Mitochondria need their inner membrane intact to turn fuel into usable energy. SS-31 is studied because it binds a fat found almost only in that membrane.
SS-31 · Mitochondrial membrane peptide
Cells need more than fuel to make energy. The machinery that converts fuel into ATP, the cell’s energy currency, sits in the inner membrane of the mitochondrion and depends on that membrane keeping its shape. SS-31 is a small synthetic peptide studied because it attaches to cardiolipin, a specialised fat in that membrane. Evidence runs from isolated mitochondria to randomised trials in rare mitochondrial disease.
SS-31, known in clinical work as elamipretide, is a synthetic tetrapeptide (four amino acids) from the Szeto-Schiller series. Its sequence alternates aromatic and positively charged residues, which lets it pass through both mitochondrial membranes and concentrate in the inner one.
There it binds cardiolipin, a phospholipid found almost exclusively in the inner mitochondrial membrane. Cardiolipin helps hold the enzyme complexes of the electron transport chain, the assembly line that passes electrons along to make ATP, in their working arrangement, and it is readily damaged by oxidative stress: reactive molecules outpacing the systems that keep them in check. SS-31 does not act on a receptor. The proposed mechanism is physical: by associating with cardiolipin it is thought to stabilise membrane structure and support electron flow, which is why it appears across cardiac, kidney, ageing and mitochondrial-disease research rather than one field (Szeto 2014).
Laboratory and animal work established the mechanism. In isolated mitochondria and in a rat model of kidney ischaemia, SS-31 was shown to interact with cardiolipin and to restore ATP production after a period without blood flow (Birk et al. 2013).
Human trials have used subcutaneous elamipretide, the pharmaceutical form. TAZPOWER, a randomised crossover trial in 12 people with Barth syndrome, a rare genetic disorder of cardiolipin metabolism, did not meet its primary endpoints in the blinded phase; improvements in six-minute walk distance and knee-extensor strength were reported in the open-label extension (Reid Thompson et al. 2021). MMPOWER-3, a phase 3 trial in 218 adults with primary mitochondrial myopathy, did not meet its primary endpoints of walk distance and fatigue (Karaa et al. 2023). PROGRESS-HF, a 28-day phase 2 trial in 71 patients with heart failure with reduced ejection fraction, found no change in ventricular volume versus placebo (Butler et al. 2020).
In September 2025 the US FDA granted accelerated approval to Forzinity (elamipretide) for Barth syndrome in patients weighing at least 30 kg, on the basis of knee-extensor strength as an endpoint reasonably likely to predict benefit, with a confirmatory randomised trial required (FDA 2025).
The approval is narrow: one rare disease, one weight threshold, one surrogate endpoint, and a confirmatory trial still owed. It does not establish that elamipretide helps recovery, energy or ageing in people without a mitochondrial disorder, and the two larger trials in broader populations missed their primary endpoints.
Every human result comes from pharmaceutical-grade elamipretide given under trial conditions. Whether cardiolipin binding produces a measurable functional change in healthy tissue is unresolved, and the mechanism-level findings come from isolated mitochondria and rodents. These findings do not establish equivalent quality, safety or clinical effects for a research-grade vial of SS-31.
SS-31 (elamipretide) is not an approved medicine in Australia. In the United States, Forzinity (elamipretide injection) received FDA accelerated approval on 19 September 2025 for Barth syndrome in patients weighing at least 30 kg, subject to a confirmatory trial; that approval applies to the pharmaceutical product and indication only, not to this research material.
Sources and status checked 2026-09-22
SS-31 — sizes and pricing