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A specimen of the Longevity drawer Drawer D · Longevity

Humanin

Research Only

A 24-amino acid mitochondria-derived peptide (MDP) discovered in 2001 that shows cytoprotective, anti-apoptotic, and neuroprotective effects in preclinical studies. Represents a novel class of signaling molecules encoded within mitochondrial DNA. Extensive academic research with emerging interest in aging, metabolic disease, and neurodegeneration, but no approved clinical applications.

HN · HNG · S14G-Humanin · HN peptide · Colivelin

Research evidence
Moderate

10 human studies

Preclinical
80%
Clinical
20%

Based on 50 cited sources

Evidence Score62/100
Emerging / moderate
Research Depth49/100
Mechanism87/100
Plausibility72/100
Global Coverage72/100
Community Experience33/100
EffectivenessNot Established

Demonstrated effect magnitude — not a recommendation or safety claim.

Research Depth 49: highest human tier is controlled observational biomarker work (Ramanjaneya 2019 n=225, 31214116; multiple correlational MDP studies), no RCTs and no therapeutic trials (1A 22); best human evidence is correlational with high RoB for causal claims (1B 5); total human N in the low-hundreds (1C 7); human data are surrogate biomarkers in the right population but not direct therapeutic outcomes (1D 6); offset by an extensive, independently replicated 20+ year preclinical program across cell/mouse/rat neuro, metabolic and cardiac models (1E 9). Mechanism 87: named, validated targets — FPRL1/2 receptor signaling (ERK1/2, STAT3) and direct BAX binding with siRNA-knockdown functional confirmation (Guo 2003 Nature, 12732850) (2A 38); downstream pathway largely mapped (2B 24); dose-dependent HNG effect in vivo (Muzumdar 2010 cardiac I/R, 20651283) (2C 15); confirmed in mammalian in-vivo models (2D 10). Plausibility 72: mechanism->surrogate biomarker established, surrogate->human clinical benefit still inferred (3A 26); coherent with mitochondrial/apoptosis/aging biology (3B 22); strong class analogy from MOTS-c and SHLPs (Cobb 2016, 27070352) (3C 17); but claims span neuro, metabolic, cardiac and aging systems, lowering specificity (3D 7). Global Coverage 72: independently reproduced across Keio (Japan), USC/Einstein/Mayo (USA), China, Qatar and Italy groups (4A 28, 4B 22); >100 studies and still growing (4C 22); no regulatory recognition anywhere (4D 0). Community Experience 33: negligible documented real-world use confined to niche enthusiast circles (5A 7, 5B 7, 5C 8), no notable adverse signal over limited exposure (5D 11). Effectiveness not established: no quantified human efficacy estimate (all human data are correlational biomarkers, no therapeutic trials) and no meaningful community effect signal.

Scored June 2026 How we rate →
~
Evidence Level
moderate
Not approved for human use by any regulatory agency
Limited human clinical trial data
Consult a healthcare provider before use
Not FDA Approved WADA Prohibited
Identity
SCALE · 1:1 N-TERMINUS C-TERMINUS 24 AA · 2,687.17 Da
Also Known As
HN • HNG • S14G-Humanin • HN peptide • Colivelin
Class
Mitochondria-Derived Peptide (MDP)
Length
24 amino acids
Mol. weight
2,687.17 Da
Sequence
MAPRGFSCLLLLTSEIDLPVKRRA
Molecular Structure
M
A
P
R
G
F
S
C
L
L
L
L
T
S
E
I
D
L
P
V
K
R
R
A
Hydrophobic
Polar
Positive
Negative

Humanin is a mitochondria-derived peptide (MDP) discovered in 2001 through its ability to rescue cells from Alzheimer’s-related death. It represents a novel class of signaling molecules encoded within mitochondrial DNA.

How It Works (Simplified)

Humanin protects cells through multiple complementary mechanisms:

Receptor Signaling

Binds FPRL1/2 receptors, activating ERK1/2 and STAT3 pathways that promote cell survival and inhibit apoptosis.

BAX Binding

Directly binds pro-apoptotic BAX protein, preventing mitochondrial permeabilization and blocking the death cascade.

Mitochondrial Support

Improves mitochondrial function, reduces oxidative stress, and prevents cytochrome c release from damaged mitochondria.

IGF Modulation

Binds IGFBP-3 to modulate insulin-like growth factor signaling, with implications for metabolism and aging.

