Triacsin C

Inhibitor of acyl-CoA synthetase CAS# 76896-80-5

Triacsin C

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Chemical structure

Triacsin C

3D structure

Chemical Properties of Triacsin C

Cas No. 76896-80-5 SDF Download SDF
PubChem ID 9576787 Appearance Powder
Formula C11H17N3O M.Wt 207.27
Type of Compound N/A Storage Desiccate at -20°C
Solubility Soluble to 25 mM in DMSO
Chemical Name N-[(E)-[(2E,4E,7E)-undeca-2,4,7-trienylidene]amino]nitrous amide
SMILES CCCC=CCC=CC=CC=NNN=O
Standard InChIKey NKTGCVUIESDXPU-YLEPRARLSA-N
Standard InChI InChI=1S/C11H17N3O/c1-2-3-4-5-6-7-8-9-10-11-12-13-14-15/h4-5,7-11H,2-3,6H2,1H3,(H,13,15)/b5-4+,8-7+,10-9+,12-11+
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Biological Activity of Triacsin C

DescriptionInhibitor of acyl-CoA synthetase. Inhibits lipid synthesis and cell proliferation in Raji lymphoma cells. Induces apoptosis in cancer cell lines and inhibits human lung cancer cell xenograft tumor growth in mice.

Triacsin C Dilution Calculator

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Triacsin C Molarity Calculator

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Preparing Stock Solutions of Triacsin C

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 4.8246 mL 24.1231 mL 48.2462 mL 96.4925 mL 120.6156 mL
5 mM 0.9649 mL 4.8246 mL 9.6492 mL 19.2985 mL 24.1231 mL
10 mM 0.4825 mL 2.4123 mL 4.8246 mL 9.6492 mL 12.0616 mL
50 mM 0.0965 mL 0.4825 mL 0.9649 mL 1.9298 mL 2.4123 mL
100 mM 0.0482 mL 0.2412 mL 0.4825 mL 0.9649 mL 1.2062 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

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References on Triacsin C

Novel triacsin C analogs as potential antivirals against rotavirus infections.[Pubmed:22365411]

Eur J Med Chem. 2012 Apr;50:311-8.

Recently our group has demonstrated that cellular triglyceride (TG) levels play an important role in rotavirus replication. In this study, we further examined the roles of the key enzymes for TG synthesis (lipogenesis) in the replication of rotaviruses by using inhibitors of fatty acid synthase, long chain fatty acid acyl-CoA synthetase (ACSL), and diacylglycerol acyltransferase and acyl-CoA:cholesterol acyltransferase in association with lipid droplets of which TG is a major component. Triacsin C, a natural ACSL inhibitor from Streptomyces aureofaciens, was found to be highly effective against rotavirus replication. Thus, novel Triacsin C analogs were synthesized and evaluated for their efficacies against the replication of rotaviruses in cells. Many of the analogs significantly reduced rotavirus replication, and one analog (1e) was highly effective at a nanomolar concentration range (ED(50) 0.1muM) with a high therapeutic index in cell culture. Our results suggest a crucial role of lipid metabolism in rotavirus replication, and Triacsin C and/or its analogs as potential therapeutic options for rotavirus infections.

Anti-atherosclerotic activity of triacsin C, an acyl-CoA synthetase inhibitor.[Pubmed:18653998]

J Antibiot (Tokyo). 2008 May;61(5):318-21.

As previously reported, Triacsin C, a selective inhibitor of acyl-CoA synthetase, inhibited the synthesis of cholesteryl ester and triacylglycerol in mouse peritoneal macrophages, leading to a reduction of lipid droplets. Therefore, the in vivo efficacy was studied. Low-density lipoprotein receptor-knockout (LDLR-/-) mice were fed a high cholesterol diet (0.15%) for two months to measure the atherogenic areas of the hearts and aortas. When Triacsin C was orally administered (10 mg/kg/day), the atherosclerotic areas were significantly reduced by 86% in aorta and 36% in hearts. The results strongly suggested that Triacsin C shows anti-atherogenic activity by inhibiting acyl-CoA synthetase activity.

Characterization of triacsin C inhibition of short-, medium-, and long-chain fatty acid: CoA ligases of human liver.[Pubmed:15122652]

J Biochem Mol Toxicol. 2004;18(2):100-6.

