In transgenic mouse models, the mitochondrial-derived peptide MOTS-c boosted intrinsic muscle mitochondrial bioenergetics and lowered ROS-related oxidative damage — requiring both PGC-1α and AMPK signalling, without increasing raw mitochondrial volume. Animal data only; a human Phase 2a trial (MOTS-MET) for prediabetes began enrolling in 2026.
Read source →Using bioinformatic and protein-docking analysis, researchers compared the mitochondrial-derived peptide humanin across mammals with different oxidative-stress profiles (deep-diving cetaceans, high-metabolism shrews, long-lived primates). Species under greater oxidative stress carried more structurally stable humanin variants, suggesting evolution has tuned the peptide's protective function and offering a template for designing humanin-based therapeutic analogs.
Read source →Preclinical work showing MOTS-c, an mtDNA-encoded peptide, restores mitochondrial respiration and energy homeostasis in a type 2 diabetic cardiac model — building the mechanistic case for its "exercise mimetic" reputation.
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