Humanin
Humanin (HN); Mitochondrial-derived peptide encoded by MT-RNR2 (16S rRNA)
This peptide has not been evaluated by the FDA. It is sold as a research chemical and has no regulatory status for human use.
A tiny natural peptide produced by mitochondria (the energy-producing parts of your cells), first discovered in 2001 in Alzheimer's disease research where it appeared to help brain cells survive. It has shown cell-protective effects in many animal and laboratory studies, but no human treatment trials have been conducted.
This entry is a cited research summary, not an established treatment reference. Dosing language is included as source context, not as medical instruction.
Safety Summary
No systematic human safety data exists. No controlled human adverse-event dataset or phase 1 tolerability study was identified. The ADDF states: 'Clinical human testing has not been conducted, and therapeutic dosing has not been established.' The most significant safety concern is humanin's anti-apoptotic effect potentially promoting tumor cell survival in certain cancer contexts. Humanin was shown to promote tumor progression in experimental TNBC by protecting tumor cells from apoptosis (PMID 32427890). A separate 2023 preprint found humanin enhanced glioblastoma progression via integrin alphaV-TGFbeta signaling (DOI 10.21203/rs.3.rs-2702693/v1). Humanin was upregulated in gastric cancer, bladder tumor cells, and pituitary tumor cells (PMID 32427890). However, HNG showed anti-tumor effects in neuroblastoma/medulloblastoma models, indicating context-dependent effects across tumor types. In preclinical animal studies, humanin was generally well-tolerated with no major adverse effects reported. Humanin transgenic mice showed decreased fertility with reduced brood size (PMID 32575077). The ADDF notes humanin effects may be sex-dependent, influenced by ovarian hormones.
Clinical check-in
If real-world use or exposure is being considered, review potential interactions, contraindications, and monitoring needs with a licensed clinician rather than relying on summary copy alone.
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