Humanin

Humanin at a Glance

Humanin is a 24-amino-acid mitochondrial-derived peptide, and the first of that class to be identified — found in a screen for factors protecting neurons from Alzheimer’s-related death. It acts mainly as a cytoprotective signal, suppressing apoptosis, and circulating levels fall with age. Work on it is almost entirely preclinical, focused on neuroprotection and metabolic health. It is not approved for anything.

History & Development

Humanin was the first mitochondrial-derived peptide ever identified - the discovery that established mitochondria send signals as well as make energy.

First described	Not established in the sources consulted for this section
Discovered / synthesised by	Not established in the sources consulted for this section
Institution	Not established in the sources consulted for this section
Origin	Endogenous 24-amino-acid mitochondrial-derived peptide, encoded within the mitochondrial genome
Key patent	Not established in the sources consulted for this section
Assignee	Not established in the sources consulted for this section
Development status	Preclinical - no human treatment trials; never approved

Discovery

Humanin is the founding member of the mitochondrial-derived peptide class - a small family of microproteins encoded inside the mitochondrial genome rather than the nucleus. Its identification opened the category that MOTS-c also belongs to, and reframed mitochondria as signalling organelles rather than only metabolic ones.

Its studied biology is cytoprotective and neuroprotective: keeping cells alive under stress, with particular interest in neurodegeneration.

Development & ownership

There is no development programme and no human treatment trial. The literature is preclinical - cell and animal work on cytoprotection - and humanin is of considerable interest as an endogenous molecule, measured as a biomarker in ageing research, which is a different activity from testing it as a drug.

That distinction matters when reading claims for it. Observational work showing humanin levels decline with age, or correlate with health, says nothing about what injecting it does.

How it reached the market

Humanin reached the peptide market straight from mitochondrial biology, sold as an injectable for longevity and neuroprotection. It has never been given to a human as a treatment in a published trial, and there is no established dose, safety record or route.

What It's Used For

Humanin is a 24-amino-acid mitochondrial-derived peptide (MDP) — the founding member of a small family of microproteins encoded not in the nucleus but inside the mitochondrial genome, humanin within the MT-RNR2 16S rRNA region. It is a genuinely endogenous human peptide: it circulates, declines with age, and is regulated by the growth-hormone/IGF-1 axis ^{9Reference 9Lee C et al. · 2014ObservationalIGF-I regulates the age-dependent signaling peptide humanin — mouse & human observational (biomarker)View study →}.

It was discovered in 2001 as a factor that rescued neurons from Alzheimer’s-related cell death, and its biology is best summarized as cytoprotective and anti-apoptotic ^{1Reference 1Hashimoto Y et al. · 2001In vitroA rescue factor abolishing neuronal cell death by a wide spectrum of familial Alzheimer’s disease genes and Abeta — in vitroView study →}.

Two facts reframe everything that follows, and both are easy to miss. First, no clinical trial has ever administered humanin to anyone. Every human study on record measures it as a biomarker; there is no interventional program, no dose, no human safety data. Second — and this is the trap in most write-ups of this compound — a large share of the animal efficacy literature does not use humanin at all. Because native humanin is weakly active and short-lived, the field engineered more potent analogues — S14G-humanin (HNG), HNGF6A, and the hybrid colivelin — and those are what many of the headline in-vivo results actually tested. An HNG result is not a humanin result. Where a study used an analogue, that is stated in the toggle. Route is likewise load-bearing: every experimental delivery is by injection (intracerebroventricular, intraperitoneal, intravenous, or local), because a 24-residue peptide has negligible oral bioavailability.

Evidence by IndicationStrength of support · Beta

Support is an experimental score I’m building — a composite weighted by study type (human > animal > in vitro > review) and study volume. It’s a beta: a fast way to rank strength of evidence at a glance, not a validated metric. For peptides it is not computed from publication counts — most of this literature is reviews and single-lab series, so raw volume does not mean independent evidence. Two things cap every row below: the human tier here is observational only (no administration study exists), and much of the in-vivo tier used a synthetic analogue rather than humanin itself, which is discounted. A low score here means “never tested in people,” not “tested and failed.” Each application links down to its write-up.

