Educational reference only. Not medical advice. Consult a healthcare provider before starting any protocol.
Humanin
Humanin (HN) — Mitochondrial-Derived Peptide
What it is
The first mitochondrial-derived peptide (MDP) ever discovered, encoded within the MT-RNR2 gene (16S rRNA region) of the mitochondrial genome. Humanin was identified in 2001 through functional expression screening of a cDNA library from the surviving occipital lobe of an Alzheimer's disease patient. It operates through both intracellular mechanisms (binding pro-apoptotic BAX and tBID to block intrinsic apoptosis, sequestering IGFBP-3) and extracellular receptor-mediated signaling (CNTFR/WSX-1/gp130 trimeric receptor activating JAK2/STAT3, and FPRL1/FPR2 activating ERK1/2). Studied in animal models across neurodegenerative, cardiovascular, metabolic, and retinal disease contexts. The S14G-Humanin (HNG) analog is approximately 1,000-fold more potent. No completed human clinical trials exist for this compound.
Community-reported ranges
Ranges sourced from community forums, biohacking protocol databases, and published preclinical literature. Not dosing guidance.
Reported dose range
500–2000 mcg
Estimated half-life
~30 min (mice), ~4 hours (rats)
Source: preclinical data (Chin et al., Endocrinology 2013)
Reported cycle length
2–4 weeks on
2-4 weeks off
Route
subcutaneous
Common vial sizes
1mg, 5mg, 10mg
Reported timing
AM or split AM/PM
Reported frequency
1-2x daily
Frequently discussed alongside
Based on community forum discussions. Not a recommendation to combine compounds.
MOTS-c
Most closely related — both are mitochondrial-derived peptides from the same genome with overlapping metabolic and longevity research contexts
SS-31 (Elamipretide)
Complementary mitochondria-targeted peptide; SS-31 targets cardiolipin in the inner mitochondrial membrane while Humanin acts on apoptotic signaling
FOXO4-DRI
Both studied in aging biology but with opposing cellular strategies — Humanin protects cells while FOXO4-DRI eliminates senescent ones
Published research
Humanin was independently discovered by three labs in 2001 — the Hashimoto/Nishimoto group (neuroprotection from Alzheimer's-related insults), the Reed lab (BAX binding), and the Cohen lab (IGFBP-3 interaction). Preclinical research spans neuroprotection against amyloid-beta and all tested familial AD mutants, cardiovascular protection (atherosclerosis, ischemia-reperfusion), central and peripheral insulin sensitization (Muzumdar et al., PLoS ONE 2009), retinal protection (AMD models), and aging biology (endogenous levels decline with age). Pharmacokinetic studies in rodents show species-dependent half-life (~30 min mice, ~4 hours rats) with IGFBP-3 binding influencing clearance. No peer-reviewed human clinical trials have been completed as of March 2026. Dosing ranges used in community settings are extrapolated from animal data and are not clinically validated.
Reported side effects
From community self-reports. Not from controlled studies.
Community users have reported generally mild effects including injection site irritation, occasional headache, fatigue at higher doses, digestive upset, and dizziness when fasting. Humanin is endogenously produced, which may contribute to its reported tolerability. Theoretical concerns center on STAT3-mediated oncogenic potential with long-term exogenous administration, as some studies have observed pro-tumoral effects in glioblastoma and gastric cancer models. Systematic safety data in humans does not exist.
Regulatory status
FDA (United States)
Not approved. Not named on the FDA Category 2 bulk drug substances list. No IND applications appear publicly listed. Research-use-only.
Health Canada
Not authorized as a therapeutic product. No DIN assigned.
WADA (Competitive Athletes)
Not specifically named on the 2025/2026 Prohibited List. Likely falls under S0 (Non-approved substances). Notably, the related MDP MOTS-c IS specifically listed under S4.4.1 as an AMPK activator.
Requires free account · 7-day trial included