Humanin G (HNG)
S14G-Humanin Enhanced Analog
Evidence grade 1 of 5, Untested. Read how the Atlas grades evidence.
HNG (S14G-Humanin) is a synthetic single-substitution analog of the mitochondrial-derived peptide humanin, reported as roughly 1,000-fold more potent than the native sequence. Every supporting result is animal or in-vitro: intranasal S14G-HN lowered amyloid and improved cognition in APPswe/PS1dE9 and 3xTg mouse models (Niikura/Yuan groups), it protected hippocampal LTP against amyloid-beta in mouse slices (PubMed 19463756), it rescued ARPE-19 cybrids from mitochondrial damage (PMC5550888), and it acted through Jak2/Stat3 in an oxygen-glucose-deprivation cell model (PubMed 29043002). There are zero completed human trials of humanin or any humanin analog, no FDA approval, and one supporting in-vitro fibril paper was later retracted, so the honest grade is 1 (animal/in-vitro only).
- FDA
- No FDA approval and no completed human trial; not on the FDA 503A or 503B compounding bulk lists. Supplied only as a research-use laboratory chemical, not for human consumption.
- WADA
- Not prohibited
Reference only. Not medical advice.
What can go wrong
Unapproved synthetic research chemical with no human safety data; reported ~1,000x potency over native humanin adds dose uncertainty, and humanin signaling has been associated with tumor progression in an experimental triple-negative breast cancer model.
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 G (HNG). 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.
An S14G-substituted humanin analog roughly 1,000x more potent than native humanin, researched for Alzheimer's resistance and insulin sensitization.
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-G (HNG, or HumaninS14G) is an engineered version of humanin, the first mitochondrial-derived peptide, with a single amino-acid change that makes it far more potent. Like humanin it is strongly cytoprotective and neuroprotective, shielding cells from stress and death, and it shows chaperone-like activity that inhibits the toxic protein misfolding seen in Alzheimer’s and type 2 diabetes. It is a research tool used to probe what amplified mitochondrial-peptide signaling can do.
Humanin G is Humanin with one substitution, a glycine swapped in at a single position, a change that increases its potency by roughly a thousandfold. It is otherwise the same mitochondrial-derived peptide, and it is the analog that appears in much of the published animal and cell research.
- Type
- Humanin analog
- Modification
- Single glycine substitution
- Potency
- About 1000x Humanin
- Human trials
- None
- Approved
- No
- Key concern
- Cancer
The Potent Humanin Analog Behind The Research
Humanin G is essentially the research workhorse form of Humanin, and the Humanin entry carries the full picture. Much of the striking preclinical data, the protection against Alzheimer’s-type and stroke injury, the lifespan and healthspan signals, was generated using this potent analog rather than the weaker natural peptide. That makes Humanin G central to the science and subject to exactly the same two cautions. First, all of it remains preclinical or observational in humans, with no completed trials, no approval and no established dosing, so the longevity use runs ahead of the evidence. Second, its core mechanism, blocking apoptosis to keep cells alive, is a double edge, and a more potent version of an anti-death signal is, if anything, a sharper version of the concern that it could also shield malignant cells. It is the strong form of a fascinating but unproven and double-edged molecule.
Safety in detail
All human-relevant claims rest on animal and cell studies; there are no completed clinical trials, no established human dose, and no purity or sterility oversight for research-chemical material. One supporting in-vitro paper was retracted. Preclinical work has also associated humanin-family signaling with tumor progression in a breast-cancer model, so a blanket safety assumption is not supported.
- Effects are documented in cell culture and animal models; there are no completed human safety or efficacy trials.
- Not approved for any use; any consumer material is gray-market research-use-only with unverified identity, dose and purity.
- As an unstudied injectable, its long-term human safety is entirely unknown.
- Best understood as a research molecule, not a therapy.
Children and teenagers
Humanin G has no validated pediatric use and is an unapproved, potent survival-signaling peptide with a cancer concern. 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 G reaches users through the longevity gray market and research-reagent suppliers, the same channels as Humanin. There is no approved product, and its market runs on potent preclinical biology with no human proof.
How we got here
Native humanin is a 24-residue mitochondrial-derived peptide identified around 2001 from the surviving neurons of Alzheimer's patients and encoded within the mitochondrial 16S rRNA region. Investigators soon engineered single-residue analogs to raise potency; substituting glycine for serine at position 14 produced S14G-Humanin, marketed and cited as HNG and reported roughly 1,000-fold more active than the parent. Groups led by Nishimoto, Matsuoka, Niikura and others then truncated and stabilized this analog into AGA-(C8R)HNG17 and, by fusing it C-terminally to the ADNF9 fragment of activity-dependent neurotrophic factor, created the femtomolar-acting hybrid Colivelin. HNG is not a natural product and has never been an approved drug; it circulates today only as a research chemical supplied by laboratory-reagent and peptide vendors, with no brand name or regional trade name because no medicine has been registered from it.
Humanin G was created as a more potent analog of Humanin to study the peptide’s effects more effectively, and a single glycine substitution proved to increase its potency roughly a thousandfold. It became the form used in much of the foundational mitochondrial-derived-peptide research.
