# GHK-Cu: The Copper Tripeptide Research Record, Sourced and Indexed > GHK-Cu, a copper(II) tripeptide present in human plasma, stimulates collagen synthesis at picomolar concentrations and modulates about 31% of human genes. A sourced literature dossier. An editorial dossier of the published literature on this copper peptide — the collagen dose-response, the gene-expression signature, the hair-count trial, and the human-data gaps, each set against its original paper. ## GHK Copper Peptide: What the Research Describes GHK-Cu is the copper(II) chelate of the tripeptide glycyl-L-histidyl-L-lysine, molecular weight 402.92 Da, CAS 89030-95-5. It is not a synthetic invention. The GHK sequence occurs naturally in human plasma, saliva, and urine, embedded in the alpha-2(I) chain of type I collagen and in the matricellular protein SPARC. Plasma GHK measures roughly 200 ng/mL at age 20 and falls to about 80 ng/mL by age 60 [3]. The peptide was first isolated in 1973 as a plasma factor that made aged human liver tissue synthesize proteins the way younger tissue does — the observation that started five decades of GHK research. The single most reproduced finding is collagen stimulation. In human fibroblast cultures, GHK-Cu increased collagen synthesis beginning between 10^-12 and 10^-11 M, peaking near 10^-9 M, with no change in cell number [1]. That last clause matters: the peptide is not driving collagen by multiplying cells. It is a specific signaling effect at concentrations a thousand-fold below a microgram. This is the kind of result that anchors a [GHK-Cu references and citations](/references) page rather than a marketing claim, because it carries a measured onset, a measured peak, and a controlled comparison. The copper is not incidental. In fibroblast cultures, GHK-Cu stimulated MMP-2 expression with concurrent TIMP-1 and TIMP-2 modulation — an effect the copper-free GHK peptide did not reproduce [7]. Copper coordination is mechanistically required for most of the documented tissue-repair activity, which is the central distinction this dossier returns to in [GHK vs GHK-Cu and the role of copper](/mechanism). ## Copper Peptide Biology: How GHK-Cu Fits the Class A copper peptide is a short peptide that carries a copper ion as a functional cargo, not as a contaminant. GHK-Cu is the archetype of the class: glycine, histidine, and lysine coordinate a single Cu(II) ion through the histidine imidazole nitrogen, the glycine alpha-amino nitrogen, and the deprotonated glycine-histidine amide nitrogen, leaving the lysine side chain free. The complex has a very high copper stability constant, log K near 16.4, which keeps free copper — the pro-oxidant form — tightly held rather than loose in solution [3]. That stability is why the peptide can act as a copper chaperone instead of a copper hazard. The bound copper enables lysyl-oxidase-mediated cross-linking of collagen and elastin and contributes superoxide-dismutase-like antioxidant behavior, while the peptide scaffold delivers it to the right place [6]. Across reviewed models GHK-Cu increases collagen, elastin, glycosaminoglycans, and the proteoglycan decorin, and rebalances matrix metalloproteinases against their TIMP inhibitors [6]. The class behavior — repair signaling plus controlled copper delivery — is exactly what the mechanism literature documents, and exactly what separates a sourced copper peptide from a generic antioxidant marketing line. The wider profile is broad. The same review documents GHK-Cu increasing VEGF, FGF-2, NGF, and neurotrophins while suppressing free radicals, thromboxane, TGF-beta-1, and TNF-alpha and chemoattracting macrophages, mast cells, and capillary cells into a wound [6]. That this profile sits on a molecule the body already makes — and makes less of with age, declining from roughly 200 ng/mL at 20 to 80 ng/mL by 60 [3] — is the reason the copper-peptide class draws the attention it does. This dossier reads that attention against the studies, sorting the strong matrix and wound data from the thinner systemic claims rather than collapsing them into one headline. ## Copper Tripeptide-1: The INCI Name for GHK-Cu Copper Tripeptide-1 is the INCI (International Nomenclature of Cosmetic Ingredients) name for GHK-Cu. If a serum or cream lists Copper Tripeptide-1, that is the same molecule this dossier covers — glycyl-L-histidyl-L-lysine chelated 1:1 to copper(II), CAS 89030-95-5. The synonym matters for label literacy: a due-diligence reader checking a product against the research record needs to know that Copper Tripeptide-1, copper peptide GHK-Cu, GHK copper complex, and prezatide copper all point to one entity. Knowing the INCI name also tells you which regulatory lane the molecule sits in. Topical Copper Tripeptide-1 is a legal cosmetic ingredient in the US, EU, and UK with a long marketing record. Injectable or systemic GHK-Cu is a different and unapproved category. The honest limits on that distinction are laid out in full in [copper peptide side effects](/side-effects). ## Copper Peptide Serum Formats Studied in the Literature The research formats GHK-Cu in creams, serums, gels, liposomes, nano-lipid carriers, ionic-liquid microemulsions, wound-dressing hydrogels, and peptide nanofibers — typically at roughly 0.05% to 2% (w/w) in topical work. Delivery is the recurring problem, not the biology: free GHK is highly hydrophilic (clogP -2.24), which limits passive penetration of the stratum corneum [5]. A human ex-vivo penetration study quantified what does get through, recording a copper permeability coefficient of 2.43 x 10^-4 cm/h and roughly 97 ug/cm^2 retained as a dermal copper depot over 48 hours [5]. This dossier describes those formats as study conditions, not as products to buy, and recommends no specific serum. --- A feature dossier on the copper tripeptide GHK-Cu, set like a magazine and sourced like a citation index — every figure attributed, every gap printed in plain sight, and nothing here clinical, prescribed, or for sale.