SS-31

SS-31, also known as Elamipretide, is a synthetic mitochondria-targeting tetrapeptide that works by selectively binding to cardiolipin — a phospholipid found in the inner mitochondrial membrane critical to mitochondrial structure and function. By stabilizing cardiolipin, SS-31 may protect mitochondrial integrity, increase ATP production, reduce reactive oxygen species (ROS), inhibit mitochondrial permeability transition pore (mPTP) opening, and reduce calcium overload. It is among the most extensively researched mitochondria-targeted compounds, with studies spanning heart failure, kidney disease, neurodegeneration, and cellular aging.

Chemical Makeup Molecular Formula: C32H52N8O6 | Molecular Weight: 639.82 g/mol | Also known as: Elamipretide, MTP-131, Bendavia

Research Highlights

• Cardiovascular Protection — SS-31 has been studied in cardiac arrest and ischemia/reperfusion injury models, where it appeared to improve survival rates and reduce myocardial damage by limiting mitochondrial dysfunction during periods of reduced oxygen supply.
• Heart Failure — Research indicates SS-31 may improve cardiac energy metabolism and contractile function in heart failure models, with studies pointing to enhanced ATP synthesis and reduced oxidative stress in cardiomyocytes.
• Kidney Disease — Studies in acute kidney injury models suggest SS-31 may reduce mitochondrial ROS accumulation and inflammation in renal tissue, potentially limiting progression of injury and supporting cellular recovery.
• Neuroprotection — Research in traumatic brain injury and neurodegenerative disease models indicates SS-31 may decrease ROS in neuronal tissue, potentially slowing mitochondrial dysfunction-related neurological decline.
• Aging & Cellular Resilience — Evidence suggests SS-31 may reduce age-related mitochondrial decline by preserving inner membrane integrity and restoring oxidative phosphorylation efficiency — with implications for longevity and cellular health research.
• Mitochondrial Disease — SS-31 has been investigated in models of Barth syndrome and primary mitochondrial myopathy, rare conditions characterized by severe mitochondrial dysfunction, with research suggesting potential improvements in energy metabolism and muscle function.

Available for research and laboratory purposes only.