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.
Regulatory & Evidence
Risk Profile
Generally considered lower risk in research contexts. Risk profile varies by individual — review contraindications before use.
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
5 sources cited · 5 moderate
3 Cohorts · 2 In vitros
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.
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.
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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
Generally considered lower risk in research contexts. Individual response varies — review all considerations before use.
Reported contraindications & considerations
Consult a qualified healthcare professional before making any health decisions. This information is educational only and does not constitute medical advice.
Where to Buy Humanin — Providers & Availability
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Questions to Ask Your Provider
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.
Reported contraindications and considerations for Humanin include none well-established. This is educational information only — consult a qualified healthcare professional before use.
8 providers in the directory currently offer Humanin.
# 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.