Humanin
24-AA Mitochondrial-Derived Peptide
Evidence grade 1 of 5, Untested. Read how the Atlas grades evidence.
Humanin is a genuine mitochondrial-derived peptide with a large mechanistic literature (about 70 studies since Hashimoto et al. identified it in 2001), but the human evidence is entirely observational: circulating humanin declines with age (Yen et al., Aging 2020) and lower levels are associated with Alzheimer's and metabolic disease while higher levels appear in centenarian offspring. Every interventional and dosing result, including the neuroprotection and insulin-secretion work on the potent HNG/HNGF6A analogs, comes from cell culture, C. elegans, rat, and mouse models; there are no completed or published human interventional trials or RCTs, so the specific supported use grades as animal/in-vitro only.
- FDA
- Not FDA approved for any indication; no completed human interventional trials. Research stage / preclinical only.
- WADA
- Not specifically named on the WADA Prohibited List, but as a non-approved peptide with claimed metabolic and growth-related activity it would fall under S0 (non-approved substances), which are prohibited at all times in sport.
Reference only. Not medical advice.
What can go wrong
No human safety, pharmacokinetic, or dosing data exist; all efficacy is animal/in-vitro, so consumer use is premature and unsupported.
Talk to a clinician before taking this, particularly if you have any history of cancer. The Atlas can tell you what has been studied about Humanin. It cannot tell you how it would interact with your body, your history, or anything else you are taking, and nothing on this page is a reason to start.
A mitochondrially-encoded peptide first identified by Japanese researchers screening for genes that confer resistance to Alzheimer's cell death. Anti-apoptotic, neuroprotective, and insulin-sensitizing; circulating levels fall with age and correlate inversely with mortality risk.
Found while hunting Alzheimer's-resistance genes. From the same mitochondrial DNA as MOTS-c.
What people take it for
These are the reasons people give for taking it. They are not effects it has been shown to have.
How it is supposed to work
Humanin is a tiny peptide your own mitochondria make, and its job is to keep stressed cells alive. It is the founding member of a class of signals encoded not in the cell’s main DNA but inside mitochondrial DNA, and it was discovered for protecting brain cells from the toxins of Alzheimer’s disease. It works by blocking a key trigger of programmed cell death and by switching on survival pathways, so cells under stress, from oxidative damage to stroke, are shielded from dying. The longevity pitch is that since the body’s humanin falls with age, supplementing it might slow aging.
Humanin is a small peptide, about 24 amino acids, encoded within a ribosomal-RNA gene of mitochondrial DNA rather than in the cell’s main genome. It is the first known mitochondrial-derived peptide, conserved from worms to humans, and it is secreted into the blood as a signal. It is sold gray-market and through compounding for off-label use, with a more potent analog called HNG used in research.
- Type
- Mitochondrial-derived peptide
- Encoded in
- Mitochondrial DNA
- Action
- Cytoprotective, anti-apoptotic
- Human trials
- None
- Approved
- No
- Key concern
- Cancer
A Survival Signal From Your Mitochondria, Untested In People
Humanin is real and important science. It was elegantly discovered by screening the surviving neurons of an Alzheimer’s brain for whatever was protecting them, and it turned out to be a peptide written into mitochondrial DNA that blocks cell death and activates survival signaling. The preclinical data is genuinely strong: it protects against Alzheimer’s-type toxicity, oxidative stress and stroke injury in animals, and the longevity associations are striking, since humanin levels fall with age, run higher in long-lived animals like the naked mole-rat and in the children of centenarians, and extend lifespan when boosted in worms. But two honest facts cut against the hype. First, all of that is preclinical or merely observational in humans; there are no completed human efficacy or safety trials, no approval and no established dosing, so the anti-aging use is well ahead of the evidence. Second, the very mechanism that makes it protective, blocking apoptosis, is a double edge, because keeping stressed cells alive can also mean shielding malignant ones, which is why it is a real concern in anyone with active or suspected cancer.
Safety in detail
Human evidence for Humanin is limited to observational associations between naturally circulating peptide levels and age or disease; there are no published human trials of injected Humanin or its HNG analog, meaning side effects, interactions, and safe dosing in people are entirely uncharacterized. Products are supplied as research chemicals not authorized for human use.
- There are no completed human safety or efficacy trials, no approved product and no established dosing.
- Its anti-apoptotic, cytoprotective mechanism could reduce the clearance of malignant cells, making it a real concern in active or suspected cancer.
