HTS 01037

HTS 01037 Property

Boiling point:

621.2±55.0 °C(Predicted)

Density 

1.493±0.06 g/cm3(Predicted)

storage temp. 

RT

solubility 

Soluble in DMSO (up to 50 mg/ml)

pka

3.39±0.10(Predicted)

form 

solid

color 

Yellow

Stability:

Stable for 1 year from date of purchase as supplied. Solutions in DMSO may be stored at -20°C for up to 2 months.

Hazard and Precautionary Statements (GHS)

HTS 01037 Chemical Properties,Usage,Production

Description

Adipocyte fatty acid binding protein (A-FABP/aP2) is a carrier protein expressed in both adipocytes and macrophages where it functions in intracellular fatty acid solubilization, trafficking, and metabolism. Molecular disruption of A-FABP/aP2 in mice results in improved insulin sensitivity and protection from atherosclerosis. HTS 01037 is a high-affinity ligand of adipocyte fatty acid binding protein (A-FABP/aP2) (K_i = 0.67 μM) that presumably competes with fatty acids for functional binding in the ligand-binding cavity of A-FABP/aP2. At a concentration of 10 μM, HTS 01037 antagonizes the protein-protein interaction of A-FABP/aP2 with hormone sensitive lipase in cultured C8PA lipocytes. HTS 01037 inhibits lipolysis in 3T3L1 adipocytes and reduces lipopolysaccharide-stimulated inflammation in bone marrow-derived macrophages, both effects of which are similar to the phenotype of A-FABP/aP2 knockout mice.

Uses

HTS 01037 is an inhibitor of fatty acid binding protein and a competitive antagonist of protein-protein interactions mediated by AFABP/aP2.

Definition

ChEBI: HTS 01037 is a ring assembly and a member of thiophenes.

References

[1] ANN V. HERTZEL. Identification and Characterization of a Small Molecule Inhibitor of Fatty Acid Binding Proteins[J]. Journal of Medicinal Chemistry, 2009, 52 19: 6024-6031. DOI:10.1021/jm900720m
[2] ERIC K. LONG . Fatty acids induce leukotriene C4 synthesis in macrophages in a fatty acid binding protein-dependent manner[J]. Biochimica et biophysica acta. Molecular and cell biology of lipids, 2013, 1831 7: Pages 1199-1207. DOI:10.1016/j.bbalip.2013.04.004
[3] HONGLIANG XU. Uncoupling lipid metabolism from inflammation through fatty acid binding protein-dependent expression of UCP2.[J]. Molecular and Cellular Biology, 2015, 35 6: 1055-1065. DOI:10.1128/mcb.01122-14
[4] K. STEEN D B Hongliang Xu. FABP4/aP2 Regulates Macrophage Redox Signaling and Inflammasome Activation via Control of UCP2[J]. Molecular and Cellular Biology, 2016, 37 1. DOI:10.1128/mcb.00282-16
[5] MARCEL BOSS. FABP4 inhibition suppresses PPARγ activity and VLDL-induced foam cell formation in IL-4-polarized human macrophages[J]. Atherosclerosis, 2015, 240 2: Pages 424-430. DOI:10.1016/j.atherosclerosis.2015.03.042