PLATE I — GHK-Cu
The Human Copper Tripeptide, Indexed.
GHK-Cu was first isolated from human plasma in 1973. Five decades later, the literature still surprises. This is an archive of what the published research actually shows — read carefully, cited honestly, with no products attached.
The short version
GHK-Cu is a tiny copper-binding peptide — three amino acids long — that your body makes naturally and that declines in your blood as you age. The compound has been studied since 1973, and the literature now covers skin repair, wound healing, hair follicles, gut health, and even brain cells. The strongest human evidence is topical: applied to skin, it measurably increases collagen and improves texture in controlled trials. Systemic (injectable or oral) uses are a separate matter — they have been studied in animals but are unapproved and not grounded in validated human pharmacokinetics. This site is a reading room, not a vendor and not a clinic. For what users and research subjects report about its effects, see the effects page.
What GHK-Cu is
GHK-Cu is a small molecule with an outsized history. Three amino acids — glycine, histidine, lysine — strung together as a tripeptide, then bound to a single copper(II) ion through the imidazole ring of histidine and the backbone of the peptide itself. Total molecular weight: 340 daltons. Net charge at physiological pH: nominally neutral once the copper sits in its coordination sphere [1].
Loren Pickart isolated it from human plasma albumin in 1973 while looking for the factor that caused aged human liver tissue to behave, in culture, like younger tissue. The factor turned out to be this tripeptide-copper complex [1]. It is endogenous: human plasma carries roughly 200 nanograms per millilitre at age twenty, declining to about 80 nanograms per millilitre by sixty. That decline is the central thread of much subsequent work.
In the International Nomenclature of Cosmetic Ingredients, the complex is registered as Copper Tripeptide-1, and that is the name under which it appears on most over-the-counter skin products.
What the research literature actually shows
The dominant signal in the published work is matrix remodeling. At one to ten nanomolar concentrations — vanishingly small — GHK-Cu applied to cultured human dermal fibroblasts shifts the cell into a tissue-repair posture: collagen and glycosaminoglycan synthesis rise, the matrix metalloproteinases that prune existing matrix rise alongside, and the inhibitors of those metalloproteinases (TIMP-1, TIMP-2) move with them [17]. The cell is not simply building. It is rebuilding.
This is consistent across surprisingly diverse systems. In cultured lung fibroblasts taken from chronic obstructive pulmonary disease patients, GHK reversed the gene-expression signature associated with emphysematous destruction and restored the cells' ability to contract collagen [2]. In dextran-sulfate-induced colitis in BALB/c mice, oral GHK-Cu at 20 mg/kg over 14 days lowered inflammatory cytokines, preserved colon length, and restored intestinal tight-junction proteins [3]. In S. aureus-infected full-thickness mouse wounds, a GHK-Cu loaded hydrogel closed the wound by day 12 at a rate above 95 percent, against ~65 percent in controls [4]. The compound's behavior is unusually general.
The scale is part of what is striking. A 2018 transcriptomic review estimated that GHK at biologically reasonable concentrations alters expression of roughly 31 percent of protein-coding genes in cultured human fibroblasts by 50 percent or more [1]. Most are nudged a few percent; a few — like the ubiquitin-specific protease USP29 — move by an order of magnitude.
Where the evidence is strongest, and where it is not
The strongest human evidence is topical and cosmetic. Multiple controlled studies of topical GHK-Cu creams have shown measurable improvements in skin thickness, wrinkle volume, and collagen deposition over 8 to 12 weeks of twice-daily use [6][7]. The 2002 Leyden comparison study found GHK-Cu cream produced collagen deposition in 70 percent of subjects versus 50 percent for vitamin C and 40 percent for retinoic acid [6]. A 2025 review further documents post-laser recovery acceleration and antimicrobial wound-dressing applications [5][4].
The weakest evidence is for systemic administration in humans. There is no large randomized controlled trial of injected or oral GHK-Cu for any indication. The rodent colitis work is genuinely promising [3], the wound-healing dressings are useful [4][5], and the gene-expression mechanism is well-described [1][2] — but the leap from a 32-mouse colitis study to a human clinical recommendation is the leap the literature has not yet made. This archive does not make that leap for it.
What is also worth understanding is the regulatory position. GHK-Cu is not FDA-approved as a drug. Topical Copper Tripeptide-1 is regulated as a cosmetic ingredient. Injectable forms exist only as compounded preparations, and in April 2026 the FDA confirmed removal of injectable GHK-Cu from Category 2 because the original bulks-list nominations had been withdrawn — leaving the compounded injectable in a regulatory gray zone pending Pharmacy Compounding Advisory Committee review [13][14].
How to read this site
Four pages do most of the work. The research page walks through the mechanism studies in detail, including the COPD lung-fibroblast paper, the 2025 colitis study, and the gene-expression review. The dosage page collects what concentrations have been studied in which species and via which routes — none of it framed as advice. The FAQ answers the questions that keep recurring in search: what GHK-Cu actually does, whether it has a half-life worth quoting, whether athletes can use it, and what 'Copper Tripeptide-1' means on a cosmetic label. The references page is the full citation list with DOIs.
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