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TUG-1375 Sale

目录号 : GC34938

TUG-1375是一种游离脂肪酸受体2(FFA2/GPR43)激动剂,pKi值为6.69。TUG-1375对FFA3,FFA4,PPARα,PPARγ,PPARδ,LXRα或LXRβ无作用。

TUG-1375 Chemical Structure

Cas No.:2247372-59-2

规格 价格 库存 购买数量
10mM (in 1mL DMSO)
¥2,673.00
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5mg
¥2,430.00
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10mg
¥4,050.00
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50mg
¥10,800.00
现货
100mg
¥18,090.00
现货

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Sample solution is provided at 25 µL, 10mM.

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产品描述

TUG-1375 is an agonist of free fatty acid receptor 2 (FFA2/GPR43), with a pKi of 6.69. TUG-1375 is inactive on FFA3, FFA4, PPARα, PPARγ, PPARδ, LXRα or LXRβ[1]. pKi: 6.69 (FFA2)[1]

TUG-1375 exhibits pEC50 of 7.11 in the cAMP FFA2 assay, also active on murine FFA2 orthologue (pEC50, 6.44 ± 0.13 in the cAMP assay)[1].

[1]. Hansen AH, et al. Discovery of a Potent Thiazolidine Free Fatty Acid Receptor 2 Agonist with Favorable Pharmacokinetic Properties. J Med Chem. 2018 Nov 8;61(21):9534-9550.

Chemical Properties

Cas No. 2247372-59-2 SDF
Canonical SMILES O=C(N1[C@@H](C2=CC=CC=C2Cl)SC[C@H]1C(O)=O)C3=CC=C(C4=C(C)ON=C4C)C=C3
分子式 C22H19ClN2O4S 分子量 442.92
溶解度 DMSO : 125 mg/mL (282.22 mM) 储存条件 Store at -20°C
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1 mM 2.2577 mL 11.2887 mL 22.5774 mL
5 mM 0.4515 mL 2.2577 mL 4.5155 mL
10 mM 0.2258 mL 1.1289 mL 2.2577 mL
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Research Update

Discovery of a Potent Thiazolidine Free Fatty Acid Receptor 2 Agonist with Favorable Pharmacokinetic Properties

Free fatty acid receptor 2 (FFA2/GPR43) is a receptor for short-chain fatty acids reported to be involved in regulation of metabolism, appetite, fat accumulation, and inflammatory responses and is a potential target for treatment of various inflammatory and metabolic diseases. By bioisosteric replacement of the central pyrrolidine core of a previously disclosed FFA2 agonist with a synthetically more tractable thiazolidine, we were able to rapidly synthesize and screen analogues modified at both the 2- and 3-positions on the thiazolidine core. Herein, we report SAR exploration of thiazolidine FFA2 agonists and the identification of 31 (TUG-1375), a compound with significantly increased potency (7-fold in a cAMP assay) and reduced lipophilicity (50-fold reduced clog P) relative to the pyrrolidine lead structure. The compound has high solubility, high chemical, microsomal, and hepatocyte stability, and favorable pharmacokinetic properties and was confirmed to induce human neutrophil mobilization and to inhibit lipolysis in murine adipocytes.

FFA2-, but not FFA3-agonists inhibit GSIS of human pseudoislets: a comparative study with mouse islets and rat INS-1E cells

The expression of short chain fatty acid receptors FFA2 and FFA3 in pancreatic islets raised interest in using them as drug targets for treating hyperglycemia in humans. This study aims to examine the efficacy of synthetic FFA2- and FFA3-ligands to modulate glucose-stimulated insulin secretion (GSIS) in human pseudoislets which display intact glucose responsiveness. The FFA2-agonists 4-CMTB and TUG-1375 inhibited GSIS, an effect reversed by the FFA2-antagonist CATPB. GSIS itself was not augmented by CATPB. The FFA3-agonists FHQC and 1-MCPC did not affect GSIS in human pseudoislets. For further drug evaluation we used mouse islets. The CATPB-sensitive inhibitory effect of 100 ?M 4-CMTB on GSIS was recapitulated. The inhibition was partially sensitive to the Gi/o-protein inhibitor pertussis toxin. A previously described FFA2-dependent increase of GSIS was observed with lower concentrations of 4-CMTB (10 and 30 ?M). The stimulatory effect of 4-CMTB on secretion was prevented by the Gq-protein inhibitor FR900359. As in human pseudoislets, in mouse islets relative mRNA levels were FFAR2 > FFAR3 and FFA3-agonists did not affect GSIS. The FFA3-agonists, however, inhibited GSIS in a pertussis toxin-sensitive manner in INS-1E cells and this correlated with relative mRNA levels of Ffar3 > > Ffar2. Thus, in humans, when FFA2-activation impedes GSIS, FFA2-antagonism may reduce glycemia.