- Its modulation of IGF-1 and IGFBP-3 has unknown long-term effects.
- Gray-market and compounded sourcing carries quality and purity risk.
- Injecting a systemic survival signal for longevity runs well ahead of the evidence.
Children and teenagers
Humanin is an unapproved survival-signaling peptide with no human trials and a real cancer concern, which makes it inappropriate for minors. There is no appropriate pediatric use.
What people get wrong
Nothing recorded here yet. There is almost certainly something people get wrong about this one, and the blank space means we have not written it down, not that the record is clean.
Who profits, and who pushes back
Nobody is named here yet, because we have not done that work on this entry. Read that as unfinished. Somebody almost certainly sells this, and somebody almost certainly disputes it. Assume both until we have checked.
Humanin’s money runs through gray-market peptide vendors and compounding pharmacies selling it and its analog for longevity, neuroprotection and metabolic use, alongside a research-reagent market and an active academic field studying mitochondrial-derived peptides. There is no approved product. The longevity-biohacking economy markets it on genuinely strong preclinical biology that has not yet been tested in humans.
How we got here
Humanin was identified in 2001 by Hashimoto and colleagues in the Nishimoto lab at Keio University while screening surviving neurons from an Alzheimer's patient's brain for factors that resist amyloid and mutant-APP toxicity, and it was named for that rescuing role. It was soon recognized as the first mitochondrial-derived peptide, encoded within the 16S ribosomal RNA (MT-RNR2) region of mitochondrial DNA rather than the nuclear genome, later joined in that family by MOTS-c (from the separate 12S rRNA region) and the SHLP series. Medicinal-chemistry work produced the far more potent analogs HNG (S14G-Humanin) and HNGF6A, which carry most of the neuroprotective and metabolic research. It has never been developed into an approved drug and today circulates through research-chemical suppliers as Humanin or Humanin HNG, sold as not for human consumption.
Humanin was discovered in 2001 by screening the surviving neurons of an Alzheimer’s brain for what protected them, becoming the first mitochondrial-derived peptide. Its anti-apoptotic and survival-signaling mechanism was mapped, and longevity data accumulated, from worm lifespan extension to the age-decline and centenarian correlations. The field expanded with MOTS-c and the SHLPs, and gray-market and compounded longevity use spread well ahead of any human trials.
- 2001Humanin is discovered as the first mitochondrial-derived peptide.
- 2000sIts anti-apoptotic and survival-signaling mechanism is mapped.
- 2010sLongevity data accumulate and the mitochondrial-peptide field expands.
- ongoingStrong preclinical and correlational human data continue, without trials.
- recentGray-market and compounded longevity use spreads ahead of the evidence.
The numbers behind the grade
- Type
- Mitochondrial-derived peptide
- Discovered
- 2001
- Action
- Cytoprotective
- Human trials
- None
- Approved
- No
- Concern
- Cancer
The people taking it
The founding mitochondrial-derived peptide, a fascinating cell-survival signal with robust preclinical and longevity-correlation data but no human trials, sold gray-market for anti-aging ahead of the evidence and carrying a real cancer concern.
Humanin’s users are longevity biohackers and anti-aging enthusiasts drawn by the centenarian and lifespan data, along with people seeking neuroprotection and cognitive longevity, metabolic and IGF-1 optimizers, and the mitochondrial-health niche. It attracts committed self-experimenters acting on preclinical promise.
A real, founding mitochondrial-derived peptide and active research focus for neuroprotection, longevity and metabolism, sold gray-market and compounded for off-label anti-aging and neuroprotection, with no human trials and a cancer concern. Not approved.
Set against the alternatives
Against MOTS-c, its sibling mitochondrial-derived peptide, humanin is the founding one, discovered in 2001 and focused on cell survival and neuroprotection, while MOTS-c came later and works on metabolism. Against FOXO4-DRI it is a striking opposite: that peptide promotes apoptosis to clear senescent cells, while humanin blocks apoptosis to keep cells alive, two opposite bets on cell death in aging. Against the other mitochondrial peptides, the SHLPs, and against longevity peptides like epithalon, humanin shares the same pattern of gray-market use running ahead of human evidence. Its strength is being a real, founding piece of biology; its weakness is being untested in people and biologically double-edged.
What we do not know
- Whether humanin and its analogs translate from strong preclinical and correlational data to real human benefit.
- Whether its anti-apoptotic mechanism is net-protective or cancer-risky in people.
- What safe human dosing, if any, would look like.
