A four-amino-acid peptide that binds cardiolipin inside mitochondria. FDA-approved in 2025 as Forzinity for Barth syndrome.
Also called Elamipretide, Forzinity, MTP-131, Bendavia, Szeto-Schiller peptide 31, D-Arg-Dmt-Lys-Phe-NH2
SS-31 is a small synthetic peptide, four amino acids long, that slips into cells and sticks to cardiolipin, a fat found almost only on the inner membrane of mitochondria. Cardiolipin holds the energy-making machinery of the cell in place. When it is damaged or abnormal, mitochondria make less ATP and leak more reactive oxygen species. SS-31 is designed to stabilize that membrane.
In September 2025 the FDA gave it accelerated approval under the brand name Forzinity for Barth syndrome, a rare inherited disease in which cardiolipin is built wrong. The approval is narrow and rests on thin data: 12 patients in a crossover trial that missed both primary endpoints, followed by an open-label extension in which knee-extensor strength rose. The company has to run a confirmatory placebo-controlled trial to keep the approval.
Outside Barth syndrome the human record is mostly negative. The largest trial, MMPOWER-3 in 218 adults with primary mitochondrial myopathy, did not beat placebo on walking distance or fatigue. Trials in heart attack and dry macular degeneration also missed their primary endpoints. The anti-aging reputation comes from mouse studies, where single doses restored muscle energy output in old animals. No trial has tested it as an anti-aging drug in healthy people.
What it binds to, and what happens inside the body after that, step by step.
SS-31 carries three positive charges that are balanced by aromatic rings, which lets it cross cell membranes and collect on the inner mitochondrial membrane. There it binds cardiolipin. Binding keeps cardiolipin from turning cytochrome c into a peroxidase that damages the membrane, and it helps keep the folds (cristae) of the inner membrane intact so the electron transport chain can make ATP.
Human results and animal results are kept apart below. A result in rats tells you a mechanism is plausible. It does not tell you what happens in a person.
Grade A here means an approved drug exists, not that the trials were positive. Most randomized trials missed their primary endpoints: mitochondrial myopathy (MMPOWER-3, 218 people), heart attack (EMBRACE STEMI), dry macular degeneration (ReCLAIM-2) and the 12-week controlled phase of the Barth syndrome trial. The approval rests on knee-extensor strength gains in 8 to 10 Barth patients during an open-label extension with no placebo arm; a separate company analysis compared them with untreated natural-history patients. The energy and anti-aging effects seen in old mice have not been tested in healthy humans.
218 adults with genetically confirmed primary mitochondrial myopathy
40 mg/day for 24 weeks did not beat placebo on 6-minute walk distance or patient-reported fatigue, the two primary endpoints.
Read the study12 patients with Barth syndrome, crossover design, then 10 in open-label extension
Neither primary endpoint was met in the 12-week placebo-controlled phase; at 36 weeks open-label, walk distance rose 95.9 m and the symptom score fell 2.1 points.
Read the study10 patients with Barth syndrome entering extension, 8 reaching week 168
6-minute walk distance improved a cumulative 96.1 m at week 168, with no placebo arm for comparison.
Read the study8 treated patients vs 19 untreated natural-history controls
Treated patients walked 91.0 m farther at week 76 and had 56.7 N more muscle strength than matched untreated patients.
Read the study30 adults with primary mitochondrial myopathy
Walk distance was 19.8 m higher on drug than placebo, not statistically significant (P = 0.08); fatigue scores improved.
Read the studyAdults with first anterior ST-elevation heart attack undergoing stenting
A 1-hour infusion did not reduce infarct size measured by CK-MB or by cardiac MRI.
Read the study176 adults aged 55+ with dry AMD and geographic atrophy
Daily 40 mg for 48 weeks missed both primary endpoints (low-light vision and atrophy growth); some secondary retinal measures favored the drug.
Read the studyAged (26-month) female mice, 8 weeks of treatment
SS-31 restored maximum mitochondrial ATP production and made old muscle more fatigue resistant, without adding more mitochondria.
Read the studyThese are questions the published research has not answered.
Approved September 19, 2025 under the accelerated approval pathway, based on knee-extensor strength as an intermediate endpoint. The FDA requires a post-approval randomized, double-blind, placebo-controlled trial to confirm real-world benefit. Approval followed a 10-6 advisory committee vote in October 2024 and a complete response letter in May 2025. Not approved for mitochondrial myopathy, heart failure, eye disease or aging. Not named on the 2026 WADA Prohibited List.
No human half-life has been published for SS-31 (Elamipretide), so we do not draw a clearance curve. Half-lives quoted online for it are usually estimates from animal data.
This table records the doses that trials and approved labels used, with the source for each row. It is a record of research, not a recommendation, and it is open to free members.
Which symptoms are expected and which mean stop and get help: side effects and red flags.
Tap a claim to see what the studies found.
Old mice given SS-31 regained muscle energy output and exercise tolerance. No human trial has measured aging outcomes, and the large human trials in muscle disease did not show clear functional gains.
MMPOWER-3, the biggest trial at 218 patients, found no improvement in walking distance or fatigue compared with placebo. Healthy people have not been studied.
It lowers mitochondrial oxidant production in lab studies, but it works by binding cardiolipin and protecting membrane structure, not by mopping up free radicals in the bloodstream.
The approval covers one rare genetic disease, Barth syndrome, on an accelerated basis, and depends on a confirmatory trial. Trials in other mitochondrial diseases, heart failure, heart attack and eye disease did not meet their main goals.
A single infusion in 36 heart failure patients briefly reduced heart volumes at the highest dose, and Barth patients showed heart volume trends in open-label follow-up. The heart attack trial showed no reduction in damage.
These pairings come up often. Almost none have been tested together in a trial, and the evidence note on each says so plainly.
Discussed online as a mitochondria pairing: SS-31 for the inner membrane, MOTS-c as a mitochondria-derived signaling peptide.
EvidenceNo study has tested the two together in humans or animals. MOTS-c has no completed human efficacy trials.
Promoted as covering both mitochondrial structure and the NAD+ supply the electron transport chain uses.
EvidenceNo combination study exists. Each has been studied on its own, and neither has shown anti-aging benefit in human trials.
The approved product is a ready-to-use solution, not a powder. No published stability data exist for research-grade lyophilized SS-31.
Forzinity label: keep unopened vials refrigerated at 2 to 8 C and do not freeze. After first use, a vial can be kept refrigerated or at 20 to 25 C and must be discarded 8 days after opening.
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