Overview
Discovered in surviving neurons of Alzheimer brains, which is a striking origin story. It is cytoprotective in a wide range of stress models, and plasma levels decline with age. None of that has yet been tested as a treatment in humans.
Not approved for human use anywhereNo approval anywhere for human use. Sold under research-use labelling. Not approved for human use.
| Regulatory status | Not approved. Preclinical neuroprotection and metabolic research compound. |
|---|---|
| Drug class | Mitochondrial-derived peptide — 24 amino acids |
| Route | Subcutaneous or intracerebroventricular (research) |
| Half-life | Short; analogs engineered for longer duration |
| Evidence rating |
1/5 Minimal
Evidence rating 1 out of 5: Minimal
Animal or laboratory data only. No human efficacy evidence. |
| Studied in | Rodent models of Alzheimer disease, stroke, myocardial infarction, and metabolic disease; human observational studies of circulating levels versus age and disease. |
How it works
Binds a trimeric receptor complex and interacts with pro-apoptotic Bcl-2 family proteins, inhibiting Bax-mediated apoptosis. Also activates STAT3 signalling and improves insulin sensitivity in animal models.
Evidence base
Rated 1 of 5 — Minimal. Animal or laboratory data only. No human efficacy evidence.
- Active academic research area; no clinical translation to date.
Benefits & potential uses
Bars indicate how well each claim is supported: three = strong human evidence, two = moderate, one = preliminary or preclinical.
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Neuroprotection in animal models Preliminary
Protects neurons against amyloid-beta toxicity and ischemic injury across multiple rodent models.
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Anti-apoptotic activity Preliminary
A well-characterised molecular mechanism inhibiting Bax-mediated cell death.
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Metabolic effects Preliminary
Improves insulin sensitivity and reduces visceral fat in rodents.
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Declines with age in humans Preliminary
Circulating levels fall with age and are higher in offspring of centenarians — an interesting association.
Risks, cons & cautions
Bars indicate seriousness: three = serious or common, two = moderate, one = minor.
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No human trials Serious
No interventional human data exists.
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Anti-apoptotic effects are double-edged Serious
Blocking programmed cell death systemically is exactly the mechanism by which damaged and pre-cancerous cells survive.
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Poor pharmacokinetics Moderate evidence
Rapid clearance and questionable CNS penetration for the native peptide.
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Unregulated supply Serious
Research-chemical market.
Who should avoid it
- Human use outside research settings
- Any cancer history
If used under medical supervision, monitor
- No validated monitoring exists
Regulatory & legal status
Not approved for human use.
Infographic
Where to read further
We link to live literature searches rather than a frozen citation list, so you always see current results — including anything published after our last review.
- PubMed — all published literature on Humanin
- PubMed — randomized controlled trials only
- ClinicalTrials.gov — registered human trials
Related peptides in Longevity & Mitochondrial
Terms used on this page
- Insulin Resistance
- Insulin resistance is a state in which a given insulin concentration produces less than the expected effect on glucose uptake, hepatic glucose output or lipolysis.
- Preclinical Study and Animal Model
- Preclinical studies are the laboratory, cell and animal experiments done before any human exposure, establishing mechanism, target engagement and the toxicology package that permits a first trial.
- Visceral Adipose Tissue (VAT)
- Visceral adipose tissue is the intra-abdominal fat surrounding the organs, metabolically distinct from subcutaneous fat and more closely linked to cardiometabolic risk.
- Central Nervous System (CNS) Penetration
- CNS penetration is the extent to which unbound drug in plasma reaches brain interstitial fluid, expressed formally as the unbound brain-to-plasma partition coefficient.
This page is educational information, not medical advice. It cannot account for your medical history, medications, or risk factors. Do not start, stop or change any treatment based on it. Speak to a qualified healthcare professional who knows your case.