01Neuroprotection & Alzheimer’s diseaseShaky44%Founding in-vitro work + defined receptor/STAT3 mechanism; mouse in-vivo efficacy largely via colivelin analogue; human data observational only ^{1,2,3,6,7Reference 1Hashimoto Y et al. · 2001In vitroA rescue factor abolishing neuronal cell death by a wide spectrum of familial Alzheimer’s disease genes and Abeta — in vitroView study →Reference 2Ying G et al. · 2004In vitroHumanin, a newly identified neuroprotective factor, uses the G protein-coupled formylpeptide receptor-like-1 as a functional receptor — in vitroView study →Reference 3Hashimoto Y et al. · 2009In vitroHumanin inhibits neuronal cell death by interacting with a cytokine receptor complex or complexes involving CNTF receptor alpha/WSX-1/gp130 — in vitroView study →Reference 6Chiba T et al. · 2005In vitroDevelopment of a femtomolar-acting humanin derivative named colivelin by attaching activity-dependent neurotrophic factor to its N terminus — in vitro & mouse (analogue colivelin)View study →Reference 7Chiba T et al. · 2006AnimalColivelin prolongs survival of an ALS model mouse — mouse (analogue colivelin)View study →}

02Insulin sensitivity & metabolic healthShaky42%Rat ICV native humanin (clamp studies) + analogue IV; human correlation only ^{8,9,10Reference 8Muzumdar RH et al. · 2009AnimalHumanin: a novel central regulator of peripheral insulin action — rat (ICV native humanin; IV arm used analogues)View study →Reference 9Lee C et al. · 2014ObservationalIGF-I regulates the age-dependent signaling peptide humanin — mouse & human observational (biomarker)View study →Reference 10Yen K et al. · 2020ObservationalThe mitochondrial derived peptide humanin is a regulator of lifespan and healthspan — C. elegans, mouse (HNG analogue) & human observationalView study →}

03Longevity & healthspanShaky36%C. elegans overexpression + HNG-treated mid-age mice + human observational (centenarian offspring, P3S variant) ^{10,21,22Reference 10Yen K et al. · 2020ObservationalThe mitochondrial derived peptide humanin is a regulator of lifespan and healthspan — C. elegans, mouse (HNG analogue) & human observationalView study →Reference 21Coradduzza D et al. · 2023Systematic reviewHumanin and its pathophysiological roles in aging: a systematic review — systematic reviewView study →Reference 22Miller B et al. · 2024In vitroHumanin variant P3S is associated with longevity in APOE4 carriers and resists APOE4-induced brain pathology — human genetics + in vitroView study →}

04Cardiovascular & endothelial protectionShaky34%Several rodent models but the key ones used analogues (HNGF6A, S14G-HN, colivelin); human = biomarker only ^{11,12,13,14Reference 11Oh YK et al. · 2011AnimalHumanin preserves endothelial function and prevents atherosclerotic plaque progression in hypercholesterolemic ApoE deficient mice — mouse (analogue HNGF6A administered, not native humanin)View study →Reference 12Zhang X et al. · 2012AnimalHumanin prevents intra-renal microvascular remodeling and inflammation in hypercholesterolemic ApoE deficient mice — mouse (4 mg/kg/day IP)View study →Reference 13Zhao Q et al. · 2023AnimalS14G-humanin confers cardioprotective effects against chronic adrenergic and pressure overload-induced heart failure in mice — mouse (analogue S14G-HN)View study →Reference 14Urban C et al. · 2022AnimalColivelin, a synthetic derivative of humanin, ameliorates endothelial injury and glycocalyx shedding after sepsis in mice — mouse (analogue colivelin)View study →}

