Rankings / Metabolic Health

TUDCA (tauroursodeoxycholic acid)

Metabolic Health · Bile acid / chemical chaperone

Tier B+

Reviewed by Read Off Label · Last reviewed · How we grade

bile-acidhepatoprotectioner-stressnafldotc
7.1 / 10
Tier B+
Ev 6 Bn 5 Sf 9

Bottom line

Read Off Label grades TUDCA (tauroursodeoxycholic acid) as B+ (7.1/10) based on moderate evidence, moderate benefit magnitude, and a low-risk safety profile.

Tauroursodeoxycholic acid is the taurine conjugate of UDCA — more hydrophilic and slightly more cytoprotective than UDCA itself.

Studied, labeled, or reported-use context: 250-500 mg/day biohacker hepatoprotection; 500-1500 mg/day clinical PBC range; 1750 mg/day in… — Approved in China and Italy for cholestatic disease; was an active ingredient (as taurursodiol) in FDA-approved Relyvrio/AMX0035 for ALS — withdrawn after PHOENIX Phase 3 failure; sold OTC in US as dietary supplement; not individualized guidance.

What the evidence says

Tauroursodeoxycholic acid is the taurine conjugate of UDCA — more hydrophilic and slightly more cytoprotective than UDCA itself. **Clinical anchors**: Ma 2016 (Medicine) n=199 China PBC trial — TUDCA non-inferior to UDCA at 500-1500 mg/day with possible superior pruritus relief; Kars 2010 (Diabetes) 1750 mg/day x 4 wk improved hepatic and muscle insulin sensitivity in obese subjects (no adipose effect). **Major 2024 negative ALS readout**: AMX0035/Relyvrio (combination of sodium phenylbutyrate + taurursodiol) was FDA-approved September 2022 for ALS based on a controversial Phase 2 signal, but the larger Phase 3 **PHOENIX** trial (n=664; 48 weeks) MISSED its primary ALSFRS-R endpoint (p=0.667) in April 2024. Amylyx discontinued marketing October 2024; FDA formally withdrew approval August 2025. The taurursodiol component was hypothesized to drive efficacy via ER-stress/UPR reduction in motor neurons — its failure substantially weakens the broader "TUDCA for neurodegeneration" narrative biohacker writeups often invoke. **Mechanism nuance**: a 2024 bioRxiv preprint (now PMC11809307) on Saccharomyces cerevisiae challenged the classical chemical-chaperone model — TUDCA may instead form micelles that reduce drug bioavailability and let cells adapt to ER stress. The cytoprotective phenotype is real but the mechanism is less settled than commonly presented. **Evidence summary**: clinical use is established for cholestatic liver disease; NAFLD and MASLD evidence is limited and uses higher monitored doses; broader "neuroprotection / longevity" claims rest largely on preclinical data and a failed ALS trial. Typical supplement-channel doses (250-1000 mg/day) are below the cholestasis-trial range. Distinct from UDCA (Ursodiol/Actigall) — UDCA is the unconjugated parent; TUDCA is the more polar taurine conjugate, marginally more potent in vitro but with similar clinical effect at equimolar doses.

Mechanism

Hydrophilic conjugated bile acid (taurine + ursodeoxycholic acid) endogenously present at trace levels in humans; acts as a chemical chaperone reducing endoplasmic reticulum stress and unfolded protein response (UPR) — blunts PERK/eIF2α/ATF4/IRE1α/JNK/CHOP signaling; activates hepatic FXR and Nrf2 pathways in cholestasis; inhibits CHOP-DR5-caspase-8 apoptotic cascade; replaces toxic hydrophobic bile acids in the bile pool; 2024 yeast study challenges the classical chaperone framing — suggests TUDCA may instead form micelles that reduce drug bioavailability and let cells adapt to ER stress

Studied, labeled, or reported dose & route

250-500 mg/day biohacker hepatoprotection; 500-1500 mg/day clinical PBC range; 1750 mg/day in insulin-sensitivity trial; ~10-13 mg/kg/day typical; food coadministration appears in reported protocols

This records doses and routes described in studies, approved labeling, clinical practice, or documented use. It is not individualized guidance and does not establish safety; context changes with indication, formulation, health history, monitoring, and other medicines.

Citations

A link means the source informed this entry; it does not mean every claim on the page comes from that source. If a citation looks wrong or you want a claim re-checked, send a correction.

Common questions

What does the evidence show about TUDCA (tauroursodeoxycholic acid)'s effects?
Read Off Label rates the evidence for TUDCA (tauroursodeoxycholic acid) as Moderate and the benefit magnitude as moderate, producing an overall grade of B+ (7.1/10). Tauroursodeoxycholic acid is the taurine conjugate of UDCA — more hydrophilic and slightly more cytoprotective than UDCA itself.
What safety findings are reported for TUDCA (tauroursodeoxycholic acid)?
TUDCA (tauroursodeoxycholic acid) has a low risk profile in the database. Low (well-tolerated; rare GI symptoms — diarrhea/bloating most common; theoretical interaction with bile acid sequestrants and insulin/insulin sensitizers; pregnancy and lactation safety data are insufficient) Legal status: Approved in China and Italy for cholestatic disease; was an active ingredient (as taurursodiol) in FDA-approved Relyvrio/AMX0035 for ALS — withdrawn after PHOENIX Phase 3 failure; sold OTC in US as dietary supplement (gray area).
What doses or routes are reported for TUDCA (tauroursodeoxycholic acid)?
250-500 mg/day biohacker hepatoprotection; 500-1500 mg/day clinical PBC range; 1750 mg/day in insulin-sensitivity trial; ~10-13 mg/kg/day typical; food coadministration appears in reported protocols This is context from studies, approved labeling, clinical practice, or documented use; it is not individualized guidance and does not establish safety.
How does TUDCA (tauroursodeoxycholic acid) work?
Hydrophilic conjugated bile acid (taurine + ursodeoxycholic acid) endogenously present at trace levels in humans; acts as a chemical chaperone reducing endoplasmic reticulum stress and unfolded protein response (UPR) — blunts PERK/eIF2α/ATF4/IRE1α/JNK/CHOP signaling; activates hepatic FXR and Nrf2 pathways in cholestasis; inhibits CHOP-DR5-caspase-8 apoptotic cascade; replaces toxic hydrophobic bile acids in the bile pool; 2024 yeast study challenges the classical chaperone framing — suggests TUDCA may instead form micelles that reduce drug bioavailability and let cells adapt to ER stress

This is an independent synthesis of published research by a non-clinician. Scores are opinions supported by citations, not prescriptions. See the full disclaimer and methodology for how this score was produced and what it does and doesn't mean.