Humanin 10mg

Most bioactive peptides are encoded in nuclear genes. Humanin is encoded within the mitochondrial genome — specifically within the 16S ribosomal RNA gene — which is an unusual location for a protein-coding sequence. This mitochondrial origin makes it the founding member of a class called mitochondria-derived peptides (MDPs). The mitochondrial genome is ancient and highly conserved, so mitochondria-derived signaling molecules have particular biological significance. Humanin’s presence in this location suggests ancient origins for mitochondria-to-nucleus and mitochondria-to-extracellular signaling.

Humanin was identified in 2001 by Nishimoto and colleagues through expression cloning from occipital cortex cDNA of an Alzheimer’s patient. The screening assay looked for factors that could protect neurons from cell death induced by familial Alzheimer’s mutations (V642I APP). Humanin potently rescued neurons from multiple Alzheimer’s-related cytotoxic stimuli including amyloid-beta peptides, ADDL oligomers, and familial AD gene mutations. Subsequent work showed it works through FPRL1/FPR2 receptor signaling and intracellular IGFBP3 binding. These neuroprotective effects are among the most replicated findings in the humanin literature.

Humanin is produced by mitochondria, and mitochondrial function and abundance decline with aging — a process called mitochondrial aging or mitochondrial dysfunction in the context of aging biology. As mitochondrial function decreases, production of mitochondria-derived peptides including humanin appears to decrease as well. Several studies have measured circulating humanin in human populations and found inverse correlations with age and with aging-related diseases. Whether declining humanin contributes to aging pathology or is simply a consequence of aging mitochondria is an active research question.