SS-31
- Energy & mitochondria
- Recovery & repair
- Longevity & anti-ageing
The mitochondrial peptide — it targets the inner membrane where energy is made, and it carries an FDA accelerated approval for Barth syndrome, a rare inherited cardiolipin disorder.
Read the published research →What SS-31 does
SS-31, developed clinically as elamipretide, concentrates about a thousand-fold in the inner membrane of mitochondria and binds cardiolipin, the phospholipid that holds that membrane's folds together. Barth syndrome is where it is approved: patients who continued into the 168-week open-label extension walked 96.1 m farther on the six-minute walk test than at that extension's baseline, with improved left ventricular volumes and monolysocardiolipin/cardiolipin ratios, and the FDA granted accelerated approval conditional on a confirmatory trial. The broader tests went the other way — across 218 adults with primary mitochondrial myopathy over 24 weeks, six-minute walk distance differed from placebo by -3.2 m and neither primary endpoint was met, and trials in heart failure and heart-attack reperfusion were also negative. The strongest energy results are in aged mice, where one dose restored resting and maximal muscle ATP production, coupling efficiency and cellular energy state to young-animal levels within an hour, and eight weeks of treatment substantially reversed age-related stiffening of the heart. Injection-site reactions dominate the safety picture: 98.2% of the treated group reported some adverse event against 76.1% on placebo in the phase 3 trial, with injection-site reactions the only category above 10%.
- Mitochondrial energy output and cellular fatigue
- Age-related decline in muscle performance
- Heart and kidney tissue in aging
- Oxidative stress inside the mitochondria
- Rare inherited mitochondrial disorders
Common areas of interest, not measured results. The findings below are the published data.
In MMPOWER-3, a 24-week phase 3 randomised, double-blind trial in 218 adults with genetically confirmed primary mitochondrial myopathy, elamipretide missed both primary endpoints: six-minute walk distance differed from placebo by -3.2 m (95% CI -18.7 to 12.3; p = 0.69) and total fatigue score on the Primary Mitochondrial Myopathy Symptom Assessment by -0.07 (95% CI -0.10 to 0.26; p = 0.37).7
In MMPOWER-2, a randomised, double-blind, placebo-controlled crossover trial in 30 adults with genetically confirmed primary mitochondrial myopathy, participants walked 398.3 +/- 134.16 m during the elamipretide period versus 378.5 +/- 125.10 m during placebo, a 19.8 m difference that was not significant (95% CI -2.8 to 42.5; p = 0.0833); patient-reported total fatigue favoured elamipretide (p = 0.0006).8
In TAZPOWER, a 28-week randomised, double-blind, placebo-controlled crossover trial in 12 patients with Barth syndrome, elamipretide separated from placebo on neither primary endpoint, with no significant improvement in six-minute walk distance or in the Barth Syndrome Symptom Assessment score.9
For laboratory research use only. Not a drug, food, or cosmetic. Not for human or veterinary use, ingestion, or any form of consumption. Sold exclusively to qualified researchers.
