GHK-Cu drives collagen synthesis at picomolar doses and modulates roughly 31% of the human genome.

What the GHK-Cu record establishes

GHK-Cu is the copper(II) complex of glycyl-L-histidyl-L-lysine, a three-amino-acid peptide first isolated from human plasma in 1973. Molecular weight: 402.92 Da. CAS: 89030-95-5. INCI name: Copper Tripeptide-1. It is a research peptide and a cosmetic ingredient — not an approved drug by any route.

The finding comes first. In human fibroblast cultures GHK-Cu raised collagen synthesis dose-dependently, with onset between 10⁻¹² and 10⁻¹¹ M and a peak near 10⁻⁹ M, and it did so without changing cell number — which marks the effect as a specific metabolic instruction rather than a crowd of new cells ^[1]. A Connectivity Map analysis reports that GHK alters expression of about 31.2% of human genes at a 50%-or-greater change threshold: 59% up, 41% down, with strong upregulation of ubiquitin-proteasome, DNA-repair and antioxidant gene sets ^[2]. The widely repeated "~4,000 genes" figure is an extrapolation; the verified threshold table reports on the order of 2,100 genes ^[2].

The sequence is not foreign to the body. GHK occurs within the alpha-2(I) chain of type I collagen and in SPARC/osteonectin, and it circulates in plasma, saliva and urine. Plasma levels fall from about 200 ng/mL at age 20 to about 80 ng/mL by age 60, tracking the slow loss of tissue-repair capacity ^[3]. That decline is the elegiac thread running under five decades of GHK research: the work reads as an attempt to restore a signal the body once carried in abundance, not to introduce something new.

This digest's recurring lens is the inflammation record. Across rodent models GHK and GHK-Cu suppress NF-kB-driven inflammation and the cytokines it controls — TNF-alpha, IL-6 and IL-1beta — in a 2025 DSS-colitis study acting through the SIRT1/STAT3 axis ^[14] and in a bleomycin pulmonary-fibrosis study acting through TGF-beta1/Smad suppression ^[7]. The anti-inflammatory and antioxidant research and the safety, tolerability and copper handling are read in full on the research page, alongside the mechanism of how GHK-Cu works. Common reader questions are gathered in the frequently asked questions.

The evidence base has a clear shape. The strongest controlled human data are topical and dermatologic — small placebo-controlled skin trials and one 6-month hair-loss trial of a combination formulation ^[3][4]. The broader systemic and gene-level claims rest largely on in-vitro and rodent work, and a substantial share of the foundational literature comes from a single investigator group ^[2]. This site leads with what each study measured and is explicit about which tier of evidence it sits in. The canonical name used throughout is GHK-Cu, and where the literature reports data on the free peptide GHK rather than the copper chelate, the distinction is flagged — it matters, because copper coordination is required for most of the documented matrix activity ^[1].

GHK Copper Peptide: What the Research Describes

The GHK copper peptide is the most-studied member of the copper-peptide class, and its defining feature is copper coordination. The Cu(II) ion binds 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 carries a very high copper stability constant — log K approximately 16.44 — far above free GHK, which is why it holds copper tightly enough to limit pro-oxidant free-copper release ^[9].

That chelation is functional, not decorative. Copper coordination enables lysyl-oxidase-mediated collagen and elastin cross-linking and superoxide-dismutase-like antioxidant chemistry, and it is required for most documented matrix-remodeling activity — the free peptide does not reproduce MMP-2 stimulation in fibroblast cultures ^[1]. Across study models the GHK copper peptide stimulates synthesis of collagen, dermatan sulfate, chondroitin sulfate and the proteoglycan decorin, while suppressing free radicals, TGF-beta-1, TNF-alpha and oxidizing-iron release and chemoattracting repair cells to the wound ^[3][6]. The picture is one molecule working on the whole repair program at once.

Copper Peptides as a Research Class

A copper peptide is a short amino-acid chain bound to a copper(II) ion, and GHK-Cu — three amino acids, one copper atom — is the archetype the class is named after. The peptide does two jobs: it acts as a copper chaperone, delivering the metal to enzymes that need it, and it acts as a signal, instructing dermal fibroblasts to rebuild the extracellular matrix ^[6].

The class earns its attention from how low the active concentrations are. The fibroblast collagen response begins in the picomolar range and peaks near 10⁻⁹ M, placing copper peptides among the more potent signaling molecules studied in dermal cells, active far below the concentrations of most cosmetic actives ^[1]. The other defining trait is copper handling: the GHK-Cu complex blocked Cu²⁺-dependent LDL oxidation completely in vitro — versus only about 20% protection from superoxide dismutase — and reduced iron release from ferritin by 87%, the antioxidant signature that distinguishes a chelated copper peptide from free copper salts ^[9].

Copper Tripeptide-1: The INCI Name and Chemical Identity

Copper Tripeptide-1 is the INCI cosmetic-ingredient name for GHK-Cu — the same molecule, labeled for skincare. On a product ingredient list, "Copper Tripeptide-1" means glycyl-histidyl-lysine copper(II) complex, CAS 89030-95-5, molecular formula C14H23CuN6O4⁺, molecular weight 402.92 Da. The free tripeptide carries its own identity (CAS 49557-75-7, MW 340.38 Da), and the two are not interchangeable in the literature ^[6].

What does a GHK-Cu peptide do?

A GHK-Cu peptide is a copper-binding tripeptide that, in research models, stimulates fibroblast synthesis of collagen and elastin, supports wound repair and angiogenesis, and modulates a broad set of repair-related genes ^[1][2]. It functions on two levels at once — as a copper chaperone supplying the metal to copper-dependent enzymes such as lysyl oxidase, and as a direct signal to dermal cells ^[6].

What is GHK-Cu and how does it work?

GHK-Cu is the glycyl-histidyl-lysine copper(II) complex. It acts as a copper chaperone and signaling molecule, altering expression of about 31.2% of human genes at a ≥50% change threshold toward repair, DNA-fidelity and antioxidant programs while suppressing NF-kB inflammation ^[2]. Copper coordination is required: the free peptide does not reproduce the key matrix effects ^[1].

What is the difference between GHK and GHK-Cu?

GHK is the free tripeptide (MW 340.38, CAS 49557-75-7); GHK-Cu is its copper(II) chelate (MW 402.92, CAS 89030-95-5) ^[6]. Copper coordination is required for most documented matrix-remodeling activity, so the form a study used matters — the free peptide does not reproduce MMP-2 stimulation in fibroblasts, yet several studies use free GHK and report systemic and gene-level effects ^[1][2]. The GHK vs GHK-Cu chemical identity distinction is the single most useful key to reading the literature.