Short-, medium-, and long-chain fatty acid:CoA ligases from human liver were tested for their sensitivity to inhibition by Triacsin C. The short-chain fatty acid:CoA ligase was inhibited less than 10% by concentrations of Triacsin C as high as 80 microM. The two mitochondrial xenobiotic/medium-chain fatty acid:CoA ligases (XM-ligases), HXM-A and HXM-B, were partially inhibited by Triacsin C, and the inhibitions were characterized by low affinity for Triacsin C (K(I) values > 100 microM). These inhibitions were found to be the result of Triacsin C competing with medium-chain fatty acid for binding at the active site. The microsomal and mitochondrial forms of long-chain fatty acid:CoA ligase (also termed long-chain fatty acyl-CoA synthetase, or long-chain acyl-CoA synthetase LACS) were potently inhibited by Triacsin C, and the inhibition had identical characteristics for both LACS forms. Dixon plots of this inhibition were biphasic. There is a high-affinity site with a K(I) of 0.1 microM that accounts for a maximum of 70% of the inhibition. There is also a low affinity site with a K(I) of 6 microM that accounts for a maximum of 30% inhibition. Kinetic analysis revealed that the high-affinity inhibition of the mitochondrial and microsomal LACS forms is the result of Triacsin C binding at the palmitate substrate site. The high-affinity Triacsin C inhibition of both the mitochondrial and microsomal LACS forms was found to require a high concentration of free Mg(2+), with the EC(50) for inhibition being 3 mM free Mg(2+). The low affinity Triacsin C inhibition was also enhanced by Mg(2+). The data suggests that Mg(2+) promotes Triacsin C inhibition of LACS by enhancing binding at the palmitate binding site. In contrast, the partial inhibition of the XM-ligases by Triacsin C, which showed only a low-affinity component, did not require Mg(2+).

Human intestinal acyl-CoA synthetase 5 is sensitive to the inhibitor triacsin C.[Pubmed:22171129]

World J Gastroenterol. 2011 Nov 28;17(44):4883-9.

AIM: To investigate whether human acyl-CoA synthetase 5 (ACSL5) is sensitive to the ACSL inhibitor Triacsin C. METHODS: The ACSL isoforms ACSL1 and ACSL5 from rat as well as human ACSL5 were cloned and recombinantly expressed as 6xHis-tagged enzymes. Ni(2+)-affinity purified recombinant enzymes were assayed at pH 7.5 or pH 9.5 in the presence or absence of Triacsin C. In addition, ACSL5 transfected CaCo2 cells and intestinal human mucosa were monitored. ACSL5 expression in cellular systems was verified using Western blot and immunofluorescence. The ACSL assay mix included TrisHCl (pH 7.4), ATP, CoA, EDTA, DTT, MgCl(2), [9,10-(3)H] palmitic acid, and triton X-100. The 200 muL reaction was initiated with the addition of solubilized, purified recombinant proteins or cellular lysates. Reactions were terminated after 10, 30 or 60 min of incubation with Doles medium. RESULTS: Expression of soluble recombinant ACSL proteins was found after incubation with isopropyl beta-D-1-thiogalactopyranoside and after ultracentrifugation these were further purified to near homogeneity with Ni(2+)-affinity chromatography. Triacsin C selectively and strongly inhibited recombinant human ACSL5 protein at pH 7.5 and pH 9.5, as well as recombinant rat ACSL1 (sensitive control), but not recombinant rat ACSL5 (insensitive control). The IC50 for human ACSL5 was about 10 mumol/L. The inhibitory Triacsin C effect was similar for different incubation times (10, 30 and 60 min) and was not modified by the N- or C-terminal location of the 6xHis-tag. In order to evaluate ACSL5 sensitivity to Triacsin C in a cellular environment, stable human ACSL5 CaCo2 transfectants and mechanically dissected normal human intestinal mucosa with high physiological expression of ACSL5 were analyzed. In both models, ACSL5 peak activity was found at pH 7.5 and pH 9.5, corresponding to the properties of recombinant human ACSL5 protein. In the presence of Triacsin C (25 mumol/L), total ACSL activity was dramatically diminished in human ACSL5 transfectants as well as in ACSL5-rich human intestinal mucosa. CONCLUSION: The data strongly indicate that human ACSL5 is sensitive to Triacsin C and does not compensate for other Triacsin C-sensitive ACSL isoforms.

p53-defective tumors with a functional apoptosome-mediated pathway: a new therapeutic target.[Pubmed:15900046]

J Natl Cancer Inst. 2005 May 18;97(10):765-77.

