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SS-31 (elamipretide)

Also known as Elamipretide, MTP-131, Bendavia, Forzinity, SS-31

Mitochondria-targeted tetrapeptide binding cardiolipin; US-approved for Barth syndrome since 2025.

early-clinical Immune & longevity approved drug

At a glance

Category
Immune & longevity
Status
approved drug
Route
subcutaneous (registered), intravenous in older studies
Half-life
approximately 2-4 hours after subcutaneous administration
Onset
weeks to months for functional endpoints
Molecular weight
approximately 639.8 g/mol (free base). The approved label gives the molecular formula as C32H49N9O5·3HCl and a molecular weight of 749.2 for the trihydrochloride salt that is actually formulated 5
Sequence
D-Arg-2',6'-dimethylTyr-Lys-Phe-NH2 (tetrapeptide containing a non-natural amino acid)

On 19 September 2025 the FDA granted accelerated approval to FORZINITY (elamipretide) injection for improving muscle strength in patients with Barth syndrome weighing 30 kg or more, the first approved treatment for that disorder 45. As a condition of the accelerated approval the FDA is requiring a post-approval randomised, double-blind, placebo-controlled trial to confirm that the change in knee muscle strength translates into patient benefit 46. That is an extremely rare genetic disorder; outside that indication elamipretide is an investigational agent. In the EU elamipretide holds only an orphan designation for Barth syndrome, granted on 20 May 2021 (EU/3/21/2430); the EMA states explicitly that orphan designation does not mean a medicine is authorised, and no marketing authorisation has followed 7. The powder sold online as 'SS-31' is not a registered medicine and falls under the research chemical trade.

Doping status: Not listed by WADA

Checked against the WADA 2026 Prohibited List. For a specific product and country, Global DRO is the lookup athletes are expected to use — the List names substances, not brand names.

Mechanism of action

Elamipretide is a small, positively charged peptide that, through its alternating aromatic and basic residues, accumulates in the inner mitochondrial membrane independently of the membrane potential. There it binds cardiolipin, the phospholipid that determines cristae architecture.

Binding to cardiolipin stabilises the interaction between cardiolipin and cytochrome c. This reduces the peroxidase activity of the cytochrome c-cardiolipin complex, limits lipid peroxidation and improves electron transport chain coupling, with more ATP production and less leakage of reactive oxygen species.

In Barth syndrome the rationale is clearest: a mutation in the TAFAZZIN gene disrupts cardiolipin remodelling. Elamipretide does not correct the underlying genetic defect, but stabilises the abnormal cardiolipin that is present.

Why the same mechanism produces a clinical effect in one mitochondrial disorder and not in another has not been explained. The post-hoc finding that patients with nuclear DNA mutations responded better than those with mtDNA mutations is a hypothesis, not an established fact.

What the research shows

Elamipretide is one of the few 'longevity' peptides to have completed a full clinical development programme, and precisely because of that the balance is easy to survey: the compound has repeatedly missed its primary endpoint in large randomised trials 13. The 2025 FDA approval rests on a surrogate endpoint (knee extensor strength) in an extremely small population, granted through the accelerated pathway and with the obligation to still confirm clinical benefit 5. For healthy people, ageing or general 'mitochondrial support' no evidence exists.

Research in humans

TAZPOWER (phase 2/3, Barth syndrome, 12 patients, cross-over): during the randomised placebo-controlled phase both primary endpoints — the six-minute walk test and a symptom score — were not met, with no indication of an effect 1. In the subsequent open-label extension out to 168 weeks, improvements in walking distance, knee extensor strength and cardiac function were reported; that phase had no placebo group and was compared with historical natural-history controls 25. MMPOWER-3 (phase 3, primary mitochondrial myopathy, 218 adults, 40 mg/day for 24 weeks): the primary endpoint (six-minute walk test and a symptom questionnaire) was not met in the total population; a pre-specified subgroup with nuclear DNA mutations did show improvement 3. Earlier studies in dry macular degeneration (ReCLAIM) and in myocardial infarction/reperfusion (EMBRACE STEMI) produced no convincing clinical benefit. In the FDA advisory committee the vote was 10 to 6 in favour of efficacy in Barth — not unanimous.