05Reproductive & gonadal protectionShaky32%Rat/mouse only; native humanin used in the testis work, HNG in the ovarian work ^{15,16,17,18Reference 15Jia Y et al. · 2013AnimalThe cytoprotective peptide humanin is induced and neutralizes Bax after pro-apoptotic stress in the rat testis — rat (intratesticular synthetic native humanin)View study →Reference 16Lue Y et al. · 2010In vitroOpposing roles of insulin-like growth factor binding protein 3 and humanin in the regulation of testicular germ cell apoptosis — rat / in vitroView study →Reference 17El Kattawy HA et al. · 2022AnimalHumanin ameliorates late-onset hypogonadism in aged male rats — rat (native humanin)View study →Reference 18Huang J et al. · 2025AnimalS14G-Humanin ameliorates ovarian dysfunction in a cyclophosphamide-induced premature ovarian insufficiency mouse model — mouse (analogue S14G-HN)View study →}

06Retinal & ocular protectionShaky20%Review of in-vitro RPE work + one non-peer-reviewed rat preprint using HNG; no human data ^{19,20Reference 19Minasyan L et al. · 2017ReviewProtective mechanisms of the mitochondrial-derived peptide humanin in oxidative and endoplasmic reticulum stress in RPE cells — review (of in-vitro human RPE work)View study →Reference 20Lin B et al. · 2026AnimalNeuroprotective effect of intraperitoneal Humanin-G in retinal degeneration of Royal College of Surgeons rats — rat (analogue HNG), preprint, not peer-reviewed. bioRxiv. https://pubmed.ncbi.nlm.nih.gov/41929020/View study →}

Mechanisms

Pharmacokinetics

Humanin is an endogenous 24-residue peptide, so like essentially all peptides its oral bioavailability is negligible — it would be digested before absorption. Every experimental study delivers it by injection: intracerebroventricular for the central insulin work ^{8Reference 8Muzumdar RH et al. · 2009AnimalHumanin: a novel central regulator of peripheral insulin action — rat (ICV native humanin; IV arm used analogues)View study →}, intraperitoneal for the vascular, renal and retinal models ^{11,12,20Reference 11Oh YK et al. · 2011AnimalHumanin preserves endothelial function and prevents atherosclerotic plaque progression in hypercholesterolemic ApoE deficient mice — mouse (analogue HNGF6A administered, not native humanin)View study →Reference 12Zhang X et al. · 2012AnimalHumanin prevents intra-renal microvascular remodeling and inflammation in hypercholesterolemic ApoE deficient mice — mouse (4 mg/kg/day IP)View study →Reference 20Lin B et al. · 2026AnimalNeuroprotective effect of intraperitoneal Humanin-G in retinal degeneration of Royal College of Surgeons rats — rat (analogue HNG), preprint, not peer-reviewed. bioRxiv. https://pubmed.ncbi.nlm.nih.gov/41929020/View study →}, intravenous for the peripheral analogue arm ^{8Reference 8Muzumdar RH et al. · 2009AnimalHumanin: a novel central regulator of peripheral insulin action — rat (ICV native humanin; IV arm used analogues)View study →}, and local intratesticular for the germ-cell work ^{15Reference 15Jia Y et al. · 2013AnimalThe cytoprotective peptide humanin is induced and neutralizes Bax after pro-apoptotic stress in the rat testis — rat (intratesticular synthetic native humanin)View study →}. Native humanin is short-lived and weakly active, and that is precisely why the field built analogues: S14G-humanin (HNG), characterized structurally as a potent rescue factor ^{5Reference 5Benaki D et al. · 2006Solution structure of Ser14Gly-humanin, a potent rescue factor against neuronal cell death in Alzheimer’s disease — structural study (analogue HNG)View study →}; HNGF6A, used in the atherosclerosis model ^{11Reference 11Oh YK et al. · 2011AnimalHumanin preserves endothelial function and prevents atherosclerotic plaque progression in hypercholesterolemic ApoE deficient mice — mouse (analogue HNGF6A administered, not native humanin)View study →}; and colivelin, an ADNF–humanin hybrid deliberately engineered for femtomolar activity ^{6Reference 6Chiba T et al. · 2005In vitroDevelopment of a femtomolar-acting humanin derivative named colivelin by attaching activity-dependent neurotrophic factor to its N terminus — in vitro & mouse (analogue colivelin)View study →}. There is no published human pharmacokinetic study of administered humanin — no absorption, distribution, half-life or clearance figure exists for it as a drug. What is measurable is the endogenous peptide: plasma levels are quantifiable, decline with age, and are suppressed by GH and IGF-1 ^{9Reference 9Lee C et al. · 2014ObservationalIGF-I regulates the age-dependent signaling peptide humanin — mouse & human observational (biomarker)View study →}, which tells you the body regulates and clears it but says nothing about the fate of an injected dose. Reconstitution and stability parameters for gray-market lyophilized product are undocumented.

