Taurochenodeoxycholic acid sodium

SKU: orb1297206

Description

Sodium taurochenodeoxycholate is a key bile acid derivative with demonstrated pro-apoptotic, anti-inflammatory, and immunomodulatory activities. It is utilized in metabolic research, particularly for studying pancreatic islet cell function, as it enhances glucose-stimulated insulin secretion and intracellular calcium signaling in α-cells.

Research Area

Cell Biology, Metabolism Research

Key Properties

• CAS Number: 6009-98-9
• MW: 521.68
• Purity: 97.00% (May vary between batches)
• Formula: C₂₆H₄₄NNaO₆S
• SMILES: [Na+].C[C@H](CCC(=O)NCCS([O-])(=O)=O)[C@H]1CC[C@H]2[C@@H]3[C@H](O)C[C@@H]4C[C@H](O)CC[C@]4(C)[C@H]3CC[C@]12C
• Target: Apoptosis,Endogenous Metabolite
• Solubility: 10% DMSO+40% PEG300+5% Tween-80+45% Saline:2 mg/mL (3.83 mM);DMSO:262.5 mg/mL (503.18 mM)

Bioactivity

• In Vitro:
  Experiments were performed with islets from wild-type, farnesoid X receptor (FXR) knockout (KO), and β-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 β-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 β-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.

Storage & Handling

• Storage: Powder: -20°C for 3 years | In solvent: -80°C for 1 year | Shipping with blue ice/Shipping at ambient temperature.
• Expiration Date: 12 months from date of receipt.
• Disclaimer: For research use only

Alternative Names

inhibit, NR8383, JNK, immune, mRNA, Inhibitor, EndogenousMetabolite, Endogenous Metabolite, Calcium Channel, caspase-3, caspase-8, bile, anti-inflammatory, apoptosis, Apoptosis, ATPase, acid, 12-Deoxycholyltaurine, TNF-α, PKC, TIMP-2, Potassium Channel, Taurochenodeoxycholic acid, Taurochenodeoxycholic acid sodium, Sodium taurochenodeoxycholate, regulation

Compound Identifiers

PubChem CID

23664008