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2 mg | ¥7,000 | ||
5 mg | ¥11,000 | ||
10 mg | ¥19,500 | ||
25 mg | ¥38,000 | ||
50 mg | ¥49,500 | ||
100 mg | ¥64,500 | ||
1 mL x 10 mM (in DMSO) | ¥12,500 |
BMS-309403 is an effective, selective and cell-permeable inhibitor of fatty acid binding protein 4 (FABP4) with a Ki of less than 2 nM. | |
Targets&IC50 | FABP3: 250 nM , FABP4:< 2 nM, FABP5: 350 nM |
In vitro | BMS-309403 binds to FABP4 with high affinity and shows over 100-fold selectivity against FABP5 as well as the heart isoform FABP3[1]. BMS-309403 interacts with the fatty-acid-binding pocket within the interior of the protein and competitively inhibits the binding of endogenous fatty acids. Treatment with BMS-309403 significantly decreased MCP-1 production from THP-1 macrophages in a dose- and time-dependent manner[2]. BMS-309403 stimulates glucose uptake in C2C12 myotubes in a temporal and dose dependent manner via activation of AMP-activated protein kinase (AMPK) signaling pathway but independent of FABPs[3]. |
In vivo | A 6 week treatment with BMS-309403 improves endothelial function, phosphorylated and total eNOS and reduced plasma triglyceride levels but does not affect endothelium-independent relaxations. In cultured human microvascular endothelial cells, lipid-induced A-FABP expression is associated with reduced phosphorylated eNOS and NO production and is reversed by BMS-309403[4]. The extent of atherosclerotic lesion area in the proximal aorta is significantly reduced in the BMS-309403-treated group compared with vehicle-treated controls in both the early and late intervention studies[2]. |
474.55 | |
C31H26N2O3 | |
CAS | 300657-03-8 |
Powder: -20°C for 3 years | In solvent: -80°C for 1 year | |||||||||||||||||||||||||||||||||||||||||
Ethanol: 20 mM, Heating is recommended. DMSO: 50 mg/mL (105.36 mM) ![]() | |||||||||||||||||||||||||||||||||||||||||
Ethanol/DMSO
DMSO
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