A materia-medica of the literature · Copper Tripeptide-1
GHK-Cu is a copper tripeptide studied for collagen, skin remodeling and hair-follicle repair across five decades.
An engraved reading of the published record: the picomolar collagen dose-response, the ~31%-of-genome gene signature, and the +71.5-hair trial delta — every quantitative claim weighed against its source and cited in place.
What the GHK-Cu literature records
GHK-Cu is the copper(II) chelate of the tripeptide glycyl-L-histidyl-L-lysine — a copper peptide first isolated by Loren Pickart in 1973 as a plasma factor that made aged human liver tissue synthesize protein like younger tissue [3]. The molecule weighs 402.92 Da; the free peptide weighs 340.38 Da [6]. In human fibroblast cultures GHK-Cu stimulated collagen synthesis at concentrations as low as 10^-12 M, with the effect peaking near 10^-9 M and occurring without any change in cell number — a specific metabolic signal, not a growth effect [1]. That single dose-response curve is the foundation of everything that follows: the GHK sequence sits inside the alpha-2(I) chain of type I collagen, so when tissue is injured the peptide is liberated locally and tells the surrounding fibroblasts to rebuild [6].
The scope of the signal is unusually broad for a three-residue peptide. A Connectivity Map analysis reports that GHK modulates expression of about 31.2% of human genes at a 50%-or-greater change threshold — 59% of those up, 41% down — with strong stimulation of the ubiquitin-proteasome system (41 genes up, 1 down) plus DNA-repair and antioxidant gene sets [2]. Across the matrix it stimulates collagen, elastin, glycosaminoglycans and the proteoglycan decorin while rebalancing matrix metalloproteinases against their TIMP inhibitors [6]. None of this is a treatment claim — it is what cell-culture and review literature have measured. For the detail on what genes GHK-Cu affects, see the mechanism overview.
GHK Copper Peptide Overview
GHK copper peptide is the same molecule under its most common alias. It is endogenous: present in human plasma, saliva and urine, with plasma GHK declining from about 200 ng/mL at age 20 to about 80 ng/mL by age 60 [3]. That age-linked decline is the narrative most consumer copper-peptide writing leans on, and it is real in the reviewed data — but it is correlation in plasma chemistry, not a demonstrated cause of aging.
The copper is not incidental. Coordination of Cu(II) is required for most documented tissue-repair activity: the free GHK peptide does not reproduce MMP-2 stimulation in fibroblast cultures [6]. The complex is also remarkably stable, with a copper stability constant of roughly log K 16.4, far above free GHK, which limits release of pro-oxidant free copper [11]. So studies on free GHK and on the copper chelate are not interchangeable — a distinction this site keeps in front of you on every page. For the full mechanism, see our GHK-Cu collagen research overview.
What Copper Peptides Are
A copper peptide is a short amino-acid chain that carries a copper ion in a fixed coordination geometry. In GHK-Cu the copper(II) is held 1:1 through the histidine imidazole nitrogen, the glycine alpha-amino nitrogen and a deprotonated amide nitrogen, leaving the lysine side chain free [6]. The cosmetic-ingredient label for this exact molecule is Copper Tripeptide-1 — the INCI name you will find on a skincare panel.
The reason copper peptides interest researchers is that copper is itself a cofactor for matrix enzymes such as lysyl oxidase, which cross-links collagen and elastin. The peptide acts as a chaperone, delivering the metal to the cell while also signaling in its own right [6]. The four GHK-Cu specimen plates at the head of this page summarize the most-cited numbers; the pages below weigh each one against the study it came from.
What does a GHK-Cu peptide do?
GHK-Cu is a copper-binding tripeptide that, at picomolar-to-nanomolar concentrations, stimulates fibroblast synthesis of collagen, elastin, glycosaminoglycans and decorin and rebalances matrix metalloproteinases against their TIMP inhibitors in research models [1][6]. The copper ion additionally enables lysyl-oxidase cross-linking and superoxide-dismutase-like antioxidant activity. These are model-level findings in cell culture and review literature, not a clinical indication.
What is GHK-Cu and how does it work?
GHK-Cu is the copper(II) chelate of the tripeptide glycyl-L-histidyl-L-lysine. It acts as both a copper chaperone and a signaling molecule, with copper coordination required for most documented matrix-remodeling activity — free GHK does not reproduce MMP-2 stimulation in fibroblast cultures [6]. In those cultures the copper complex drove collagen synthesis dose-dependently from 10^-12 M [1].
What is the difference between GHK and GHK-Cu?
GHK is the free tripeptide (MW 340.38); GHK-Cu is its copper(II) chelate (MW 402.92) [6]. Copper coordination is required for most tissue-repair activity, so studies on the free peptide and the copper complex are not interchangeable. Much published work uses free GHK and reports systemic or gene-level effects, so the form a study used always matters — see GHK vs GHK-Cu framing throughout this digest.