Modified Urolithin A Compound Extends Survival, Improves Movement in ALS Mice
A lab-modified version of the gut-microbiome compound urolithin A, called UA-30, extended median survival by 8.5 days and improved motor performance in mice with an ALS-like disease, according to a study published September 15, 2026, in the Journal of Clinical Investigation.
Researchers gave SOD1G93A mice, a standard ALS model, UA-30 by mouth once daily for 6 weeks, starting at 13 weeks of age after motor decline had begun. Doses of 25, 50 or 100 mg/kg were compared with the ALS drug riluzole (10 mg/kg) and a saline placebo. Treated mice lived a mean of 171.5 days versus 161.9 days for untreated mice, an 8.5-day gain in median survival. The high dose beat the low dose by 19.36% on pole-climbing, 22.11% on wire-hang endurance and 8.39% on rotarod balance, and beat riluzole by up to 64.5% on wire-hang endurance in males. UA-30 also cut muscle scarring, preserved spinal motor neurons and reached the brain and spinal cord within an hour of a single oral dose.
UA-30 Extends Mean Survival to 171.5 Days vs 161.9 Days in ALS Mice
UA-30 is a lab-modified version of urolithin A, a compound gut bacteria make from polyphenols in foods like pomegranates, walnuts and berries; natural urolithin A absorbs poorly into the bloodstream and brain, prompting the redesign. UA-30 blocked a protein called RalA, lowering signaling through the ERK pathway and stabilizing FOXO3a, a protein that switches on genes for PINK1 and Parkin — the proteins that tag damaged mitochondria, the cell's energy factories, for recycling, a process called mitophagy. Blocking that cleanup process with a separate drug, Mdivi-1, erased UA-30's benefits on movement, survival, muscle and nerve preservation, confirming mitophagy as the mechanism.
This is a mouse study of a synthetic compound not available to humans, and animal results often fail to predict outcomes in people with ALS. The survival benefit reached significance mainly in male mice, and higher doses did not consistently outperform lower ones. Funding and conflicts were not reported in the available record; UA-30 was synthesized at Sichuan University.
Data Panel
- Who
- SOD1G93A transgenic mice, a genetic model of ALS; male and female cohorts analyzed separately; treatment started at 13 weeks of age
- Design
- Placebo-controlled preclinical study; oral gavage once daily for 6 weeks; UA-30 (25, 50 or 100 mg/kg) compared with riluzole (10 mg/kg) and a saline placebo
- Dose
- UA-30 25, 50 or 100 mg/kg by mouth once daily for 6 weeks; riluzole comparator 10 mg/kg
- Primary result
- Mean lifespan 171.5 ± 8.7 days with UA-30 (100 mg/kg) vs 161.9 ± 8.1 days without, an 8.5-day gain in median survival
- Secondary
- High-dose UA-30 beat low-dose by 19.36% on pole-climbing, 22.11% on wire-hang endurance, 2.30% on grip strength and 8.39% on rotarod; beat riluzole by 64.5% (males) and 39.7% (females) on wire-hang endurance
- Funding / conflicts
- Not reported in the available record; UA-30 was synthesized by the State Key Laboratory of Biotherapy, West China Hospital, Sichuan University
Dr. Axe's Take
This tracks with core ALS biology: mitochondria wear out and never get cleared, and UA-30 restores the cleanup crew — PINK1 and Parkin — through a pathway involving RalA and FOXO3a. UA-30 is a synthetic drug candidate, not a supplement, and I would not chase urolithin A products expecting the same effect, since researchers built UA-30 specifically because natural urolithin A barely reaches the brain. For mitochondrial support today, eat polyphenol-rich foods — pomegranate, walnuts, berries — to feed the gut bacteria that make urolithin A, and keep moving; exercise independently supports mitophagy.
— Dr. Axe