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Taurochenodeoxycholic acid Caspase activator

Cat.No.S3865

Taurochenodeoxycholic acid (Taurochenodeoxycholate, TCDCA, Chenodeoxycholyltaurine), a bile acid formed in the liver of most species, is used as a cholagogue and choleretic.
Taurochenodeoxycholic acid Caspase activator Chemical Structure

Chemical Structure

Molecular Weight: 499.70

Quality Control

Chemical Information, Storage & Stability

Molecular Weight 499.70 Formula

C26H45NO6S

Storage (From the date of receipt)
CAS No. 516-35-8 -- Storage of Stock Solutions

Synonyms Taurochenodeoxycholate, TCDCA, 12-Deoxycholyltaurine, Chenodeoxycholyltaurine, Chenyltaurine Smiles CC(CCC(=O)NCCS(=O)(=O)O)C1CCC2C1(CCC3C2C(CC4C3(CCC(C4)O)C)O)C

Solubility

In vitro
Batch:

DMSO : 100 mg/mL (200.12 mM)
(Moisture-contaminated DMSO may reduce solubility. Use fresh, anhydrous DMSO.)

Water : 100 mg/mL

Ethanol : Insoluble

Molarity Calculator

Mass Concentration Volume Molecular Weight

In vivo
Batch:

In vivo Formulation Calculator (Clear solution)

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Working concentration: mg/ml;

Method for preparing DMSO master liquid: mg drug pre-dissolved in μL DMSO ( Master liquid 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 master liquid, next addμL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O, mix and clarify.

Method for preparing in vivo formulation: Take μL DMSO master liquid, next add μL Corn oil, mix and clarify.

Note: 1. Please make sure the liquid is clear before adding the next solvent.
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Mechanism of Action

In vitro
Taurochenodeoxycholic acid (TUDCA) induces dissociation of CD34+ HSCs from stromal cells by decreasing adhesion molecule expression. It induces bone marrow stem cell mobilization and differentiation into endothelial progenitor cells (EPCs) and enhances EPC proliferation, invasion, and tube formation via Akt and ERK activation[1]. TCDCA induces the apoptosis process through the activation of caspase cascade in macrophages, and this process may be involved in PKC/JNK signaling pathway[2].
In vivo
TUDCA has neuroprotective effects in neuronal cultures and positive effects on ischemia reperfusion in animal models, reducing infarct area and inflammation via attenuation of endoplasmic reticulum (ER) stress. TUDCA is incorporated into target cells via organic anion transporter (OATP) 2, OATP8, and the Na+‐taurocholate cotransporting polypeptide (NTCP). TUDCA inhibits neointimal hyperplasia by promoting apoptosis of smooth muscle cells via induction of MAP kinase phosphatase‐1 (MKP‐1) expression. In addition, TUDCA protects the hepatocytes and restores glucose homeostasis by reducing ER stress. TUDCA enhances neovascularization in vivo[1]. TCDCA in dosages of 0.05 and 0.1g/kg can extremely significantly decrease the pulmonary coefficient in the model mice. TCDCA in a dosage of 0.2g/kg significantly decreases the pulmonary coefficient in the model mice (P<0.05); TCDCA in dosages of 0.05 and 0.1g/kg significantly reduce the pathological damages on their lungs; TCDCA can extremely significantly decrease the expression levels of TNF-α and TIMP-2 in pulmonary tissues in the pulmonary fibrosis mice (P>0.01), the expression level of MMP-9 extremely significantly increased (P>0.01), while it has no significant effects on MMP2. Thus, TCDCA has antagonistic actions on pulmonary fibrosis in mice[3].
References

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