TUDCA (tauroursodeoxycholic acid, also called taurursodiol or ursodoxicoltaurine) is a bile acid. It is ursodeoxycholic acid (UDCA) joined to the amino acid taurine, and the human liver makes small amounts of it on its own. In Italy it is a licensed drug for disorders of bile production, and in the US it is sold as a dietary supplement that is often promoted as “liver support” for people using oral steroids.
Its best-known clinical story is in amyotrophic lateral sclerosis (ALS). A small trial in 2016 looked promising, and TUDCA was one of the two ingredients in Relyvrio, which FDA approved for ALS in 2022. Then two large phase 3 trials, TUDCA-ALS and PHOENIX, both missed their primary endpoints in 2024, and FDA formally withdrew Relyvrio’s approval in August 2025. No controlled trial has tested TUDCA for liver protection in people taking anabolic steroids.
This page summarizes what the clinical trials, the former FDA label and regulators report. It is for education only and is not medical advice.
| Property | Detail |
|---|---|
| Class | Hydrophilic bile acid; the taurine conjugate of ursodiol (UDCA) |
| Formula | C₂₆H₄₅NO₆S, molecular weight 499.7 g/mol (PubChem CID 9848818) |
| Route | Oral (capsules, tablets, powder) |
| Doses used in trials | 500–1,500 mg/day in liver disease; 1,750 mg/day in an insulin-sensitivity study; 1 g twice daily (2 g/day) in ALS trials |
| Approved products | Tudcabil (Italy, bile-flow disorders); in the US, only as one ingredient of Relyvrio (1 g per packet), approved 2022 and withdrawn 2025 |
| Pharmacokinetics | Median peak at 4.5 h, 98% protein bound (Relyvrio label); no plasma half-life is given on the label |
| ALS evidence | Positive 34-patient phase 2 trial; 336-patient phase 3 TUDCA-ALS trial missed its primary endpoint |
| US status | Sold as a dietary supplement; not an FDA-approved drug on its own; not a controlled substance |
| WADA status | Not named on the 2026 Prohibited List |
The library also has pages for ursodiol (UDCA), the FDA-approved form of the parent bile acid, and for UDCA as a supplement. This page covers the taurine-conjugated form.
What it is
TUDCA is formed when the liver attaches taurine to ursodeoxycholic acid. The former Relyvrio label describes taurursodiol as “the taurine conjugate of ursodiol” and as an ambiphilic (partly water-attracting, partly fat-attracting) bile acid. It is a bitter white powder, freely soluble in alcohol and sparingly soluble in water (Relyvrio label; PubChem).
| Compound | Relationship | Library page |
|---|---|---|
| Ursodiol (UDCA), prescription | Unconjugated parent bile acid; FDA-approved for gallstones and primary biliary cholangitis | Ursodiol (UDCA) |
| UDCA, supplement | Same molecule as ursodiol, listed as a supplement | UDCA |
| TUDCA | UDCA conjugated with taurine | This page |
Why the conjugate was studied. Researchers studied TUDCA in the 1990s as an alternative to UDCA for cholestatic liver disease (disease where bile flow is impaired). In patients with primary biliary cirrhosis (now called primary biliary cholangitis, PBC), oral TUDCA was partly deconjugated and reconjugated as it cycled between gut and liver. Gut bacteria converted less of it than UDCA, so the bile acid pool shifted further toward the hydrophilic (water-attracting) form (Setchell et al., Gut 1996).
Proposed mechanisms. Like UDCA, TUDCA displaces more toxic, hydrophobic bile acids in bile. In mouse models it reduced endoplasmic reticulum (ER) stress, the cell’s response to misfolded proteins, and this is the basis for its testing in neurodegenerative and metabolic disease (Kars et al., Diabetes 2010). In the one human study that measured it, markers of ER stress in muscle and fat did not change on TUDCA. The Relyvrio label stated that the drug’s mechanism in ALS was unknown.
