Peptide Profile
Humanin
HN · MART
Humanin is a mitochondrially encoded 21-amino-acid peptide originally identified through its capacity to suppress neuronal apoptosis induced by familial Alzheimer's disease gene products, now recognized as a founding member of…
- Half-life
- ~2-4 hours
- Routes
- subcutaneous, intranasal
Educational research information — not medical advice. Review primary sources and consult a qualified professional before any decision.
Educational research tools — not medical advice.
What Humanin is
About Humanin
Mitochondria-derived peptide; binds gp130 receptor, activates STAT3/JAK pathway; inhibits BAX-mediated apoptosis; improves insulin sensitivity
Humanin is a mitochondrially encoded 21-amino-acid peptide originally identified through its capacity to suppress neuronal apoptosis induced by familial Alzheimer's disease gene products, now recognized as a founding member of the class of mitochondrial-derived peptides (MDPs) with broad cytoprotective actions in neurons, cardiomyocytes, and other metabolically stressed cell types. Humanin exerts its cytoprotective effects through multiple mechanisms: extracellularly, it binds insulin-like growth factor-binding protein 3 (IGFBP-3) to regulate IGFBP-3's interaction with nuclear import machinery and modulate its proapoptotic signaling; intracellularly, it inhibits c-Jun NH2-terminal kinase (JNK) activation through SH3-binding protein 5 to suppress stress-induced apoptotic cascades. PNAS research established that humanin interacts with IGFBP-3 to regulate cell survival and apoptosis, characterizing a molecular basis for its anti-apoptotic activity, and subsequent work identified JNK inhibition as an additional neuroprotective mechanism in humanin-treated neuronal preparations. Humanin is a research compound with no regulatory approval in any jurisdiction; published evidence is predominantly from in vitro and preclinical models, and no human clinical trials have been completed to establish pharmacokinetic, safety, or efficacy parameters for exogenous humanin administration.
Humanin Benefits & Research Areas
Research Signals
Commonly researched in the context of
Population research notes
These signals reflect research interest areas, not treatment indications.
Humanin half-life
Why no half-life is shown
Published half-life data for humanin is limited to animal studies and varies widely by analogue and species. No reliable human plasma half-life has been established.
What the evidence says about Humanin
Research Evidence
based on 11 studies · most recent 2026
Regulatory Status
- Availability Status
- Research Only
- FDA Status
- Not Evaluated
Mitochondria-derived 21-aa cytoprotective peptide encoded in 12S rRNA. No FDA approval, no NDA or IND. Research interest in aging and neuroprotection. Research use only.
Regulatory status reflects publicly available information and may change. This is not legal or medical advice.
Research Sources
11 sources cited · 11 moderate
9 Cohorts · 2 In vitros
Humanin and MOTS-c Attenuate Atrial Fibrillation by Suppressing Fibrosis and Mitochondrial Dysfunction.
Biomedicines · 2026
# Summary Research found that humanin and MOTS-c, mitochondrial-derived peptides that are reduced in atrial fibrillation patients, can attenuate the condition by suppressing atrial fibrosis, reducing mitochondrial dysfunction, and lowering inflammatory markers in mouse models. This study demonstrated that these peptides work through distinct mechanisms—humanin primarily via cell adhesion pathways and MOTS-c through metabolic processes—and showed an inverse correlation between peptide levels and disease severity in human AF patients.
Humanin Mitigates Aβ-Induced Retinal Pigment Epithelium Injury via AMPK-Beclin1-Dependent Mitophagy.
Aging Cell · 2026
Humanin Restores Metabolic Hormone Homeostasis of Leptin, Ghrelin, Irisin and Asprosin in Streptozotocin-Induced Diabetic Mice.
Metabolites · 2026
Show 8 more sources ↓
Mitochondrial-derived Peptides and Cytoprotection in ARDS: Emerging Therapeutic Promise of Humanin.
Am J Respir Cell Mol Biol · 2026
Neuroprotective Effect of Intraperitoneal Humanin-G in Retinal Degeneration of Royal College of Surgeons Rats.
Res Sq · 2026
# Research Summary Research found that Humanin-G, a mitochondrial-derived peptide, modulated gene expression related to apoptosis, oxidative stress, and inflammation in the retinas of rats with retinal degeneration, and improved visual acuity in treated animals. This study demonstrated that Humanin-G may have potential as a therapeutic approach for retinal degeneration diseases through its cytoprotective effects on retinal tissue.
Neuroprotective Effect of Intraperitoneal Humanin-G in Retinal Degeneration of Royal College of Surgeons Rats.
Res Sq · 2026
Humanin-G protects septic ARDS by mediating mitochondrial function in lung vascular endothelial cells.