Clinical & regulatory status

Humanin is an unapproved research chemical — it has no FDA, EMA, TGA or PMDA approval, is not an approved dietary supplement, and is not a scheduled or controlled substance anywhere. No registered clinical trial has ever administered humanin as an intervention. A ClinicalTrials.gov search returns only studies that measure it: completed observational work on humanin isoforms in cardiac muscle and plasma around cardiac surgery (NCT03431844, n=106, completed 2019, no results posted as of July 2026), plasma humanin in acute kidney injury (NCT06105229 and NCT06125249, both status unknown), muscle biopsies in cerebral palsy (NCT05506228), and IVF outcomes in PCOS (NCT04104958). Two interventional records mention humanin — a comparison of general versus combined spinal-epidural anesthesia (NCT07678073) and a high-intensity exercise study in a diabetic population (NCT07438002) — but in both, the intervention is the anesthetic or the exercise and humanin is only an outcome measure. There is therefore no phase-based development program, no efficacy readout, and no controlled human safety data.

Last checked: July 2026.

Sourcing, Route & Legal Status

Regulatory status. Humanin is not approved as a drug or dietary supplement in any jurisdiction, holds no marketing authorization anywhere, and has never held one — so there is no label, withdrawn or current, to cite. It is not a scheduled or controlled substance. No sponsor has ever sought approval to administer it; the only registered human studies measure it in patients (see Clinical & regulatory status). Being an endogenous human peptide does not make the injected research-grade product a supplement — your body making a molecule says nothing about the safety or legality of injecting a synthesized copy of it.

How it’s supplied & administered. Gray-market vendors sell it as lyophilized (freeze-dried) powder requiring reconstitution, as either native humanin or the analogue HNG (S14G-humanin) — and the distinction between those two products is routinely blurred in marketing copy even though it is the single most important thing about the compound. Vendor-suggested routes are subcutaneous or intraperitoneal injection. Note the mismatch: subcutaneous dosing is essentially unstudied for humanin. The animal literature used intracerebroventricular, intraperitoneal, intravenous and local intratesticular delivery — a route nobody has characterized is being sold as the standard one. Oral, sublingual, nasal or topical “humanin” products have no basis at all, since peptide oral bioavailability is negligible.

Sourcing reality (a safety issue). Because humanin sits outside every regulatory framework, each quality risk falls on the buyer. There is no manufacturing oversight and no batch accountability: sequence identity, peptide content, purity and bacterial endotoxin load are all unverified. Independent testing of the gray-market peptide sector routinely finds under-dosing, mislabeling, degraded material and endotoxin contamination — a particular hazard for injectables, where contaminants bypass the gut entirely. For humanin there is an additional, compound-specific identity risk: native humanin and HNG are different molecules with different potency, and a vial can contain either. Third-party certificates of analysis (mass-spec identity, HPLC purity, endotoxin testing) are the only partial check available, and even those can be fabricated. No vendors are recommended or linked here; the sourcing environment is itself a reason for caution independent of the pharmacology.

Safety

No trial has ever given humanin to a person, so there is no adverse-event profile, no dose-limiting toxicity and no dose range. The one concern worth stating plainly is mechanistic: its defining property is broad suppression of apoptosis.

