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Peptides for Mitochondrial Dysfunction Research Compared: Mechanism Comparison
SS-31 (elamipretide) Cardiolipin binding, cristae stabilization Inner membrane (intermembrane space) Ischemia-reperfusion injury, Barth syndrome ATP/ADP ratio, cristae morphology (EM), cytochrome c retention First mitochondrial-targeting peptide to reach Phase
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- SS-31 (elamipretide)
- Cardiolipin binding, cristae stabilization
- Inner membrane (intermembrane space)
- Ischemia-reperfusion injury, Barth syndrome
- ATP/ADP ratio, cristae morphology (EM), cytochrome c retention
- First mitochondrial-targeting peptide to reach Phase 3 trials. Directly addresses membrane architecture rather than upstream signaling
- MOTS-c
- AMPK activation, PGC-1α upregulation
- Cytoplasm → nucleus (retrograde signaling)
- Metabolic dysfunction, sarcopenia
- Mitochondrial DNA copy number, citrate synthase activity, oxygen consumption rate
- Biogenesis-focused. Requires time to show effect but increases total mitochondrial capacity rather than preserving existing organelles
- Humanin
- STAT3 activation, Bax inhibition
- Cytoplasmic (anti-apoptotic signaling)
- Neurotoxicity models, ischemic injury
- Caspase-3 activation, TUNEL staining, cell viability
- Prevents apoptotic commitment without restoring bioenergetics. Protective in acute injury but doesn't address chronic ATP deficits
- HLDF-6 (humanin analog)
- Enhanced STAT3 binding (1000× potency vs humanin)
- Cytoplasmic
- Alzheimer's models, stroke
- Neuronal survival, infarct volume
- Synthetic analog with improved receptor affinity. Used when humanin shows subthreshold effects in specific tissue types