Humanin

Overview

Humanin was discovered in 2001 by Nishimoto et al. while searching for factors that could rescue neurons from Alzheimer's disease-associated amyloid toxicity. Like MOTS-c, it is encoded by mitochondrial DNA (specifically within the 16S rRNA gene) rather than nuclear DNA, making it a mitochondrial-derived peptide (MDP). Circulating humanin levels are reported to decline with age and are lower in individuals with Alzheimer's disease and cardiovascular disease.

Humanin and its more potent variant HNG (S14G-humanin) have demonstrated cytoprotective effects in neuronal, cardiovascular, and metabolic contexts. It activates the gp130/IL-6 receptor family and interacts with IGFBP-3 to regulate cell survival. Its role as a potential longevity biomarker (the offspring of centenarians have higher humanin levels) has generated interest in aging research.

Mechanism of Action

Humanin binds to a heterotrimeric receptor consisting of CNTFR, WSX-1, and gp130, activating JAK-STAT3 and PI3K/Akt signaling to promote cell survival. It also binds to and inhibits the pro-apoptotic protein BAX and neutralizes IGFBP-3-mediated apoptosis. Its metabolic effects involve IGF-1 signaling modulation and AMPK activation.

Research Areas

• ●Alzheimer's disease neuroprotection
• ●Mitochondrial-derived peptide biology
• ●Longevity and aging biomarkers
• ●Cardiovascular cytoprotection
• ●Insulin sensitivity and diabetes models
• ●Retinal ganglion cell protection

Storage & Handling

For Research Use Only. This information is provided for educational and research purposes. Humanin is not approved for human consumption, veterinary use, or clinical application. All research must be conducted in accordance with applicable laws and institutional guidelines.