Safety at a Glance

❔ Toxicity unknown

• No human safety data at all. Humanin has never been administered to a person in a trial, at any dose, for any duration.
• It suppresses apoptosis broadly. Evading apoptosis is a general survival mechanism of malignant cells, so a systemic anti-apoptotic peptide carries a theoretical oncological concern.
• Not assessed in pregnancy or breastfeeding. No human or dedicated animal reproductive-safety studies — see the box below.
• Current or prior malignancy. The anti-apoptotic mechanism is the specific reason for concern.
• No interaction study of any kind exists. Humanin sits on the GH/IGF-1 axis and signals through gp130/STAT3, so interactions are conceivable but untested.
• Injection and sourcing risks dominate. Injection-site reactions, infection from non-sterile technique, and endotoxin in impure material.

Full Safety & Interactions Detail

What’s actually known: nothing, in humans. There are no human safety data from administering humanin — no trial has ever given it to a person, so there is no adverse-event profile, no dose-limiting toxicity, and no dose-ranging study. Everything below is drawn from animal work and from the peptide’s mechanism, and is labeled as such.

• Animal tolerability. In rodent studies humanin and its analogues were generally tolerated at the doses used, with reported effects being protective rather than toxic. But these are short-term efficacy experiments, not toxicology studies; most used analogues rather than native peptide; and absence of reported harm is not evidence of safety.
• A mechanism-based caution worth stating plainly. Humanin’s defining property is that it suppresses apoptosis broadly. Evasion of apoptosis is a general survival mechanism of pre-malignant and malignant cells, so a systemically administered anti-apoptotic peptide carries a theoretical oncological concern. This is inference from mechanism, not an observed harm — but it is the kind of concern that a human trial would exist to resolve, and no such trial exists.
• Endocrine-axis interactions. Humanin sits on the GH/IGF-1 axis and signals through gp130/STAT3 cytokine receptors ^{3,9Reference 3Hashimoto Y et al. · 2009In vitroHumanin inhibits neuronal cell death by interacting with a cytokine receptor complex or complexes involving CNTF receptor alpha/WSX-1/gp130 — in vitroView study →Reference 9Lee C et al. · 2014ObservationalIGF-I regulates the age-dependent signaling peptide humanin — mouse & human observational (biomarker)View study →}, so interactions with drugs acting on those pathways are conceivable. No interaction study of any kind has been performed — do not represent any specific interaction as established.
• Injection-specific risks. As a reconstituted injectable of unregulated origin, the dominant real-world hazards are not the peptide’s pharmacology but the delivery: injection-site reactions, infection from non-sterile technique or contaminated product, and systemic reaction to endotoxin in impure material.
• Who should avoid it. Anyone pregnant or breastfeeding; anyone with a current or prior malignancy, given the anti-apoptotic mechanism; and in general anyone unwilling to accept an entirely untested investigational peptide from an unregulated supply.

Scope disclosure (not a claim):

• Human data? None from administration. The human literature is entirely observational — levels, correlations and genotypes — and cannot establish what giving the peptide does.
• Interactions assessed? No. No formal interaction studies. The endocrine-axis note above is inferred from mechanism, not tested.
• Pregnancy/lactation assessed? No. Not studied; avoid.
• Long-term safety established? No. There are no human safety data of any duration. Do not infer safety from the absence of reports — the peptide simply has not been given to people.

Never imply safety from silence. Where humanin “wasn’t studied,” that is stated rather than treating no-news as good-news.

Pregnancy & Lactation

? Not established in pregnancy? Not established in lactation

Not assessed / not established. There are no human or dedicated animal reproductive-safety studies of administered humanin, and no label statement exists. (Animal work has studied humanin analogues for protecting gonadal tissue against chemotherapy — that is a protection experiment, not a pregnancy-safety evaluation.) Should be avoided in pregnancy and lactation on the default-caution principle for unapproved peptides.

