Longevity is the only goal on this site whose endpoint cannot be measured by any study in the literature. A lifespan trial in humans takes decades. Nothing cited on this page — or on any competitor’s page — has run for decades. Batch certificates are published at /coa.
GHK peptide as a natural modulator of multiple cellular pathways in skin regeneration. PMC4508379; The potential of GHK as an anti-aging peptide. PMC8789089; Effects of NMN on glucose and lipid metabolism: meta-analysis of RCTs. PMID 39531138; Safety and metabolism of long-term NIAGEN (nicotinamide riboside chloride). PMC6611812; The mitochondrial-derived peptide MOTS-c: a player in exceptional longevity? PMID 26289118
What “longevity research” actually studies
Since lifespan cannot be an endpoint in a practical human trial, the field works on proxies: biomarkers thought to track biological ageing, or age-related declines that can be measured over months.
That is legitimate science and it is also a substitution. A compound that moves a proxy has moved a proxy. Whether that translates into more years, or better years, is precisely the question the proxy exists because nobody can answer directly.
Every longevity claim in this category rests on that substitution. Most pages don’t mention it.
The age-decline observation, and its limit
GHK occurs naturally in human plasma and reported levels fall with age — around 200 ng/ml at 20, roughly 80 ng/ml by 60. That decline is the observation the regenerative interest is built on (see the GHK-Cu overview).
It is an association. A molecule declining with age does not establish that restoring it reverses anything, and correlation between a falling biomarker and ageing is exactly the kind of evidence that looks stronger than it is.
The same caution applies more sharply still: natural presence at nanogram concentrations says nothing about the safety of a manufactured, far higher-concentration, injected form.
Where the GHK-Cu evidence actually sits
The best-characterised finding is collagen synthesis in fibroblast culture. Reviews describe GHK modulating collagen and glycosaminoglycan turnover and influencing metalloproteinases.
Human work has concerned topical skincare programmes and a specific wound gel — those results address the formulations they used, not an injectable pen (more under peptides for skin). Formulation is not incidental for this molecule: GHK-Cu is a defined copper coordination complex whose behaviour depends on pH, concentration and counter-ions.
Where the NAD+ evidence sits
NAD+ is a coenzyme, not a peptide (what NAD+ is), and its human trial literature is mostly about the oral precursors NMN and nicotinamide riboside rather than NAD+ itself; it is also listed on the energy goal page.
Those trials show the biomarker moves reliably — dose-dependent increases in cellular NAD+ in humans. The downstream outcomes are inconsistent by endpoint: a meta-analysis of NMN trials found no significant benefit on fasting glucose, insulin, HbA1c or lipids, while a separate review reported improvements in physical performance measures.
For a longevity claim that pattern is the whole problem in miniature. The proxy responds. What the proxy is standing in for remains unmeasured.
MOTS-c and the longevity literature
MOTS-c (what MOTS-c is) appears in papers explicitly asking whether it plays a role in exceptional longevity. That framing is a research question, not a finding, and the underlying work is preclinical — cell culture and rodent models, with no published human efficacy trial.
Why this page is shaped this way
We could write a confident longevity page. The mechanistic material is there, the biomarkers are real, and nobody would be able to disprove it within the lifetime of the claim — which is precisely why it would be irresponsible.
What we can evidence is what is in the pen: identity, content, purity, sterility, batch traceability, third-party tested per lot with the certificate reachable from its QR code. Neither compound holds a marketing authorisation.
Further reading: what are peptides?, mitochondrial peptides, why these compounds are not EMA-authorised.