Pharmacokinetics
Most human data come from bile studies in liver disease and from the Relyvrio label, where TUDCA was given together with sodium phenylbutyrate.
| Parameter | Finding | Source |
|---|---|---|
| Time to peak (fasting, healthy adults) | Median 4.5 h | Relyvrio label |
| Effect of a high-fat meal | Peak level unchanged; total exposure (AUC) up 39% | Relyvrio label |
| Plasma protein binding | 98% | Relyvrio label |
| Major metabolites | Ursodiol and glyco-ursodiol (UDCA conjugated with glycine) | Relyvrio label |
| Share of UDCA in bile after 6 months (PBC) | 34% at 500 mg/day, 33% at 1,000 mg/day, 42% at 1,500 mg/day | Setchell et al., Gut 1996 |
| Mass balance and plasma half-life | Not studied or not reported on the label | Relyvrio label |
Because TUDCA is partly converted back to UDCA and recycled through the gut and liver, its effects in the liver overlap heavily with those of ursodiol. A plain plasma half-life is of limited use for a bile acid that cycles this way, and we found no verified human half-life figure for TUDCA.
Approved medical use
TUDCA is licensed in Italy, and in some non-European countries such as Turkey and China, under the brand name Tudcabil for disorders of bile production by the liver. The European Medicines Agency granted it orphan drug designation for ALS in February 2017 (EU/3/17/1844). Orphan designation is a status for drugs under development for rare diseases; it is not a marketing approval (Albanese et al., Front Neurol 2022).
In the US, TUDCA has never been approved as a standalone drug. Its only US approval was as one ingredient of Relyvrio (sodium phenylbutyrate 3 g and taurursodiol 1 g per packet), approved for ALS in adults on September 29, 2022. Approval was withdrawn on August 29, 2025 (Federal Register 2025). The ALS section below explains why.
What the research shows
ALS: the phase 2 TUDCA trial
In a double-blind pilot trial in Italy, 34 patients with ALS already taking riluzole were randomized to TUDCA 1 g twice daily or placebo for 54 weeks, after a 3-month lead-in period (Elia et al., Eur J Neurol 2016). Five patients dropped out before treatment started, leaving 29 in the analysis.
| Outcome | TUDCA | Placebo |
|---|---|---|
| Responders (at least 15% improvement in ALSFRS-R slope vs lead-in) | 87% | 43% (p = 0.021) |
| ALSFRS-R at study end, baseline-adjusted | Higher on TUDCA (p = 0.007) | — |
| Deaths during the study | 1 | 3 |
| Mild diarrhea | 2 patients | 2 patients |
The ALSFRS-R (ALS Functional Rating Scale–Revised) scores daily function from 0 to 48; higher is better. The trial was small, and the study drug was supplied by its Italian manufacturer, Bruschettini.
ALS: the phase 3 TUDCA-ALS trial
TUDCA-ALS was designed to confirm the phase 2 result. It was an EU-funded, investigator-led, double-blind, placebo-controlled trial at 25 centers in seven European countries (Albanese et al., Front Neurol 2022; ClinicalTrials.gov NCT03800524).
| Design element | Detail |
|---|---|
| Participants | 336 adults with ALS on riluzole (ClinicalTrials.gov lists 337 enrolled); recruitment ran February 2019 to December 2021 |
| Treatment | TUDCA 1 g twice daily (four 250 mg capsules twice daily) or matching placebo, for 18 months |
| Lead-in | 3 months on riluzole alone to measure each patient’s own rate of decline |
| Primary endpoint | Share of responders, defined as at least 20% improvement in ALSFRS-R slope during treatment vs the lead-in period |
| Secondary endpoints | Survival without tracheostomy, quality of life, breathing capacity, muscle strength, biomarkers such as neurofilament light chain |
Secondary endpoints are listed in the EU project record (CORDIS). The responder threshold was raised from the 15% used in phase 2 to 20% on advice from the EMA’s orphan medicines committee (Albanese et al., Front Neurol 2022; Lombardo et al., Trials 2023).
Results. In March 2024 the consortium announced that the trial did not meet its primary endpoint. There was also no significant difference between TUDCA and placebo in secondary outcomes, including survival and neurofilament light chain (ALS Canada 2024; MND Scotland 2024). The COVID-19 pandemic slowed recruitment below the original target of 440 participants (CORDIS). In our searches of PubMed and Europe PMC, we found no peer-reviewed publication of the full results.
