Taurodeoxycholate-d6 sodium salt is an anionic detergent related to bile salts. It is formed in the liver by conjugating deoxycholic acid with taurine. This compound is utilized for the separation of membrane proteins, including those in the mitochondrial inner membrane. Taurodeoxycholate-d6 (TDCA) exhibits anti-inflammatory and neuroprotective properties.

Taurodeoxycholate-d 6 sodium salt (Taurodeoxycholic acid form) exhibits agonistic activity on human TGR5 expressed in CHO cells, with an EC₅₀ value of 0.79 μM, as determined by a luciferase assay. In HEK293 cells expressing wild-type and Y89A mutant human TGR5, it acts as an agonist with EC₅₀ values of 0.68 and 8.9 μM, respectively, based on elevated intracellular cAMP levels. At concentrations of 50-100 μM over 4 hours, this compound increases oligomeric DNA fragmentation and nuclear apoptosis in primary human hepatocytes. When applied at 400 μM for 18-24 hours, it induces apoptosis through increased DNA fragmentation and PARP cleavage in human liver-derived Huh7 cells. Furthermore, Taurodeoxycholate-d 6, ranging from 0.05 to 1.00 mM over 1-6 days, stimulates intestinal epithelial cell proliferation. At 0.05-1.00 mM for 24 hours, it induces a significant increase in S-phase concentration and a decrease in G1-phase concentration, thereby elevating the expression of c-myc protein and mRNA in IEC-6 cells. Additionally, at concentrations of 25-400 ng/mL, with fourfold dilutions over 3 hours, it inhibits NF-κB activation in lipopolysaccharide-stimulated bone marrow-derived macrophages (BMDMs) by activating the cAMP-PKA axis.

Taurodeoxycholate-d6 sodium salt can ameliorate colitis in mice induced by dextran sulfate sodium (DSS) when administered orally at doses ranging from 1.25 to 5 mg/kg over 6 days. Administered intraperitoneally at 50 mg/kg daily for 34 days in its Taurodeoxycholic acid form, it prevents neuropathology and associated behavioral deficits in rat models of Huntington's disease (HD). Subcutaneous administration at 500 mg/kg every 3 days for 7 weeks significantly reduces striatal neuropathology in R6/2 transgenic HD mice. When given as a single intravenous dose of 0.5 mg/kg, it protects C57BL/6N mice with sepsis, but lacks protective effect in TGR5 KO mice with sepsis.