BAY-876 is an orally active, selective inhibitor of glucose transporter 1 (GLUT1, IC50= 2 nM), exhibiting over 130-fold greater selectivity for GLUT1 than GLUT2, GLUT3, and GLUT4. It also inhibits glycolytic metabolism and ovarian cancer growth.

GLUT1:0.002 μM

METHODS: HNSCC cell lines SCC47 and RPMI2650 were treated with BAY-876 (0.01-100 µM) for 24 h. Cell viability was detected by crystal violet staining.
RESULTS: After 24 h, BAY-876 reduced the viable SCC47 and RPMI2650 cells. [1]
METHODS: Ovarian cancer cells SKOV-3, OVCAR-3 and HEY were treated with BAY-876 (25-75 nM) for 24 h. The rate of glycolysis was detected by Glycolysis Assay.
RESULTS: Incubation with BAY-876 dose-dependently decreased the rate of glycolysis in SKOV-3, OVCAR-3 and HEY cells. Although this anti-glycolytic effect of BAY-876 was detectable at single-digit nanomolar concentrations, half-maximal inhibition was achieved at 25-50 nM of the compound. [2]

METHODS: To detect the antitumor activity in vivo, BAY-876 (1.5-4.5 mg/kg, 0.5% hydroxypropyl methyl cellulose and 0.1% Tween 80) was administered by gavage to NSG mice bearing SKOV-3 xenografts once a day for four weeks.
RESULTS: BAY-876 showed a significant dose-dependent inhibitory effect on tumorigenicity. The maximum effect was observed in the 4.5 mg/kg/day treatment group. After 2 weeks of treatment, tumors were significantly reduced. At the endpoint, final mean tumor volume and tumor weight decreased by 68% and 66%, respectively, compared to the excipient control group. However, the dose of 4.5 mg/kg/day was toxic to NSG mice. [2]