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2-(Tetradecylthio)acetic acid Sale

(Synonyms: 十四烷基硫代乙酸) 目录号 : GC65414

2-Tetradecylthio acetic acid 是一种泛过氧化物酶体增殖物激活受体 (pan-PPAR) 激活剂。2-Tetradecylthio acetic acid 诱导低血脂。2-Tetradecylthio acetic acid 可降低啮齿动物的血浆脂质并增强肝脏脂肪酸氧化。2-Tetradecylthio acetic acid 增加参与脂肪酸摄取、活化、积累和氧化的基因的表达。

2-(Tetradecylthio)acetic acid Chemical Structure

Cas No.:2921-20-2

规格 价格 库存 购买数量
5mg
¥450.00
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10mg
¥720.00
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25mg
¥1,260.00
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50mg
¥1,980.00
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100mg
¥3,060.00
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产品描述

2-Tetradecylthio acetic acid is a pan-peroxisome proliferator activated receptor (pan-PPAR) activator. 2-Tetradecylthio acetic acid induces hypolipidemia. 2-Tetradecylthio acetic acid reduces plasma lipids and enhances hepatic fatty acid oxidation in rodents. 2-Tetradecylthio acetic acid increases the expression of genes involved in fatty acid uptake, activation, accumulation, and oxidation[1][2].

[1]. Vaagenes H, et al. Methylated eicosapentaenoic acid and tetradecylthioacetic acid: effects on fatty acid metabolism. Biochem Pharmacol. 1999 Oct 1;58(7):1133-43.

Chemical Properties

Cas No. 2921-20-2 SDF Download SDF
别名 十四烷基硫代乙酸
分子式 C16H32O2S 分子量 288.49
溶解度 储存条件 4°C, stored under nitrogen
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1 mg 5 mg 10 mg
1 mM 3.4663 mL 17.3316 mL 34.6632 mL
5 mM 0.6933 mL 3.4663 mL 6.9326 mL
10 mM 0.3466 mL 1.7332 mL 3.4663 mL
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Research Update

The molecular structure of thio-ether fatty acids influences PPAR-dependent regulation of lipid metabolism

Bioorg Med Chem 2016 Mar 15;24(6):1191-203.PMID:26874397DOI:10.1016/j.bmc.2016.01.045

Thio-ether fatty acids (THEFAs), including the parent 2-(Tetradecylthio)acetic acid (TTA), are modified fatty acids (FAs) that have profound effects on lipid metabolism given that they are blocked for β-oxidation, and able to act as peroxisome proliferator-activated receptor (PPAR) agonists. Therefore, TTA in particular has been tested clinically for its therapeutic potential against metabolic syndrome related disorders. Here, we describe the preparation of THEFAs based on the TTA scaffold with either a double or a triple bond. These are tested in cultured human skeletal muscle cells (myotubes), either as free acid or following esterification as phospholipids, lysophospholipids or monoacylglycerols. Metabolic effects are assessed in terms of cellular bioavailabilities in myotubes, by FA substrate uptake and oxidation studies, and gene regulation studies with selected PPAR-regulated genes. We note that the inclusion of a triple bond promotes THEFA-mediated FA oxidation. Furthermore, esterification of THEFAs as lysophospholipids also promotes FA oxidation effects. Given that the apparent clinical benefits of TTA administration were offset by dose limitation and poor bioavailability, we discuss the possibility that a selection of our latest THEFAs and THEFA-containing lipids might be able to fulfill the therapeutic potential of the parent TTA while minimizing required doses for efficacy, side-effects and adverse reactions.