Taurocholic acidCAS# 81-24-3 |
Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
| Cas No. | 81-24-3 | SDF | Download SDF |
| PubChem ID | 6675 | Appearance | Powder |
| Formula | C26H45NO7S | M.Wt | 515.70 |
| Type of Compound | Steroids | Storage | Desiccate at -20°C |
| Solubility | Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc. | ||
| Chemical Name | 2-[[(4R)-4-[(3R,5S,7R,8R,9S,10S,12S,13R,14S,17R)-3,7,12-trihydroxy-10,13-dimethyl-2,3,4,5,6,7,8,9,11,12,14,15,16,17-tetradecahydro-1H-cyclopenta[a]phenanthren-17-yl]pentanoyl]amino]ethanesulfonic acid | ||
| SMILES | CC(CCC(=O)NCCS(=O)(=O)O)C1CCC2C1(C(CC3C2C(CC4C3(CCC(C4)O)C)O)O)C | ||
| Standard InChIKey | WBWWGRHZICKQGZ-HZAMXZRMSA-N | ||
| Standard InChI | InChI=1S/C26H45NO7S/c1-15(4-7-23(31)27-10-11-35(32,33)34)18-5-6-19-24-20(14-22(30)26(18,19)3)25(2)9-8-17(28)12-16(25)13-21(24)29/h15-22,24,28-30H,4-14H2,1-3H3,(H,27,31)(H,32,33,34)/t15-,16+,17-,18-,19+,20+,21-,22+,24+,25+,26-/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 | 1. Rectal administration of taurocholic acid can stimulate glucagon-like peptide-1 and peptide YY by TGR5 receptor activation, which may have potential for the management of type 2 diabetes and obesity. 2. Taurocholic acid feeding prevents tumor necrosis factor-alpha-induced damage of cholangiocytes by a PI3K-mediated pathway. 3. Taurocholic acid feeding shows cytoprotective effects on the biliary tree after adrenergic denervation of the liver. 4. High concentraction of taurocholic acid can induce apoptosis in HTR-8/SVneo cells via overexpression of ERp29 and activation of p38. |
| Targets | TNF-α | PI3K | Akt | p38MAPK | Caspase |
Taurocholic acid Dilution Calculator
Taurocholic acid Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 1.9391 mL | 9.6956 mL | 19.3911 mL | 38.7822 mL | 48.4778 mL |
| 5 mM | 0.3878 mL | 1.9391 mL | 3.8782 mL | 7.7564 mL | 9.6956 mL |
| 10 mM | 0.1939 mL | 0.9696 mL | 1.9391 mL | 3.8782 mL | 4.8478 mL |
| 50 mM | 0.0388 mL | 0.1939 mL | 0.3878 mL | 0.7756 mL | 0.9696 mL |
| 100 mM | 0.0194 mL | 0.097 mL | 0.1939 mL | 0.3878 mL | 0.4848 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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Taurocholic acid feeding prevents tumor necrosis factor-alpha-induced damage of cholangiocytes by a PI3K-mediated pathway.[Pubmed:17609511]
Exp Biol Med (Maywood). 2007 Jul;232(7):942-9.
Cholangiopathies, such as primary biliary cirrhosis and primary sclerosis cholangitis, are characterized at the end stage by ductopenia due to increased cholangiocyte apoptosis and decreased cholangiocyte proliferation. Although cholangiocyte proliferation is associated with an increased number of intra-hepatic bile ducts and secretin-stimulated ductal secretion, ductopenia is coupled with decreased ductal mass and secretin-induced ductal secretory activity. We have shown that a single injection of actinomycin D + tumor necrosis factor-alpha (TNF-alpha ) to bile duct-ligated (BDL) rats induces cholangiocyte injury, which is characterized by loss of cholangiocyte proliferation, and secretory activity and by an increase in cholangiocyte apoptosis. We also have shown that Taurocholic acid both in vivo and in vitro stimulates cholangiocyte proliferation. We hypothesize that Taurocholic acid feeding protects cholangiocytes against TNF-alpha -induced apoptosis through a phosphatidylinositol-3-kinase (PI3K)-dependent pathway. Immediately after BDL, rats were fed Taurocholic acid or control diet in the absence/presence of daily injections of wortmannin for 1 week. Seven days later, control-fed or Taurocholic acid-fed rats were treated with a single intraperitoneal injection of actinomycin D + TNF-alpha . Twenty-four hours later we evaluated: (i) cholangiocyte apoptosis and proliferation in liver sections and (ii) basal and secretin-stimulated bile and bicarbonate secretion in bile fistula rats. Taurocholic acid feeding prevented TNF-alpha -induced increases in cholangiocyte apoptosis and decreases in growth and secretin-stimulated bile and bicarbonate secretion, changes that were blocked by PI3K inhibition. The PI3K survival pathway is important in bile acid protection against immune-mediated cholangiocyte injury in cholestatic liver diseases.