- What therapeutic potential the broader mitochondrial-derived-peptide family holds.
What could change
Mitochondrial signalingThe broader field reframes mitochondria as active signaling organelles.Analog developmentMore potent humanin analogs are studied in the lab.Human trialsGenuine human efficacy and safety trials remain pending.Cancer double-edgeIts survival mechanism is studied for benefit versus cancer risk.
Legal status
Humanin is not approved and has no legal prescribing pathway as of 2026, with no completed human trials. It is sold gray-market and through compounding for off-label longevity, neuroprotection and metabolic use. The cancer concern and absence of established dosing are serious cautions.
Status current as of July 2026. Regulatory positions change, sometimes quickly.
The market for this
What follows describes how this is bought and sold. It is not a buying guide and it is not an endorsement of any seller.
Available only through gray-market vendors and compounding pharmacies, with no approval, no human safety or efficacy data, no established dosing and a real cancer concern. There is no validated route. The mitochondrial-peptide field is a fascinating, legitimate research frontier, but injecting humanin for longevity is unproven and biologically double-edged, and especially risky for anyone with cancer risk. This is research-stage biology, not a therapy.
Gray-market and compounded humanin is moderately to highly priced, with research-grade material more expensive. The cost buys a research-stage compound, not a validated therapy.
Synthesized overseas, mainly in China, and supplied gray-market or through compounding, with no human-grade quality assurance.
China and research vendorsSupply gray-market and research-use-only material.Compounding pharmaciesProvide off-label humanin for longevity and neuroprotection.Research reagentsHumanin and its analog are sold for laboratory study.
At a glance
- Encoded in
- Mitochondrial 16S rRNA
- Discovered via
- Alzheimer's resistance screen
- Trend
- Falls with age
- Correlation
- Inverse w/ mortality
What this entry does not yet cover
What follows is unfinished work on our side, not a finding about Humanin.
Nothing outstanding on this one.
Sources
Humanin is a 24-amino-acid mitochondrial-derived peptide encoded in the MT-RNR2 (16S rRNA) region of mtDNA, discovered in a 2001 screen for factors that rescue neurons from Alzheimer's-related cell death
Humanin regulates lifespan/healthspan; C. elegans overexpression extends lifespan via daf-16/FoxO, but midlife mouse treatment improved metabolic parameters without extending lifespan; human data is observational only
Review confirming humanin is encoded in mitochondrial 16S rRNA, that circulating levels decline with age across mice, monkeys and humans, and that MOTS-c is encoded separately in the 12S rRNA region
Miller et al., mitochondrial-derived peptides in aging, GeroScience 2020
The potent humanin analog HNGF6A enhances glucose-stimulated insulin secretion, but exclusively in isolated pancreatic islets, a murine betaTC3 cell line, rats, and mice, with no human data
Emerging role of humanin in cellular stress resistance and cytoprotection, summarizing anti-apoptotic mechanism and analog development (HNG / S14G)
Gong et al., mitochondrial-derived peptide humanin in stress resistance, PMC
Detailed characterization of humanin neuroprotection against Alzheimer's-relevant insults, all in neuronal cell-culture models
Neuroprotection by rescue factor humanin against AD-relevant insults, PMC
Humanin and MOTS-c expression studied as markers alongside telomere length in Alzheimer's disease, an observational human association study
Marker potential of humanin and MOTS-c in Alzheimer's disease, PMC
US patent describing a method of treating type-1 diabetes with a humanin analogue, documenting the peptide is at the patent/preclinical stage rather than an approved therapy
Humanin has no FDA approval and no completed human interventional/RCT trials; it is sold through research-chemical suppliers not authorized for human use
The studies that matter
Discovery2001
Humanin was found by screening the surviving neurons of an Alzheimer’s brain for resistance to amyloid-beta toxicity, the first mitochondrial-derived peptide.
Mechanismpreclinical
It blocks a key apoptosis trigger, antagonizes IGFBP-3 and lowers IGF-1, and activates STAT3, AKT and ERK survival signaling.
Neuroprotectionanimal models
It protects against amyloid-beta, oxidative and stroke injury, and improved learning while reducing plaques in Alzheimer’s mouse models.
Longevity dataanimal and observational
Boosting it extends lifespan in worms, an analog improves mouse healthspan, and levels fall with age while running higher in long-lived animals and centenarians’ children.
Human gap and cancer concern2026
Human data is only observational with no trials, and the anti-apoptotic mechanism could shield malignant cells, a real concern in cancer.