BACKGROUND: Although cancer cells appear to maintain the machinery for intrinsic apoptosis, defects in the pathway develop during malignant transformation, preventing apoptosis from occurring. How to specifically induce apoptosis in cancer cells remains unclear. METHODS: We determined the apoptosome activity and p53 status of normal human cells and of lung, colon, stomach, brain, and breast cancer cells by measuring cytochrome c-dependent caspase activation and by DNA sequencing, respectively, and we used COMPARE analysis to identify apoptosome-specific agonists. We compared cell death, cytochrome c release, and caspase activation in NCI-H23 (lung cancer), HCT-15 (colon cancer), and SF268 (brain cancer) cells treated with Triacsin C, an inhibitor of acyl-CoA synthetase (ACS), or with vehicle. The cells were mock, transiently, or stably transfected with genes for Triacsin C-resistant ACSL5, dominant negative caspase-9, or apoptotic protease activating factor-1 knockdown. We measured ACS activity and levels of cardiolipin, a mitochondrial phospholipid, in mock and ACSL5-transduced SF268 cells. Nude mice carrying NCI-H23 xenograft tumors (n = 10) were treated with Triacsin C or vehicle, and xenograft tumor growth was assessed. Groups were compared using two-sided Student t tests. RESULTS: Of 21 p53-defective tumor cell lines analyzed, 17 had higher apoptosome activity than did normal cells. Triacsin C selectively induced apoptosome-mediated death in tumor cells (caspase activity of Triacsin C-treated versus untreated SF268 cells; means = 1020% and 100%, respectively; difference = 920%, 95% CI = 900% to 940%; P<.001). Expression of ACSL5 suppressed Triacsin C-induced cytochrome c release and subsequent cell death (cell survival of Triacsin C-treated mock- versus ACSL5-transduced SF268 cells; means = 40% and 83%, respectively; difference = 43%, 95% CI = 39% to 47%; P<.001). ACS was also essential to the maintenance of cardiolipin levels. Finally, Triacsin C suppressed growth of xenograft tumors (relative tumor volume on day 21 of Triacsin C-treated versus untreated mice; means = 4.6 and 9.6, respectively; difference = 5.0, 95% CI = 2.1 to 7.9; P = .006). CONCLUSIONS: Many p53-defective tumors retain activity of the apoptosome, which is therefore a potential target for cancer chemotherapy. Inhibition of ACS may be a novel strategy to induce the death of p53-defective tumor cells.

Evidence for an essential role of long chain acyl-CoA synthetase in animal cell proliferation. Inhibition of long chain acyl-CoA synthetase by triacsins caused inhibition of Raji cell proliferation.[Pubmed:1999415]

J Biol Chem. 1991 Mar 5;266(7):4214-9.

Triacsins A, B, C, and D are new inhibitors of long chain acyl-CoA synthetase (EC 6.2.1.3) and possess different inhibitory potencies against the enzyme (Tomoda, H., Igarashi, K., and Omura, S. (1987) Biochim. Biophys. Acta 921, 595-598). Acyl-CoA synthetase activity in the membrane fraction of Raji cells was also inhibited by triacsins. The same hierarchy of inhibitory potency as that against the enzyme from other sources, Triacsin C greater than triacsin A much greater than triacsin D greater than or equal to triacsin B, was observed. When Raji cells were cultivated in the presence of triacsins, cell proliferation was inhibited in a dose-dependent fashion. The drug concentrations required for 50% inhibition of cell growth at day 2 were calculated to be 1.8 microM for triacsin A, much greater than 20 microM for triacsin B, 1.0 microM for Triacsin C, and much greater than 15 microM for triacsin D, demonstrating a hierarchy for inhibitory potency of triacsins similar to that against the acyl-CoA synthetase activity. To understand the role of long chain acyl-CoA synthetase in animal cells, the effect of triacsins on the lipid metabolism of Raji cells was studied. When intact Raji cells were incubated with [14C]oleate in the presence of individual triacsins, the incorporation of [14C]oleate into each of the lipid fractions such as phosphatidylcholine, phosphatidylethanolamine, and triacylglycerol was inhibited to an analogous extent. A common hierarchy, Triacsin C greater than triacsin A much greater than triacsin D greater than triacsin B, was shown for the inhibition in each synthesis of the three lipids, which was identical with that for acyl-CoA synthetase. These findings indicate that the inhibition of acyl-CoA synthetase is well correlated with the inhibition of lipid synthesis. Taken together, the data strongly suggest that the inhibition of acyl-CoA synthetase by triacsins leads to the inhibition of lipid synthesis and eventually to the inhibition of proliferation of Raji cells.

Description

Triacsin C (WS 1228A), a natural intracellular long-chain acyl-CoA synthetases (ACSL) inhibitor, is from Streptomyces aureofaciens. Triacsin C inhibits TAG accumulation into lipid droplets (LD) by suppressing ACSL activity. Triacsin C is found to be highly effective against rotavirus replication.

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