Fasentin

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]. 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].