Understand the source comparison
SS-31 vs SS-LUP-332: Research Model Comparison
Ischaemia-reperfusion injury Reduces infarct size 15–25%, prevents cytochrome c release, maintains ATP production during reperfusion No protective effect. Insufficient time for transcriptional changes Hours SS-31 is the only viable option Metabolic syndrome mo
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- Ischaemia-reperfusion injury
- Reduces infarct size 15–25%, prevents cytochrome c release, maintains ATP production during reperfusion
- No protective effect. Insufficient time for transcriptional changes
- Hours
- SS-31 is the only viable option
- Metabolic syndrome models
- No effect on insulin sensitivity, glucose uptake, or mitochondrial density in non-stressed tissue
- Improves insulin sensitivity 25–40%, increases mitochondrial respiration, shifts substrate utilisation toward fat oxidation
- 14–21 days
- SS-LUP-332 addresses the metabolic root cause
- Exercise performance enhancement
- Modest improvements (8–12%) only when combined with actual training stimulus
- 40–50% improvement in untrained animals, mimics training adaptations at molecular level
- 10–14 days
- SS-LUP-332 shows stronger standalone effect
- Neurodegenerative disease models
- Mixed results. Mitochondrial protection evident, but poor BBB penetration limits CNS delivery
- Untested in CNS models due to uncertain brain penetration
- N/A
- Neither peptide has strong CNS translational data
- Cardiac dysfunction (chronic heart failure)
- Failed primary endpoints in Phase 3 trials despite mitochondrial improvements
- Preclinical data shows increased cardiac output and oxidative capacity in non-ischaemic models
- 21+ days
- SS-LUP-332 may address chronic remodelling better, but clinical data lacking
- Acute mitochondrial toxin exposure
- Dose-dependent protection against rotenone, antimycin A, oligomycin toxicity
- No protection. Can't rescue acutely poisoned mitochondria
- Minutes to hours
- SS-31 is protective; SS-LUP-332 is not