Dosage

There is no established human dose for humanin, and none is recommended here. It is not an approved supplement or drug, no human has ever been dosed with it in a registered study, and no human pharmacokinetic data exist to anchor a figure to.

Animal doses circulate online and are sometimes presented as a starting point — they are not one. Rodent work used model-specific injected amounts (for example 4 mg/kg/day intraperitoneally in the ApoE mouse renal study ^{12Reference 12Zhang X et al. · 2012AnimalHumanin prevents intra-renal microvascular remodeling and inflammation in hypercholesterolemic ApoE deficient mice — mouse (4 mg/kg/day IP)View study →}), delivered by routes that do not apply to human self-administration, and in many cases used HNG or another analogue rather than humanin, so even the milligram figure refers to a different molecule with different potency. Allometric conversion of a rodent dose to a human one is not a validated exercise for an untested peptide. Vendor-suggested reconstitution and injection amounts are derived from no trial at all. Because oral bioavailability is negligible, any oral, sublingual or topical “humanin” product has no basis for a dose in the first place (see Sourcing, Route & Legal Status). This entry is informational only and is not a protocol.

References

1. Hashimoto Y, Niikura T, Tajima H, et al. (2001). A rescue factor abolishing neuronal cell death by a wide spectrum of familial Alzheimer’s disease genes and Abeta — in vitro. Proc Natl Acad Sci USA. https://pubmed.ncbi.nlm.nih.gov/11371646/
2. Ying G, Iribarren P, Zhou Y, et al. (2004). Humanin, a newly identified neuroprotective factor, uses the G protein-coupled formylpeptide receptor-like-1 as a functional receptor — in vitro. J Immunol. https://pubmed.ncbi.nlm.nih.gov/15153530/
3. Hashimoto Y, Kurita M, Aiso S, et al. (2009). Humanin inhibits neuronal cell death by interacting with a cytokine receptor complex or complexes involving CNTF receptor alpha/WSX-1/gp130 — in vitro. Mol Biol Cell. https://pubmed.ncbi.nlm.nih.gov/19386761/
4. Ikonen M, Liu B, Hashimoto Y, et al. (2003). Interaction between the Alzheimer’s survival peptide humanin and insulin-like growth factor-binding protein 3 regulates cell survival and apoptosis — in vitro. Proc Natl Acad Sci USA. https://pubmed.ncbi.nlm.nih.gov/14561895/
5. Benaki D, Zikos C, Evangelou A, et al. (2006). Solution structure of Ser14Gly-humanin, a potent rescue factor against neuronal cell death in Alzheimer’s disease — structural study (analogue HNG). Biochem Biophys Res Commun. https://pubmed.ncbi.nlm.nih.gov/16945331/
6. Chiba T, Yamada M, Hashimoto Y, et al. (2005). Development of a femtomolar-acting humanin derivative named colivelin by attaching activity-dependent neurotrophic factor to its N terminus — in vitro & mouse (analogue colivelin). J Neurosci. https://pubmed.ncbi.nlm.nih.gov/16267233/
7. Chiba T, Yamada M, Sasabe J, et al. (2006). Colivelin prolongs survival of an ALS model mouse — mouse (analogue colivelin). Biochem Biophys Res Commun. https://pubmed.ncbi.nlm.nih.gov/16564029/
8. Muzumdar RH, Huffman DM, Atzmon G, et al. (2009). Humanin: a novel central regulator of peripheral insulin action — rat (ICV native humanin; IV arm used analogues). PLoS One. https://pubmed.ncbi.nlm.nih.gov/19623253/
9. Lee C, Wan J, Miyazaki B, et al. (2014). IGF-I regulates the age-dependent signaling peptide humanin — mouse & human observational (biomarker). Aging Cell. https://pubmed.ncbi.nlm.nih.gov/25040290/