ALS: TUDCA with sodium phenylbutyrate (Relyvrio, AMX0035)
Relyvrio combined TUDCA with sodium phenylbutyrate, a separate drug.
| Trial | Design | Result |
|---|---|---|
| CENTAUR (Paganoni et al., NEJM 2020) | n = 137, randomized 2:1, 24 weeks; 3 g sodium phenylbutyrate plus 1 g TUDCA once daily for 3 weeks, then twice daily | ALSFRS-R decline −1.24 vs −1.66 points per month (difference 0.42, 95% CI 0.03–0.81; p = 0.03); secondary outcomes not significantly different |
| CENTAUR long-term follow-up (Paganoni et al., Muscle Nerve 2021) | Post hoc survival analysis; placebo patients who completed 24 weeks could switch to the active drug | Median survival 25.0 vs 18.5 months (HR 0.56, 95% CI 0.34–0.92) |
| PHOENIX (study A35-004; Jomaa et al., 2026) | n = 664, 48 weeks, global phase 3 | Did not meet its primary or secondary endpoints |
FDA approved Relyvrio in September 2022 on the CENTAUR data. After PHOENIX failed, the company told FDA it would stop marketing the drug as of October 31, 2024, and asked FDA to withdraw approval on the basis of the PHOENIX results (Federal Register 2025). A 2026 meta-analysis pooling CENTAUR and PHOENIX (801 patients) found no significant effect on ALSFRS-R decline (mean difference 1.51, 95% CI −1.01 to 4.02) or survival (HR 0.90, 95% CI 0.73–1.11). It rated the certainty of evidence as very low and noted that PHOENIX had been reported only as a conference abstract (Jomaa et al., Ann Indian Acad Neurol 2026).
An Italian registry study matched 86 ALS patients who took TUDCA with 172 who did not. Median survival was 49.6 vs 36.2 months, and patients taking at least 1,000 mg/day had a lower risk of death (HR 0.56, 95% CI 0.38–0.83) (Zucchi et al., EClinicalMedicine 2023). This was an observational study, and the authors called it exploratory. The randomized TUDCA-ALS trial later found no survival difference.
Liver disease
Most liver trials of TUDCA are small, short, and measured blood tests rather than clinical outcomes.
| Condition | Trial | Dose and duration | Result |
|---|---|---|---|
| PBC | Crosignani et al., Dig Dis Sci 1996; n = 24, randomized by dose | 500, 1,000 or 1,500 mg/day, 6 months | Liver enzymes fell with all doses, no significant difference between doses; total and HDL cholesterol fell at the two higher doses; diarrhea the only side effect |
| PBC | Larghi et al., Aliment Pharmacol Ther 1997; n = 23, crossover vs UDCA | 500 mg/day, two 6-month periods | Enzymes improved on both; no significant difference between TUDCA and UDCA |
| PBC | Ma et al., Medicine 2016; n = 199, double-blind vs UDCA | 250 mg three times daily, 24 weeks | Alkaline phosphatase fell over 25% in 76% (TUDCA) vs 81% (UDCA), p = 0.453; itching rose from 1.4% to 10.0% on UDCA but not on TUDCA |
| Hepatitis C–related chronic hepatitis | Crosignani et al., Hepatogastroenterology 1998; n = 150, placebo-controlled | 500 or 750 mg/day, 6 months | Aminotransferases (ALT, AST) fell more than on placebo (p under 0.001) |
| Liver disease from intravenous feeding in newborns | Heubi et al., J Pediatr 2002; 22 treated vs 30 controls | 30 mg/kg/day | No difference in bilirubin, ALT, alkaline phosphatase or bile acids; judged ineffective |
Taken together, TUDCA lowers liver enzymes in cholestatic and inflammatory liver disease about as well as UDCA, which is consistent with its partial conversion to UDCA. None of these trials showed effects on cirrhosis, transplant or survival.
Steroid-related liver injury
We found no clinical trial or case series testing TUDCA in people taking anabolic-androgenic steroids. The claim that it protects the liver during oral steroid use rests on its use in other cholestatic diseases and on studies of UDCA. Even for UDCA, the evidence in steroid-related liver injury is limited to case reports with mixed results (see ursodiol (UDCA)).
About “liver protection.” TUDCA is often sold as making oral 17α-alkylated steroids such as oxymetholone or stanozolol safe for the liver. No study has tested this. Lower liver enzymes on a bile acid do not by themselves show that the underlying injury has stopped.