The numbers behind the grade
- Type
- Mitochondrial peptide analog
- Based on
- Humanin
- Effect
- Neuroprotective (potent)
- Stage
- Preclinical
- Approved
- No
- Use
- Research tool
The people taking it
Best known as the potent research analog of humanin, widely used in mitochondrial-peptide and neuroprotection studies, but not a consumer therapy.
Humanin G’s users are longevity biohackers and neuroprotection seekers drawn by the research data, plus the mitochondrial-peptide research community itself.
Used in research as a potent humanin analog for neuroprotection and anti-misfolding studies; it has no approved or established human use and appears only as a research peptide.
Set against the alternatives
Humanin G is the potent form of Humanin and the headliner of the mitochondrial-derived-peptide research, sitting alongside the sibling peptide MOTS-c and the SHLPs. Against the senolytic FOXO4-DRI, which promotes cell death to clear senescent cells, it is the opposite bet, blocking cell death, in an even stronger form than natural Humanin. Its profile is Humanin’s, amplified.
What we do not know
- Whether the strong neuroprotective effects of HNG translate into any human benefit in neurodegeneration or metabolic disease.
- What the long-term effects of amplifying this mitochondrial signal would be.
- Whether it offers anything beyond a research tool.
Legal status
Not approved anywhere and not available as a therapeutic. It exists as a research compound and, where sold to consumers, as research-use-only material that is not for human use. The evidence is preclinical.
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.
There is no approved route. It is available only as research-use-only material from peptide vendors, which is not intended for human use; given the absence of human data, self-experimentation is not advisable.
Not produced as a drug; any consumer-facing material is research-use-only, typically synthesized overseas in China, with no quality assurance and frequently no certificate of analysis.
What this entry does not yet cover
What follows is unfinished work on our side, not a finding about Humanin G (HNG).
- Timeline. We have not built the dated record of research and regulatory events.
- Supply chain. We have not mapped where it is made.
- What could change. No forward-looking summary yet.
Sources
S14G-humanin (HNG) is a synthetic analog with Ser14-to-Gly substitution, reported ~1,000x more potent than native humanin at rescuing neurons from Alzheimer-specific insults
Solution structure of Ser14Gly-humanin (Biochem Biophys Res Commun)
Intranasal S14G-HN improved cognitive deficits and reduced amyloid pathology in middle-aged APPswe/PS1dE9 transgenic mice (animal model, not human)
S14G-Humanin improves cognitive deficits, APPswe/PS1dE9 mice (Neurobiol Aging / ScienceDirect)
A humanin derivative reduced amyloid-beta accumulation and ameliorated memory deficit in triple-transgenic (3xTg) AD mice
A Humanin Derivative Reduces Amyloid Beta in Triple Transgenic Mice (PMC3022031)
S14G-humanin protected against amyloid-beta-induced LTP inhibition in mouse hippocampal slices (in-vitro/ex-vivo electrophysiology)
Protective effect of S14G-humanin against beta-amyloid LTP inhibition (PubMed 19463756)
S14G-humanin was neuroprotective against oxygen-glucose deprivation/reoxygenation by reactivating Jak2/Stat3 signaling (cell model)
S14G-humanin neuroprotection via Jak2/Stat3 (PubMed 29043002)
Humanin G (HNG) protected age-related macular degeneration transmitochondrial ARPE-19 cybrids from mitochondrial and cellular damage (human cell model, in-vitro)
Colivelin is a synthetic fusion of ADNF9 with the potent humanin derivative AGA-(C8R)HNG17 (which carries the S14G substitution), acting at femtomolar range; documents the HNG-analog lineage
Development of colivelin, a femtomolar-acting humanin derivative (PubMed 16267233)
Structural characterization confirming Colivelin is built on the AGA-(C8R)HNG17 humanin analog containing the S14G change; family/lineage evidence
ADNF determines structure of Colivelin, ADNF9-Humanin analog fusion (PubMed 17994638)
Consensus/secondary review: no humanin analog (including HNG and Colivelin) is FDA approved; evidence is predominantly preclinical/animal with very limited human data
Humanin and Humanin Analogs, Cognitive Vitality review (Alzheimer's Drug Discovery Foundation)
HNG (Gly14-Humanin G) is catalogued and sold as a research-grade laboratory chemical, not a therapeutic product, consistent with unapproved research-chemical status
Retraction notice on an in-vitro S14G-humanin amyloid-fibril paper; data-integrity caution justifying exclusion from efficacy count
Retracted: S14G-humanin inhibits Abeta1-42 fibril formation (J Peptide Science, Wiley)
The studies that matter
Potent humanin analog development2000s
HumaninS14G was created and shown to have markedly enhanced neuroprotective activity compared with natural humanin, making it the standard potent analog in research.
Chaperone and anti-misfolding studies2017
HNG inhibited the misfolding and aggregation of amyloid proteins involved in diabetes and neurodegeneration, in a dose-dependent way.
Cell-protection models2010s-2020s
HNG protected neuronal and retinal cell models against cellular and mitochondrial damage, reinforcing humanin biology.