| CAS Number | 14605-22-2 |
|---|---|
| Molecular Formula | C26H45NO6S |
| Molecular Weight | 499.7 |
| Regulatory Status | Dietary Supplement (OTC) |
| Typical Dose | 250–500 mg/day |
| Mechanism Class | Chemical Chaperone / Bile Acid |
| Parent Compound | Ursodeoxycholic Acid (UDCA) |
Tauroursodeoxycholic acid (TUDCA) is the taurine conjugate of ursodeoxycholic acid (UDCA), a bile acid naturally produced in the human body. It was first isolated from bear bile, where it serves as a major bile component, though modern TUDCA is synthesized commercially without animal sources. Structurally, TUDCA consists of UDCA conjugated with a taurine molecule via an amide bond, which increases its water solubility relative to the unconjugated form. Its molecular formula is C26H45NO6S with a molecular weight of 499.7 g/mol. The CAS registry number is 14605-22-2.
TUDCA is not FDA-approved as a prescription drug. It is sold in the United States and internationally as a dietary supplement available over the counter (OTC). This distinguishes it from its parent compound UDCA (ursodiol), which holds FDA approval for primary biliary cholangitis (PBC) and gallstone dissolution. TUDCA does not hold a formal FDA GRAS determination. Its current OTC status rests on its presence as a minor endogenous bile acid in humans and the extensive clinical safety record of UDCA, its parent compound. The bile acid pool in healthy adults contains TUDCA at roughly 2–4% of total biliary bile acids, with UDCA representing less than 5% in individuals not taking UDCA supplementation.
Interest in TUDCA has grown substantially over the past decade, driven by preclinical research demonstrating its activity as a chemical chaperone that reduces endoplasmic reticulum (ER) stress, independent of its bile acid function. This mechanism has implications for neurodegenerative diseases, metabolic disorders, and liver conditions. As of July 2026, Google search volume for "TUDCA" exceeds 27,000 searches per month, reflecting growing consumer and professional interest.
TUDCA exerts biological effects through multiple pathways, making it a pleiotropic compound. The four most rigorously documented mechanisms are:
TUDCA stabilizes protein folding in the endoplasmic reticulum lumen by binding to exposed hydrophobic regions of misfolded proteins. This reduces the unfolded protein response (UPR), a cellular stress pathway triggered when ER protein folding capacity is overwhelmed. Chronic ER stress is implicated in insulin resistance, beta-cell dysfunction in type 2 diabetes, and neurodegenerative protein aggregation diseases. Research published in Science (Ozcan et al., 2006) demonstrated that TUDCA treatment normalized hyperglycemia and restored insulin sensitivity in obese and diabetic mice by reducing ER stress in the hypothalamus, liver, and adipose tissue.
TUDCA inhibits the intrinsic (mitochondrial) apoptotic pathway through three specific actions: (1) blocking Bax translocation from the cytosol to the mitochondrial outer membrane, (2) preventing mitochondrial cytochrome c release into the cytoplasm, and (3) reducing activation of caspase-3, caspase-9, and caspase-12. These effects have been confirmed in hepatocyte models exposed to hydrophobic bile acids, ethanol, and TGF-beta, as well as in neuronal cell models. Unlike broad-spectrum caspase inhibitors, TUDCA acts upstream at the mitochondrial level, preserving cellular energy metabolism while preventing apoptosis.
TUDCA directly inhibits reactive oxygen species (ROS) production and upregulates endogenous antioxidant defenses. In primary hepatocyte cultures, TUDCA at concentrations of 50–200 µM reduced ROS levels by 40–60% following oxidative challenge. This effect is partially mediated through PI3K/Akt pathway activation, which promotes cell survival and suppresses pro-oxidant enzyme expression.
TUDCA suppresses NF-kB activation and reduces expression of pro-inflammatory cytokines including TNF-alpha, IL-1beta, and IL-6. In a murine colitis model, TUDCA administration reduced intestinal inflammation scores and preserved epithelial barrier integrity. In neural tissue, TUDCA attenuates microglial activation, which contributes to its neuroprotective profile.
