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

Name	N-[4-chloro-3-(trifluoromethyl)phenyl]-3-oxobutanamide
Synonyms	Fasentin Fasentin NEW N-[4-chloro-3-(trifluoromethyl)phenyl]-3-oxobutanamide
CAS	392721-37-8

Molecular Formula	C11H9ClF3NO2
Molar Mass	279.64
Solubility	DMSO: >10mg/mL
Appearance	powder
Color	white to off-white
Storage Condition	room temp
Stability	Stable for 2 years from date of purchase as supplied. Solutions in DMSO may be stored at -20° for up to 3 months.
Use	Fasentin is an inhibitor of glucose transport. It partially inhibits glucose uptake in U937 and DU145 cells when used at concentrations ranging from 15 to 80 µM. Fasentin sensitizes PPC-1 prostate cancer and U937 leukemia cells, but not DU145 prostate cancer cells, to cell death induced by the Fas receptor activator CH-11 activating anti-Fas antibody (FAS). It also increases the expression of AspSyn and PCK2, genes associated with glucose deprivation, in PPC-1 cells and halts the cell cycle at the G0/G1 phase in U937 cells when used at concentrations of 50 and 40 µM, respectively.

Last Update：2024-01-02 23:10:35

biological activity	Fasentin is a potent glucose uptake inhibitor that inhibits the GLUT-1/GLUT-4 transporter. Fasentin preferentially inhibited GLUT4 (IC50=68 μm). Fasentin is a death receptor-stimulating (FAS) sensitizer that sensitizes cells to FAS-induced cell death. Fasentin is also a sensitizer that induces tumor necrosis factor (TNF) apoptosis ligand. Fasentin blocks glucose uptake in cancer cell lines and has anti-angiogenic activity.
Cell Line:	Three types of endothelial cells ECs (HMEC, human microvascular endothelial cells; HUVEC, human umbilical vein endothelial cells; and BAEC, bovine aortic endothelial cells), three human tumour cell lines (MDA-MB-231 and MCF7 breast carcinoma cells, and HeLa cervix adenocarcinoma cells), and human gingival fibroblasts (HGF) HMECs PPC-1 cells [2]
Concentration:	0.1, 1, 10, 100, 1000 μM 25, 50, 100 μM 50 μM
Incubation Time:	72 hours 16, 24 hours 16 hours
Result:	Inhibited endothelial, tumour and fibroblast cell growth (IC 50 =26.3-111.2 μM) without inducing cell death. Induced a cell cycle arrest in G0/G1 phase and reduced the cell number in S phase in a dose-dependent manner. Did not increase the subG1 population. Altered expression of genes associated with glucose deprivation such as AspSyn and PCK-2 not FLIP mRNA expression.