Peptides studied across the aging axis — senescence, NAD+, and resilience.
Longevity research examines peptides that act on the hallmarks of aging: cellular senescence, mitochondrial decline, telomere maintenance, NAD+ metabolism, and the gradual loss of circadian and hormonal regulation. The goal in most models is healthspan — preserving function — rather than a single disease endpoint.
Compounds studied here often originate as endogenous regulatory peptides whose expression falls with age. Because aging endpoints are slow and multifactorial, this area leans heavily on biomarker studies, model organisms, and mechanistic work rather than large outcome trials.
Mitochondrially-encoded peptide with reported insulin-sensitizing activity.
View profileSynthetic tetrapeptide investigated for telomerase activity and circadian effects.
View profileSmall-molecule NNMT inhibitor (often catalogued alongside peptides).
View profileEssential redox cofactor central to mitochondrial bioenergetics and sirtuin activity.
View profileThe hallmarks of aging — cellular senescence, mitochondrial decline, telomere maintenance, NAD+ metabolism, and loss of circadian and hormonal regulation — usually with healthspan as the goal.
Aging endpoints are slow and multifactorial, so research relies on biomarkers, model organisms, and mechanistic work rather than large outcome trials.
Many are endogenous regulatory peptides whose expression falls with age, studied as candidates to restore more youthful signaling.
How to weigh this evidence
Preclinical, observational, and randomized findings carry very different weight. The evidence hierarchy shows how to rank what you read before drawing conclusions.