# MOTS-c as a Metabolic Healthspan Peptide

MOTS-c has measurable metabolic and functional effects in rodent models; benefit from administering native MOTS-c to humans for healthspan remains unestablished.

Overall Γ follows preregistered primary human-administered SC3. Partial native molecular SC1 is Γ and explicitly scoped rodent metabolic/functional pharmacology SC2 is Ε under a declared phenotype adaptation. Controlled model benefit is retained; neither endogenous exercise-marker induction, K14Q population association nor an analogue program supplies native human healthspan causality.

Species, background, sex, age, baseline metabolic status, tissue, dose/route and functional endpoint are measurable before results. Published post-hoc activity/age strata need prospective replication, not responder-defined rescue of the broad claim. Rodent insulin handling, acute running performance, cast atrophy and mouse late-life walking are separate endpoints; none establishes human healthspan.