SS-31 · MOTS-c · NAD+ · 5-Amino-1MQ — Complete Mitochondrial Optimisation
The most comprehensive mitochondrial optimisation protocol available — addressing mitochondrial structure (SS-31), metabolic signalling (MOTS-c), energy substrate supply (NAD+) and degradation prevention (5-amino-1MQ) simultaneously. Each compound targets a different aspect of mitochondrial function for a synergistic effect greater than any single intervention.
Mitochondrial dysfunction is now widely recognised as a central driver of aging and age-related disease. The Mito Stack addresses this through four distinct but complementary mechanisms — each targeting a different aspect of how mitochondria produce energy and maintain their function over time.
SS-31 addresses the physical structure of the inner mitochondrial membrane. By binding cardiolipin — the lipid that organises the electron transport chain complexes — SS-31 stabilises the membrane architecture that all mitochondrial energy production depends on. Damaged cardiolipin is now understood to be a primary mechanism of age-related mitochondrial dysfunction. SS-31's FDA approval for Barth Syndrome validates the mechanism in humans.
MOTS-c is a mitochondrial-derived peptide that activates AMPK — the master metabolic switch — through the AICAR pathway. This upstream signalling activation improves glucose uptake, enhances fat oxidation, promotes mitochondrial biogenesis and produces exercise-mimicking metabolic adaptations. MOTS-c levels decline with age correlating with metabolic dysfunction — exogenous MOTS-c replaces this declining signal.
NAD+ is the essential electron carrier that mitochondria use to convert nutrients into ATP. Without adequate NAD+, the electron transport chain cannot function efficiently regardless of structural integrity or signalling. NAD+ levels decline approximately 50% by age 60 — making supplementation foundational to any mitochondrial optimisation protocol. SubQ NAD+ provides superior bioavailability to oral NMN or NR.
While NAD+ supplements increase supply, 5-amino-1MQ addresses the demand side — blocking CD38, the primary enzyme that degrades NAD+. CD38 activity increases with age and inflammation, driving NAD+ decline faster than supplementation alone can counter. By blocking degradation simultaneously with increasing supply, the combination produces significantly greater NAD+ elevation than either approach alone.