10. Yen K, Mehta HH, Kim S-J, et al. (2020). The mitochondrial derived peptide humanin is a regulator of lifespan and healthspan — C. elegans, mouse (HNG analogue) & human observational. Aging (Albany NY). https://pubmed.ncbi.nlm.nih.gov/32575074/
11. Oh YK, Bachar AR, Zacharias DG, et al. (2011). Humanin preserves endothelial function and prevents atherosclerotic plaque progression in hypercholesterolemic ApoE deficient mice — mouse (analogue HNGF6A administered, not native humanin). Atherosclerosis. https://pubmed.ncbi.nlm.nih.gov/21763658/
12. Zhang X, Urbieta-Caceres VH, Eirin A, et al. (2012). Humanin prevents intra-renal microvascular remodeling and inflammation in hypercholesterolemic ApoE deficient mice — mouse (4 mg/kg/day IP). Life Sci. https://pubmed.ncbi.nlm.nih.gov/22820173/
13. Zhao Q, et al. (2023). S14G-humanin confers cardioprotective effects against chronic adrenergic and pressure overload-induced heart failure in mice — mouse (analogue S14G-HN). Heliyon. https://pubmed.ncbi.nlm.nih.gov/38045183/
14. Urban C, et al. (2022). Colivelin, a synthetic derivative of humanin, ameliorates endothelial injury and glycocalyx shedding after sepsis in mice — mouse (analogue colivelin). Front Immunol. https://pubmed.ncbi.nlm.nih.gov/36119052/
15. Jia Y, Lue Y-H, Swerdloff R, et al. (2013). The cytoprotective peptide humanin is induced and neutralizes Bax after pro-apoptotic stress in the rat testis — rat (intratesticular synthetic native humanin). Andrology. https://pubmed.ncbi.nlm.nih.gov/23686888/
16. Lue Y, Swerdloff R, Liu Q, et al. (2010). Opposing roles of insulin-like growth factor binding protein 3 and humanin in the regulation of testicular germ cell apoptosis — rat / in vitro. Endocrinology. https://pubmed.ncbi.nlm.nih.gov/19952275/
17. El Kattawy HA, Abozaid ER, Abdullah DM (2022). Humanin ameliorates late-onset hypogonadism in aged male rats — rat (native humanin). Curr Mol Pharmacol. https://pubmed.ncbi.nlm.nih.gov/35086467/
18. Huang J, et al. (2025). S14G-Humanin ameliorates ovarian dysfunction in a cyclophosphamide-induced premature ovarian insufficiency mouse model — mouse (analogue S14G-HN). Mol Hum Reprod. https://pubmed.ncbi.nlm.nih.gov/40811024/
19. Minasyan L, Sreekumar PG, Hinton DR, Kannan R (2017). Protective mechanisms of the mitochondrial-derived peptide humanin in oxidative and endoplasmic reticulum stress in RPE cells — review (of in-vitro human RPE work). Oxid Med Cell Longev. https://pubmed.ncbi.nlm.nih.gov/28814984/
20. Lin B, et al. (2026). Neuroprotective effect of intraperitoneal Humanin-G in retinal degeneration of Royal College of Surgeons rats — rat (analogue HNG), preprint, not peer-reviewed. bioRxiv. https://pubmed.ncbi.nlm.nih.gov/41929020/
21. Coradduzza D, et al. (2023). Humanin and its pathophysiological roles in aging: a systematic review — systematic review. Biology (Basel). https://pubmed.ncbi.nlm.nih.gov/37106758/
22. Miller B, et al. (2024). Humanin variant P3S is associated with longevity in APOE4 carriers and resists APOE4-induced brain pathology — human genetics + in vitro. Aging Cell. https://pubmed.ncbi.nlm.nih.gov/38520065/

View all 22 references▾

Registered studies (ClinicalTrials.gov) — none administers humanin; all measure it.

• NCT03431844 — Humanin isoforms in cardiac muscle and blood plasma and major complications after cardiac operation (observational, n=106, completed 2019, no results posted). https://clinicaltrials.gov/study/NCT03431844
• NCT06105229 / NCT06125249 — plasma humanin in acute kidney injury (observational, status unknown).