Sodium taurochenodeoxycholateCAS# 6009-98-9 |
2D Structure
- Sodium Tauroursodeoxycholate (TUDC)
Catalog No.:BCC6516
CAS No.:35807-85-3
Quality Control & MSDS
3D structure
Package In Stock
Number of papers citing our products
Cas No. | 6009-98-9 | SDF | Download SDF |
PubChem ID | 23664008 | Appearance | Powder |
Formula | C26H44NNaO6S | M.Wt | 521.68 |
Type of Compound | Steroids | Storage | Desiccate at -20°C |
Solubility | Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc. | ||
Chemical Name | sodium;2-[[(4R)-4-[(3R,5S,7R,8R,9S,10S,13R,14S,17R)-3,7-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]pentanoyl]amino]ethanesulfonate | ||
SMILES | CC(CCC(=O)NCCS(=O)(=O)[O-])C1CCC2C1(CCC3C2C(CC4C3(CCC(C4)O)C)O)C.[Na+] | ||
Standard InChIKey | IYPNVUSIMGAJFC-HLEJRKHJSA-M | ||
Standard InChI | InChI=1S/C26H45NO6S.Na/c1-16(4-7-23(30)27-12-13-34(31,32)33)19-5-6-20-24-21(9-11-26(19,20)3)25(2)10-8-18(28)14-17(25)15-22(24)29;/h16-22,24,28-29H,4-15H2,1-3H3,(H,27,30)(H,31,32,33);/q;+1/p-1/t16-,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. Sodium taurochenodeoxycholate can increase glucose-induced insulin secretion and stimulate the electrical activity of β-cells and enhance cytosolic Ca(2+) concentration ([Ca(2+)](c)). |
Targets | ATPase | Potassium Channel | Calcium Channel |
Sodium taurochenodeoxycholate Dilution Calculator
Sodium taurochenodeoxycholate Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 1.9169 mL | 9.5844 mL | 19.1688 mL | 38.3377 mL | 47.9221 mL |
5 mM | 0.3834 mL | 1.9169 mL | 3.8338 mL | 7.6675 mL | 9.5844 mL |
10 mM | 0.1917 mL | 0.9584 mL | 1.9169 mL | 3.8338 mL | 4.7922 mL |
50 mM | 0.0383 mL | 0.1917 mL | 0.3834 mL | 0.7668 mL | 0.9584 mL |
100 mM | 0.0192 mL | 0.0958 mL | 0.1917 mL | 0.3834 mL | 0.4792 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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Bile acids acutely stimulate insulin secretion of mouse beta-cells via farnesoid X receptor activation and K(ATP) channel inhibition.[Pubmed:22492528]
Diabetes. 2012 Jun;61(6):1479-89.
Type 2 diabetes mellitus is associated with alterations in bile acid (BA) signaling. The aim of our study was to test whether pancreatic beta-cells contribute to BA-dependent regulation of glucose homeostasis. Experiments were performed with islets from wild-type, farnesoid X receptor (FXR) knockout (KO), and beta-cell ATP-dependent K(+) (K(ATP)) channel gene SUR1 (ABCC8) KO mice, respectively. Sodium taurochenodeoxycholate (TCDC) increased glucose-induced insulin secretion. This effect was mimicked by the FXR agonist GW4064 and suppressed by the FXR antagonist guggulsterone. TCDC and GW4064 stimulated the electrical activity of beta-cells and enhanced cytosolic Ca(2+) concentration ([Ca(2+)](c)). These effects were blunted by guggulsterone. Sodium ursodeoxycholate, which has a much lower affinity to FXR than TCDC, had no effect on [Ca(2+)](c) and insulin secretion. FXR activation by TCDC is suggested to inhibit K(ATP) current. The decline in K(ATP) channel activity by TCDC was only observed in beta-cells with intact metabolism and was reversed by guggulsterone. TCDC did not alter insulin secretion in islets of SUR1-KO or FXR-KO mice. TCDC did not change islet cell apoptosis. This is the first study showing an acute action of BA on beta-cell function. The effect is mediated by FXR by nongenomic elements, suggesting a novel link between FXR activation and K(ATP) channel inhibition.