BAY-876 | GLUT1 inhibitor
NMR (Conforms)
Available Options
| Size: | Price | Quantity | |
|---|---|---|---|
| 5 mg | $80.00 | ||
| 25 mg | $245.00 |
BAY-876 (1799753-84-6) is a potent inhibitor (IC50 = 2 nM) of the facilitative glucose transporter GLUT1, an enzyme frequently overexpressed in many cancers.1 It shows greater than 100-fold selectivity over GLUT2-4. BAY-876 displayed potent antitumor activity in ovarian cancer xenograft models2 and in triple negative breast cancer cells displaying high glycolytic and low oxidative phosphorylation rates3. It reduced CD4+ T cell proliferation and IFN-γ secretion via GLUT1 inhibition suggesting utility against auto-inflammatory diseases.4 BAY-876 induces disulfidptosis in SLCA11high cancer cells.5
References/Citations:
- Siebeneicher et al. (2016), Identification and Optimization of the First Highly Selective GLUT1 Inhibitor BAY-876; ChemMedChem., 11 2261
- Ma et al. (2018), Ovarian Cancer Relies on Glucose Transporter 1 to Fuel Glycolysis and Growth: Anti-Tumor Activity of BAY-876; Cancers (Basel), 11 33
- Wu et al. (2020) GLUT1 inhibition blocks growth of RB1-positive triple negative breast cancer; Nat. Commun. 11 4205
- Chen et al. (2023), Characterization of the effect of the GLUT-1 inhibitor BAY-876 on T cells and macrophages; Eur. J. Pharmacol., 945 175552
- Liu et al. (2023), Actin cytoskeleton vulnerability to disulfide stress mediates disulfidptosis; Nat. Chem. Biol., 25 404
NMR (Conforms)
Safety Data Sheet:
Product Data Sheet:
Materials provided by Focus Biomolecules are for laboratory research use only and are not intended for human or veterinary applications. Please note that we do not sell to individuals and that all orders placed by non-research organizations will incur a $20 restocking/refund fee
BAY-876 (1799753-84-6) is a potent inhibitor (IC50 = 2 nM) of the facilitative glucose transporter GLUT1, an enzyme frequently overexpressed in many cancers.1 It shows greater than 100-fold selectivity over GLUT2-4. BAY-876 displayed potent antitumor activity in ovarian cancer xenograft models2 and in triple negative breast cancer cells displaying high glycolytic and low oxidative phosphorylation rates3. It reduced CD4+ T cell proliferation and IFN-γ secretion via GLUT1 inhibition suggesting utility against auto-inflammatory diseases.4 BAY-876 induces disulfidptosis in SLCA11high cancer cells.5
References/Citations:
- Siebeneicher et al. (2016), Identification and Optimization of the First Highly Selective GLUT1 Inhibitor BAY-876; ChemMedChem., 11 2261
- Ma et al. (2018), Ovarian Cancer Relies on Glucose Transporter 1 to Fuel Glycolysis and Growth: Anti-Tumor Activity of BAY-876; Cancers (Basel), 11 33
- Wu et al. (2020) GLUT1 inhibition blocks growth of RB1-positive triple negative breast cancer; Nat. Commun. 11 4205
- Chen et al. (2023), Characterization of the effect of the GLUT-1 inhibitor BAY-876 on T cells and macrophages; Eur. J. Pharmacol., 945 175552
- Liu et al. (2023), Actin cytoskeleton vulnerability to disulfide stress mediates disulfidptosis; Nat. Chem. Biol., 25 404
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