Am J Respir Cell Mol Biol · 2026
# Summary Research found that Humanin-G (HNG), a mitochondrial peptide, protects lung blood vessel cells from damage in septic acute respiratory distress syndrome by restoring mitochondrial function and reducing inflammation through inhibition of the IL-6/STAT3 signaling pathway. This study demonstrated that HNG treatment reduced inflammatory markers, restored mitochondrial structure and energy production, and prevented cell death in both animal models and laboratory settings of septic ARDS.
Humanin improved the rotenone-induced reactive oxygen species formation in PC12 cells by modulating the SIRT3/Nrf2/HO-1 signaling pathway.
Toxicol Ind Health · 2026
# Summary Research found that Humanin, a mitochondrial peptide, protected PC12 cells from rotenone-induced damage by reducing reactive oxygen species formation through activation of the SIRT3/Nrf2/HO-1 signaling pathway. This study demonstrated that Humanin's protective mechanism involved increasing cellular antioxidant defenses and enhancing the cells' ability to counteract oxidative stress.
Mitochondrial-derived Peptides and Cytoprotection in ARDS: Emerging Therapeutic Promise of Humanin.
Am J Respir Cell Mol Biol · 2026
SH3BP5 mediates the neuroprotective effects of humanin by inhibiting c-Jun N-terminal kinase
Journal of Biological Chemistry · 2013
Research identified SH3 domain-binding protein 5 (SH3BP5) as a downstream effector of humanin that directly binds and inhibits c-Jun N-terminal kinase (JNK) via kinase interaction motifs, suppressing pro-apoptotic signaling in neurons exposed to Alzheimer's disease-related insults and establishing a mechanistic pathway for humanin's neuroprotective activity.
Humanin inhibits neuronal cell death by interacting with a cytokine, IGFBP-3
Proceedings of the National Academy of Sciences · 2003
Research identified that humanin binds insulin-like growth factor binding protein-3 (IGFBP-3) with high affinity, inhibiting IGFBP-3-induced neuronal apoptosis; IGFBP-3 in turn potentiated humanin's protective rescue of neurons from amyloid-beta toxicity, revealing a bidirectional neuroprotective interaction relevant to Alzheimer's disease pathology.
Humanin Side Effects & Safety Considerations
Research-use compound with limited human data. Evidence strength varies — see the Evidence section.
No established clinical contraindications. This is an investigational compound with limited human data and has not been evaluated by the FDA for safety in this context. Consult a qualified clinician.
Consult a qualified healthcare professional before making any health decisions. This information is educational only and does not constitute medical advice.
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Frequently Asked Questions — Humanin
Humanin is a mitochondrially encoded 21-amino-acid peptide originally identified through its capacity to suppress neuronal apoptosis induced by familial Alzheimer's disease gene products, now recognized as a founding member of the class of mitochondrial-derived peptides (MDPs) with broad cytoprotective actions in neurons, cardiomyocytes, and other metabolically stressed cell types. Humanin exerts its cytoprotective effects through multiple mechanisms: extracellularly, it binds insulin-like growth factor-binding protein 3 (IGFBP-3) to regulate IGFBP-3's interaction with nuclear import machinery and modulate its proapoptotic signaling; intracellularly, it inhibits c-Jun NH2-terminal kinase (JNK) activation through SH3-binding protein 5 to suppress stress-induced apoptotic cascades.
neuroprotection, anti-apoptotic, metabolic improvement, cardiovascular protection.
Research on Humanin primarily documents effects related to neuroprotection and anti-apoptotic and metabolic improvement and cardiovascular protection. These are areas covered in preclinical and clinical literature — individual response varies and effects depend on context of use.
For Humanin, its FDA status is not evaluated by the FDA, and it is designated for research use only. Regulatory status reflects publicly available information and may change. This is not legal or medical advice.
8 providers in the directory currently offer Humanin.
Humanin is tracked across 3 research vendors on PeptideBase, with per-mg prices ranging $9.79–$11.47. This reflects research-use vendor pricing, not clinical or prescription costs.
# Summary Research found that humanin and MOTS-c, mitochondrial-derived peptides that are reduced in atrial fibrillation patients, can attenuate the condition by suppressing atrial fibrosis, reducing mitochondrial dysfunction, and lowering inflammatory markers in mouse models. This study demonstrated that these peptides work through distinct mechanisms—humanin primarily via cell adhesion pathways and MOTS-c through metabolic processes—and showed an inverse correlation between peptide levels and disease severity in human AF patients.
How to get Humanin
Market Pricing
3 vendorsPrice per mg varies by quantity, vendor type, and formulation. Research use only.
Data verified July 2026 · Humanin price intelligence
Where to buy Humanin
8 providersClinics
7 providersDenver Wellness & Aesthetics Center
Englewood, United StatesView →Hormone & Peptide Therapy Greenville SC
Greenville, United StatesView →Vital Infusions and Performance
Las Vegas, United StatesView →Maryland Trim Clinic
Laurel, United StatesView →Meeting Point Health
Philadelphia, United StatesView →The Hormone Zone
Scottsdale, United StatesView →MATTR
United StatesView →
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