Insulin sensitivity
In a randomized, placebo-controlled study, 20 obese adults took TUDCA 1,750 mg/day or placebo for 4 weeks (Kars et al., Diabetes 2010). Liver and muscle insulin sensitivity rose by about 30% on TUDCA (p under 0.05) and did not change on placebo. Fat-tissue insulin sensitivity did not change, and neither did markers of ER stress in muscle or fat. The study was small and short, and it did not measure blood sugar control over time.
Side effects and risks
Common side effects
Across trials, TUDCA was generally well tolerated. Diarrhea is the most consistently reported side effect:
- In PBC, diarrhea was the only side effect at 500–1,500 mg/day (Crosignani et al., Dig Dis Sci 1996).
- In the phase 2 ALS trial, mild diarrhea occurred in 2 patients on TUDCA and 2 on placebo (Elia et al., Eur J Neurol 2016). The TUDCA-ALS protocol allowed a temporary dose cut to 0.5 g twice daily for diarrhea.
- In the Italian ALS registry, 8.1% of patients stopped TUDCA because of side effects, mostly mild and gastrointestinal (Zucchi et al., EClinicalMedicine 2023).
In CENTAUR, diarrhea (25% vs 19%), abdominal pain (21% vs 13%) and nausea (18% vs 13%) were more common on Relyvrio than placebo. These rates reflect the combination with sodium phenylbutyrate, not TUDCA alone (Relyvrio label).
Interactions
The Relyvrio label listed these interactions for its bile acid component:
- Bile acid sequestrants (cholestyramine, colestipol, colesevelam) may block TUDCA absorption.
- Aluminum-based antacids bind bile acids in vitro and may reduce absorption.
- Strong inhibitors of the bile salt export pump (BSEP), such as cyclosporine, may cause conjugated bile salts to build up in the liver. The label advised monitoring liver tests if the combination could not be avoided.
Who should be cautious
The Relyvrio label warned that people with disorders of bile circulation (such as biliary infection or active cholecystitis), severe pancreatic disease, or intestinal disease that alters bile acids (such as ileal resection) may have worsening diarrhea or poor absorption. These patients were excluded from its trial. The same cautions that apply to ursodiol, such as complete biliary obstruction, are relevant because TUDCA is partly converted to UDCA in the body.
Legal status and quality
In the US, TUDCA is sold as a dietary supplement. FDA does not approve dietary supplements before they are marketed, and manufacturers generally do not have to show FDA evidence of safety or effectiveness (FDA). We found no published independent testing of TUDCA supplement content. The only US-approved product containing TUDCA, Relyvrio, has been withdrawn.
TUDCA is not a controlled substance and is not named on the WADA 2026 Prohibited List.
Key takeaways
- A taurine-conjugated form of UDCA. TUDCA is partly converted back to UDCA in the body, and its effects on liver tests closely match those of ursodiol.
- ALS hopes did not hold up. A 34-patient phase 2 trial was positive, but the 336-patient TUDCA-ALS phase 3 trial missed its primary endpoint and showed no survival benefit.
- Relyvrio is gone. The TUDCA–sodium phenylbutyrate combination was approved by FDA in 2022 and withdrawn in 2025 after the PHOENIX phase 3 trial failed.
- Liver data are about enzymes, not outcomes. Small trials show lower liver enzymes in PBC and chronic hepatitis, roughly matching UDCA, with no trials on hard clinical outcomes.
- No evidence for “on-cycle” liver protection. No study has tested TUDCA in people using anabolic steroids.
- Generally well tolerated. Diarrhea and other mild gastrointestinal effects are the main reported side effects at 0.5–2 g/day.
Sources
- Amylyx Pharmaceuticals. RELYVRIO (sodium phenylbutyrate and taurursodiol) for oral suspension, prescribing information, NDA 216660, 2022. FDA.
- Food and Drug Administration. Amylyx Pharmaceuticals, Inc.; Withdrawal of Approval of New Drug Application for RELYVRIO (Sodium Phenylbutyrate and Taurursodiol) for Suspension, 3 Gram/Packet and 1 Gram/Packet. Federal Register. August 29, 2025;90:42251 (FR Doc 2025-16646). Federal Register.
- National Center for Biotechnology Information. Tauroursodeoxycholic acid, PubChem CID 9848818. PubChem.
