Humanin
Dosage Protocol
Humanin is a 21-amino acid peptide encoded within the mitochondrial 16S rRNA genome — one of a family of mitochondria-derived peptides (MDPs). Circulating humanin levels decline with age and various diseases. It signals through FPRL1, CNTFR, and gp130 receptors to exert cytoprotective, anti-apoptotic, anti-inflammatory, and insulin-sensitizing effects.
What is Humanin?
Humanin was discovered in 2001 by Hashimoto and colleagues while screening mitochondrial genome sequences for factors that could rescue neurons from Alzheimer's disease-related apoptosis. It is one of the first identified mitochondria-derived peptides (MDPs) — a class of small peptides encoded in the mitochondrial genome that function as endocrine-like signals.
Circulating humanin levels are positively correlated with health and longevity — higher levels are found in centenarians' offspring, and lower levels are associated with metabolic syndrome, cardiovascular disease, and cognitive decline. It acts on multiple receptor complexes to promote cell survival, improve insulin sensitivity, reduce inflammation, and protect against oxidative stress.
Dosing Schedule
Parameters documented in published preclinical and clinical research.
| Phase | Dose | Frequency | Duration | Notes |
|---|---|---|---|---|
| Research | 0.5 mg | 2× weekly SubQ | Weeks 1–4 | Conservative start based on mouse-scaled pharmacology. |
| Working dose | 1–2 mg | 2–3× weekly | Weeks 4–12 | Most research protocols use 2 mg/week in divided SubQ doses. |
| HNG analog | 0.1–0.5 mg | 2× weekly | Per protocol | HNG (S14G-Humanin) is ~1000× more potent — dose accordingly. |
| Off cycle | — | — | 4–8 weeks | Limited human data — periodic assessment recommended. |
Safety & Side Effects
Academic References
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[1]
Hashimoto Y, et al. (2001). A rescue factor abolishing neuronal cell death by a wide spectrum of familial Alzheimer's disease genes and Aβ. Proc Natl Acad Sci USA. 98(11):6336–41. PubMed ↗
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[2]
Muzumdar RH, et al. (2009). Acute humanin therapy attenuates myocardial ischemia and reperfusion injury in mice. Arterioscler Thromb Vasc Biol. 30(10):1940–8. PubMed ↗
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[3]
Lee C, et al. (2015). The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance. Cell Metab. 21(3):443–54. PubMed ↗
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[4]
Sreekumar PG, et al. (2019). The emerging role of senescence in ocular disease. Oxid Med Cell Longev. 2019:1438951. PubMed ↗