SS-31

SS-31 is a synthetic, mitochondria-targeted tetrapeptide engineered to support mitochondrial bioenergetics and protect against oxidative stress. It selectively localizes to the inner mitochondrial membrane by binding to cardiolipin, a phospholipid essential for electron transport chain stability.

By stabilizing cardiolipin and mitochondrial complexes, SS-31 helps preserve mitochondrial structure, reduce reactive oxygen species (ROS), and maintain mitochondrial membrane potential—optimizing ATP production and cellular energy efficiency.

(Preclinical + investigational human research; not FDA-approved for therapeutic use.)

Mechanism of Action

  • Cardiolipin Stabilization: Maintains inner mitochondrial membrane integrity
  • Oxidative Stress Reduction: Lowers mitochondrial ROS and lipid peroxidation
  • Bioenergetic Optimization: Preserves ATP synthesis during metabolic or ischemic stress
  • Cell Survival Support: Helps protect mitochondrial structure and function

Clinical References

  1. Szeto, H.H. (2014). First-in-class cardiolipin-protective compound as a therapeutic agent to restore mitochondrial bioenergetics. British Journal of Pharmacology, 171(8), 2029–2050.
  2. Birk, A.V., et al. (2013). SS-31 re-energizes ischemic mitochondria by interacting with cardiolipin. J Am Soc Nephrol, 24(8), 1250–1261.
  3. Chiao, Y.A., et al. (2020). Late life restoration of mitochondrial function reverses cardiac dysfunction in old mice. eLife, 9:e55513.
  4. Thompson, M., et al. (2021). Phase 2/3 trial of elamipretide in Barth syndrome. Genetics in Medicine, 23(3), 471–478.
  5. Szeto, H.H., Liu, S. (2018). Cardiolipin-targeted peptides for mitochondrial protection and tissue regeneration during aging. Archives of Biochemistry and Biophysics, 660, 137–148.

*Based on preclinical and investigational human data—no implied clinical claims.

  • Mitochondrial Function: Supports ATP production and energy output under stress
  • Oxidative Stress: Reduces ROS generation and lipid peroxidation
  • Cell Survival: Stabilizes mitochondria and decreases apoptosis during stress
  • Organ Function: Helps maintain cardiac, renal, and skeletal muscle performance
  • Degenerative Processes: Slowed progression of muscle atrophy, cardiomyopathy, and neurodegenerative changes in models
  • Recovery from Injury: Potentially improves recovery in ischemia-reperfusion, acute kidney injury, and metabolic stress
  • Exercise Tolerance: Supports muscle function and reduces fatigue in mitochondrial dysfunction models

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