Source comparison
MOTS-c vs Other Mitochondrial Peptides: Comparison
MOTS-c AMPK activation, mitochondrial biogenesis Insulin sensitivity, glucose uptake, fat oxidation Rodent + small human pilots Strongest insulin resistance data; age-related decline makes it compensatory rather than performance-enhancing Humanin Cytoprotectiv
This comparison does not assign a generated winner or score.
- MOTS-c
- AMPK activation, mitochondrial biogenesis
- Insulin sensitivity, glucose uptake, fat oxidation
- Rodent + small human pilots
- Strongest insulin resistance data; age-related decline makes it compensatory rather than performance-enhancing
- Humanin
- Cytoprotective signalling, apoptosis inhibition
- Neuroprotection, metabolic syndrome
- Phase II human trials
- Broader cytoprotective role but weaker direct metabolic effects than MOTS-c
- SS-31 (Elamipretide)
- Cardiolipin stabilisation, ROS reduction
- Mitochondrial membrane integrity
- FDA Fast Track for heart failure
- Targets structure over signalling; complementary to MOTS-c, not overlapping
- SHLP2
- Stress response, mitochondrial unfolded protein response
- Metabolic stress adaptation
- Preclinical only
- Least characterised; mechanistic overlap with MOTS-c unclear
- MOTS-c distinguishes itself through direct AMPK engagement and proven insulin sensitivity improvements. Humanin operates upstream at the apoptosis checkpoint, making it relevant for neurodegeneration but less targeted for metabolic dysfunction. SS-31 repairs mitochondrial membranes but doesn't activate metabolic pathways. It stabilises function without increasing capacity. Researchers focused specifically on glucose metabolism, insulin resistance, or age-related metabolic slowdown should prioritise MOTS-c. Those addressing broader mitochondrial dysfunction or oxidative stress may find complementary peptides like Cerebrolysin more relevant depending on study design.