- Setchell KD, Rodrigues CM, Podda M, et al. Metabolism of orally administered tauroursodeoxycholic acid in patients with primary biliary cirrhosis. Gut. 1996;38(3):439–446. PubMed.
- Crosignani A, Battezzati PM, Setchell KD, et al. Tauroursodeoxycholic acid for treatment of primary biliary cirrhosis. A dose-response study. Dig Dis Sci. 1996;41(4):809–815. PubMed.
- Larghi A, Crosignani A, Battezzati PM, et al. Ursodeoxycholic and tauro-ursodeoxycholic acids for the treatment of primary biliary cirrhosis: a pilot crossover study. Aliment Pharmacol Ther. 1997;11(2):409–414. PubMed.
- Ma H, Zeng M, Han Y, et al. A multicenter, randomized, double-blind trial comparing the efficacy and safety of TUDCA and UDCA in Chinese patients with primary biliary cholangitis. Medicine (Baltimore). 2016;95(47):e5391. PubMed.
- Crosignani A, Budillon G, Cimino L, et al. Tauroursodeoxycholic acid for the treatment of HCV-related chronic hepatitis: a multicenter placebo-controlled study. Hepatogastroenterology. 1998;45(23):1624–1629. PubMed.
- Heubi JE, Wiechmann DA, Creutzinger V, et al. Tauroursodeoxycholic acid (TUDCA) in the prevention of total parenteral nutrition-associated liver disease. J Pediatr. 2002;141(2):237–242. PubMed.
- Kars M, Yang L, Gregor MF, et al. Tauroursodeoxycholic Acid may improve liver and muscle but not adipose tissue insulin sensitivity in obese men and women. Diabetes. 2010;59(8):1899–1905. PubMed.
- Elia AE, Lalli S, Monsurrò MR, et al. Tauroursodeoxycholic acid in the treatment of patients with amyotrophic lateral sclerosis. Eur J Neurol. 2016;23(1):45–52. PubMed.
- Albanese A, Ludolph AC, McDermott CJ, et al. Tauroursodeoxycholic acid in patients with amyotrophic lateral sclerosis: The TUDCA-ALS trial protocol. Front Neurol. 2022;13:1009113. PubMed.
- Lombardo FL, Spila Alegiani S, Mayer F, et al. A randomized double-blind clinical trial on safety and efficacy of tauroursodeoxycholic acid (TUDCA) as add-on treatment in patients affected by amyotrophic lateral sclerosis (ALS): the statistical analysis plan of TUDCA-ALS trial. Trials. 2023;24(1):792. PubMed.
- TUDCA-ALS Consortium. Safety and efficacy of tauroursodeoxycholic acid (TUDCA) as add-on treatment in patients affected by amyotrophic lateral sclerosis (ALS), NCT03800524. ClinicalTrials.gov.
- European Commission. TUDCA-ALS, grant agreement 755094: fact sheet and periodic reporting. CORDIS; CORDIS reporting.
- ALS Canada. TUDCA trial did not meet its endpoints. April 4, 2024. ALS Canada.
- MND Scotland. MND charities respond to TUDCA trial results. March 27, 2024. MND Scotland.
- Paganoni S, Macklin EA, Hendrix S, et al. Trial of Sodium Phenylbutyrate-Taurursodiol for Amyotrophic Lateral Sclerosis. N Engl J Med. 2020;383(10):919–930. PubMed.
- Paganoni S, Hendrix S, Dickson SP, et al. Long-term survival of participants in the CENTAUR trial of sodium phenylbutyrate-taurursodiol in amyotrophic lateral sclerosis. Muscle Nerve. 2021;63(1):31–39. PubMed.
- Jomaa AM, Khalid H, Abozait HJ, et al. Efficacy of Sodium Phenylbutyrate-Taurursodiol in Amyotrophic Lateral Sclerosis: A Systematic Review and Meta-Analysis. Ann Indian Acad Neurol. 2026;29(3):343–352. PubMed.
- Zucchi E, Musazzi UM, Fedele G, et al. Effect of tauroursodeoxycholic acid on survival and safety in amyotrophic lateral sclerosis: a retrospective population-based cohort study. EClinicalMedicine. 2023;65:102256. PubMed.
- Food and Drug Administration. Questions and Answers on Dietary Supplements. FDA.
- World Anti-Doping Agency. The 2026 Prohibited List. WADA 2026 Prohibited List.