# GHK-Cu Clinic — A research-data working file on the copper tripeptide GHK-Cu > GHK-Cu is a three-amino-acid copper(II) complex first isolated from human plasma in 1973. This site indexes the published research literature on its mechanism, doses studied, and regulatory status. Glycyl-L-histidyl-L-lysine bound to Cu(II). First isolated from human plasma in 1973. A fifty-year literature, indexed in plain type. ## § 00 · THE SHORT VERSION GHK-Cu is a three-amino-acid copper complex — glycine, histidine, lysine bound to a single copper ion — that the human body produces naturally. Blood levels fall by roughly 60% between age 20 and age 60. In the published literature, the copper-bound form (not the plain peptide) stimulates skin cells called fibroblasts to make more collagen at concentrations as low as one picomole — a vanishingly small amount. Topical copper peptide serums and creams carry a long cosmetic history and a handful of small human trials showing measurable skin and hair changes. Injectable or systemic use is a separate matter: there is no approved drug form and no validated human dosing data. This site indexes what the peer-reviewed record actually shows — the doses used, the species studied, the mechanism proposed, and the gaps the research has not yet closed. For the human side — what people in skincare communities say about using it — see [what people report](/effects). ## the molecule GHK-Cu is a tripeptide-copper complex. The peptide backbone is three amino acids — glycine, histidine, lysine — coordinated to a single divalent copper ion. Molecular weight of the free peptide is 340.38 Da; the copper complex is 403.93 Da. The Cu(II) is held by the imidazole nitrogen of histidine, the alpha-amino nitrogen of glycine, and the deprotonated amide nitrogen of the Gly–His peptide bond, with a fourth coordination position available for axial ligands [1]. The sequence is not synthetic in origin. Loren Pickart isolated GHK from human plasma in 1973 while studying age-related changes in liver cell behavior. Plasma concentrations fall with age — approximately 200 ng/mL at age 20 declining to roughly 80 ng/mL by age 60 [1]. The same Gly-His-Lys motif appears in the alpha-2(I) chain of type I collagen and is thought to be released by proteolytic cleavage during tissue injury, which gives the molecule a plausible endogenous role as a damage-released signal. ## what the literature actually shows GHK-Cu is unusual because the published evidence base is both old and broad. Three observations recur across fifty years of in vitro and animal work. First, GHK-Cu modulates a large fraction of the transcriptome. Connectivity Map analyses estimate it influences expression of roughly 31% of human genes, with consistent upregulation of tissue-repair, antioxidant, and DNA-repair programs and downregulation of inflammatory and pro-fibrotic signaling [2]. A 2012 *Genome Medicine* study identified GHK as the single compound — out of the entire Broad Institute screening library — capable of reversing 127 emphysema-associated gene-expression changes in human lung tissue [2]. Second, the dose-response on dermal fibroblasts is established at extremely low concentrations. The 1988 Maquart paper in *FEBS Letters* showed measurable collagen induction beginning at 10⁻¹² M and saturating at 10⁻⁹ M [3]. That picomolar-to-nanomolar window has been the working range for most subsequent fibroblast and wound-healing studies. Third, the human clinical record exists but is small. A 12-week trial in 71 women showed increases in skin density and thickness with daily topical application [4]. A 1998 head-to-head comparison reported topical GHK-Cu outperformed vitamin C and retinoic acid on collagen induction in 70% of subjects [5]. A randomized trial of 2% topical gel in diabetic foot ulcers increased wound-closure rates versus placebo [6]. No large injectable GHK-Cu trials in humans have been published. ## what this site is GHK-Cu Clinic is an independent editorial publisher. The work is a working file: a typographic index of the GHK-Cu research literature — primary studies, dose ranges, mechanistic claims, recent reviews, and the regulatory frame — organized to be read. The site does not provide medical advice. It does not sell GHK-Cu or any related product. It is not a clinic in the patient-facing sense; the modifier is editorial — the position the publisher occupies relative to the science. Every quantitative claim on the site is sourced. The references page carries the full citation index with DOIs and PubMed links. If you came here looking for a vendor, you are in the wrong place. If you came here looking for what the research actually says — the doses, the species, the mechanism, the gaps — the rest of the site is for you. ## where to start [The literature](/research) — mechanism, fibroblast studies, the Connectivity Map result, CNS work, fibrosis models. [Doses studied](/dosage) — the picomolar fibroblast range, intraperitoneal rodent doses, intranasal CNS doses, topical concentrations. All research-context. [Questions](/faq) — what people ask about GHK-Cu and what the published record answers. [References](/references) — full citation list, sortable and searchable. --- An independent working file on the published GHK-Cu literature — not a clinic, not a vendor, not a prescription.