HumaninMitochondrial PeptideSafety Rating 6/10

TypeMitochondrial-derived peptide
CAS330936-69-1
MW≈2,687 g/mol
AAs24
Primary research areaCytoprotective / longevity research

Research-literature reference data, NOT patient instructions. Not for human use. Consult a licensed clinician for any human application.

Research dose rangeLimited clinical data; mouse studies used ~4 mg/kg IP twice weekly (HNG analog)source ↗
AdministrationIntraperitoneal (mice); no established human route
Half-lifeNot well characterized in humans
Safety6/10 · Not FDA-approved
NCAA D1Not listed

Price Comparison

Compare vendors · per 10mg

3 vendors competing

VendorPrice$ / mgUpdated
PureRawzBest $/mgCOA ✓ · 3P$92.92$9.29May 14, 2026Buy →
Core PeptidesCOA ✓ · 3P$147.00$14.70Apr 16, 2026Buy →
Modern AminosCOA ✓ · 3P$148.00$14.80May 14, 2026Buy →

Overview

About Humanin

Mechanism of action

Mitochondria-derived peptide (MTDP); binds FPRL1/Bax; anti-apoptotic; neuroprotective against Alzheimer's-related toxicity; activates STAT3 and AMPK; insulin sensitizing.

Safety profile

Very limited human data. Generally well-tolerated in early research. Long-term safety profile not established. · Endogenous peptide; cytoprotective; animal studies favorable; no proven harms

Storage

Stability & handling

❄️Lyophilized (powder)−20°Clong-term stable
💉Reconstituted2–8°Cwithin 30 days
📈

Price tracking starts now.

Set an alert to get notified when this peptide drops.

Related pages

More on Humanin

Stack & Compare

Frequently Researched Together

Research

Studies & key findings

  • Humanin is a 21-amino-acid peptide encoded within the mitochondrial 16S rRNA region and first identified in 2001 as a neuroprotective factor from surviving neurons in Alzheimer's disease brains; circulating humanin levels decline with age across species, and children of human centenarians show substantially elevated humanin compared to age-matched controls.
  • Mechanistically, humanin binds IGFBP-3 and blocks amyloid-beta aggregation; in the presence of IGFBP-3 the protective interaction with Aβ is abolished and amyloid oligomer formation increases, identifying IGFBP-3 as a physiological regulator of humanin's neuroprotective capacity and a potential Alzheimer's disease risk modifier.

7 peer-reviewed sources cited — clinical, preclinical, and regulatory.

Read full research →
Failed to fetch