SS-31

SS-31 selectively binds cardiolipin, a phospholipid found almost exclusively in the inner mitochondrial membrane. By stabilising cardiolipin it improves the efficiency of the electron transport chain, reduces electron leak and therefore reactive oxygen species production. It concentrates in mitochondria at roughly a thousand-fold over cytosolic levels.

• Phase 2 and 3 trials in primary mitochondrial myopathy and Barth syndrome
• Improved mitochondrial respiration and reduced oxidative stress in multiple tissue models
• Studied in heart failure, ischaemia-reperfusion injury and dry age-related macular degeneration
• Neuroprotection in animal models of neurodegeneration

• Primary endpoints have been missed in several late-stage trials
• No approval to date
• No trial in depression or cognition

Clinical trials used approximately 40 mg/day subcutaneously in adults, under supervision.

Routes studied

Subcutaneous

Half-life

Roughly 2–4 hours in plasma; tissue mitochondrial retention is far longer

Cycle length in the literature

Trials ran continuous daily dosing over weeks to months

Working out a draw volume from a vial? Use the free reconstitution calculator.

Reported side effects

Do not use if

SS-31 makes existing mitochondria run cleaner; exercise makes more of them. The two mechanisms are complementary rather than redundant, which is one of the few genuinely well-founded synergy arguments in this space.

• Fuel →
• Rest →

What amplifies it

• Mitochondria & mental energyWhy depression tracks with impaired cellular energy production, and what mitochondrial peptides, nutrition and sleep actually do about it.
• Nerve regenerationPeripheral nerves regenerate at roughly a millimetre a day. The central nervous system largely does not. What that means for peptides and practice.

• Mitochondrial resetFor flatness and fatigue that sleep does not fix: the three distinct mitochondrial mechanisms, and which compounds hit which.