Overview
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In plain language
Humanin is a small, natural peptide of 24 amino acids. Its genetic instructions are found in mitochondria, the energy factories inside our cells, rather than in the main DNA in the nucleus.
It was discovered in 2001 while scientists studied brain cells that survived Alzheimer's disease. In cells and animals it appears to protect cells from stress and damage. It has not been tested as a treatment in people and is not FDA-approved.
For students
Humanin (MAPRGFSCLLLLTSEIDLPVKRRA, about 2,687 Da) was identified by Nishimoto's group in 2001 through a cDNA screen for factors that protected neurons from Alzheimer's-related insults. It is encoded within the mitochondrial MT-RNR2 (16S rRNA) gene, making it the first described mitochondrial-derived peptide.
It is reported to act both inside cells (for example binding the pro-apoptotic protein BAX) and outside cells through receptors including FPRL1 and a CNTFR/WSX-1/gp130 complex. Circulating levels have been reported to fall with age in some studies.
For researchers and instructors
Analogues. HNG (S14G-humanin) is about 1,000-fold more potent in some assays and is the form used in many animal studies.
Evidence. Protective effects are reported in models of neurodegeneration, ischemia, diabetes and atherosclerosis. Human data are limited to observational measurements of circulating levels.
Open questions. Nuclear genome pseudogenes (NUMTs) can encode humanin-like sequences, complicating attribution of its true origin.
Status. Not FDA-approved; graded Preclinical.
Molecular identity
- Amino acids
- 24
- Molecular weight
- ~2,687.3 Da
- Formula
- C₁₁₉H₂₀₄N₃₄O₃₂S₂
- Sequence
- MAPRGFSCLLLLTSEIDLPVKRRA
Sequence map
Hydropathy
Kyte–Doolittle score per residue. Positive values are water-repelling.
Origin and history
Humanin was discovered in 2001 by Ikuo Nishimoto’s lab at Keio University in Tokyo. They searched brain tissue from a person with Alzheimer’s disease for genes that protected nerve cells and found a 24-amino-acid peptide that shielded them from Alzheimer’s-related damage.
Two other labs found it independently in 2003, binding cell-death and growth proteins. Surprisingly, its gene sits in mitochondrial DNA. It was the first “mitochondrial-derived peptide,” opening the field that later produced MOTS-c and the SHLPs.
Key people
- Ikuo NishimotoKeio University, Tokyo
- Pinchas CohenUSC; mitochondrial peptide research
Timeline
- 2001
Humanin discovered
- 2003
Independent discoveries of its binding partners
- 2015–16
Related mitochondrial peptides (MOTS-c, SHLPs) found
See every peptide on one history timeline.
Human evidence
Human research is observational, linking blood levels with age or disease. No controlled treatment trials establish benefit.
Registration and enrollment are not proof of benefit; check study results directly.
Explore original publications and distinguish preclinical findings from controlled human evidence.
Safety and regulatory status
See every compound on the regulatory tracker.
Not FDA-approved.
This profile is educational and does not provide treatment, dosing or sourcing guidance.
Sources
- PubMed literature search: Humanin
- PubChem compound search: Humanin
- Hashimoto et al. 2001, PNAS
- ClinicalTrials.gov search: Humanin
Hernandez Gener, E. (2026, November 7). Humanin: molecular data, research history and evidence. VALREXA Biosciences. https://valrexa.com/peptides/humanin.html
APA style · Last reviewed November 7, 2026 · Our editorial standardsLast reviewed November 7, 2026. Trial and regulatory status can change; confirm in the linked registries. This profile is educational and is not medical advice, a treatment recommendation, or dosing or sourcing guidance. Report an error · Corrections policy