SML2374
HTS01037
≥98% (HPLC)
别名:
(E)-4-(5-(Methoxycarbonyl)-2,2′-bithiophen-4-ylamino)-4-oxobut-2-enoic acid, 4-[(3-Carboxy-1-oxo-2-propenyl)amino]-[2,2′-bithiophene]-5-carboxylic acid 5-methyl ester, 4-{[2-(Methoxycarbonyl)-5-(2-thienyl)-3-thienyl]amino}-4-oxo-2-butenoic acid, HTS 01037, HTS-01037
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关于此项目
经验公式（希尔记法）:
C14H11NO5S2
化学文摘社编号:
分子量:
337.37
UNSPSC Code:
12352200
MDL number:
NACRES:
NA.21
SMILES string
[s]1c(cc(c1C(=O)OC)NC(=O)C=CC(=O)O)c2[s]ccc2
InChI
1S/C14H11NO5S2/c1-20-14(19)13-8(15-11(16)4-5-12(17)18)7-10(22-13)9-3-2-6-21-9/h2-7H,1H3,(H,15,16)(H,17,18)
InChI key
GJODSFZNKNHKML-UHFFFAOYSA-N
assay
≥98% (HPLC)
form
powder
color
white to beige
solubility
DMSO: 2 mg/mL, clear
storage temp.
−20°C
Biochem/physiol Actions
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.
存储类别
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
法规信息
新产品
此项目有
Marcel Boss et al.
Atherosclerosis, 240(2), 424-430 (2015-04-22)
Macrophages, converted to lipid-loaded foam cells, accumulate in atherosclerotic lesions. Macrophage lipid metabolism is transcriptionally regulated by peroxisome proliferator-activated receptor gamma (PPARγ), and its target gene fatty acid binding protein 4 (FABP4) accelerates the progression of atherosclerosis in mouse models.
Cayla M Duffy et al.
Molecular and cellular neurosciences, 80, 52-57 (2017-02-20)
Hypothalamic inflammation contributes to metabolic dysregulation and the onset of obesity. Dietary saturated fats activate microglia via a nuclear factor-kappa B (NFκB) mediated pathway to release pro-inflammatory cytokines resulting in dysfunction or death of surrounding neurons. Fatty acid binding proteins
Ann V Hertzel et al.
Journal of medicinal chemistry, 52(19), 6024-6031 (2009-09-17)
Molecular disruption of the lipid carrier AFABP/aP2 in mice results in improved insulin sensitivity and protection from atherosclerosis. Because small molecule inhibitors may be efficacious in defining the mechanism(s) of AFABP/aP2 action, a chemical library was screened and identified 1
The possible factors affecting microglial activation in cases of obesity with cognitive dysfunction.
Titikorn Chunchai et al.
Metabolic brain disease, 33(3), 615-635 (2017-11-23)
Obesity has reached epidemic proportions in many countries around the world. Several studies have reported that obesity can lead to the development of cognitive decline. There is increasing evidence to demonstrate that microglia play a crucial role in cognitive decline
Hongliang Xu et al.
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.
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