NMN (nicotinamide mononucleotide) is a direct NAD+ precursor that replenishes intracellular nicotinamide adenine dinucleotide pools through salvage pathway kinases, restoring substrate availability for NAD+-dependent enzymes including sirtuins, PARPs, and CD38/CD157. This mechanism addresses the age-related decline in NAD+ levels, thereby modulating multiple hallmarks of aging including mitochondrial dysfunction, genomic instability, and cellular senescence through sirtuin and PARP-mediated pathways. Published evidence demonstrates improvements in metabolic parameters, exercise capacity, and muscle insulin sensitivity in human trials, while preclinical studies report extended lifespan in rodent models accompanied by enhanced mitochondrial biogenesis and improved stress resistance; however, human longevity data remain limited to surrogate biomarkers and intermediate outcomes without prospective lifespan confirmation.
NMN (nicotinamide mononucleotide) is sold as a dietary supplement in the United States and is not FDA-approved as a drug for any indication, including longevity.
Available human data (e.g., Yoshino 2021) has focused on surrogate endpoints such as insulin sensitivity rather than hard outcomes like mortality. See the full profile for the current paper count and study details.
Current published human evidence is limited to surrogate endpoints and small trials. No pooled mortality or major-outcome hazard ratio currently exists for NMN in longevity contexts.
Published human trials to date have not identified major safety signals at studied doses, though long-term safety data and standardized dosing remain limited compared to approved pharmaceuticals.
Both target NAD+ repletion through different metabolic pathways. Evidence tiers are currently similar (Emerging) for both, based on surrogate-endpoint human data. See the NR profile for direct comparison.