Urolithin A is a postbiotic metabolite derived from dietary ellagitannins that activates mitophagy—the selective autophagy of dysfunctional mitochondria—primarily through PINK1/Parkin pathway signaling and potentially via direct mTORC1 inhibition. By clearing senescent mitochondria and restoring mitochondrial quality control, it targets the hallmark aging process of mitochondrial dysfunction and bioenergetic decline. In preclinical models, urolithin A extends lifespan in C. elegans and improves mitochondrial respiration and exercise capacity in aged rodents and humans; limited human data from Phase 2 trials demonstrate improvements in muscle strength and mitochondrial function in older adults, though effects on longevity endpoints remain to be established. Its mechanism positions it as an indirect modulator of multiple aging pathways including energy metabolism, oxidative stress, and cellular senescence through restoration of mitochondrial homeostasis.
Urolithin A is sold as a dietary supplement and is not FDA-approved as a drug for any indication. It is studied as a mitophagy activator.
Phase II muscle-outcome data (Amazentis) has been published. Geroevidence's profile is currently under editorial review as additional trial data is indexed.
Urolithin A is mechanistically distinct from NAD+ precursors like NMN and NR but is often discussed alongside them in mitochondrial-health longevity research.
Available Phase II data has not identified major safety signals at studied doses; broader long-term human safety data remains limited.
Urolithin A acts on mitophagy rather than NAD+ metabolism directly, but is often studied alongside NMN and NR in mitochondrial-health longevity research. See the NMN profile for comparison.