# GHK-Cu: A Copper Peptide Studied for Skin and Matrix Repair

> GHK-Cu, the copper(II) chelate of the glycyl-histidyl-lysine tripeptide, stimulates fibroblast collagen and elastin synthesis at picomolar-to-nanomolar doses. A research digest that labels every finding established, limited, context, or safety.

What the picomolar collagen data, the 70-percent procollagen comparison, and the hair-count trial actually established, and where the human evidence stops. Every finding is tagged established, limited, context, or safety.

## What GHK-Cu is, in one paragraph

GHK-Cu is the copper(II) chelate of the tripeptide glycyl-L-histidyl-L-lysine, a short three-amino-acid sequence (Gly-His-Lys) that binds a single copper ion and turns up naturally in human plasma, saliva, and urine. At picomolar-to-nanomolar concentrations it stimulates dermal fibroblast synthesis of collagen, elastin, glycosaminoglycans, and the proteoglycan decorin [2][6]. It carries the INCI label [copper tripeptide-1](/) on skincare ingredient lists, the molecular formula C14H23CuN6O4+, a molecular weight of 402.92 Da, and the CAS number 89030-95-5 [2]. Plasma GHK is not fixed for life: it declines from roughly 200 ng/mL at age 20 to about 80 ng/mL by age 60, which is part of why the peptide is read as a repair signal that fades with age [2]. This site is a digest of the published GHK-Cu record. It is editorial, not a clinic, and it labels each finding by how strong the evidence behind it is.

## What Is GHK Copper Peptide?

The phrase GHK copper peptide names the same molecule as GHK-Cu: the copper-bound form of the Gly-His-Lys tripeptide. The copper is not incidental. In fibroblast cultures, GHK-Cu stimulated matrix metalloproteinase-2 expression and concurrently raised the tissue inhibitors TIMP-1 and TIMP-2, and that effect was reproduced by the copper-bound complex but not by the free GHK peptide [3]. Copper coordination also enables lysyl-oxidase-mediated collagen and elastin cross-linking and a superoxide-dismutase-like antioxidant activity that the bare peptide does not provide [6]. Loren Pickart first isolated GHK in 1973 as a plasma factor that caused aged human liver tissue to synthesize proteins like younger tissue, and the copper complex is what most of the documented tissue-repair work has used since [6]. The single most important reading rule for this literature: check whether a study used free GHK or the copper chelate, because for matrix remodeling the two are not interchangeable [3].

## Copper Peptides and the GHK Sequence

A copper peptide is, broadly, a short peptide that carries a copper ion; the GHK sequence is the best-studied endogenous example. The Gly-His-Lys tripeptide occurs naturally inside the alpha-2(I) chain of type I collagen and in the matrix protein SPARC/osteonectin, so the body already builds it into its own scaffolding [2]. When tissue is injured, GHK liberated from broken collagen is thought to act as a local repair signal, binding copper and switching fibroblasts toward synthesis. The foundational dose-response work showed collagen synthesis in human fibroblast cultures beginning between 10^-12 and 10^-11 M, peaking near 10^-9 M, and occurring without any change in cell number, which means the peptide changed what the cells did rather than simply making more of them [1]. That specificity, at vanishingly low concentrations, is the core of why the GHK sequence anchors the whole copper-peptide category. The deeper mechanism is set out under [GHK-Cu mechanism of action](/research).

## Copper Tripeptide-1 (INCI name)

Copper Tripeptide-1 is the INCI (International Nomenclature of Cosmetic Ingredients) name for GHK-Cu, the label used to declare copper-peptide content on a skincare ingredient list [2]. The research compound and the cosmetic ingredient are the same molecule: the copper(II) chelate of glycyl-histidyl-lysine, MW 402.92 Da, CAS 89030-95-5 [2]. Topical Copper Tripeptide-1 is a legal, widely marketed cosmetic ingredient with a long safety record, which is a different regulatory status from injectable or systemic GHK-Cu, which is unapproved and research-only [2]. When this site uses "GHK-Cu" and a product label uses "Copper Tripeptide-1," they are naming the same thing for two different audiences.

## What does a GHK-Cu peptide do?

GHK-Cu is a copper-binding tripeptide that, at picomolar-to-nanomolar levels, stimulates fibroblast synthesis of collagen, elastin, glycosaminoglycans, and decorin while rebalancing matrix metalloproteinases against their TIMP inhibitors [2][3]. Beyond skin, it behaves as a broad gene-modulating signaling molecule: gene-expression analyses report that GHK alters about 31% of human genes at a 50-percent-or-greater change threshold, favoring wound-repair, DNA-repair, and antioxidant programs [5]. It also chemoattracts repair cells and suppresses several inflammatory and oxidative signals in wound models [6]. The strongest direct human skin data is for [copper peptide skin research](/skin-research), and the full slate of documented [copper peptide benefits](/copper-peptide-benefits) is weighted by evidence on its own page.

## What is GHK-Cu and how does it work?

GHK-Cu is the copper(II) chelate of the glycyl-histidyl-lysine tripeptide. It works on two tracks at once. As a copper chaperone it delivers copper for lysyl-oxidase cross-linking of collagen and elastin and for SOD-like antioxidant chemistry [6]. As a signaling molecule it drives wound-repair, DNA-repair, and antioxidant gene programs while suppressing NF-kB-driven inflammation [5][6]. The copper form matters: MMP-2 stimulation in fibroblasts is produced by GHK-Cu but not by the free peptide, which is the clearest single demonstration that the metal is doing mechanistic work, not just riding along [3]. The full pathway map, with its established and limited claims separated, is on the [GHK-Cu mechanism of action](/research) page.

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The GHK-Cu copper-peptide record, read with each finding labelled by how much it can bear — established, limited, context, or safety — and legible to every reader; no clinic, no counter, nothing here to sell.
