BMS-309403 sodium |
رقم الكتالوجGC61783 |
BMS-309403 الصوديوم عبارة عن مثبط قوي ، نشط عن طريق الفم ، وانتقائي للأحماض الدهنية الدهنية (المعروف أيضًا باسم FABP4 ، aP2) ، مع Kis <2 ، 250 ، و 350 نانومتر لـ FABP4 ، FABP3 ، و FABP5 ، على التوالي
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Cas No.: 2802523-05-1
Sample solution is provided at 25 µL, 10mM.
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.
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