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Dr. Pickart had me post this for your reading enjoyment.


In 1984, I observed that GHK-Cu possesses a mild antioxidant activity similar to the enzyme superoxide dismutase, which manifests itself as a calming of red and irritated skin. Steve Aust’s lab at Utah State University discovered that GHK-Cu blocks the damage-induced release of oxidizing iron molecules from ferritin. Further discoveries followed. Vinci et al. at the University of Catalina in Italy reported that GHK-Cu blocks tissue damage by interleukin-1.


Vinci C, Caltabiano V, Santoro AM, Rabuazzo AM, Buscema M, Purrello R, Rizzarelli E. Copper addition prevents the inhibitory effects of interleukin 1-beta on rat pancreatic islets, Diabetologia, 1995; 38:39-45


Soon after, Robert Koch’s lab at Stanford University reported that GHK- Cu shuts down the production, by normal and keloid fibroblasts, of the scar- forming protein TGF-ß-1. Interestingly, they also found that retinoic acid, which is thought to trigger remodeling, actually increases this scar-forming factor.


McCormack MC, Nowak KC, Koch RJ. The effect of copper tripeptide and tretinoin on growth factor production in a serum-free fibroblast model, Arch. Facial. Plast Surg 2001;3:28-32


Canapp et al. found GHK-Cu suppresses the tissue damaging cytokine TNF-alpha (tumor necrosis factor-alpha) and shifts the balance of proteases that dissolve proteins, and anti-proteases toward more anti-protease activity.


Canapp SO Jr, Farese JP, Schultz GS, Gowda S, Ishak AM, Swaim SF, Vangilder J, Lee-Ambrose L, Martin FG. The effect of topical tripeptide-copper complex on healing of ischemic open wounds. Vet Surg. 2003;32(6):515-23.


In wound healing models, biotinylated GHK increases the production of anti-inflammatory proteins such as copper, zinc-superoxide dismutase that detoxifies oxygen radicals. GHK-Cu also acts to detoxify some dangerous products of free radical reactions. Beretta et al. discovered these effects of GHK-Cu and proposed that this molecule may be useful in preventing many degenerative diseases of aging such as Alzheimer’s disease, neuropathy, retinopathy, atherosclerosis and diabetes. They demonstrated that GHK binds alpha,beta-4-hydroxy-trans-2- nonenal—a toxic product of fatty acids lipid peroxidation that plays an important role in the pathogenesis of several age related conditions.


Beretta G, Artali R, Regazzoni L, Panigati M, Facino RM. Glycyl-histidyl-lysine (GHK) is a quencher of alpha,beta- 4-hydroxy-trans-2-nonenal: a comparison with carnosine. insights into the mechanism of reaction by electrospray ionization mass spectrometry, 1H NMR, and computational techniques. Chem Res Toxicol. 2007 Sep;20(9):1309- 14.

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