Genuinely novel biology — a peptide written into mitochondrial DNA rather than the nucleus, which was not thought to happen. The science is interesting. The human evidence is about as early as it gets.
Regulatory status. Research compound — no FDA approval. Very early human research stage. That is the app’s own field, reproduced here rather than summarised. It means no regulator has reviewed a manufacturer’s evidence for identity, purity, potency or safety in people for this compound, so nothing below is a marketing claim about a product you can buy.
Purity, identity and concentration are therefore unverified by anyone but whoever made the vial. The storage rule in the fact box below is general practice for this formulation rather than a specification for a particular product: General handling practice for this formulation. Your supplier’s own insert or COA overrides anything here.
This page names no vendor, no clinic and no testing service, and there is no discount code anywhere on this site — the moment a page like this recommends where to buy, it stops being information.
Established clinical use Mitochondria carry their own small genome, and it was long assumed to encode only the handful of proteins needed for the electron transport chain. MOTS-c is one of a small family of mitochondrial-derived peptides — short sequences encoded within mitochondrial DNA that act as signalling molecules elsewhere in the cell and in circulation. That was a real addition to the picture of how mitochondria communicate with the rest of the body, and it is why the discovery attracted attention beyond the longevity field.
Animal-only or theoretical Functionally, MOTS-c is reported to activate AMPK and to improve glucose uptake in skeletal muscle through a route that does not depend on insulin. That is the basis for the exercise-mimetic framing: AMPK activation is one of the things exercise does, and circulating MOTS-c rises with exercise and declines with age. Animal work reports improved metabolic measures and, in mice, extended healthspan.
The app records no half-life, because none has been published for the material in circulation, which is why the fact box above carries no pharmacokinetic rows.
Animal-only or theoretical The peptide was described in 2015. Human data consists of observational work — circulating levels correlating with metabolic status, age and exercise — and a small amount of early interventional work. There is no published randomised controlled trial reporting a clinical outcome from administering it.
That is a much thinner base than the enthusiasm around it suggests, and the app’s own drawbacks list is right to lead with it. "Very early human research stage" is the accurate description, and a compound at that stage sold on animal healthspan data is the familiar pattern this site keeps flagging.
The observational finding is also worth reading carefully. Higher circulating MOTS-c in metabolically healthier, more active people is consistent with it being a marker of mitochondrial function rather than a cause of it. Administering the marker does not necessarily produce the state, and distinguishing those two is exactly what an interventional trial is for.
The app’s panel is glucose-focused — fasting glucose, HbA1c, a metabolic panel — which follows the proposed mechanism sensibly. The HbA1c page covers why those two markers can disagree. Exercise capacity assessed consistently is the other honest measure, and consistently is the operative word.
Animal-only or theoretical There is no approved product and no reference standard. Identity and purity rest entirely with whoever made the vial, and for a sixteen-residue peptide sold into an enthusiastic market, that is not a small caveat. This site names no vendor and no testing service.
The reasonable position is that this is real and novel biology at a stage where nobody can say what administering it does to a person over months. Anyone using it should be treating their own record as the only data available, and anyone with a metabolic condition should be raising it with the clinician managing that.
Off-label or community practice Reproduced from the app’s reference so you can see what it holds, not as a recommendation. Which row applies to a particular person, if any, is a clinical decision this page does not make — and rows describing supraphysiological or post-cycle use are filtered out before this table is built, so what you see here is a subset.
| Label | Amount | Route and frequency | Duration recorded |
|---|---|---|---|
| Research protocol | 5-10mg | SubQ 2-3x weekly | 4-8 weeks |
The panel below is the app’s own monitoring note for MOTS-c, verbatim. The analytes in it that have a page here are linked; those pages cover what each one measures, which assay produced it and how to read a trend.
From the app’s own entry, and the first two items are the honest summary of everything else on this page.
From the app’s interaction data, filtered so no rule naming a compound this site does not publish appears. Not exhaustive, and not a safety clearance: a combination that is not listed is one nobody has documented here, which is not the same as one that is fine. The combination checker has the rest.
SS-31 targets the inner mitochondrial membrane (cardiolipin) while MOTS-c activates AMPK and nuclear gene expression. Together they address mitochondrial function at two distinct levels — membrane integrity and metabolic signaling.
What to watch: Energy and exercise capacity self-assessment, VO2 max if available, fasting glucose.
It activates one of the pathways exercise activates, in animal and cell work. Exercise does a great many other things at the same time, and no human trial has compared them. "Exercise mimetic" is a mechanism claim being used as an outcome claim.
Observational work relating circulating levels to metabolic status, and early interventional work. No published randomised trial reporting a clinical outcome from administering it.
Because none has been published for the material people are using, so the app holds none.
That is the hypothesis and it is not established. A level that tracks mitochondrial health may be a marker rather than a cause, and administering a marker does not necessarily produce the state it marks.
Named rather than linked. Publisher URLs move, and a citation that resolves to a 404 two years from now is worse than one you can search for by name — every entry below is findable from the title and year alone.
At this stage of evidence, your own dated record is the entire dataset. TherapyLog keeps it beside the metabolic panel.
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