GHK-Cu is a copper tripeptide benchmarked across collagen, hair, and anti-inflammatory research.

GHK-Cu, measured

GHK-Cu is the copper(II) chelate of the glycyl-histidyl-lysine tripeptide, and its research record reads like a benchmark sheet. It stimulates human fibroblast collagen synthesis at picomolar-to-nanomolar concentrations, with onset between 10^-12 and 10^-11 M and a peak near 10^-9 M, all without any change in cell number ^[1]. Gene-expression analysis reports that the parent GHK peptide alters roughly 31.2% of human genes at a 50%-or-greater change threshold — 59% up, 41% down — pushing tissue-repair, DNA-repair, antioxidant and ubiquitin-proteasome programs ^[2].

The compound is endogenous. Loren Pickart first isolated GHK in 1973 as a plasma factor that made aged human liver tissue synthesize proteins like younger tissue, and plasma GHK falls from about 200 ng/mL at age 20 to about 80 ng/mL by age 60 ^[3]. That decline is the framing the whole literature works against: a signaling tripeptide that the body makes less of with age, studied for what it does to collagen, hair, wounds, and inflammation.

This site is an editorial console for that record. It reports what each study measured, in which species, at which dose and route — and it names the gaps plainly. There is no approved therapeutic indication for GHK-Cu by any route, and no validated human pharmacokinetic data for systemic use ^[6]. The numbers below are findings, not instructions.

What Is GHK Copper Peptide?

GHK copper peptide is the popular name for GHK-Cu — the same molecule the cosmetic industry labels Copper Tripeptide-1. Structurally it is a linear three-amino-acid chain, glycine-histidine-lysine, bound 1:1 to a copper(II) ion through the histidine imidazole nitrogen, the glycine alpha-amino nitrogen, and a deprotonated amide nitrogen, leaving the lysine side chain free (molecular formula C14H23CuN6O4+, 402.92 Da) ^[6].

The GHK sequence is not synthetic in origin. It occurs naturally inside the alpha-2(I) chain of type I collagen and in the matricellular protein SPARC/osteonectin, and it is found free in human plasma, saliva and urine ^[6]. The working model across the literature is that when tissue is injured, proteases liberate GHK from collagen breakdown, and the freed tripeptide — once it picks up copper — signals the repair response ^[1][6]. That is why a fragment of collagen ends up driving the synthesis of new collagen.

Copper Peptides and the GHK Sequence

Copper peptide is the category; GHK is the sequence that defines it. A copper peptide is any short peptide carrying a bound copper(II) ion, and GHK is the endogenous one with the deepest research record — the prototype the whole class is named after. Copper coordination is not incidental: it is required for most documented activities. In fibroblast culture, the copper-loaded GHK-Cu form stimulates MMP-2, while the free GHK peptide does not reproduce that effect ^[6].

That distinction governs how the literature should be read. GHK is the free tripeptide (340.38 Da, CAS 49557-75-7); GHK-Cu is the copper chelate (402.92 Da, CAS 89030-95-5) ^[6]. Many gene-level and behavioral studies use the copper-free peptide, while most matrix-remodeling work uses the chelate. Throughout this site, the form a given study actually used is stated, because it changes what the result means. For the full mechanistic picture, see the GHK-Cu mechanism of action.

Copper Tripeptide-1 (INCI name)

Copper Tripeptide-1 is the INCI name — the standardized cosmetic-ingredient label — for GHK-Cu. When a serum or cream lists "Copper Tripeptide-1," it is declaring GHK-Cu content ^[6]. This is the one form of the compound with regulatory standing: topical Copper Tripeptide-1 is a legal, widely marketed cosmetic ingredient with a long safety record.

That standing is topical only. Injectable, oral and other systemic uses of GHK-Cu carry no approved indication and no validated human pharmacokinetic basis ^[6]. The split matters for reading the research: the dermatology evidence sits behind a marketed, regulated ingredient, while the systemic rodent and in vitro work sits in research-only territory. This site keeps the two clearly separated.

What the record shows — and where it stops

The strongest GHK-Cu evidence is concentrated in three areas, and this site is organized around them. Skin is the deepest file: dose-resolved fibroblast collagen synthesis ^[1] and small placebo-controlled topical trials reporting collagen gains in 70% of treated women versus 50% for vitamin C and 40% for retinoic acid ^[3][13] — see the copper peptide skin research. Hair has one controlled human anchor, a 6-month trial in 45 men where a GHK-containing topical raised hair count by up to 71.5 versus 9.6 for placebo ^[4] — covered in the copper peptide hair research. And the anti-inflammatory work spans lung, gut and gene-reversal models ^[8][9][14] — detailed under GHK-Cu and inflammation.

The record stops at human systemic data. Most mechanistic evidence is in vitro or rodent with small sample sizes; the human trials are topical; and a large share of the foundational review literature traces to a single investigator, which limits independent replication of the broadest claims ^[2][6]. There is no validated human pharmacokinetic profile for injectable or systemic GHK-Cu and no approved therapeutic indication by any route ^[6]. Stating both halves — the reproducible findings and the missing human data — is the whole point of reading this compound as a benchmark sheet rather than a brochure.

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 ^[3][6]. Beyond the matrix, it behaves as a broad gene-modulating signaling molecule, shifting expression across thousands of genes toward repair, DNA-fidelity and antioxidant programs ^[2].

What is GHK-Cu and how does it work?

GHK-Cu is the copper(II) chelate of the glycyl-histidyl-lysine tripeptide. It works as both a copper chaperone — enabling lysyl-oxidase collagen cross-linking and superoxide-dismutase-like antioxidant activity — and a signaling molecule that drives wound-repair, DNA-repair and antioxidant gene programs while suppressing NF-kB-driven inflammation ^[2][6][7].