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Research-onlyVendors pendingFacts verified · 2026-05-25

Humanin

Also known as humanin · Wikipedia

Humanin is a 24-amino-acid mitochondrial-derived peptide first identified in 2001 by the Hashimoto laboratory in surviving neurons from an Alzheimer's-disease brain (Hashimoto et al., Proc Natl Acad Sci USA 2001). It is encoded by a short open reading frame within the mitochondrial 16S rRNA (MT-RNR2) gene and acts as a cytoprotective, anti-apoptotic signalling peptide with neuroprotective, metabolic, and IGF-axis-modulating properties in preclinical models (Lee, Cohen et al.). Circulating endogenous humanin declines with age. There are no completed human clinical trials of synthetic humanin or its analogs; all therapeutic claims remain preclinical. Vendors sell unmodified native sequence as a research chemical.

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Mechanism of action

Humanin is a 24-amino-acid peptide encoded within a short open reading frame in the mitochondrial 16S rRNA gene (MT-RNR2). It signals through a trimeric cell-surface receptor complex (CNTFR/WSX-1/gp130) and the formyl peptide receptor-like-1 (FPRL1/FPR2) to activate STAT3, JAK2, and ERK survival pathways (Hashimoto et al.

Humanin is a 24-amino-acid peptide encoded within a short open reading frame in the mitochondrial 16S rRNA gene (MT-RNR2). It signals through a trimeric cell-surface receptor complex (CNTFR/WSX-1/gp130) and the formyl peptide receptor-like-1 (FPRL1/FPR2) to activate STAT3, JAK2, and ERK survival pathways (Hashimoto et al., 2001; Ying et al., 2004). Intracellularly, humanin binds and antagonises pro-apoptotic Bax and BimEL, preventing mitochondrial outer-membrane permeabilisation and caspase activation. It also binds IGFBP-3, modulating IGF-1 bioavailability and signalling (Ikonen et al., 2003; Cohen laboratory). Net preclinical effects are neuroprotection (Alzheimer/ischaemia models), improved insulin sensitivity, suppression of mitochondrial-stress-induced apoptosis, and modulation of the IGF-1 axis.

Pharmacokinetic properties

Half-life

Plasma half-life ~30 minutes (native humanin); analogs like S14G-humanin and HNG (HumaninG) are 1000x more potent and have extended activity

Routes

subcutaneous · intramuscular · intranasal · intravenous

Bioavailability

Not orally bioavailable. Endogenous circulating humanin declines with age. Synthetic analogs (HNG, S14G) used in most preclinical research outperform native peptide.

Amino-acid sequence

(21-aa mitochondria-derived peptide; full 21-aa sequence: MAPRGFSCLLLLTSEIDLPVI)

Use & research dosing

No human clinical dose has been established. Most published efficacy studies use the synthetic S14G-humanin (HNG) analog, reported to be ~1000-fold more potent than native humanin (Hashimoto et al., 2001) - this is not what most vendors sell. Preclinical rodent studies have used 1-10 mg/kg/day parenterally. Self-experimentation protocols commonly report 5-10 mg subcutaneously 2-3 times per week, sometimes paired with MOTS-c. These doses are not supported by controlled human PK or safety data.

Research-use framing only. SavePeptides sells nothing for human consumption. Doses above reflect reported research / self-experimentation ranges, not clinical recommendations.

Editorial perspective

Humanin was the first identified mitochondrial-derived peptide (Hashimoto et al., 2001) and anchors a peptide family that now includes MOTS-c and the SHLPs. Most of the strongest preclinical efficacy data come from the synthetic HNG (S14G-humanin) analog, which is roughly 1000-fold more potent than the native sequence - a crucial caveat because most vendor product is unmodified native humanin. There is no IND-stage human clinical program. All current human use is gray-market self-experimentation.

— SavePeptides editorial desk · last updated 2026-05-25

Cautions & contraindications

Before researching this compound, note:

  • No completed human clinical trials; long-term safety unknown
  • IGFBP-3 binding could alter IGF-1 axis - theoretical concern in active malignancy or anabolic stacks
  • Anti-apoptotic mechanism is theoretically concerning in established malignancy (could promote cancer-cell survival)
  • Most published efficacy data are with the HNG/S14G analog, not the native sequence that vendors typically sell
  • Injection-site reactions; intranasal route causes local irritation
  • Avoid in pregnancy and breastfeeding (no safety data)
  • Not characterised in renal or hepatic impairment
  • Research-grade material purity and endotoxin content highly variable
  • Unknown immunogenicity with chronic administration

Facts verified

2026-05-25

Confidence

low

What this means

  • no completed human clinical trials
  • most published efficacy data use HNG/S14G analog, not native sequence sold by vendors
  • anti-apoptotic mechanism theoretically risky in active malignancy

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