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Merck
CN

SML2374

Sigma-Aldrich

HTS01037

≥98% (HPLC)

Synonym(s):

(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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About This Item

Empirical Formula (Hill Notation):
C14H11NO5S2
CAS Number:
682741-29-3
Molecular Weight:
337.37
MDL number:
MFCD02681826
UNSPSC Code:
12352200

Key Documents

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Assay

≥98% (HPLC)

form

powder

color

white to beige

solubility

DMSO: 2 mg/mL, clear

storage temp.

−20°C

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

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.

Storage Class Code

11 - Combustible Solids

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Regulatory Information

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Certificates of Analysis (COA)

Lot/Batch Number
0000061328
0000061329
0000048997

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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
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
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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