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| Cas No.: | 300657-03-8 |
| Chemical Name: | 2-[[2'-(5-ethyl-3,4-diphenyl-1H-pyrazol-1-yl)[1,1'-biphenyl]-3-yl]oxy]-acetic acid |
| Synonyms: | BMS 309403,BMS309403 |
| SMILES: | CCC1=C(C2=CC=CC=C2)C(C3=CC=CC=C3)=NN1C4=CC=CC=C4C5=CC=CC(OCC(O)=O)=C5 |
| Formula: | C31H26N2O3 |
| M.Wt: | 474.6 |
| Sotrage: | 2 years -20°C Powder, 2 weeks 4°C in DMSO, 6 months -80°C in DMSO |
| Description: | BMS-309403 is a potent, selective and cell-permeable inhibitor of fatty acid binding protein 4 (FABP4) with a Ki of less than 2 nM. |
| 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]. |
| 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]. |
MSDS
COA
| LOT NO. | DOWNLOAD |
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| 2018-0101 |
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| 2018-0101 |
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