SS-31 (Elamipretide) is a mitochondria-targeted tetrapeptide that selectively concentrates in the inner mitochondrial membrane. Research has characterized it as a cardiolipin-interacting compound that stabilizes electron transport chain complex organization and reduces mitochondrial ROS production. It is among the most studied mitochondria-targeted research peptides available.
SS-31 (Elamipretide) is a mitochondria-targeted tetrapeptide that selectively concentrates in the inner mitochondrial membrane. Research has characterized it as a cardiolipin-interacting compound that stabilizes electron transport chain complex organization and reduces mitochondrial ROS production. It is among the most studied mitochondria-targeted research peptides available.
SS-31 (Elamipretide) is supplied strictly as a reference material for in vitro and preclinical investigation. All characterization data described here is drawn from peer-reviewed literature and laboratory analysis; nothing herein constitutes a claim of clinical effect in humans.
The following domains summarize directions explored across published studies and laboratory models. Each reflects observations reported in rodent models, in vitro systems, or the peer-reviewed record.
SS-31 has been shown to bind cardiolipin, the signature phospholipid of the inner mitochondrial membrane. Research has documented its ability to stabilize cardiolipin organization and prevent peroxidation in cell culture and animal models.
SS-31 has been extensively studied in cardiac ischemia-reperfusion injury models. Research has documented significant reductions in infarct size, mitochondrial dysfunction markers, and cardiomyocyte death in rodent models.
Studies have examined SS-31's effects on mitochondrial morphology and function in aged tissues, with documented improvements in cristae structure, Complex I activity, and ATP production in aged rodent models.
Research has examined SS-31 in models of acute kidney injury and chronic kidney disease, with studies documenting preserved tubular cell function and reduced oxidative stress markers in rodent subjects.
Mechanistic steps below are hypothesized from in vitro assays and animal-model data reported in the literature. They describe biochemical interactions observed under controlled experimental conditions.
SS-31 selectively accumulates in the inner mitochondrial membrane where it binds cardiolipin with high affinity. Cardiolipin stabilization prevents cytochrome c release and maintains electron transport chain supercomplex organization.
The Dmt (dimethyltyrosine) residue in SS-31 provides antioxidant activity by scavenging mitochondrial reactive oxygen species. Research has documented reductions in mitochondrial superoxide and hydrogen peroxide production in treated cells.
By stabilizing cardiolipin and electron transport chain supercomplexes, SS-31 maintains efficient electron transfer through Complexes I–IV, reducing electron leak, ROS production, and supporting ATP synthesis efficiency.
Studies have documented SS-31's ability to preserve mitochondrial membrane potential (ΔΨm) under stress conditions, a key indicator of mitochondrial health and a prerequisite for oxidative phosphorylation.
| Amino Acid Sequence | D-Arg-Dmt-Lys-Phe-NH₂ |
|---|---|
| Molecular Weight | 639.8 g/mol |
| Molecular Formula | C₃₂H₄₉N₉O₅ |
| CAS Number | 736992-21-5 |
| Storage | −20°C long-term, 4°C short-term up to 4 weeks |
The following peer-reviewed references informed the research summaries on this page. Citations are provided for scientific context only.
This product is intended strictly for laboratory research purposes only. It is not a drug, food, cosmetic, or dietary supplement and is not intended to diagnose, treat, cure, or prevent any disease. It is not for human or animal consumption. All information presented is derived from published scientific literature and is provided for educational reference only. By purchasing, the buyer affirms they are a qualified researcher or institution and assume full responsibility for the safe and lawful handling of this material.