Animal and lab research

Preclinically the picture is far more positive: in models of heart failure, ischaemia-reperfusion, kidney injury, sarcopenia and ageing in mouse, rat and dog, elamipretide improved mitochondrial function, exercise capacity and tissue damage. These models use acute or greatly magnified injury and repeatedly failed to translate into clinical endpoints in humans — a classic example of the gap between preclinical and clinical research.

Caveats. TAZPOWER had 12 participants 1; that is too small for a reliable effect estimate. Almost all the positive results come from unblinded extension phases and comparisons with historical controls, where expectation effects and selection play a role. The registered endpoint (knee extensor strength) is an intermediate endpoint; whether it translates into survival or daily functioning still has to be confirmed 5. Virtually all the research has been funded by the developer.

What it is used for

  • Barth syndrome: improvement of muscle strength in patients weighing 30 kg or more (the registered indication in the US) 45
  • Primary mitochondrial myopathy (studied, primary endpoint not met)
  • Dry age-related macular degeneration and Leber's hereditary optic neuropathy (investigational)
  • Heart failure with preserved ejection fraction and ischaemia-reperfusion injury (studied, no convincing result)
  • Off-label: 'mitochondrial support', fatigue, ageing — without supporting evidence

Dosing

Dose
40 mg per day subcutaneously — the registered dose in Barth syndrome for people weighing 30 kg or more
Frequency
once daily
Route
subcutaneous in the abdomen (at least 5 cm from the navel) or the thigh, rotating the injection site daily
Duration
In Barth syndrome an ongoing treatment; clinical studies ran 12 to 168 weeks
  • 40 mg per day is also the dose used in MMPOWER-3, where it showed no effect on the primary endpoint — a registered dose is therefore no guarantee of effect in a different condition.
  • No dose has been established for children under 30 kg 5.
  • The approved label halves the dose in renal impairment: 20 mg subcutaneously once daily if eGFR is below 30 mL/min and the patient is not on dialysis, against 40 mg once daily at eGFR 30 mL/min or above 56. No adjustment is required for mild or moderate impairment, and the label states elamipretide has not been studied in patients with renal failure on dialysis 5. The reason for the reduction is exposure: AUC rose by 39%, 75% and 125% at creatinine clearances of 60-89, 30-59 and below 30 mL/min respectively 5.
  • Lower doses circulating in user protocols (for example 5-10 mg per day) have no clinical basis whatsoever.
  • Doses are described here on the basis of the approved product information and published studies; this is not treatment advice.

These figures describe what the literature and published protocols report. They are not advice and not a dosing instruction.

Protocols

Barth syndrome (FORZINITY)

approved product information

Source: FDA prescribing information for FORZINITY (elamipretide), 2025, as published on DailyMed

Once daily, ongoing40 mg by subcutaneous injection, in patients weighing 30 kg or more
Renal impairment, eGFR below 30 mL/min and not on dialysis20 mg by subcutaneous injection once daily

Injected into the abdomen at least 5 cm (the label says 2 inches) from the navel, or the outer thigh, rotating the site daily, at the same time each day. The label gives no dose for patients on dialysis, citing insufficient information. This is an accelerated approval for improving muscle strength in Barth syndrome and nothing else; no dose is established below 30 kg. The powder sold online as 'SS-31' is not this product.

Primary mitochondrial myopathy (MMPOWER-3)

published trial

Source: Neurology, 2023 - MMPOWER-3 randomised clinical trial

Randomised treatment period40 mg once daily by subcutaneous injection

The same 40 mg daily dose that is now registered for Barth syndrome showed no effect on the primary endpoint here. It is a worked example of the difference between a dose that is documented and a dose that works: the two are not the same claim.

Grey-market 'mitochondrial' use (user-reported)

user protocol — not validated

Source: The pattern repeated across longevity, biohacking and peptide forums together with research-chemical vendor labelling of 'SS-31' powder

This is not a validated schedule. It is a pattern that circulates among users and sellers, reproduced because it is what people actually follow — not because it has been tested. No trial established these doses, this interval or this duration, and nobody is checking what is in the vial. Treat every number below as an assertion, not a finding.

