Almost everything else in this reference acts on a receptor at the cell surface. This one accumulates inside the mitochondrion and binds a specific lipid there, which is a genuinely different kind of intervention and has a genuinely different evidence base.
Regulatory status. Phase II clinical trials ongoing (Barth syndrome, heart failure). Not FDA approved. Research compound. 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 Cardiolipin is a phospholipid found almost exclusively in the inner mitochondrial membrane, where it shapes the cristae and organises the electron transport chain complexes into functional supercomplexes. When cardiolipin is damaged — by oxidation, or by a genetic defect in the enzyme that remodels it — the membrane architecture degrades, electron transport becomes inefficient, and the mitochondrion leaks more reactive oxygen species, which damages more cardiolipin. It is a self-reinforcing failure.
SS-31, also called elamipretide, is a four-amino-acid peptide with an alternating aromatic-cationic structure that causes it to concentrate in the inner mitochondrial membrane at concentrations far above the surrounding cytosol, where it associates with cardiolipin. The proposed effect is to stabilise the architecture and interrupt that cycle. Animal-only or theoretical Preclinical work across ischaemia-reperfusion, heart failure and age-related mitochondrial decline supports it consistently.
Established clinical use This compound has had a real clinical programme, which distinguishes it sharply from most research peptides. It has been studied in primary mitochondrial myopathy, in Barth syndrome — a rare genetic disorder of cardiolipin remodelling, which is about as clean a test of the mechanism as biology offers — and in heart failure and other indications.
The results have been mixed rather than triumphant. A phase III trial in primary mitochondrial myopathy did not meet its primary endpoint. The Barth syndrome work, conducted in a very small population with extension data, produced signals that the sponsor pursued toward approval. Heart failure trials have not delivered a clear positive. The overall picture is a well-founded mechanism that has been hard to convert into endpoints, which is a common outcome for mitochondrial therapeutics and not a disqualification of the idea.
That is a far more informative position than "promising preclinical data", and it is the reason this page can say something concrete. It also means the longevity framing — which the app’s entry reflects — runs ahead of the evidence: nothing in the programme measured ageing, and the populations studied had specific diseases.
Animal-only or theoretical There is no approved product. What is available is research-supply material, and for a compound whose entire function depends on a precise aromatic-cationic sequence reaching an intracellular compartment, purity is not a peripheral concern. This site names no vendor and no testing service. The app’s own drawbacks list flags sourcing and expense before anything else, which is the right ordering.
The app records no half-life or time to peak, because none is published for the preparations in circulation, which is why the fact box above has no pharmacokinetic rows. It also records no meaningful monitoring: there is no blood test that reflects mitochondrial function well enough to follow a trend against, and the honest assessment markers are exercise capacity and how you actually feel, measured the same way each time.
The dosing rows above include a performance-framed entry that survives this site’s filters, and it is worth saying that nothing in the trial programme studied that use. The amounts in trials were set for disease indications under monitoring that does not exist outside one. Anyone considering this should be having that conversation with a clinician who knows their cardiac history in particular, given where the trials were run.
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 |
|---|---|---|---|
| Longevity and Mitochondrial | 5-10mg | SubQ 3-5x weekly | 4-8 weeks on / 4 weeks off |
| Clinical trial dose | 4mg/kg IV in trials | Physician administered | Study protocol |
| Research Protocol | 1–3mg/day | SubQ injection | 4–12 weeks |
The panel below is the app’s own monitoring note for SS-31, verbatim. None of the analytes it names has a page here yet.
From the app’s own entry, and it is honest: cost, sourcing and the absence of established dosing are the practical barriers, ahead of any adverse effect.
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.
Mixed. The phase III in primary mitochondrial myopathy missed its primary endpoint; the Barth syndrome work in a very small population produced signals the sponsor pursued; heart failure trials have not delivered a clear positive. A real programme with an unresolved result is still far more than most compounds here have.
Nothing in the clinical programme measured ageing. The longevity framing comes from the mechanism — mitochondrial decline is a hallmark of ageing — and from preclinical work, not from a human outcome.
Because the app holds none for the material in circulation. Duration figures quoted elsewhere are not coming from a characterisation of what people are actually using.
Nothing on a routine panel reflects mitochondrial function usefully. Exercise capacity measured consistently is the honest proxy, which means measuring it the same way each time rather than comparing impressions.
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.
With no marker to follow, a consistent measure of what you can actually do is the whole dataset. TherapyLog keeps it beside the dose.
Save this dose to your log