Source comparison
Comparison: MOTS-c + 5-Amino-1MQ Synergy vs Monotherapy
MOTS-c alone (5–10mg daily) AMPK activation increases glucose uptake and fatty acid oxidation; insulin sensitisation High NAD+ demand from increased mitochondrial activity without replenishment mechanism Moderate—limited by baseline NAD+ availability during su
This comparison does not assign a generated winner or score.
- MOTS-c alone (5–10mg daily)
- AMPK activation increases glucose uptake and fatty acid oxidation; insulin sensitisation
- High NAD+ demand from increased mitochondrial activity without replenishment mechanism
- Moderate—limited by baseline NAD+ availability during sustained activity
- Moderate—downstream signalling initiates biogenesis but cofactor limitation reduces maximum effect
- Effective for insulin resistance and acute metabolic flexibility but plateaus without NAD+ support
- 5-Amino-1MQ alone (50–100mg daily)
- NNMT inhibition preserves NAD+ by preventing nicotinamide methylation
- Elevated NAD+ pools but no direct mitochondrial activation signal
- Low to moderate—NAD+ preservation supports existing oxidative capacity but doesn't increase demand
- Minimal—NAD+ availability alone doesn't trigger biogenesis without AMPK or SIRT1 activation
- Best for baseline metabolic health and energy production but lacks the activation signal to drive adaptation
- Combined protocol (4–6 hour offset)
- Sequential NNMT inhibition followed by AMPK activation—NAD+ supply precedes NAD+ demand
- Optimised—5-Amino-1MQ preloads NAD+ before MOTS-c increases mitochondrial workload
- High—MOTS-c drives oxidative demand while 5-Amino-1MQ ensures cofactor availability
- High—AMPK activation triggers biogenesis with sufficient NAD+ to sustain new mitochondrial synthesis
- Maximum synergy—each compound compensates for the other's limitation when dosed in sequence