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10,12-Tricosadiynoic acid Sale

(Synonyms: 10,12-二十三联炔酸) 目录号 : GC38881

10,12-Tricosadiynoic acid 是一种高特异性,选择性,高亲和力且具有口服活性的酰基辅酶 A 氧化酶-1 (ACOX1) 抑制剂。10,12-Tricosadiynoic acid 可通过改善线粒体脂质和 ROS 代谢来治疗高脂饮食或肥胖引起的代谢性疾病。

10,12-Tricosadiynoic acid Chemical Structure

Cas No.:66990-30-5

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10mM (in 1mL DMSO)
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10mg
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25mg
¥720.00
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50mg
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100mg
¥1,260.00
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产品描述

10,12-Tricosadiynoic acid is a highly specific, selective, high affinity and orally active acyl-CoA oxidase-1 (ACOX1) inhibitor. 10,12-Tricosadiynoic acid can treat high fat diet- or obesity-induced metabolic diseases by improving mitochondrial lipid and ROS metabolism[1].

10,12-Tricosadiynoic acid-CoA rapidly inhibits ACOX1 activity in a time- and concentration-dependent manner. The activity of ACOX1 decreases by nearly 95% after 5 min of incubation with 10 eq of 10,12-Tricosadiynoic acid-CoA. ACOX1 activity is inhibited only if free 10,12-Tricosadiynoic Acid is activated as the CoA thioester, the substrate form. Inhibition of ACOX1 by 10,12-Tricosadiynoic acid-CoA is irreversible. And the kinetics parameters KI and kinact are calculated to be 680 nm and 3.18 min-1, respectively[1]. 10,12-Tricosadiynoic acid is the precursor of 10,12-Tricosadiynoic acid-CoA and is transformed into 10,12-Tricosadiynoic acid-CoA by peroxisomal very long chain acyl-CoA synthetase (VLACS) after entering into cells, and it inhibits ACOX1 in vivo[1].

10,12-Tricosadiynoic acid (100 μg/kg; oral gavage; daily; for 8 weeks; male Wistar rats) treatment increases hepatic mitochondrial fatty acid oxidation (FAO) via activation of the SIRT1-AMPK (adenosine 5′-monophosphate-activated protein kinase) pathway and proliferator activator receptor α and reduces hydrogen peroxide accumulation in high fat diet-fed rats, which significantly decreases hepatic lipid and ROS contents, reduces body weight gain, and decreases serum triglyceride and insulin levels[1]. Animal Model: Male Wistar rats (210-230 g) fed with high fat diet[1]

[1]. Zeng J, et al. Specific Inhibition of Acyl-CoA Oxidase-1 by an Acetylenic Acid Improves Hepatic Lipid and Reactive Oxygen Species (ROS) Metabolism in Rats Fed a High Fat Diet. J Biol Chem. 2017 Mar 3;292(9):3800-3809.

Chemical Properties

Cas No. 66990-30-5 SDF
别名 10,12-二十三联炔酸
Canonical SMILES CCCCCCCCCCC#CC#CCCCCCCCCC(O)=O
分子式 C23H38O2 分子量 346.55
溶解度 DMSO : 100 mg/mL (288.56 mM) 储存条件 Store at 4°C
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1 mM 2.8856 mL 14.4279 mL 28.8559 mL
5 mM 0.5771 mL 2.8856 mL 5.7712 mL
10 mM 0.2886 mL 1.4428 mL 2.8856 mL
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Research Update

Dual colorimetric response of polydiacetylene/zinc oxide nanocomposites to low and high pH

J Colloid Interface Sci 2014 Mar 15;418:43-51.PMID:24461816DOI:10.1016/j.jcis.2013.11.083.

This contribution presents our continuation work on the color-transition behaviors of polydiacetylene(PDA)/ZnO nanocomposites prepared by using three types of monomers, 5,7-hexadecadiynoic acid (HDDA), 10,12-Tricosadiynoic acid (TCDA) and 10,12-pentacosadiynoic acid (PCDA). The color-transition behaviors of these nanocomposites upon exposure to acid and base are investigated by utilizing UV/vis absorption spectroscopy. We have found that these PDA/ZnO nanocomposites exhibit colorimetric response at both low and high pH regions. The addition of acid causes the poly(HDDA)/ZnO, poly(TCDA)/ZnO and poly(PCDA)/ZnO nanocomposites to change color from blue to red at pH~5, 3.5 and 2, respectively. The color of pure PDA vesicles, on the other hand, is hardly affected at this pH range. At high pH region, the pure poly(TCDA) vesicles change color at pH~8 while it requires much higher pH to induce color transition of the PDA/ZnO nanocomposites. The mechanism responsible for color transition of the PDA/ZnO nanocomposites is explored by various techniques including infrared spectroscopy, zeta potential analyzer and light scattering. Our result provides a new approach for controlling the colorimetric response to pH of PDA-based materials.

