BMS-309403 | FABP4 inhibitor
NMR (Conforms)
Available Options
| Size: | Price | Quantity | |
|---|---|---|---|
| 5 mg | $60.00 | ||
| 25 mg | $225.00 |
BMS-309403 (300657-03-8) is a potent (Ki <2 nM FABP4, Ki = 250 nM FABP3, Ki = 350 nM FABP5) and selective inhibitor of the fatty-acid-binding protein aP2 (FABP4).1,2 It demonstrated marked reductions in atherosclerotic lesions in an Apoe-/- mouse model and improved glucose metabolism, reduced inflammation, and increased insulin sensitivity in a Lepob/obmouse model. BMS-309403 stimulated glucose uptake in myotubes via activation of AMPK.3 It decreased ER stress-associated inflammation in skeletal muscle4 and suppressed inflammation and oxidative stress in mouse and cell models of acute lung injury5.
References/Citations:
1) Furuhashi et al. (2007), Treatment of diabetes and atherosclerosis by inhibiting fatty-acid-binding protein aP2; Nature 447 959
2) Sulsky et al. (2007), Potent and selective biphenyl azole inhibitors of adipocyte fatty acid binding protein (aFABP); Bioorg. Med. Chem. Lett., 17 3511
3) Lin et al. (2012), BMS309403 stimulates glucose uptake in myotubes through activation of AMP-activated protein kinase; PLoS One, 7 e44570
4) Bosquet et al. (2018), FABP4 inhibitor BMS3409403 decreases saturated-fatty-acid-induced endoplasmic reticulum stress-associated inflammation in skeletal muscle by reducing p38 MAPK activation; Biochim. Biophys. Acta Mol. Cell Biol. Lipids, 1863 604
5) Gongl et al. (2018), FABP4 inhibitors suppress inflammation and oxidative stress in murine and cell models of acute lung injury; Biochem. Biophys. Res. Commun., 496 1115
NMR (Conforms)
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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
BMS-309403 (300657-03-8) is a potent (Ki <2 nM FABP4, Ki = 250 nM FABP3, Ki = 350 nM FABP5) and selective inhibitor of the fatty-acid-binding protein aP2 (FABP4).1,2 It demonstrated marked reductions in atherosclerotic lesions in an Apoe-/- mouse model and improved glucose metabolism, reduced inflammation, and increased insulin sensitivity in a Lepob/obmouse model. BMS-309403 stimulated glucose uptake in myotubes via activation of AMPK.3 It decreased ER stress-associated inflammation in skeletal muscle4 and suppressed inflammation and oxidative stress in mouse and cell models of acute lung injury5.
References/Citations:
1) Furuhashi et al. (2007), Treatment of diabetes and atherosclerosis by inhibiting fatty-acid-binding protein aP2; Nature 447 959
2) Sulsky et al. (2007), Potent and selective biphenyl azole inhibitors of adipocyte fatty acid binding protein (aFABP); Bioorg. Med. Chem. Lett., 17 3511
3) Lin et al. (2012), BMS309403 stimulates glucose uptake in myotubes through activation of AMP-activated protein kinase; PLoS One, 7 e44570
4) Bosquet et al. (2018), FABP4 inhibitor BMS3409403 decreases saturated-fatty-acid-induced endoplasmic reticulum stress-associated inflammation in skeletal muscle by reducing p38 MAPK activation; Biochim. Biophys. Acta Mol. Cell Biol. Lipids, 1863 604
5) Gongl et al. (2018), FABP4 inhibitors suppress inflammation and oxidative stress in murine and cell models of acute lung injury; Biochem. Biophys. Res. Commun., 496 1115
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