A synthetic four-amino-acid peptide that concentrates inside mitochondria, researched for mitochondrial dysfunction, heart failure, ischemia-reperfusion injury and rare mitochondrial disease.
FDA accelerated approval (19 Sep 2025) as Forzinity — for muscle strength in Barth syndrome only. Every other use, including anti-aging and performance, is investigational.
Also known as: Elamipretide, MTP-131, Bendavia, Forzinity
Its alternating aromatic-cationic structure lets SS-31 cross membranes and selectively accumulate on the inner mitochondrial membrane, where it binds the phospholipid cardiolipin. Binding cardiolipin stabilises cristae architecture and holds the electron-transport-chain supercomplexes together, improving electron flow and ATP output. That tighter electron flow reduces electron leak, so less reactive oxygen species (ROS) are produced at the source. It also helps keep cytochrome c attached and limits opening of the mitochondrial permeability transition pore (mPTP), reducing cell-death signalling under stress. Notably it is not a receptor drug — the effect is structural.
In September 2025 elamipretide received FDA accelerated approval (Forzinity) to improve muscle strength in Barth syndrome — the first mitochondria-targeted drug approved. The wider picture is more mixed and rarely mentioned by sellers: a randomised crossover trial in primary mitochondrial myopathy showed no significant improvement in six-minute walk distance or fatigue at its primary endpoint, and cardiovascular trials were largely negative at primary endpoints, though open-label extensions reported sustained function. Preclinical data in heart failure, ischemia-reperfusion and age-related mitochondrial decline remain strong across 150+ publications.
We report both positive and negative trial results. For exact study protocols, read the sources — we cite them rather than repackage them.
Bars reflect the strength & volume of research evidence for each use — not a guarantee of results.
Generally well tolerated in trials; the most commonly reported problem was injection-site reaction. No prominent drug-specific toxicity emerged in published clinical data, but long-term safety outside the Barth syndrome population is not established.
MOTS-c — complementary: SS-31 stabilises and repairs existing mitochondria, MOTS-c drives biogenesis of new ones. NAD+ / NMN — discussed alongside because they replenish the redox cofactor pool the improved electron transport depends on. Urolithin A — discussed for mitophagy (clearing damaged mitochondria) as a counterpart to repairing intact ones.
Mechanistic context only — we don't publish combinations, amounts or protocols.
Unlike antioxidant supplements such as CoQ10 or MitoQ, which scavenge ROS after they form, SS-31 acts structurally at the membrane to prevent excess ROS being generated in the first place and to preserve supercomplex assembly.
Yes, but narrowly — accelerated approval in September 2025 as Forzinity, for muscle strength in Barth syndrome patients of at least 30 kg. It is the first approved mitochondria-targeted drug. No other indication is approved.
No. It works physically, by binding cardiolipin in the inner mitochondrial membrane, rather than through a cell-surface receptor.
Largely no. Cardiovascular and primary mitochondrial myopathy trials were mixed or negative at their primary endpoints, which is why approval came first in a narrow rare-disease indication.
No reviews yet. If you've used SS-31, be the first to share what it helped with and any side effects.
⚠️ Educational research information only — not medical advice. Many peptides are sold strictly for laboratory research and are not approved treatments. The evidence scores reflect research interest and strength, not efficacy or safety for any individual. Always consult a qualified professional.