GHK (Glycyl-Histidyl-Lysine)

Research-Grade

GHK (Glycyl-L-Histidyl-L-Lysine) is a naturally occurring tripeptide first isolated from human plasma in 1973 by Loren Pickart during studies on why older serum was less effective at stimulating liver cell growth than younger serum. The peptide was identified as a key factor that declined with age — plasma concentrations drop from approximately 200 ng/mL at age 20 to 80 ng/mL by age 60. GHK is the precursor and apo-form of the widely studied GHK-Cu complex, but importantly, the unmetallated tripeptide retains significant biological activity independent of copper binding. Gene expression microarray studies have revealed that GHK modulates the expression of approximately 4,000 human genes — roughly 6% of the genome — in patterns associated with tissue remodeling, anti-inflammatory signaling, antioxidant defense, and stem cell biology. Among the most notable effects: suppression of TGF-β-driven fibrosis, upregulation of DNA repair enzymes, increased production of antioxidant proteins (superoxide dismutase, glutathione-S-transferase), and modulation of genes associated with the ubiquitin-proteasome pathway. These gene-level effects suggest GHK has systemic significance beyond its well-known role as a copper chaperone. In wound healing contexts, GHK accelerates re-epithelialization, stimulates collagen synthesis, and promotes angiogenesis. It also demonstrates chemoattractant properties, recruiting mast cells and macrophages to wound sites. While GHK-Cu is the more commonly studied and commercially available form, research into the apo-peptide continues to reveal that many of GHK's biological effects are mediated by the peptide backbone itself, with copper binding amplifying rather than initiating these activities.