High concentraction of taurocholic acid induced apoptosis in HTR-8/SVneo cells via overexpression of ERp29 and activation of p38.[Pubmed:24780196]
Placenta. 2014 Jul;35(7):496-500.
INTRODUCTION: Intrahepatic cholestasis of pregnancy (ICP) is a pregnancy-specific disease associated with a significant risk of fetal complications. Our previous study using an iTRAQ-based proteomics approach showed that ERp29 was overexpressed in the placenta tissue of ICP patients, which was an apoptosis-related protein and has not been investigated in the pathogenesis of ICP. The aim of this study was to explore the role of ERp29 in the mechanism of apoptosis in the placenta of ICP. METHODS: HTR-8/SVneo cells were cultured and treated with different concentrations of Taurocholic acid (TCA) (0, 10, 50 and 100 muM). The apoptotic index and cell cycle were detected by flow cytometry; furthermore, the expression levels of ERp29 and p-p38 were detected by western blot. The ERp29-siRNA was also used to confirm the role of ERp29 in TCA induced-apoptosis. RESULTS: ERp29 expression and the apoptotic index were significantly increased in HTR-8/SVneo cells exposed to 100 muM TCA; so were p-p38 and caspase-3 activity, compared with the 50 muM, 10 muM TCA groups and negative control group (P < 0.05, respectively). The induction of apoptosis by TCA and the expression of p-p38 were reduced in HTR-8/SVneo cells after treatment with ERp29-siRNA, compared with controls (P < 0.05, respectively). CONCLUSIONS: This study suggested that overexpression of ERp29 may play a key role in TCA-induced apoptosis in HTR-8/SVneo cells via activation of p38, which may participate in the pathogenesis of ICP and may represent a novel target for ICP treatment.
Effects of rectal administration of taurocholic acid on glucagon-like peptide-1 and peptide YY secretion in healthy humans.[Pubmed:23181598]
Diabetes Obes Metab. 2013 May;15(5):474-7.
Glucagon-like peptide-1 (GLP-1) and peptide YY (PYY), secreted by enteroendocrine L-cells located most densely in the colon and rectum, are of fundamental importance in blood glucose and appetite regulation. In animal models, colonic administration of bile acids can stimulate GLP-1 and PYY by TGR5 receptor activation. We evaluated the effects of Taurocholic acid (TCA), administered as an enema, on plasma GLP-1 and PYY, as well as gastrointestinal sensations in 10 healthy male subjects, and observed that rectal administration of TCA promptly stimulated secretion of both GLP-1 and PYY, and increased fullness, in a dose-dependent manner. These observations confirm that topical application of bile acids to the distal gut may have potential for the management of type 2 diabetes and obesity.
Cytoprotective effects of taurocholic acid feeding on the biliary tree after adrenergic denervation of the liver.[Pubmed:17403196]
Liver Int. 2007 May;27(4):558-68.
BACKGROUND: Cholangiopathies impair the balance between proliferation and apoptosis of cholangiocytes leading to the disappearance of bile ducts and liver failure. Taurocholic acid (TC) is essential for cholangiocyte proliferative and functional response to cholestasis. Bile acids and neurotransmitters co-operatively regulate the biological response of the biliary epithelium to cholestasis. Adrenergic denervation of the liver during cholestasis results in the damage of bile ducts. AIM: To verify whether TC feeding prevents the damage of the biliary tree induced by adrenergic denervation in the course of cholestasis. METHODS: Rats subjected to bile duct ligation (BDL) and to adrenergic denervation were fed a TC-enriched diet, in the absence or presence of daily administration of the phosphatidyl-inositol-3-kinase (PI3K) inhibitor wortmannin for 1 week. RESULTS: TC prevented the induction of cholangiocyte apoptosis induced by adrenergic denervation. TC also restored cholangiocyte proliferation and functional activity, reduced after adrenergic denervation. TC prevented AKT dephosphorylation induced by adrenergic denervation. The cytoprotective effects of TC were abolished by the simultaneous administration of wortmannin. SUMMARY/CONCLUSIONS: TC administration prevents the damage of the biliary tree induced by the adrenergic denervation of the liver. These novel findings open novel perspectives in the understanding of the potential of bile acids especially in post-transplant liver disease.