Key Research: Hashimoto Y et al. (2001) characterized humanin’s ability to rescue cells from familial Alzheimer’s disease (FAD) gene toxicity and amyloid-beta. PMID:11717357

Important Limitations

  • No therapeutic trials — Despite 20+ years of research, no human treatment studies
  • Complex biology — Multiple mechanisms complicate drug development
  • Cancer question — Anti-apoptotic effects could theoretically promote tumor survival
  • Delivery challengesPeptide stability and pharmacokinetics not optimized
  • All human data correlativeBiomarker studies, not cause-and-effect
i. FPRL Receptor Signaling · Anti-Apoptotic
HumaninFPRL1/2 receptorGαi/o couplingERK1/2 activationSTAT3 signalingAnti-apoptotic gene expression
ii. BAX Inhibition Pathway · Cytoprotection
HumaninDirect BAX bindingBlocks BAX oligomerizationPrevents mitochondrial permeabilizationInhibits cytochrome c releaseCell survival
Mechanism FPRL1/2 receptor binding activating ERK1/2 and STAT3 anti-apoptotic signaling
Established 15 direct studies
Benefit shown to protect cells from apoptotic death
Evidence Level
Moderate
20 Animal
25 In Vitro
Mechanism Direct BAX and Bid binding blocking mitochondrial apoptosis cascade
Established 8 direct studies
Benefit appears to provide neuroprotection in disease models
Evidence Level
Moderate
15 Animal
12 In Vitro
Mechanism Improved mitochondrial function and reduced oxidative stress
Supported 10 direct studies
Benefit may improve metabolic function
Evidence Level
Low
5 Human
12 Animal
8 In Vitro
Mechanism IGFBP-3 binding modulating IGF signaling pathway
Supported 6 direct studies
Benefit suggested to modulate aging-related signaling pathways
Evidence Level
Low
8 Human
6 Animal
5 In Vitro
Mechanism Confidence
Established
Supported
Emerging
Evidence Level
High
Moderate
Low
Very Low
Phase 01 1
Acute

Humanin binds FPRL receptors rapidly, activating ERK1/2 and STAT3 signaling within minutes. Anti-apoptotic effects are immediate in cellular models. In vivo distribution and kinetics not fully characterized.

PMID:11717357
Phase 02 2
Days to weeks

Preclinical studies typically administer humanin or HNG for days to weeks. Neuroprotective effects in AD models observed over weeks of treatment. Metabolic improvements in diabetic mice seen within weeks.

PMID:28731445
Phase 03 3
Long-term

Endogenous humanin levels decline with age (from higher levels in youth to lower in elderly). Long-term effects of exogenous supplementation are not characterized. No human chronic administration data available.

PMID:31214116

Research-based observations

This timeline reflects observations from published clinical and preclinical studies. Individual responses may vary significantly. This is not a guarantee of effects or a dosing schedule. Consult qualified healthcare providers for personalized guidance.

Good Signs (6 indicators)
White to off-white lyophilized powder
Complete dissolution in appropriate solvent
Certificate of analysis showing >95% purity
HPLC verification of identity
Mass spectrometry confirmation
Proper vacuum seal on vial
Warning Signs (5 indicators)
Slightly off-white coloration
Slow dissolution time
No third-party testing verification
Purity below 95%
Limited supplier documentation
Bad Signs (5 indicators)
Discolored powder (yellow, brown)
Particles or cloudiness after dissolution
No certificate of analysis
Cannot verify source or identity
Compromised vial seal
Positive quality indicator
Requires evaluation
Potential quality issue

For Research Evaluation Only

These quality indicators are general guidelines based on typical peptide characteristics. Professional laboratory testing (HPLC, mass spectrometry) provides definitive quality verification. This checklist is for initial visual evaluation only.

Synergistic
Compatible
Caution
Avoid

Both are mitochondria-derived peptides with complementary mechanisms. Humanin is cytoprotective while MOTS-c is metabolic. May provide synergistic longevity benefits through different pathways.

Ss-31

Compatible
Compatible

Both target mitochondrial function. SS-31 acts on cardiolipin while humanin signals through FPRL receptors. Non-overlapping mechanisms with potential complementary benefits.

Different anti-aging mechanisms - humanin provides cytoprotection while epithalon targets telomerase. No known interactions.

Different protective mechanisms - humanin acts on apoptosis pathways while BPC-157 promotes angiogenesis and tissue repair.

Both have neuroprotective properties through different mechanisms. Humanin inhibits apoptosis while cerebrolysin provides neurotrophic factors.

Research Note: Interaction data is based on published literature, mechanistic understanding, and theoretical considerations. Most peptide combinations lack direct clinical study. This information is for educational purposes only and does not constitute medical advice. Always consult qualified healthcare providers.

This dossier synthesizes available evidence from peer-reviewed literature, regulatory documents, and clinical trial registries. Evidence strength ratings follow a modified GRADE approach.

For complete methodology details, see our Methodology page.

Important Disclaimer

This dossier is for educational purposes only and does not constitute medical advice. Always consult a qualified healthcare provider before making health decisions.

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