SS-31: Benefits & Research

SS-31's primary benefit is direct protection and restoration of mitochondrial function. The peptide binds to cardiolipin in the inner mitochondrial membrane — a unique phospholipid essential for organizing the electron transport chain complexes. In aged or damaged mitochondria, cardiolipin becomes oxidized and loses its structural integrity, leading to electron leak, reduced ATP production, and increased reactive oxygen species (ROS).

SS-31 stabilizes cardiolipin interactions with cytochrome c, restoring efficient electron transport, improving ATP synthesis, and reducing ROS generation. This mechanism is distinct from antioxidants that merely scavenge ROS — SS-31 prevents their formation at the source.

Mitochondrial dysfunction is recognized as a primary hallmark of aging. SS-31 has demonstrated the ability to reverse age-related mitochondrial decline in multiple tissues. In aged mice, SS-31 treatment improved cardiac function, restored skeletal muscle performance, enhanced renal function, and improved insulin sensitivity — all by targeting the underlying mitochondrial dysfunction.

For complementary anti-aging approaches, see NAD+ (mitochondrial cofactor), epitalon (telomere maintenance), and MOTS-c (mitochondrial signaling peptide). Visit anti-aging peptides for a complete overview.

SS-31 has been extensively studied in cardiac models. Research demonstrates protection against ischemia-reperfusion injury, improvement in heart failure models, and reversal of age-related cardiac decline. The heart is particularly dependent on mitochondrial function, with cardiac cells containing thousands of mitochondria that generate the ATP needed for continuous contraction.

The kidneys are among the most metabolically active organs and are highly vulnerable to mitochondrial dysfunction. SS-31 has shown renal protective effects in models of acute kidney injury, diabetic nephropathy, and age-related renal decline. Clinical trials are investigating elamipretide for renal conditions.

SS-31 (as elamipretide) has advanced furthest in clinical development for Barth syndrome — a rare genetic disorder caused by mutations in the tafazzin gene that impair cardiolipin remodeling. Clinical trials demonstrated improvements in cardiac and skeletal muscle function, validating the cardiolipin-targeting mechanism in human patients.