[CAS NO. 300657-03-8] BMS-309403
PRODUCTS SPECIFICATIONS [300657-03-8]
DESCRIPTION [300657-03-8]
Overview
| MDL | MFCD09991687 |
|---|---|
| Molecular Weight | 474.55 |
| Molecular Formula | C31H26N2O3 |
| SMILES | O=C(O)COC1=CC(C2=CC=CC=C2N3N=C(C4=CC=CC=C4)C(C5=CC=CC=C5)=C3CC)=CC=C1 |
11 Publications Citing Use of MCE
- [1]Bone Res. 2022 Jun 22;10(1):45.
- [2]Cell Death Dis. 2019 May 16;10(6):382.
- [3]Free Radic Biol Med. 2022 Jul 15;S0891-5849(22)00474-9.
- [4]Am J Cancer Res. 2019 Oct 1;9(10):2140-2155.
- [5]Antioxidants (Basel). 2023, 12(1), 74.
- [6]Int J Biol Sci. 2021 Oct 11;17(15):4207-4222.
- [7]J Proteomics. 2020 Feb 10;212:103570.
- [8]Br J Nutr. 2021 Mar 5;1-27.
- [9]Comp Biochem Physiol B Biochem Mol Biol. 2022 Jan 6;110715.
- [10]Iran J Basic Med Sci. 07 September 2022.
- [11]Parasitol Res. 2019 Jun;118(6):1919-1926.
Summary
BMS-309403 is a potent, orally active and selective adipocyte fatty acid binding protein (also known as FABP4, aP2) inhibitor with K i s of <2, 250, and 350 nM for FABP4, FABP3, and FABP5, respectively. BMS-309403 interacts with the fatty-acid-binding pocket within the interior of the protein and competitively inhibits the binding of endogenous fatty acids. BMS-309403 improves endothelial function in apolipoprotein E-deficient mice and in cultured human endothelial cells [1] [2] [3] .
IC50 & Target
Ki: less than 2 nM (FABP4), 250 nM (FABP3), 350 nM (FABP5) [1]
In Vitro
Treatment with BMS-309403 significantly decreased MCP-1 production from THP-1 macrophages in a dose- and time-dependent manner [2] .
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
In Vivo
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] .
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
| Animal Model: | C57BL/6J mice (ApoE −/− mice) [3] |
| Dosage: | 15 mg/kg |
| Administration: | Chronic treatment ; daily for 6 weeks |
| Result: | Significantly increased the phosphorylated eNOS (Ser1177) and total eNOS but not the phosphorylated to total eNOS ratio in aortae of 18 weeks old ApoE −/− mice. |
Appearance
Solid
Shipping
Room temperature in continental US; may vary elsewhere.
Storage
| Powder | -20°C | 3 years |
|---|---|---|
| 4°C | 2 years | |
| In solvent | -80°C | 6 months |
| -20°C | 1 month |
Solvent & Solubility
DMSO : 100 mg/mL ( 210.73 mM ; Need ultrasonic and warming)
H 2 O : < 0.1 mg/mL (ultrasonic;warming;heat to 60°C) (insoluble)
Stock Solutions
| Concentration Solvent Mass | 1 mg | 5 mg | 10 mg |
|---|
| 1 mM | 2.1073 mL | 10.5363 mL | 21.0726 mL |
| 5 mM | 0.4215 mL | 2.1073 mL | 4.2145 mL |
| 10 mM | 0.2107 mL | 1.0536 mL | 2.1073 mL |
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Add each solvent one by one: 10% DMSO >> 90% corn oil
Solubility: ≥ 2.08 mg/mL (4.38 mM); Clear solution
References
- [1] Sulsky R, et al. Potent and selective biphenyl azole inhibitors of adipocyte fatty acid binding protein (aFABP). Bioorg Med Chem Lett. 2007 Jun 15;17(12):3511-5.
- [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 Apr;162(7):1564-76.