Most commonly reported daily amount5-10 mg subcutaneously once daily
Reported cycleruns of a few weeks to a few months, often stacked with other 'mitochondrial' or longevity peptides, with no consistent off-period

The gap between label and practice here is one of the widest on the site, and it is a gap of purpose as much as of dose. The label directs 40 mg a day for a single ultra-rare genetic disorder, Barth syndrome; the circulating use is general 'mitochondrial support', fatigue and anti-ageing in healthy people, at roughly 5-10 mg a day — a purpose the drug was never approved for and a dose several-fold below the registered one. That lower figure has no published basis: no study used it, and the compound repeatedly failed its primary endpoint in the large trials that did exist. The material is research-chemical 'SS-31' powder of unverified identity and purity, not the registered product. Injection-site reactions were near-universal in the controlled trial and should be expected; 'no effect' is the likely honest outcome for the population using it, and the absence of reported harm from an unmonitored group is not evidence of safety.

Schedules are reproduced as their source states them. Units, IU and milligrams explains why the figures are not interchangeable between products.

Reconstitution

Vial sizes
10 mg, 50 mg
Solvent
The registered product does not need to be reconstituted. At 80 mg/ml the 40 mg dose is 0.5 ml drawn from the vial; the vial is not a single dose. Unregistered lyophilised powder is in practice dissolved in bacteriostatic water (0.9% benzyl alcohol).
Storage
Registered product: store refrigerated according to the package leaflet. Reconstituted powder in practice at 2-8 °C and used within a few weeks; unopened powder in the freezer, protected from light.

Worked example

50 mg vial + 2 ml bacteriostatic water = 25 mg/ml; 10 mg then corresponds to 0.4 ml (40 units on a U100 insulin syringe). Be clear about what that 10 mg is: it is a grey-market figure with no clinical basis, not the dose in any study. The registered and trial dose is 40 mg daily, which at 25 mg/ml would be 1.6 ml — 160 units, more than a U100 insulin syringe holds in one draw.

Do not shake. The quality and purity of non-pharmaceutical material is not controlled; the actual content of such vials is unknown.

Work it out for SS-31 (elamipretide)

Safety

Side effects

  • Injection site reaction — very common, and the most frequently reported side effect 45. In the placebo-controlled crossover trial every one of the 12 patients on elamipretide had a local administration reaction, against 8 of 12 on placebo; injection site erythema occurred in 12 of 12 versus 3 of 12, induration and pruritus in 8 of 12 each versus 2 of 12, and pain in 9 of 12 versus 5 of 12 5
  • Eosinophilia — the label reports frequent increases in absolute eosinophil count when dosing ran 30 days or longer, peaking around 90 days (mean rise from baseline of roughly 0.5-0.6 x 10^3/uL) and returning to baseline after 6 to 12 months of continued exposure or on stopping, without clinical manifestations 5
  • Headache
  • Dizziness
  • Nausea, abdominal complaints
  • Hypersensitivity reactions (rarely reported); the label carries hypersensitivity as a warning and precaution 5

Do not use if

  • Serious hypersensitivity to elamipretide or to any of the ingredients — the only contraindication in the approved label 5
  • Neonates: the product contains benzyl alcohol as a preservative and the label directs that it not be used in neonates because of the risk of benzyl alcohol toxicity 5
  • Pregnancy and breastfeeding: the label notes there are no data in pregnant women, since Barth syndrome is X-linked recessive and unlikely to affect females 5
  • Children under 30 kg: no established dose 5
  • Use outside a diagnosed mitochondrial disorder rests on no clinical basis whatsoever

Interactions

Largely negative on the classical axes, and that is documented rather than assumed. The approved label reports that no hepatic metabolism was observed in vitro, that elamipretide neither inhibits CYP1A, 2D6, 2E1, 2B6, 2C8, 2C9, 2C19 or 3A nor induces CYP1A2, 2B6 or 3A4, and that it does not inhibit OCT2, BCRP, OAT1, OAT3, OATP1B1, OATP1B3, P-gp or MATE2-K 5. There is one positive in-vitro finding that is easy to miss: elamipretide is an inhibitor of the MATE1 transporter, with an IC50 of 3.53 micromolar 5. Clinically, co-administration with aspirin and with clopidogrel was studied and did not affect their pharmacokinetics or, for aspirin, its antiplatelet activity 5. Beyond these, no interaction studies have been carried out.

Sources