No. 037 · Longevity & Immune · Longevity Peptide
Humanin
Also known as: HNMT-RNR2-encoded peptide
- Not FDA approved
- WADA ✗ S0
- Nonpolar 14
- Polar 4
- Positive charge 4
- Negative charge 2
Each dot is a residue placed around the ring from N- to C-terminus; its distance from the centre reflects its chemistry.
Evidence
- D In vitro
- C Animal
- B Human pilot
- A RCT
- S Approved
TIER C — Evidence comes mostly from animal studies.
Evidence comes from cell and animal (mostly rodent) studies. Human data only link circulating levels to age and disease; no interventional human trials have been published.
Tiers rate the strength of published evidence — not effectiveness, safety, or a recommendation.
At a glance
- Residues
- 24 amino acids, N→C
- Molecular weight
- 2,687.2 Da
- Formula
- C119H204N34O32S2
- Discovered
- 2001 Identified by Hashimoto et al. from a cDNA library of an Alzheimer’s-disease brain region as a factor that protects neurons from death.
- Routes studied
- Subcutaneous, Intramuscular Routes used in published research
- FDA
- Not approved
- WADA
- Prohibited · S0 Non-approved substances
Sequence
Note Encoded within the mitochondrial 16S rRNA gene (MT-RNR2). Many animal studies use the more potent S14G analogue (HNG).
Overview
A mitochondrial-derived peptide that protects cells from apoptosis and oxidative stress. It is associated with longevity in centenarian studies and is explored for Alzheimer neuroprotection.
Research status Published observational human data linking levels to longevity; preclinical interventional studies ongoing
Mechanism
Humanin is a 24-amino-acid peptide encoded in the mitochondrial 16S rRNA gene. It inhibits apoptosis by binding to Bax and preventing its translocation to mitochondria, and also interacts with IGFBP-3 to modulate apoptotic signaling. It binds the CNTFR/WSX-1/gp130 tripartite receptor to activate STAT3 survival pathways.
Effects reported in research
Reported outcomes, not promises. These come mostly from preclinical (cell or animal) research and have not been confirmed in human trials.
- Cytoprotection against oxidative stress
- Neuroprotective anti-apoptotic signaling
- Improved mitochondrial function
- Associated with healthy aging biomarkers
Safety & unknowns
Endogenous mitochondrial-derived peptide with circulating levels correlated to longevity in humans. No formal human interventional safety data. Preclinical studies show good tolerability. Not FDA-approved. Theoretical concerns about anti-apoptotic mechanisms and cancer.
Unknowns. No randomized controlled trials in humans have been published, so human safety has not been established in controlled studies.
Informational only — not medical advice. peptidemeta publishes no dosing, protocols, or sourcing. Talk to a qualified clinician about any treatment decision.
Studies [2]
- Review 2013
Humanin: a harbinger of mitochondrial-derived peptides?
Review of humanin, a mitochondrially encoded peptide with cytoprotective actions in many stress and disease models, as the first of a class of mitochondrial-derived peptides.
- Preclinical 2001
A rescue factor abolishing neuronal cell death by a wide spectrum of familial Alzheimer's disease genes and Abeta
Discovery paper identifying humanin from an Alzheimer brain cDNA library as a peptide that protected cultured neurons against death caused by familial Alzheimer disease genes and amyloid-beta.
Status sources
Sources behind the tier, regulatory status, sequence and dates on this page.
- Hashimoto et al. 2001 — discovery of humanin (PNAS) pubmed.ncbi.nlm.nih.gov
- UniProt Q8IVG9 — Humanin uniprot.org
- PubChem CID 16131438 (humanin) pubchem.ncbi.nlm.nih.gov
- WADA 2026 Prohibited List — S0 non-approved substances wada-ama.org
Cite this entry
peptidemeta. (2026). Humanin. In peptidemeta: The peptide library, ranked by evidence. Retrieved November 8, 2026, from https://peptidemeta.com/p/humanin/
@misc{peptidemeta-humanin,
title = {Humanin},
author = {{peptidemeta}},
year = {2026},
howpublished = {\url{https://peptidemeta.com/p/humanin/}},
note = {Accessed 2026-11-08}
} Accessed date reflects when you opened this page. Cite primary studies for scientific claims.