BMS-309403sodium是一种有效的选择性脂肪细胞脂肪酸结合蛋白aFABP,也称为FABP4，aP2抑制剂，对FABP4，FABP3和FABP5的Ki分别为<2nM，250nM，350nM。BMS-309403sodium与蛋白质内部的脂肪酸结合口袋相互作用，竞争性地抑制内源性脂肪酸的结合。BMS-309403sodium可改善载脂蛋白E缺乏症小鼠和培养的人内皮细胞的内皮功能。
货号:ajcx32446
CAS:N/A
分子式:C31H25N2NaO3
分子量：496.53
溶解度:H2O: 100 mg/mL (201.40 mM); DMSO: 50 mg/mL (100.70 mM)
纯度：98%
存储：Store at -20°C
库存：现货

Background:

BMS-309403 sodium is a potent, orally active, and selective adipocyte fatty acid binding protein (also known as FABP4, aP2) inhibitor, with Kis of<2, 250, and 350 nM for FABP4, FABP3, and FABP5, respectively. BMS-309403 sodium interacts with the fatty-acid-binding pocket within the interior of the protein and competitively inhibits the binding of endogenous fatty acids. BMS-309403 sodium improves endothelial function in apolipoprotein E-deficient mice and in cultured human endothelial cells[1][2][3].

Treatment with BMS-309403 significantly decreased MCP-1 production from THP-1 macrophages in a dose- and time-dependent manner[1].

BMS-309403 sodium (15 mg/kg; chronic treatment; daily for 6 weeks) improves endothelial function, phosphorylated and total eNOS and reduced plasma triglyceride levels but did not affect endothelium-independent relaxations[3]. Animal Model: C57BL/6J mice (ApoE-/- mice)[3]

[1]. Sulsky R, et al. Potent and selective biphenyl azole inhibitors of adipocyte fatty acid binding protein (aFABP). Bioorg Med Chem Lett. 2007;17(12):3511-3515. [2]. Lin W, et al. BMS309403 stimulates glucose uptake in myotubes through activation of AMP-activated protein kinase. PLoS One. 2012;7(8):e44570. [3]. Lee MY, et al. Chronic administration of BMS309403 improves endothelial function in apolipoprotein E-deficient mice and in cultured human endothelial cells. Br J Pharmacol. 2011;162(7):1564-1576.