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Longevity & Anti-Aging

Peptides targeting hallmarks of aging including mitochondrial decline, cellular senescence, and tissue homeostasis.

Clinical Overview

Longevity & Anti-Aging

Peptides targeting hallmarks of aging including mitochondrial decline, cellular senescence, and tissue homeostasis.

3 peptides0 FDA-approvedSubcutaneous injection (SC) · intramuscular injection (IM) · intranasal (investigational) · IV · SC · IM · intranasal (oral NAD+ poorly absorbed; use NR · NMN precursors) · Topical (most common)Last reviewed · April 22, 2026

Longevity-focused peptides target the biological hallmarks of aging — mitochondrial dysfunction, cellular senescence, telomere attrition, and loss of proteostasis. Clinical use should focus on validated symptomatic endpoints rather than unproven claims of lifespan extension.

Mechanism Classes

  • Mitochondrial-targeted peptides

    SS-31 / elamipretide (Phase 3 for mitochondrial myopathy and dry AMD) and humanin (cytoprotective, anti-apoptotic) act directly on mitochondrial function and energetics.

  • Telomere / sirtuin modulators

    Epithalon is a synthetic tetrapeptide studied for telomerase activation and circadian/sleep effects. NAD+ (a coenzyme, not a peptide) fuels sirtuin signaling and is included here for common co-prescribing.

  • Tissue-homeostasis peptides

    GHK-Cu (copper-binding tripeptide) modulates broad gene-expression networks involved in tissue repair and antioxidant defense.

Regulatory Status

FDA-Approved

None FDA-approved in this category.

Investigational / Off-Label

  • Epithalon
  • NAD+
  • Humanin
  • SS-31 / Elamipretide
  • GHK-Cu

No peptide is FDA-approved for longevity indications. SS-31 is in Phase 3 for mitochondrial myopathy — the most advanced regulatory pathway in this class.

Evidence Base

Heterogeneous. SS-31 has multi-year Phase 3 safety and efficacy data. NAD+ has growing human data for metabolic and cognitive endpoints. Epithalon and humanin remain predominantly preclinical. No peptide has demonstrated human lifespan extension in controlled trials.

Primary-Literature References

37

Across 3 linked monographs

Prescribing Considerations

  1. 1Frame as investigational; do not position as disease-modifying or lifespan-extending.
  2. 2Focus on measurable endpoints: energy, sleep, cognition, body composition, inflammatory markers.
  3. 3Baseline labs: CMP, CBC, lipid panel, HbA1c, thyroid function, hs-CRP; consider IGF-1 and biological-age markers.
  4. 4Structure as time-limited cycles with periodic reassessment — avoid indefinite continuous therapy without clinical justification.
  5. 5NAD+ is administered IV, SC, or IM in compounded forms; oral precursors (NMN, NR) are supplements rather than prescribed peptides.
  6. 6Document informed consent around investigational long-term use.
Peer-reviewed clinical references · last reviewed April 22, 2026PeptidePrescriber · Clinical Reference

Peptides in this category(3)

Clinical monographs for each agent — dosing ranges, safety profile, evidence, and prescribing considerations.

LongevityLimited EvidenceIV · SC · IM · intranasal (oral NAD+ poorly absorbed; use NR/NMN precursors)

NAD+

Cellular energetics and mitochondrial support in age-related decline, metabolic dysfunction, and post-exertional recovery (all investigational; no FDA-approved indication for injectable NAD+)

Primary indication: Cellular energetics and mitochondrial support in age-related decline, metabolic dysfunction, and post-exertional recovery (all investigational; no FDA-approved indication for injectable NAD+)

NAD+ is a central redox coenzyme required for oxidative phosphorylation, glycolysis, the TCA cycle, and beta-oxidation. Beyond its redox role, NAD+ is a substrate consumed by three major enzyme families: sirtuins (SIRT1-7, NAD+-dependent deacylases regulating stress response, mitochondrial biogenesis, and metabolic homeostasis); poly-ADP-ribose polymerases (PARPs, which consume NAD+ during DNA damage repair); and CD38 (a cell-surface ectoenzyme that degrades NAD+ and increases with age). Age-related decline in tissue NAD+ is driven by increased CD38 activity and chronic PARP activation, contributing to mitochondrial dysfunction and cellular senescence. Exogenous NAD+ replenishment — via IV administration, or indirectly through oral NAD+ precursors nicotinamide riboside (NR) and nicotinamide mononucleotide (NMN) — is hypothesized to restore sirtuin activity, improve mitochondrial function, and attenuate age-related metabolic decline.

Read full guide

2 additional monographs in this category are in clinical review and will be published soon.

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