The strongest clinical evidence for TUDCA is in liver disease. A 3-month clinical trial in chronic hepatitis patients demonstrated that TUDCA supplementation significantly reduced alanine aminotransferase (ALT), aspartate aminotransferase (AST), and gamma-glutamyl transferase (GGT) levels compared to baseline. The hepatoprotective mechanism combines anti-apoptotic activity (protecting hepatocytes from bile acid-induced death), choleretic effects (stimulating bile flow), and direct antioxidant action. For cholestatic liver diseases, TUDCA's ability to displace toxic hydrophobic bile acids from the bile acid pool provides additional benefit distinct from simple ER stress reduction.
Three lines of preclinical evidence support TUDCA's neuroprotective potential:
As of mid-2026, the sole completed Phase 3 trial for a neurological indication — the TUDCA-ALS trial (NCT03800524) — did not demonstrate efficacy on its primary endpoint. All other neuroprotective evidence remains preclinical except the small ALS pilot trial and a Phase 1/2 progressive MS safety trial (2025, n=47).
TUDCA improves insulin sensitivity through ER stress reduction in peripheral tissues. In a proof-of-concept human study, TUDCA 1,750 mg/day for 4 weeks increased hepatic insulin sensitivity by approximately 30% and muscle insulin sensitivity by approximately 25% in obese individuals, as measured by hyperinsulinemic-euglycemic clamp. This finding positions TUDCA as a compound of interest for metabolic syndrome and type 2 diabetes, though long-term outcome data are lacking.
| Parameter | TUDCA | UDCA |
|---|---|---|
| Full Name | Tauroursodeoxycholic Acid | Ursodeoxycholic Acid |
| FDA Status | Dietary supplement (OTC) | FDA-approved prescription drug |
| Water Solubility | Higher (taurine conjugate) | Lower (unconjugated) |
| Blood-Brain Barrier Penetration | Documented in animal models | Minimal to none |
| Clinical Evidence Level | Limited human trials; strong preclinical | Multiple phase III RCTs; FDA approved |
| Typical Human Dose | 250–1,500 mg/day | 8–15 mg/kg/day |
| Insurance Coverage | Not covered (supplement) | Covered for approved indications |
| Cost (approximate) | $0.50–$2.00/day (supplement) | $3–$8/day (generic); $15–$30/day (brand) |
TUDCA and UDCA are structurally related but not interchangeable. TUDCA's taurine conjugation confers higher aqueous solubility and the ability to cross the blood-brain barrier — a property that drives its investigation in neurological conditions where UDCA is ineffective. For liver indications, UDCA has the advantage of extensive clinical trial data and FDA labeling, while TUDCA's liver evidence, though promising, comes mainly from smaller studies. See our detailed comparison at TUDCA vs UDCA: Differences, Benefits & Which to Choose.
China is the dominant producer of TUDCA raw material, using the same cholic acid supply chain that supports UDCA manufacturing. When sourcing TUDCA from China, buyers should verify whether the product is pharmaceutical-grade or supplement-grade — a critical distinction that affects pricing, regulatory acceptance, and quality documentation. As a TUDCA supplier China, KingWish provides TUDCA with full documentation support including CoA, MSDS, and GMP certificates. For buyers seeking tudca powder supplier or exploring buy tudca bulk options, contact our team for specifications and pricing. Common procurement terms include MOQ starting at 25 kg for pharmaceutical-grade material, with smaller trial quantities available for initial quality evaluation.
TUDCA dosing varies significantly by intended use. All dosing recommendations below are based on published clinical literature; they are not medical advice. Anyone considering TUDCA supplementation should consult a licensed healthcare provider.
For detailed dosing guidance, see TUDCA Dosage Guide: Evidence-Based Dosing Recommendations.
TUDCA has a generally favorable safety profile based on available human data, with several important caveats:
Full safety details: TUDCA Side Effects & Safety: What the Research Shows.
TUDCA quality in the supplement market varies widely. As a compound not regulated as a pharmaceutical, TUDCA supplements are not subject to FDA pre-market approval. Key quality considerations include:
For procurement guidance, see How to Source TUDCA: Quality, Suppliers & Procurement Guide.