Humanin
Metabolic
ABOUT
Humanin is a mitochondrial-derived peptide. Human studies cited here measure endogenous circulating levels in response to physiological or disease contexts; they do not establish a therapeutic use for administered Humanin.
EVIDENCE OVERVIEW
Reasoned from mechanism, not measured in people
WHAT THIS MEANS
Theoretical. Review the research and limitations before relying on this record.
IDENTITY
HALF-LIFE
HOW IT IS THOUGHT TO WORK
Humanin is a mitochondrial-derived peptide encoded in the 16S rRNA region, described as acting in autocrine, paracrine and endocrine fashion. Reported cytoprotective signalling runs through the JAK/STAT pathway and interaction with BCL-2 family proteins, and it inhibits mitochondrial complex I activity, limiting oxidative stress.
PHARMACOKINETICS
No pharmacokinetic data is available. Endogenous humanin is detectable in circulation, but that does not describe the handling of an administered dose.
REVIEW
PUBLISHED PAIR RECORDS
with MOTS-c
Converging on mitochondrial functionMOTS-c and Humanin both act on mitochondrial biology, so their proposed effects converge rather than complement. MOTS-c and humanin are both mitochondrial-derived peptides encoded in mitochondrial DNA and described as retrograde signals to the nucleus; their reported metabolic and cytoprotective effects overlap substantially, and human data for both is observational - circulating levels associated with age and disease - with no interventional trial for either. No study has characterised this combination. Peppy reports curated pharmacology, not a safety verdict. A prescriber or pharmacist should review any intended combination.
Reviewed 21 Aug 2026with SS-31
Converging on mitochondrial functionHumanin and Elamipretide (SS-31) both act on mitochondrial biology, so their proposed effects converge rather than complement. Elamipretide is the only one of this group tested in a large controlled human trial, and MMPOWER-3 did not meet either primary endpoint; the mitochondrial-derived peptide in this pair has no interventional human data at all. Their mechanisms differ within the same organelle - cardiolipin binding on the inner membrane versus retrograde signalling to the nucleus - so overlap is at the level of target tissue rather than target molecule. No study has characterised this combination. Peppy reports curated pharmacology, not a safety verdict. A prescriber or pharmacist should review any intended combination.
Reviewed 21 Aug 2026HUMAN EVIDENCE
Human evidence is observational: circulating humanin declines with age and has been proposed as a marker of mitochondrial function in cardiovascular disease. No interventional human trial has been reported. The disease associations across cancer, diabetes, neurodegeneration and cardiovascular disease all derive from cell-culture and animal work.
REPORTED EFFECTS
No human safety data exists. Note that a substantial part of this literature carries a commercial conflict of interest disclosure tied to a company developing humanin analogues. No regulator has approved this substance for the use described here, so there is no label-verified dose, purity standard, or safety monitoring requirement behind it.
RESEARCH LIMITATIONS
Observational biomarker findings do not demonstrate benefit or safety of supplementation. No dose, protocol, or interaction conclusion is provided.
CURATED SOURCES · 4