Fasentin

  Cat. No.:  DC20381   Featured
Chemical Structure
392721-37-8
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More than 5000 active chemicals with high quality for research!
Field of application
Fasentin is a novel inhibitor of glucose uptake (GLUT) that sensitizes cancer cells to FAS-induced cell death, preferentially inhibits GLUT4 (IC50=68 uM) over GLUT1.
Cas No.: 392721-37-8
Chemical Name: N-[4-Chloro-3-(trifluoromethyl)phenyl]-3-oxobutanamide
SMILES: ClC1C=CC(NC(=O)CC(=O)C)=CC=1C(F)(F)F
Formula: C11H9ClF3NO2
M.Wt: 279.643
Purity: >98%
Sotrage: 2 years -20°C Powder, 2 weeks 4°C in DMSO, 6 months -80°C in DMSO
Description: Fasentin, a potent glucose uptake inhibitor, inhibits GLUT-1/GLUT-4 transporters. Fasentin preferentially inhibits GLUT4 (IC50=68 μM) over GLUT1. Fasentin is a death receptor stimuli (FAS) sensitizer and sensitizes cells to FAS-induced cell death. Fasentin is also a tumor necrosis factor (TNF) apoptosis-inducing ligand sensitizer. Fasentin blocks glucose uptake in cancer cell lines and has anti-angiogenic activity[1][2][3].
Target: GLUT4:68 μM (IC50) GLUT1
In Vitro: Fasentin (0.1-1000 μM; 72 hours) inhibits endothelial, tumour and fibroblast cell growth without inducing cell death[1]. Fasentin (25-100 μM; 16-24 hours) induces a cell cycle arrest in G0/G1 phase and reduces the cell number in S phase in a dose-dependent manner[1]. Fasentin (50 μM; 16 hours) alters expression of genes associated with glucose deprivation such as AspSyn and PCK-2[2]. Fasentin (15, 30, 80 μM; pretreatment 1 hour) induces glucose deprivation, partially blocks glucose uptake in PPC-1, DU145, and U937 cells[2]. Fasentin (100 μM; 16 hours) does not affect the migratory capability of endothelial cells[1]. Fasentin (25-100 μM; 16 hours) lowers levels of phospho-ERK in HMECs, indicating a partial inhibition on the ERK signalling pathway, even though the effect is not statistically significant. Fasentin does not inhibit the tyrosine kinase activity of VEGFR2[1]. Fasentin interacts with a unique site in the intracellular channel of GLUT1[3]. Cell Viability Assay[1] 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) Concentration: 0.1, 1, 10, 100, 1000 μM Incubation Time: 72 hours Result: Inhibited endothelial, tumour and fibroblast cell growth (IC50=26.3-111.2 μM) without inducing cell death. Cell Cycle Analysis[1] Cell Line: HMECs Concentration: 25, 50, 100 μM Incubation Time: 16, 24 hours Result: 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. RT-PCR[2] Cell Line: PPC-1 cells[2] Concentration: 50 μM Incubation Time: 16 hours Result: Altered expression of genes associated with glucose deprivation such as AspSyn and PCK-2 not FLIP mRNA expression.
References: [1]. Mª Carmen Ocaña, et al. Fasentin diminishes endothelial cell proliferation, differentiation and invasion in a glucose metabolism-independent manner. Sci Rep. 2020 Apr 9;10(1):6132. [2]. Tabitha E Wood, et al. A novel inhibitor of glucose uptake sensitizes cells to FAS-induced cell death. Mol Cancer Ther. 2008 Nov;7(11):3546-55. [3]. Qin Wu, et al. GLUT1 inhibition blocks growth of RB1-positive triple negative breast cancer. Nat Commun. 2020 Aug 21;11(1):4205.
MSDS
COA
LOT NO. DOWNLOAD
2018-0101
2018-0101
2018-0101
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