SS31

SS-31 (Elamipretide) is a mitochondria-targeted tetrapeptide designed to selectively bind cardiolipin within the inner mitochondrial membrane. In research settings, SS-31 is studied for its effects on mitochondrial bioenergetics, oxidative stress modulation, ATP production efficiency, and protection against mitochondrial dysfunction in cardiac, skeletal muscle, and metabolic disease models. For research use only.

10MG | PHYSICIAN USE ONLY

$164.90

Confirm compounded formula & unique dosing are necessary for the patient

Research Profile

At a Glance

  • Type: Mitochondria-Targeted Tetrapeptide
  • Also Known As: Elamipretide; Bendavia; MTP-131
  • Sequence: D-Arg-2’,6’-dimethylTyr-Lys-Phe-NH₂
  • Length: 4 amino acids
  • Molecular Weight: ~639.8 Da
  • Primary Target: Cardiolipin within the inner mitochondrial membrane
  • Research Focus: Mitochondrial bioenergetics, oxidative stress regulation, ATP production, cardiac and skeletal muscle mitochondrial function
  • Regulatory Status: Investigational; not FDA-approved; Research Use Only (RUO) outside clinical trials
  • Categories: Anti-Aging Research; Metabolic Research; Recovery & Repair; Hormone Research

What Research Shows

  • Demonstrates selective binding to cardiolipin, stabilizing mitochondrial inner membrane structure in preclinical models.
  • Improves mitochondrial respiration and ATP production efficiency in models of cardiac and skeletal muscle dysfunction.
  • Reduces mitochondrial reactive oxygen species (ROS) production and oxidative stress markers in experimental systems.
  • Studied in heart failure and ischemia-reperfusion models, showing preservation of mitochondrial structure and function.
  • Investigated in age-related and metabolic dysfunction models where mitochondrial impairment is a contributing factor.

Mechanistic Notes

  • Cardiolipin interaction: SS-31 binds cardiolipin, a phospholipid essential for electron transport chain organization.
  • Electron transport chain stabilization: Improves coupling efficiency of oxidative phosphorylation in mitochondrial membranes.
  • ROS modulation: Reduces excessive mitochondrial ROS production under stress conditions.
  • Mitochondrial structural integrity: Preserves cristae architecture and prevents cardiolipin peroxidation in injury models.
  • Energy metabolism enhancement: Associated with improved ATP synthesis efficiency in mitochondrial dysfunction research.

What Remains Unknown

  • Long-term outcomes outside controlled clinical trials
  • Tissue-specific variability in mitochondrial response
  • Optimal dosing paradigms across different disease models
  • Translational consistency across aging populations