1. Metabolic Enzyme/Protease GPCR/G Protein Epigenetics Cell Cycle/DNA Damage Apoptosis NF-κB Stem Cell/Wnt TGF-beta/Smad
  2. Endogenous Metabolite G protein-coupled Bile Acid Receptor 1 PARP Apoptosis NF-κB PKA
  3. Taurodeoxycholate-d6 sodium salt

Taurodeoxycholate-d6 sodium salt is a bile salt-related anionic detergent. Taurodeoxycholate-d6 sodium salt is formed in the liver by conjugation of deoxycholate with Taurine (HY-B0351). Taurodeoxycholate-d6 sodium salt is used for isolation of membrane proteins including inner mitochondrial membrane proteins. Taurodeoxycholate-d6 (TDCA) exhibits anti-inflammatory and neuroprotective effects.

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Taurodeoxycholate-d<sub>6</sub> sodium salt Chemical Structure

Taurodeoxycholate-d6 sodium salt Chemical Structure

CAS No. : 2687960-92-3

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Description

Taurodeoxycholate-d6 sodium salt is a bile salt-related anionic detergent. Taurodeoxycholate-d6 sodium salt is formed in the liver by conjugation of deoxycholate with Taurine (HY-B0351). Taurodeoxycholate-d6 sodium salt is used for isolation of membrane proteins including inner mitochondrial membrane proteins. Taurodeoxycholate-d6 (TDCA) exhibits anti-inflammatory and neuroprotective effects[1][2][3][9][10].

In Vitro

Taurodeoxycholate-d6 sodium salt (Taurodeoxycholic acid form) shows agonist activity at human TGR5 expressed in CHO cells by luciferase assay, with an EC50 of 0.79 μM[4].
Taurodeoxycholate-d6 sodium salt (Taurodeoxycholic acid form, 16 h) shows agonist activity at wild type and Y89A mutant human TGR5 expressed in HEK293 cells assessed as rise in intracellular cAMP level, with EC50s of 0.68 and 8.9 μM, respectively[5].
Taurodeoxycholate-d6 sodium salt (Taurodeoxycholic acid form, 50 μM, 100 μM; 4 h) increases oligonucleosomal DNA cleavage and apoptotic nuclei in primary human hepatocytes[6].
Taurodeoxycholate-d6 sodium salt (Taurodeoxycholic acid form, 400 μM, 18-24 h) increases DNA fragmentation and PARP cleavage in human liver-derived cell line Huh7 cells, thus induces apoptosis[8].
Taurodeoxycholate-d6 (0.05-1.00 mM; 1-6 days) sodium salt stimulates intestinal epithelial cell proliferation[8].
Taurodeoxycholate-d6 (0.05-1.00 mM; 24 h) sodium salt induces a significant increase in S-phase concentration and a significant decrease in G1-phase concentration of the cell cycle, increases c-myc protein and mRNA expression in IEC-6 cells[8].
Taurodeoxycholate-d6 (25-400 ng/mL, with a four-fold dilution, 3 h) sodium salt inhibits the activation of NF-κB in lipopolysaccharide-activated bone marrow-derived macrophages (BMDMs) by activating the cAMP-PKA axis[9].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Cell Proliferation Assay[8]

Cell Line: IEC-6 and caco-2 cells
Concentration: 0, 0.05, 0.50, and 1.00 mM
Incubation Time: 1, 2, 4 and 6 days
Result: Significantly stimulated intestinal epithelial cell proliferation in a dose-dependent manner.

Cell Cycle Analysis[8]

Cell Line: IEC-6 cells
Concentration: 0, 0.05, 0.50, and 1.00 mM
Incubation Time: 24 h
Result: Significantly increased cells in S phase and decreased cells in G1-phase.

Western Blot Analysis[8]

Cell Line: IEC-6 cells
Concentration: 0.5 mM
Incubation Time: 1 and 6 days
Result: Significantly increased c-myc protein expression.
In Vivo

Taurodeoxycholate-d6 (1.25-5 mg/kg, p.o., 6 days) sodium salt ameliorates dextran sodium sulfate (DSS)-induced colitis in mice[9].
Taurodeoxycholate-d6 sodium salt (Taurodeoxycholic acid form, 50 mg/kg; i.p.; once daliy for 34 d) prevents neuropathology and associated behavioral deficits in the 3-nitropropionic acid rat model of Huntington's disease (HD) [10].
Taurodeoxycholate-d6 sodium salt (Taurodeoxycholic acid form, 500 mg/kg; s.c.; once every 3 d for 7 weeks) leads to a significant reduction in striatal neuropathology of the R6/2 transgenic HD mouse[11].
Taurodeoxycholate-d6 (0.5 mg/kg; i.v., once) sodium salt confers protection to C57BL/6N mice with sepsis, but does not protect TGR5 KO mice under sepsis[12].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: A mouse colitis model (fed with 3% (w/v) DSS in drinking water for the first seven days and then switched to normal drinking water for an additional two days)[9]
Dosage: 1.25, 2.5, and 5 mg/kg
Administration: Oral gavage (p.o.), from day 3 to day 8, once a day
Result: Prevented loss of body weight, shortening of the colon, production of pro-inflammatory cytokines, infiltration of pro-inflammatory cells, and mucosal ulceration in the colon.
Animal Model: Huntington's disease model in mouse[10]
Dosage: 50 mg/kg
Administration: Intraperitoneal injection; once daliy for 34 d, injected 3-NP at 6 hr after Taurodeoxycholic acid treatment
Result: Reduced striatal atrophy, decreased striatal apoptosis, as well as fewer and smaller size ubiquitinated neuronal intranuclear huntingtin inclusions.
Significantly improved locomotor and sensorimotor deficits.
Animal Model: C57BL/6N mice, Lipopolysaccharides (HY-D1056) injection model of sepsis[12]
Dosage: 0.5 mg/kg
Administration: Intravenous injection, 30 min or 24 h after LPS injection
Result: Improved the survival rate of mice with sepsis.
Decreased liver and kidney damage in septic mice.
Ameliorated systemic inflammation and normalized blood pressure in septic mice.
Molecular Weight

528.73

Formula

C26H39D6NNaO6S

CAS No.
Unlabeled CAS
SMILES

C[C@@]12[C@](CC[C@]2([H])[C@H](C)CCC(NCCS(=O)(O)=O)=O)([H])[C@@]3([H])[C@@](C([2H])([2H])[C@@H]1O)([H])[C@@]4([C@](C([2H])([2H])[C@@H](C([2H])([2H])C4)O)([H])CC3)C.[Na]

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  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

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Taurodeoxycholate-d6 sodium salt
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