BM0015
BMS-309403
≥98% (HPLC)
Synonym(s):
2-[[2′-(5-Ethyl-3,4-diphenyl-1H-pyrazol-1-yl)[1,1′-biphenyl]-3-yl]oxy]acetic acid, BMS 309403
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About This Item
Empirical Formula (Hill Notation):
C31H26N2O3
CAS Number:
Molecular Weight:
474.55
MDL number:
UNSPSC Code:
12352200
PubChem Substance ID:
NACRES:
NA.77
Assay
≥98% (HPLC)
form
powder
color
white to beige
solubility
DMSO: 10 mg/mL, clear
storage temp.
room temp
SMILES string
O=C(O)COC1=CC(C2=CC=CC=C2N3C(CC)=C(C4=CC=CC=C4)C(C5=CC=CC=C5)=N3)=CC=C1
Biochem/physiol Actions
BMS-309403 is a potent and selective inhibitor of fatty acid binding protein 4 (FABP4), also known as adipocyte FABP (A-FABP, aP2). 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. BMS309403 interacts with the fatty-acid-binding pocket within the interior of FABP4 and has been shown to competitively inhibit fatty acid binding with a Ki value < 2 nM. BMS309403 is orally active and has been shown to reduce atherosclerosis in mice studies.
BMS-309403 is a potent and selective inhibitor of fatty acid binding protein 4 (FABP4).
Features and Benefits
BMS-309403 is available through a partnership with Bristol-Myers Squibb (BMS). To learn more and view other BMS compounds, visit sigma.com/BMS.
Legal Information
Sold for research purposes only under agreement from BMS.
Storage Class Code
13 - Non Combustible Solids
WGK
WGK 3
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
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Mohammed Haider et al.
Biomedicines, 9(11) (2021-11-28)
Atherosclerosis is a chronic degenerative disorder characterized by lipid-dense plaques and low-grade inflammation affecting arterial walls. Foamy macrophages are important in the formation of atherosclerotic plaques and the induction of low-grade inflammation. The presence of lipid-laden macrophages has occurred in
Yuxian Guo et al.
Nature communications, 12(1), 7094-7094 (2021-12-09)
Oxidative stress contributes to the pathogenesis of acute lung injury. Protein S-glutathionylation plays an important role in cellular antioxidant defense. Here we report that the expression of deglutathionylation enzyme Grx1 is decreased in the lungs of acute lung injury mice.
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