Deoxycholic acidCAS# 83-44-3 |
Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
| Cas No. | 83-44-3 | SDF | Download SDF |
| PubChem ID | 222528 | Appearance | White powder |
| Formula | C24H40O4 | M.Wt | 392.57 |
| Type of Compound | Steroids | Storage | Desiccate at -20°C |
| Synonyms | Cholanoic Acid; Desoxycholic acid | ||
| Solubility | DMSO : ≥ 100 mg/mL (254.73 mM) *"≥" means soluble, but saturation unknown. | ||
| Chemical Name | (4R)-4-[(3R,5R,8R,9S,10S,12S,13R,14S,17R)-3,12-dihydroxy-10,13-dimethyl-2,3,4,5,6,7,8,9,11,12,14,15,16,17-tetradecahydro-1H-cyclopenta[a]phenanthren-17-yl]pentanoic acid | ||
| SMILES | CC(CCC(=O)O)C1CCC2C1(C(CC3C2CCC4C3(CCC(C4)O)C)O)C | ||
| Standard InChIKey | KXGVEGMKQFWNSR-LLQZFEROSA-N | ||
| Standard InChI | InChI=1S/C24H40O4/c1-14(4-9-22(27)28)18-7-8-19-17-6-5-15-12-16(25)10-11-23(15,2)20(17)13-21(26)24(18,19)3/h14-21,25-26H,4-13H2,1-3H3,(H,27,28)/t14-,15-,16-,17+,18-,19+,20+,21+,23+,24-/m1/s1 | ||
| 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. |
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| 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. |
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| 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. | ||
| Description | Deoxycholic acid is a strong promoter of hepatocarcinogenesis with possible complete carcinogenicity in the liver and promotion potential for tumor development in the small intestine. Loss of deoxycholic acid-induced EGFR/Ras/MAPK pathway function potentiates deoxycholic acid-stimulated FAS-induced hepatocyte cell death via a reduction in the expression of c-FLIP isoforms. |
| Targets | EGFR | MAPK | MEK | Caspase | PI3K | Ras | c-FLIP |
Deoxycholic acid Dilution Calculator
Deoxycholic acid Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 2.5473 mL | 12.7366 mL | 25.4732 mL | 50.9463 mL | 63.6829 mL |
| 5 mM | 0.5095 mL | 2.5473 mL | 5.0946 mL | 10.1893 mL | 12.7366 mL |
| 10 mM | 0.2547 mL | 1.2737 mL | 2.5473 mL | 5.0946 mL | 6.3683 mL |
| 50 mM | 0.0509 mL | 0.2547 mL | 0.5095 mL | 1.0189 mL | 1.2737 mL |
| 100 mM | 0.0255 mL | 0.1274 mL | 0.2547 mL | 0.5095 mL | 0.6368 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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Deoxycholic acid is specifically responsible for activating the G protein-coupled bile acid receptor TGR5 that stimulates brown adipose tissue (BAT) thermogenic activity.
In Vitro:Deoxycholic acid (DCA) and chenoDeoxycholic acid (CDCA), as the common ingredients of duodenal reflux, act synergistically in many physiological and pathological processes. The cells are repeatedly exposed to 100 μM CDCA and Deoxycholic acid at pH 5.5 for up to 120 min. To simulate chronic local recurrent disease in vitro, the gastric cancer cell line MGC803 is exposed to acidified medium (pH 5.5) containing 100 μM Deoxycholic acid and CDCA. An untreated log-growth MGC803 cell line is generated to be used as a control in normal pH media. After daily 10 min exposure to the acidified bile acids for 60 weeks, MGC803-resistant cells are able to survive and proliferate after 120 min exposure[2].
References:
[1]. Somm E, et al. β-Klotho deficiency protects against obesity through a crosstalk between liver, microbiota, and brown adipose tissue. JCI Insight. 2017 Apr 20;2(8). pii: 91809.
[2]. Wang X, et al. Acidified bile acids enhance tumor progression and telomerase activity of gastric cancer in micedependent on c-Myc expression. Cancer Med. 2017 Apr;6(4):788-797.
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Positive influence of dietary deoxycholic acid on development of pre-neoplastic lesions initiated by N-methyl-N-nitrosourea in rat liver.[Pubmed:3370752]
Carcinogenesis. 1988 Jun;9(6):1103-5.
