MOTS-c

One of the more scientifically interesting mitochondrial-derived peptides. Mouse metabolic data are real. Jumping from that to a self-administered longevity drug is not.

A 16-residue peptide encoded in the mitochondrial 12S rRNA region. In rodents it influences AMPK-related metabolic signaling and exercise-like adaptations. Human circulating MOTS-c is measurable; pharmacology of injected synthetic MOTS-c in people is early.

Lee, Cohen, and colleagues established MOTS-c as a mitochondrial-encoded metabolic regulator in animal and cell systems. Human work is mostly observational (levels vs age/metabolic status) plus early interventional exploration. Not an outcomes literature.

Not FDA-approved. Research chemical. Academic material, not a medicine.

Academic research material, not a medicine. July 2026 PCAC recommended 503A listing (non-binding). No FDA-approved product. Legitimate human exposure is observational sampling or a trial — not a vendor protocol.

Same four pathways as the Sourcing guide.

None.

Longevity-market injectables appeared years ahead of any human interventional evidence. Sequence on a vial label is not Lee and Cohen's laboratory material.

Strand does not list vendors. See the grey market.

Human dosing is not established. Mitochondrial peptides could, in principle, perturb metabolic set-points in unexpected ways. Gray-market injectables add identity risk.

• Human interventional dosing is not established.
• Mitochondrial peptides can, in principle, perturb metabolic set-points.
• Grey-market identity risk is the immediate practical harm.

• Lee et al. · 2015 · Cell Metab

  The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance. PMID 25738455.

• Human observational follow-up

  Circulating MOTS-c versus age and insulin sensitivity — not an interventional literature.