Overview
Humanin is a small peptide encoded within the mitochondrial 16S rRNA gene, identified for its protective effects against Alzheimer-related neurotoxicity.
- Endogenously produced from mitochondrial DNA
- Synthesized for research
- Subcutaneous injection (research)
Mechanism of action
Binds formyl peptide receptor-like 1 and IGFBP-3 to suppress apoptosis pathways and improve mitochondrial bioenergetics under stress.
- · BAX inhibition (anti-apoptotic)
- · IGFBP-3 binding
- · Insulin sensitivity
How it acts on the body
Humanin sits in a small but growing family of mitochondrial-derived peptides (MOTS-c is another) that act as signaling molecules between mitochondria and the rest of the cell. Its best-known effect is protecting neurons from amyloid-beta toxicity, which was the context of its discovery.
Beyond neuroprotection, humanin improves insulin sensitivity, modulates inflammation, and declines with age in human plasma — a pattern shared with several other longevity-related peptides. Whether replacement is meaningful in humans is still being explored.
Hormonal & endocrine impact
How this peptide is reported to shift specific hormones and signaling molecules. Directionality reflects research literature and preclinical models, not clinical prescribing data.
Curves are schematic shapes (sigmoid for increases/decreases, damped oscillation for modulation/stabilization) anchored to a 100% baseline. They communicate direction and tempo of change reported in research literature — not absolute hormone concentrations.
Effects on the body
Organ system effects
Neuroprotection against amyloid-beta toxicity.
Insulin sensitivity and IGFBP-3 modulation.
Reported effects
Drawn from preclinical research, anecdote, and small-scale clinical observation. No evidence grades are assigned — most peptides on this page lack rigorous human trials.
- Neuroprotective signaling
- Mitochondrial / longevity research interest
Potential side effects
- · Injection-site reactions
- · Mild fatigue
- · Limited human data
Drug interactions
No notable interactions reported.
Pairing context
- MOTS-cComplementary mitochondrial signaling.
- Unsupervised long-term useSafety profile not characterized.