N-[4-chloro-3-(trifluoromethyl)phenyl]-3-oxobutanamide
[Molecular Formula]

C11H9ClF3NO2
[MDL Number]

MFCD01001285
[MOL File]

392721-37-8.mol
[Molecular Weight]

279.64
Chemical PropertiesBack Directory
[Boiling point ]

394.2±42.0 °C(Predicted)
[density ]

1.411±0.06 g/cm3(Predicted)
[storage temp. ]

room temp
[solubility ]

DMSO: >10mg/mL
[form ]

powder
[pka]

10.76±0.46(Predicted)
[color ]

white to off-white
[Stability:]

Stable for 2 years from date of purchase as supplied. Solutions in DMSO may be stored at -20° for up to 3 months.
Safety DataBack Directory
[Hazard Codes ]

Xn
[Risk Statements ]

22
[WGK Germany ]

3
Hazard InformationBack Directory
[Description]

Fasentin (392721-37-8) is a novel inhibitor of glucose uptake which acts via inhibition of the glucose transporter GluT1 and GluT4 (IC50=68 μM).1?Inhibition of glucose uptake is cell type specific2?and is a promising approach to new cancer therapeutics3. Rescues cardiac progenitor cell dysfunction and mitochondrial fission induced by high glucose.4?Sensitizes cells to FAS-induced cell death.5,6
[Uses]

Fasentin has been used as a glucose transporter (GLUT1) inhibitor to assess its effects on the vulnerability of a wide range of triple-negative breast cancer (TNBC) cell lines and to study its effects on cytotoxic drugs induced by hydrocortisone (HC).
[Uses]

Fasentin is a novel glucose transport inhibitor that blocks glucose uptake and is also a chemical sensitizer to the death receptor stimuli FAS and tumor necrosis factor apoptosis-inducing ligand.
[Biochem/physiol Actions]

Fasentin is a novel inhibitor of glucose uptake, GluT1 inhibitor. Fasentin is a novel inhibitor of glucose uptake that sensitizes cells to FAS-induced cell death. Fasentin selectively sensitized to death ligands, but did not decrease FLIP expression. It alters expression of genes associated with nutrient and glucose deprivation. Fasentin interacted with a unique site in the intracellular channel of the glucose transport protein GLUT1.
[IC 50]

GLUT4: 68 μM (IC50); GLUT1
[storage]

Store at -20°C
[References]

1) Granchi?et al.?(2016),?Anticancer agents interacting with membrane glucose transporters; Med. Chem. Comm.,?7?1716 2) Kraus?et al. (2018),?Targeting glucose transport and the NAD pathway in tumor cells with STF-31: a re-evaluation; Cell. Oncol. (Dordr),?41?485 3) Adekola?et al. (2012),?Glucose transporters in cancer metabolism; Curr. Opin. Oncol.,?24?650 4) Choi?et al.?(2016),?High Glucose Causes Human Cardiac Progenitor Cell Dysfunction by Promoting Mitochondrial Fission: Role of a GLUT1 Blocker; Prog. Biomol. Ther. (Seoul),?24?363 5) Schimmer?et al.?(2006),?Identification of small molecules that sensitize resistant tumor cells to tumor necrosis factor-family death receptors; Cancer Res.,?66?2367 6) Wood?et al.?(2008),?A novel inhibitor of glucose uptake sensitizes cells to FAS-induced cell death; Mol. Cancer Ther.,?7?3546
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