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50mg |
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Purity: ≥98%
Sodium Tauroursodeoxycholate (TUDC) is a water soluble bile salt, which is used for the treatment of gallstones and liver cirrhosis. Tauroursodeoxycholate exhibits protective and reversing effects in vitro against the impairment of the cVA-of-CLF brought on by 17βEG. Tauroursodeoxycholate reduces cell growth in Mz-ChA-1 cholangiocarcinoma cells through pathways that depend on Ca2+-, PKC, and MAPK. Tauroursodeoxycholate inhibits bile acid-induced apoptosis in isolated rat hepatocytes by causing the formation of cAMP through the β1-integrin.
Targets |
ERK; Caspase-3; Caspase-12; Human Endogenous Metabolite
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ln Vitro |
Tauroursodeoxycholate (TUDCA) reduces the viability and migration of vascular smooth muscle cells (VSMCs) by inhibiting the phosphorylation of ERK and by inducing mitogen-activated protein kinase phosphatase-1 (MKP-1) via PKCα. By blocking ERK through Ca2+-dependent PKC translocation, tauroursodeoxycholate prevents the VSMCs from proliferating and migrating. Platelet-derived growth factor (PDGF) and MMP-9 expression brought on by vascular injury are both prevented by tauroursodeoxycholate. Tauroursodeoxycholate (200 μM) reduced VSMC viability, which suggests that Tauroursodeoxycholate's ability to inhibit cell proliferation depended on MKP-1 expression[1]. MKP-1 expression can be reduced by using specific si-RNA to knock it down.
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ln Vivo |
Immunohistochemistry is used to examine the impact of tauroursodeoxycholate (TUDCA) on the proliferation and apoptosis of VSMCs in vivo. Tauroursodeoxycholate (10, 50, and 100 mg/kg) increases the caspase 3 activity of injured tissues in a dose-dependent manner, suggesting that it causes VSMCs in the neointima to undergo apoptosis. At one week after injury, additional testing and comparison of the phosphorylation level of ERK and MMP-9 expression is done using the injured tissues in comparison to normal controls. Both ERK phosphorylation and MMP-9 expression were upregulated in the tissues after balloon injury. Tauroursodeoxycholate (10, 50, and 100 mg/kg) inhibits the expression of MMP-9 and ERK in a dose-dependent manner[1]. Tauroursodeoxycholate (TUDCA) is a hydrophilic bile acid. By lowering ER stress and apoptosis, tauroursodeoxycholate, a cytoprotective agent, enhances liver function and can prevent hepatocellular carcinoma. In Ang II-induced ApoE-/- mice, tauroursodeoxycholate significantly decreases expression of apoptosis molecules like caspase-3, caspase-12, C/EBP homologous protein, c-Jun N-terminal kinase (JNK), activating transcription factor 4 (ATF4), X-box binding protein (XBP), and eukaryotic initiation factor 2α (eIF2; p<0.05). In ApoE-/- mice, tauroursodeoxycholate prevents the development of abdominal aortic aneurysms (AAAs) brought on by Ang II. Tauroursodeoxycholate is administered to ApoE-/- mice (ER stress inhibitor group) at a dose of 0.5 g/kg/day. Total cholesterol levels (663.6±88.7 mg/dL vs 655.7±65.4 mg/dL; p>0 .05) and systolic blood pressure (141.3±5.6 mmHg vs 145.98.9 mmHg; p>0.05) were comparable between the AAA model group and the Tauroursodeoxycholate group. Additionally, when compared to the AAA model group, the Tauroursodeoxycholate group's maximum aortic diameter was significantly lower (0.95±0.03 mm vs 1.79±0.04 mm; p<0.05). The AAA lesion areas in the Tauroursodeoxycholate group are also smaller than those in the AAA model group (0.37±0.03 mm2 vs 1.51±0.06 mm2; p<0.05)[2].
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Cell Assay |
Ez-Cytox is used to assess the viability and growth of cells. Smooth Muscle Cell Growth Medium 2 (SMCGM2) is used to seed and cultivate VSMCs (5×103 cells) on 96-well plates. After serum starvation, Tauroursodeoxycholate (0, 50, 100, and 200 μM) is added to the hVSMCs, with or without 1,2-bis(o-aminophenoxy) ethane-N,N,N′,N′-tetraacetic acid tetra(acetoxymethyl) ester (BAPTA, 10 μM) and 7-hydroxystaurosporine (H7, 10 μM) and cultured for 24 h. HVSMCs are seeded onto 96-well plates and cultured to determine the impact of tauroursodeoxycholate on the PDGF-stimulated hVSMC proliferation. Tauroursodeoxycholate (0, 50, 100, and 200 μM) is added to the hVSMCs after serum starvation, with or without PDGF-BB (50 ng/mL), and the cells are then cultured. The optical density at 450 nm is used to assess cell viability after the addition of 10 μL of Ez-Cytox into each well[1].
