Background of Copper Peptides
GHK-Cu emerged during my attempts 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 of blood in the microcirculation.
I found that the albumin fraction of human blood plasma has a suppressive action on fibrinogen synthesis and also improved the survival of the cultured liver cells that produce fibrinogen. Further isolations found these activities concentrated in a low molecular weight fraction that contained GHK-Cu. 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.
Later research found that Iamin is generated during tissue damage and suggests 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.