AG-CR1-3640-M0011 mgCHF 45.00
AG-CR1-3640-M0055 mgCHF 80.00
AG-CR1-3640-M02525 mgCHF 320.00
|Synonyms||BMS309403; BMS 309403; FABP4 Inhibitor; 2-[[2'-(5-Ethyl-3,4-diphenyl-1H-pyrazol-1-yl)[1,1'-biphenyl]-3-yl]oxy]acetic acid|
|Purity Chemicals||≥98% (HPLC)|
|Appearance||White to off-white solid.|
|Solubility||Soluble in DMSO (25mg/ml), ethanol (30mg/ml), dimethylformamide (30mg/ml) or methanol. Almost insoluble in water.|
|Identity||Determined by 1H-NMR.|
|Shipping and Handling|
|Short Term Storage||+4°C|
|Long Term Storage||-20°C|
Keep cool and dry.
Protect from moisture.
|Use/Stability||Stable for at least 2 years after receipt when stored at -20°C.|
|Product Specification Sheet|
- Cell permeable, potent and selective fatty acid binding protein 4 (FABP4; A-FABP; ALBP; adipocyteP2 protein) inhibitor that competitively targets the fatty acid-binding pocket (Ki= <2nM). Inhibits FABP3 (muscle) and FABP5 (epidermal) with lower affinity (Ki=250nM and 350nM, respectively). FABP4 is an intracellular lipid-binding protein responsible for the transportation of fatty acids. It is expressed primarily in adipose tissue and is associated with inflammation, obesity, diabetes and cardiovascular diseases.
- Glucose uptake stimulator. Reduces blood glucose levels and increases insulin sensitivity in a mouse model of obesity. Protects against the development of insulin resistance associated with genetic or diet-induced obesity in mice.
- Anti-atherosclerotic. Decreases fatty acid uptake in adipocytes in vitro and reduces atherosclerotic lesion area in a mouse model of atherosclerosis.
- Potent and selective biphenyl azole inhibitors of adipocyte fatty acid binding protein (aFABP): R. Sulsky, et al.; Bioorg. Med. Chem. Lett. 17, 3511 (2007)
- Treatment of diabetes and atherosclerosis by inhibiting fatty-acid-binding protein aP2: M. Furuhashi, et al.; Nature 447, 959 (2007)
- BMS309403 stimulates glucose uptake in myotubes through activation of AMP-activated protein kinase: W. Lin, et al.; PLoS One 7, e44570 (2012)
- FABP4 attenuates PPARγ and adipogenesis and is inversely correlated with PPARγ in adipose tissues: T. Garin-Shkolnik, et al.; Diabetes 63, 900 (2014)
- FABP4 inhibition suppresses PPARγ activity and VLDL-induced foam cell formation in IL-4-polarized human macrophages: M. Boss, et al.; Atherosclerosis 240, 424 (2015)