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Animal Protocol |
Rats: Ketamine (70 mg/kg) and Xylazine (7 mg/kg) are combined to anesthetize Sprague-Dawley rats. For two weeks, tauroursodeoxycholate is given orally once daily at various concentrations (e.g., vehicle, 10, 50, and 100 mg/kg). The carotid arteries are preserved by perfusion with 4% formaldehyde, followed by paraffin embedding and H&E staining of sections (8 μm)[1].
Mice: Thirty C57BL/6 male ApoE-/- mice are divided into three groups at random, each with ten mice, and they are eight weeks old. (i) ApoE-/- mice are implanted with mini-osmotic pumps to release Ang II (1000 ng/kg/min) over the course of 28 days (AAA model group); (ii) AAA model mice are treated with Tauroursodeoxycholate daily for 4 weeks at a dosage of 0.5 g/kg/day in drinking water (Tauroursodeoxycholate group). Following a 28-day Ang II infusion, mice are sacrificed[2]. |
References |
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Molecular Formula |
C26H44NNAO6S
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Molecular Weight |
521.69
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Elemental Analysis |
C, 59.86; H, 8.50; N, 2.68; Na, 4.41; O, 18.40; S, 6.15
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CAS # |
35807-85-3
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Related CAS # |
Tauroursodeoxycholate;14605-22-2;Tauroursodeoxycholate-d4 sodium;2410279-95-5;Tauroursodeoxycholate dihydrate;117609-50-4
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Appearance |
Solid powder
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SMILES |
C[C@H](CCC(=O)NCCS(=O)(=O)[O-])[C@H]1CC[C@@H]2[C@@]1(CC[C@H]3[C@H]2[C@H](C[C@H]4[C@@]3(CC[C@H](C4)O)C)O)C.[Na+]
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InChi Key |
IYPNVUSIMGAJFC-JUWYWQLMSA-M
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InChi Code |
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
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Chemical Name |
sodium;2-[[(4R)-4-[(3R,5S,7S,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
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Synonyms |
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HS Tariff Code |
2934.99.9001
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Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month Note: Please store this product in a sealed and protected environment, avoid exposure to moisture. |
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Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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Solubility (In Vitro) |
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Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.5 mg/mL (4.79 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: ≥ 2.5 mg/mL (4.79 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly. Preparation of 20% SBE-β-CD in Saline (4°C,1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution. View More
Solubility in Formulation 3: ≥ 2.5 mg/mL (4.79 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. Solubility in Formulation 4: 100 mg/mL (191.68 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with ultrasonication. |
Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
1 mM | 1.9168 mL | 9.5842 mL | 19.1685 mL | |
5 mM | 0.3834 mL | 1.9168 mL | 3.8337 mL | |
10 mM | 0.1917 mL | 0.9584 mL | 1.9168 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration: mg/mL;
Method for preparing DMSO stock solution: mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation::Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O,mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
NCT Number | Recruitment | interventions | Conditions | Sponsor/Collaborators | Start Date | Phases |
NCT00771901 | Completed | Drug: tauroursodeoxycholic acid Other: placebo |
Insulin Resistance Diabetes |
Washington University School of Medicine |
February 2008 | Not Applicable |
The uptake of TUDCA in hVSMCs was mediated by OATP2. Cardiovasc Res . 2011 Nov 1;92(2):307-16. td> |
TUDCA suppressed viability of hVSMCs by inhibition of ERK phosphorylation, through induction of MKP-1 via PKCα. Cardiovasc Res . 2011 Nov 1;92(2):307-16. td> |
TUDCA inhibited both the proliferation and migration of PDGF-stimulated hVSMCs. Cardiovasc Res . 2011 Nov 1;92(2):307-16. td> |
TUDCA reduced neointimal hyperplasia after vascular injury. Cardiovasc Res . 2011 Nov 1;92(2):307-16. td> |
Tauroursodeoxycholic acid (TUDCA) attenuated endoplasmic reticulum stress (ERS) mediated apoptosis of aortas in angiotensin II induced apolipoprotein E−/− mice. Eur J Vasc Endovasc Surg . 2017 Mar;53(3):337-345. td> |