Impaired peroxisomal fat oxidation induces hepatic lipid accumulation and oxidative damage in Nile tilapia

Fish Physiol Biochem 2020 Aug;46(4):1229-1242.PMID:32144523DOI:10.1007/s10695-020-00785-w.

Many metabolic diseases in fish are often associated with lowered peroxisomal fatty acid (FA) β-oxidation. However, the physiological role of peroxisomal FA oxidation in lipid metabolism in fish still remains unclear. In the present study, a specific peroxisomal FA β-oxidation inhibitor, 10,12-Tricosadiynoic acid (TDYA), was used to investigate the effects of impaired peroxisomal β-oxidation on growth performance, health status, and lipid metabolism in Nile tilapia. The results showed that the dietary TDYA treatment did not affect weight gain, but significantly decreased peroxisomal β-oxidation in the liver, and increased body fat accumulation. The fish with impaired peroxisomal β-oxidation exhibited higher contents of serum lipid and peroxidation products, and alanine aminotransferase activity, and significantly lowered hepatic activities of superoxide dismutase and catalase. The inhibited peroxisomal β-oxidation did not enhance mitochondrial β-oxidation activity, but compensatorily upregulated FA β-oxidation-related gene expression, and downregulated the gene expressions in lipolysis and lipogenesis. Taken together, TDYA treatment markedly induced lipid accumulation and hepatic oxidative damage via systemically depressing lipid catabolism and antioxidant capacity. Our findings reveal the pivotal roles of peroxisomal β-oxidation in maintaining health and lipid homeostasis in fish, and could be helpful in understanding metabolic diseases in fish.

Peroxisomal β-oxidation stimulates cholesterol biosynthesis in the liver in diabetic mice

J Biol Chem 2022 Feb;298(2):101572.PMID:35007532DOI:10.1016/j.jbc.2022.101572.

Although diabetes normally causes an elevation of cholesterol biosynthesis and induces hypercholesterolemia in animals and human, the mechanism linking diabetes to the dysregulation of cholesterol biosynthesis in the liver is not fully understood. As liver peroxisomal β-oxidation is induced in the diabetic state and peroxisomal oxidation of fatty acids generates free acetate, we hypothesized that peroxisomal β-oxidation might play a role in liver cholesterol biosynthesis in diabetes. Here, we used erucic acid, a specific substrate for peroxisomal β-oxidation, and 10,12-Tricosadiynoic acid, a specific inhibitor for peroxisomal β-oxidation, to specifically induce and suppress peroxisomal β-oxidation. Our results suggested that induction of peroxisomal β-oxidation increased liver cholesterol biosynthesis in streptozotocin-induced diabetic mice. We found that excessive oxidation of fatty acids by peroxisomes generated considerable free acetate in the liver, which was used as a precursor for cholesterol biosynthesis. In addition, we show that specific inhibition of peroxisomal β-oxidation decreased cholesterol biosynthesis by reducing acetate formation in the liver in diabetic mice, demonstrating a crosstalk between peroxisomal β-oxidation and cholesterol biosynthesis. Based on these results, we propose that induction of peroxisomal β-oxidation serves as a mechanism for a fatty acid-induced upregulation in cholesterol biosynthesis and also plays a role in diabetes-induced hypercholesterolemia.

Chromatic immunoassay based on polydiacetylene vesicles

Colloids Surf B Biointerfaces 2004 Oct 10;38(1-2):29-33.PMID:15465301DOI:10.1016/j.colsurfb.2004.08.010.

A new approach of chromatic immunoassay based on polydiacetylene vesicles is described. Antibodies were covalently coupled with mixed vesicles of 10,12-Tricosadiynoic acid (TCDA) and dimyristoylphosphatidycholine (DMPC). The vesicle-antibody conjugates were irradiated with UV light to yield a blue-colored polydiacetylene. After antigen injection, specific immunoreactions took place at the vesicle surface alter polydiacetylene conformation and lead to a color change from blue to red. The chromatic immunoassay described here is simple, rapid, sensitive; the color change was readily discernible by naked eye when the concentration of antigen is 1 ng/mL. Incorporation of DMPC in the mixed vesicles increases the sensitivity of the chromatic immunoassay.

The deconvolution analysis of ATR-FTIR spectra of diacetylene during UV exposure

Spectrochim Acta A Mol Biomol Spectrosc 2019 Aug 5;219:23-32.PMID:31030044DOI:10.1016/j.saa.2019.04.030.

We performed a detailed deconvolution analysis of ATR-FTIR peaks of a common diacetylene, 10,12-Tricosadiynoic acid (TRCDA) during the polymerization and the blue-to-red transition. Based on the analysis and the solvent dependence on the IR signals, we found that the triple peak from CC stretching mode that has been previously suspected as a consequence of Fermi resonance is rather associated with the macromolecular assembly of TRCDA. Besides these CC triple peaks, we found that the background in the region increased during the UV exposure due to the CC signals from polymers. In addition, the anisotropic compression during polymerization was also detected, which supports the proposed interpretation of X-ray data reported previously. These results are the benefits from the deconvolution analysis.