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Humanin

HN, S14G-Humanin

Quick Stats
Studies 491
Trials 100
Score 2
2010 pubmed

Humanins, the neuroprotective and cytoprotective peptides with antiapoptotic and anti-inflammatory properties.

Zapała. Barbara B; Kaczyński. Łukasz Ł; Kieć-Wilk. Beata B; Staszel. Teresa T; Knapp. Anna A; Thoresen. G Hege GH; Wybrańska. Iwona I; Dembińska-Kieć. Aldona A

Key Findings

  • Humanin is a 24‑amino‑acid peptide that blocks cell death pathways (Bax, JNK) and reduces inflammation.
  • It acts through receptors FPRL1/FPRL2 and interacts with IGFBP3 and STAT3, offering broad cytoprotection beyond the brain.
  • Pre‑clinical work suggests it may help prevent Alzheimer‑related damage, mitochondrial disease effects, and protect pancreatic beta cells.

Practical Outcomes

  • Humanin looks promising as a neuro‑ and cell‑protective agent, but without human trials or dosage guidelines it’s not ready for a concrete supplement protocol. Biohackers might watch for future clinical data or consider it only in the context of experimental use with professional supervision.

Summary

Humanin is a tiny protein that helps protect brain cells and other cells from dying, mainly by blocking stress pathways and inflammation. It’s been shown in lab and animal studies to guard against things like Alzheimer’s‑type damage, mitochondrial disorders, and even damage to insulin‑producing cells, but there’s no clear human dosing or proven benefit yet.

Abstract

Humanin (HN) is a newly discovered 24-amino acid peptide, which may suppress neuronal cell death. HN cDNA includes an open reading frame (HN-ORF) of 75 bases located 950 bases downstream of the 5' end of the HN cDNA. It has been demonstrated that HN cDNA is 99% identical to the mitochondrial DNA (mtDNA) sequence. HN homologs have been identified as expressed sequence tags (ESTs) in both rats and nematodes. Certain regions that are homologous to the HN cDNA exist on human chromosomes. HN forms homodimers and multimers and this action seems to be essential for peptide function. HN acts as a ligand for formyl peptide receptor-like 1 (FPRL1) and 2 (FPRL2). It has been demonstrated that HN plays a protective role through its antiapoptotic activity that interferes with Bax activation, which suppresses Bax-dependent apoptosis. HN has also been shown to suppress the c-Jun N-terminal kinase (JNK) and ASK/JNK-mediated neuronal cell death. Several studies have also confirmed that HN could be important in the prevention of angiopathy-associated Alzheimer's disease dementia, diseases related to mitochondrial dysfunction (MELAS), and other types of β-amyloid accumulation-associated neurodegeneration. Avery recent study demonstrated a pluripotent cytoprotective effect and mechanisms of HNs in cells not from the CNS, such as germ cells or pancreatic β-cells, and the potent physiological consequences that result from HN interaction with IGFBP3 and STAT3. In vivo studies suggest that HN may also protect against cognitive impairment due to ischemia/reperfusion injury.

Study Information

Provider

pubmed

Year

2010

DOI

10.1016/s1734-1140(10)70337-6