Peptide class
Compounds investigated for their potential to influence fundamental aging mechanisms — telomere maintenance, epigenetic regulation, NAD+ metabolism, and mitochondrial function — rather than treating specific diseases.
| Compound | Mechanism | Primary Use | Profile |
|---|---|---|---|
| Epitalon (Epithalon) | Telomerase activation; pineal gland regulation; epigenetic modulation | Longevity research, telomere biology, pineal/melatonin regulation | View |
| GHK-Cu | Copper-mediated gene expression; collagen synthesis; antioxidant | Anti-aging skin research, wound healing, gene expression modulation | View |
| NAD+ (NMN / NR precursors) | NAD+ biosynthesis; sirtuin activation; mitochondrial function; DNA repair | Longevity research, metabolic health, cognitive aging, mitochondrial support | View |
Note: NAD+ precursors (NMN/NR) are small molecules rather than peptides, included here for research context given their mechanistic overlap with longevity peptide research.
Unlike disease-specific compounds, longevity-oriented peptides target fundamental mechanisms that are conserved across the biology of aging: telomere shortening (associated with replicative senescence), epigenetic drift (changes in gene expression patterns with age), declining NAD+ levels (which reduce sirtuin activity and DNA repair capacity), and mitochondrial dysfunction (impaired energy production and increased ROS). These are among the "hallmarks of aging" described by López-Otín et al. (2013) and updated subsequently. Compounds in this class target one or more of these hallmarks rather than specific organ pathology.
Epitalon (Ala-Glu-Asp-Gly) was developed by Vladimir Khavinson's group at the St. Petersburg Institute of Bioregulation and Gerontology from peptide extracts of the pineal gland. Research has reported telomerase activation and telomere lengthening in human somatic cell cultures, alongside regulation of melatonin production by the pineal gland and modulation of gene expression in aging tissues. GHK-Cu has been documented to modulate the expression of over 4,000 human genes toward a younger expression pattern in Broad Institute GEO analyses, suggesting epigenetic-adjacent effects through transcription factor interaction.
NAD+ (nicotinamide adenine dinucleotide) declines substantially with age — by approximately 50% between the ages of 40 and 60 in many tissues. NAD+ is an essential cofactor for sirtuins (SIRT1–7, deacetylases with roles in DNA repair, metabolic regulation, and stress resistance), PARPs (DNA repair enzymes), and CD38 (an NADase whose activity increases with age). NMN and NR are biosynthesis precursors that restore NAD+ levels and have been investigated in human trials, showing increases in blood NAD+ and some downstream biomarker changes, though long-term hard endpoint data (mortality, disease incidence) is not yet available.
The scientific field of longevity biology has expanded substantially since the identification of sirtuins, mTOR, and AMPK as conserved aging-regulatory pathways in the 2000s–2010s. Human trials of longevity-targeting compounds including NMN, NR, metformin (via TAME trial), and rapamycin analogues are ongoing. Epitalon's clinical research comes primarily from Khavinson's Russian group and has not been replicated in large Western trials.
Research has investigated compounds in this class for their potential role in extending healthspan (quality of life in aging) rather than necessarily lifespan — reducing age-related decline in muscle function, cognitive function, metabolic health, and tissue integrity. The compounds in this class are commonly reported in research contexts together (e.g. Epitalon + NMN, or Epitalon + GHK-Cu) by researchers pursuing multi-mechanism longevity intervention.
A tetrapeptide with the most specific telomerase-activation research profile of any compound on this site. Published research has investigated Epitalon for its potential role in telomerase activation in human cell cultures and animal models, with some human skin aging data from Khavinson's group. Commonly reported in cyclic protocols — typically 10–20 days of SubQ or IM injection once or twice annually in anecdotal research contexts.
Included here for its gene-expression-modulating properties that intersect with anti-aging biology, alongside its primary classification as a copper peptide. Plasma GHK levels decline with age, making restoration a longevity research rationale.
Small molecules (not strictly peptides) included for mechanistic completeness given substantial overlap with longevity peptide research contexts. Research has investigated NMN for its potential role in NAD+ restoration in multiple human trials at doses of 250–1000 mg/day oral, with results showing safe NAD+ restoration. Longer-term outcome data is pending.