The effect of Deoxycholic acid (DCA) treatment subsequent to initiation of F344 male rats with N-methyl-N-nitrosourea (MNU), a wide spectrum carcinogen inducing tumors in many organs, was investigated. Rats were initially given four doses of MNU (50 mg/kg) i.p. within a 2-week period combined with a two-thirds partial hepatectomy performed at day 7 and then placed on basal diet containing DCA at concentrations of 0.313, 0.125, 0.050 and 0.020% for 21 weeks prior to final sacrifice. All organs studied were carefully examined histologically and histochemically for development of neoplastic and pre-neoplastic lesions. DCA enhanced the induction of glutathione S-transferase positive (GST-P+) liver cell foci in a dose-related manner. Furthermore groups of rats given DCA without prior MNU administration also developed dose-dependent numbers of pre-neoplastic liver lesions. In addition, increased numbers of small intestine tumors were apparent in DCA-treated animals although the difference was not significant. Induction of tumors in the thyroids, Zymbal glands, skin and peripheral nerves was not affected. The results indicate that DCA is a strong promoter of hepatocarcinogenesis with possible complete carcinogenicity in the liver and promotion potential for tumor development in the small intestine.
In vitro investigation of self-assembled nanoparticles based on hyaluronic acid-deoxycholic acid conjugates for controlled release doxorubicin: effect of degree of substitution of deoxycholic acid.[Pubmed:25837468]
Int J Mol Sci. 2015 Mar 31;16(4):7195-209.
Self-assembled nanoparticles based on a hyaluronic acid-Deoxycholic acid (HD) chemical conjugate with different degree of substitution (DS) of Deoxycholic acid (DOCA) were prepared. The degree of substitution (DS) was determined by titration method. The nanoparticles were loaded with doxorubicin (DOX) as the model drug. The human cervical cancer (HeLa) cell line was utilized for in vitro studies and cell cytotoxicity of DOX incorporated in the HD nanoparticles was accessed by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. In addition, cellular uptake of fluorescently labeled nanoparticles was also investigated. An increase in the degree of Deoxycholic acid substitution reduced the size of the nanoparticles and also enhanced their drug encapsulation efficiency (EE), which increased with the increase of DS. A higher degree of Deoxycholic acid substitution also lead to a lower release rate and an initial burst release of doxorubicin from the nanoparticles. In summary, the degree of substitution allows the modulation of the particle size, drug encapsulation efficiency, drug release rate, and cell uptake efficiency of the nanoparticles. The herein developed hyaluronic acid-Deoxycholic acid conjugates are a good candidate for drug delivery and could potentiate therapeutic formulations for doxorubicin-mediated cancer therapy.
A phase 1 pharmacokinetic study of ATX-101: serum lipids and adipokines following synthetic deoxycholic acid injections.[Pubmed:25684122]
J Cosmet Dermatol. 2015 Mar;14(1):33-9.
BACKGROUND: ATX-101 (Deoxycholic acid injection, Kythera Biopharmaceuticals, Inc.) is a proprietary formulation of pure synthetic Deoxycholic acid (DCA). It is undergoing clinical investigation as an injectable drug for contouring the submental area by reducing submental fat (SMF). When injected into subcutaneous fat, ATX-101 causes focal adipocytolysis, the targeted destruction of fat cells. OBJECTIVES: This phase 1 study evaluated the safety, pharmacokinetics (PK), and pharmacodynamic effects of ATX-101 (100-mg total dose). METHODS: Following PK evaluation of baseline endogenous DCA, lipids, and adipokines in the initial stage of the study (samples collected at hours 0.25, 0.5, 1, 1.5, 2, 4, 6, 12, 15.5, and 24.5), 10 subjects received subcutaneous injections of ATX-101 into abdominal fat. PK evaluation of DCA, lipids, and adipokines was repeated in the second phase of the study. RESULTS: After ATX-101 injections, plasma concentration of DCA increased transiently, reached a maximum plasma concentration rapidly, and returned to endogenous concentrations within 12 h postdose. ATX-101 injection was not associated with any clinically meaningful changes in systemic concentrations of total cholesterol, total triglycerides, free fatty acids, C-reactive protein, or interleukin-6. Adverse events were mild in severity, transient, and showed a temporal relationship to dosing. CONCLUSIONS: This study demonstrated favorable safety and PK profiles, and no clinically meaningful changes in DCA, lipids, and proinflammatory cytokines following subcutaneous injection of ATX-101. Our results support continued clinical investigation of ATX-101 as an injectable drug to reduce SMF.
