TUDCA (Tauroursodeoxycholic Acid) for ALS
Also known as: Tauroursodeoxycholic acid, Taurursodiol
A bile acid with potent anti-apoptotic and ER stress-reducing properties studied independently and as part of Relyvrio for ALS.
Mechanism of Action
TUDCA stabilizes the mitochondrial membrane by preventing BAX translocation and cytochrome c release. It also acts as a chemical chaperone, reducing ER stress-induced unfolded protein response (UPR) activation. In ALS, these dual actions protect motor neurons from the convergent stress pathways.
General mechanism: Bile acid with anti-apoptotic (mitochondrial stabilization) and chemical chaperone (ER stress reduction) properties.
Current Evidence
Independent pilot studies demonstrated changes in outcome measures trending toward slower decline. As part of AMX0035/Relyvrio, the CENTAUR trial reported outcomes in clinical trials. Available as a supplement. Optimal dosing for neurological applications is still being established in ongoing research.
Clinical Status: Available as a supplement. Was part of FDA-approved Relyvrio combination. Independent trials for ALS ongoing.
Safety Profile
Very well-tolerated. Mild GI effects at high doses. Long history of safe use as a supplement and in bile acid replacement.
Key Research Questions
- What is the optimal standalone TUDCA dose for neuroprotection?
- Does TUDCA penetrate the blood-brain barrier sufficiently at oral doses?
- Can TUDCA biomarkers (bile acid profiles) predict response?