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First, by enhancing fatty acid transport into the mitochondria, it theoretically ensures that a greater proportion of the energy deficit is filled by fat oxidation rather than muscle protein breakdown

While the drug initially showed promise in a Phase 2 study, a large Phase 3 trial failed to meet its primary endpoint, raising major doubts about efficacy.24 No trials of TUDCA alone have shown clear clinical benefit in ALS, and regulatory approvals for the combo have already been withdrawn in the U.S

Depletion of mitochondrial glutathione is associated with mitochondrial dysfunction, reduced ATP production, and increased cellular susceptibility to apoptosis

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