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.
IC50 & Target
68 μM (IC50)
体外研究 (In Vitro)
Fasentin (0.1-1000 μM; 72 hours) inhibits endothelial, tumour and fibroblast cell growth without inducing cell death. 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. Fasentin (50 μM; 16 hours) alters expression of genes associated with glucose deprivation such as AspSyn and PCK-2. Fasentin (15, 30, 80 μM; pretreatment 1 hour) induces glucose deprivation, partially blocks glucose uptake in PPC-1, DU145, and U937 cells. Fasentin (100 μM; 16 hours) does not affect the migratory capability of endothelial cells. 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. Fasentin interacts with a unique site in the intracellular channel of GLUT1.
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
Cell Viability Assay
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)
0.1, 1, 10, 100, 1000 μM
Inhibited endothelial, tumour and fibroblast cell growth (IC50=26.3-111.2 μM) without inducing cell death.
Cell Cycle Analysis
25, 50, 100 μM
16, 24 hours
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.
Room temperature in continental US; may vary elsewhere.