SS-31

SS-31 (elamipretide) is a synthetic cell-permeable tetrapeptide developed by Hazel Szeto at Weill Cornell Medical College. It is designed to target the inner mitochondrial membrane by selectively binding to cardiolipin, a unique phospholipid found almost exclusively in the inner mitochondrial membrane. Cardiolipin plays a critical structural role in organizing electron transport chain (ETC) complexes into supercomplexes (respirasomes) that enable efficient electron transfer. By binding cardiolipin, SS-31 stabilizes the cristae structure and ETC supercomplex organization, improving the efficiency of oxidative phosphorylation. This reduces electron leak and consequently decreases mitochondrial reactive oxygen species (ROS) production. Importantly, SS-31 does not act as a conventional antioxidant that scavenges ROS after they are produced — instead, it prevents excess ROS generation at the source by optimizing ETC function. SS-31 has shown therapeutic potential across multiple organ systems in preclinical and clinical studies. It reduces infarct size in cardiac ischemia-reperfusion injury, protects renal tubular cells from ischemic damage, improves skeletal muscle function in aged animals, and reverses age-related mitochondrial dysfunction. It has advanced to Phase II/III clinical trials for heart failure (Barth syndrome, primary mitochondrial myopathy, and heart failure with preserved ejection fraction).

SS-31 (elamipretide) is a synthetic cell-permeable tetrapeptide developed by Hazel Szeto at Weill Cornell Medical College. It is designed to target the inner mitochondrial membrane by selectively binding to cardiolipin, a unique phospholipid found almost exclusively in the inner mitochondrial membrane. Cardiolipin plays a critical structural role in organizing electron transport chain (ETC) complexes into supercomplexes (respirasomes) that enable efficient electron transfer. By binding cardiolipin, SS-31 stabilizes the cristae structure and ETC supercomplex organization, improving the efficiency of oxidative phosphorylation. This reduces electron leak and consequently decreases mitochondrial reactive oxygen species (ROS) production. Importantly, SS-31 does not act as a conventional antioxidant that scavenges ROS after they are produced — instead, it prevents excess ROS generation at the source by optimizing ETC function. SS-31 has shown therapeutic potential across multiple organ systems in preclinical and clinical studies. It reduces infarct size in cardiac ischemia-reperfusion injury, protects renal tubular cells from ischemic damage, improves skeletal muscle function in aged animals, and reverses age-related mitochondrial dysfunction. It has advanced to Phase II/III clinical trials for heart failure (Barth syndrome, primary mitochondrial myopathy, and heart failure with preserved ejection fraction).

Clinical trials used 0.01-0.25 mg/kg IV or 4-40 mg SC daily. Mouse studies used 1-3 mg/kg IP. The typical research dose in preclinical cardiac studies is 0.1-3 mg/kg.

Store lyophilized (freeze-dried) powder at -20°C to 4°C in a dry environment protected from light. Unreconstituted peptide is stable for extended periods when stored properly.

Once reconstituted with bacteriostatic water or an appropriate solvent, store at 2-8°C and use within the timeframe specified on the Certificate of Analysis. Avoid repeated freeze-thaw cycles.

A Certificate of Analysis documenting purity, identity, and recommended storage conditions is included with every order.