Background of Regenerative Copper Peptides (1962 to 2016)
GHK-Cu emerged during my graduate work at the University of Minnesota from 1962-1965, and later at the Sansum Institute in Santa Barbara, California. I was attempting to reverse certain changes that occur during human aging. The goal was to suppress the synthesis of the blood fibrinogen, a protein that rises with age and rises even more after myocardial infraction. Its blood concentration is an excellent predictor of mortality. Elevated fibrinogen levels increase blood coagulation and decrease tissue perfusion, by increasing the thixotropic properties (toothpaste-like) of blood in the microcirculation.
I found that the albumin fraction of human blood plasma had a suppressive action on fibrinogen synthesis and also improved the survival of the cultured liver cells that produce fibrinogen. Later during Ph.D. thesis work at the University of California at San Francisco (1969-1973), I found that these activities concentrated from albumin into a low molecular weight fraction that contained GHK-Cu. In 1979, I moved to Seattle where subsequent work defined the three dimensional solution structure of GHK-Cu and the binding affinities between GHK and copper (II). My colleagues at the University of Washington (Seattle) and I used the structure of GHK-Cu to create analogs that were very potent cell growth inhibitors, inhibiting fibroblast replication at concentrations equivalent to chemotherapeutic drugs such as cisplatin and bleomycin. During surgical procedures to test these inhibitors on the suppression of tumor growth in mice, GHK-Cu was used as a control substance. It became apparent that GHK-Cu was rapidly healing the surgical incisions needed in these procedures.
Later research found that GHK is generated during tissue damage or normal tissue turnover, and suggested that, after tissue damage, GHK-Cu serves as a human feedback signal that has potent tissue protective properties and stimulates tissue remodeling after the initial phase of wound healing. It is postulated that a localized generation of GHK-Cu after tissue damage causes an influx of skin repair cells called macrophages which initiate skin repair mechanisms. The decrease in the blood concentrations of GHK-Cu during human aging may be a factor in the decreased tissue repair and subsequent increased organ failure that occurs during aging.
By 2009, I published a paper viewing GHK as a factor that might reverse many of the degenerative diseases of human aging. By 2010 to 2012, the Broad Institute published huge amounts of data on GHK's effects on human gene expression. This led to studies that predicted that GHK would to be the most effective bioactive molecule, of 1,309 tested, to treat aggressive, metastatic cancer and also COPD (chronic obstructive pulmonary disease). GHK was found the reset genes of diseased cells from patients with cancer patients or COPD to a more healthy state. Very small amounts of GHK caused cancer cells reset their programmed cell death system while COPD patients cells shut down tissue distructive genes and activated repair and remodeling activities.
During human aging there is an increase in the activity of inflammatory, cancer promoting, and tissue destructive genes plus a decrease in the activity of regenerative and reparative genes. The human blood tripeptide GHK possesses many positive effects but declines with age. It improves wound healing and tissue regeneration (skin, hair follicles, stomach and intestinal linings, boney tissue), increases collagen, decorin, angiogenesis, and nerve outgrowth, possesses anti-oxidant and anti-inflammatory effects, increases cellular stemness and the secretion of trophic factors by mesenchymal stem cells. GHK may become a general treatment for many diseases of aging.