HTS01037 is a selective, high-affinity fatty acid-binding protein FABP4 (AFABP; aP2) antagonist (aP2 Ki = 0.67 μM; EFABP/HF/IFABP/LFABP Ki = 3.40/9.07/6.57/8.17 μM) that targets aP2 long-chain fatty acid-binding site. HTS01037 is shown to downregulate basal and fatty acid-stimulated LTC4 levels in primary murine peritoneal macrophages (0.2-20 μM), upregulate murine macrophage RAW 264.7 intracellular free fatty acids and uncoupling protein 2 (UCP2) mRNA levels (30 μM), as well as suppress PPARγ target genes expression in IL-4 polarized human primary macrophages (10-25 μM).
Selective, high-affinity fatty acid-binding protein FABP4 (AFABP; aP2) antagonist that blocks aP2-mediated responses in human and murine macrophages.
Storage Class
11 - Combustible Solids
wgk_germany
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
Choose from one of the most recent versions:
Certificates of Analysis (COA)
Lot/Batch Number
It looks like we've run into a problem, but you can still download Certificates of Analysis from our Documents section.
Molecular and cellular biology, 37(2) (2016-11-01)
Obesity-linked metabolic disease is mechanistically associated with the accumulation of proinflammatory macrophages in adipose tissue, leading to increased reactive oxygen species (ROS) production and chronic low-grade inflammation. Previous work has demonstrated that deletion of the adipocyte fatty acid-binding protein (FABP4/aP2)
Biochimica et biophysica acta, 1831(7), 1199-1207 (2013-04-16)
Obesity results in increased macrophage recruitment to adipose tissue that promotes a chronic low-grade inflammatory state linked to increased fatty acid efflux from adipocytes. Activated macrophages produce a variety of pro-inflammatory lipids such as leukotriene C4 (LTC4) and 5-, 12-
Pflugers Archiv : European journal of physiology, 469(9), 1177-1188 (2017-04-14)
Fatty acid-binding protein (FABP) 4 is an adipocytokine mainly expressed in adipocyte and macrophage. Blood FABP4 is related not only to metabolic disorders including insulin resistance and atherosclerosis but also increased blood pressure. We tested the hypothesis that FABP4 plays
Journal of lipid research, 55(5), 808-815 (2014-03-13)
Adipose TG lipase (ATGL) catalyzes the rate-limiting step in TG hydrolysis in most tissues. We have shown that hepatic ATGL preferentially channels hydrolyzed FAs to β-oxidation and induces PPAR-α signaling. Previous studies have suggested that liver FA binding protein (L-FABP)
Molecular and cellular biology, 35(6), 1055-1065 (2015-01-15)
Chronic inflammation in obese adipose tissue is linked to endoplasmic reticulum (ER) stress and systemic insulin resistance. Targeted deletion of the murine fatty acid binding protein (FABP4/aP2) uncouples obesity from inflammation although the mechanism underlying this finding has remained enigmatic.
Our team of scientists has experience in all areas of research including Life Science, Material Science, Chemical Synthesis, Chromatography, Analytical and many others.
