# GHK-Cu: An Audited Ledger of the Copper-Tripeptide Research > GHK-Cu is the glycyl-histidyl-lysine copper(II) complex (MW 402.92). A dated, sourced ledger of the collagen, skin and hair-growth research, with every quantitative claim cited. Every collagen figure, skin trial, hair-count result and regulatory status, dated and sourced. The verified facts, the preclinical-only findings, and the no-human-data gaps are marked separately. ## The compound, stated as a line item GHK-Cu is the glycyl-L-histidyl-L-lysine copper(II) complex — a three-amino-acid peptide (glycine-histidine-lysine) carrying a single copper(II) ion, molecular weight 402.92 Da, cosmetic-ingredient name Copper Tripeptide-1 [3]. It was first isolated from human plasma by Loren Pickart in 1973 as a factor that caused aged human liver tissue to synthesize proteins like younger tissue [6]. This page reads the GHK-Cu literature the way a statement reads an account: each finding posted as a line, each number reconciled to its source, each regulatory status flagged with a badge. The headline figures of that ledger are quantitative. 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 — a specific metabolic effect, not a proliferation artifact [1]. Gene-expression analysis reports that GHK shifts roughly 31.2% of human genes at a 50%-or-greater change threshold toward repair, DNA-fidelity and antioxidant programs [2]. Topical formulations raised procollagen synthesis in 70% of treated subjects, against 50% for vitamin C and 40% for retinoic acid in the same comparison [3]. And in a six-month controlled hair trial of 45 men, a 5-aminolevulinic-acid plus GHK complex increased hair count by 71.5 at the 50 mg/mL dose versus 9.6 for placebo [4]. The boundaries are stated with the same precision as the findings. There is no FDA- or EMA-approved drug product for GHK-Cu by any route [3]. Topical Copper Tripeptide-1 is a legal cosmetic ingredient in the US, EU and UK. No validated human pharmacokinetic data — half-life, Cmax, bioavailability — exist for injectable or systemic use; the closest peer-reviewed pharmacokinetics is a rat study showing free GHK is rapidly metabolized in plasma to the dipeptide histidyl-lysine [10]. That separation — verified fact in one column, preclinical signal in another, no-human-data gap in a third — is the whole point of reading this compound as a ledger rather than a brochure. ## What a copper peptide is A copper peptide is a short chain of amino acids bound to a copper(II) ion, where the metal is not an impurity but a functional part of the molecule. In GHK-Cu the copper sits in a square-planar coordination held by the histidine imidazole nitrogen, the glycine alpha-amino nitrogen and a deprotonated amide nitrogen, leaving the lysine side chain free [6]. The complex forms at a 1:1 copper-to-peptide ratio with a very high stability constant (log K around 16.4), which keeps free, pro-oxidant copper from being released [3]. That distinction matters because copper coordination is required for most of the documented activity. The free tripeptide GHK (MW 340.38) and the copper chelate GHK-Cu (MW 402.92) are frequently conflated in the literature, but the free peptide does not reproduce the matrix-remodeling effects of the complex in fibroblast cultures [3]. When this site reports a finding, it tracks which form the underlying study used. The endogenous version of this molecule declines with age: plasma GHK falls from roughly 200 ng/mL at age 20 to about 80 ng/mL by age 60 [3], the observation that started the research program. ## GHK copper peptide: what the research describes The GHK copper peptide is best understood as two things at once: a copper chaperone and a pleiotropic signaling molecule. As a chaperone it enables copper-dependent reactions — lysyl-oxidase-mediated collagen and elastin cross-linking, and superoxide-dismutase-like antioxidant activity [6]. As a signal it directly stimulates dermal fibroblasts to synthesize collagen, elastin, glycosaminoglycans and the proteoglycan decorin, while rebalancing matrix metalloproteinases against their TIMP inhibitors toward controlled remodeling rather than tissue breakdown [3][6]. The research record across this molecule spans several tissue systems. In skin it is the most studied: collagen and matrix synthesis, photoaging repair, and small placebo-controlled facial trials [3]. In hair it has one controlled human signal — the ALAVAX hair-count trial — and preclinical anagen-induction work [4]. Beyond the surface, reviews document angiogenic (VEGF, FGF-2), anti-inflammatory (NF-kB suppression) and neurotrophic effects, largely in cell-culture and rodent models [6]. The reading list that follows sorts those domains and cites each one. Start with the [GHK-Cu research summary](/research), or jump to the [copper peptide skin research](/skin-research) and [copper peptide serum research](/serum-research) pages. ## How to read this ledger Three rules govern every page here. First, the headline is the number. Each section opens with what was measured — the dose, the percentage, the count, the species — and the attribution follows. Second, the form is tracked: where a study used free GHK rather than the copper complex, the entry says so, because the two are not interchangeable in the evidence [3]. Third, the evidence class is marked, not blurred. A human placebo-controlled result, an in-vitro dose-response, and a single rodent behavioral study are different grades of evidence, and a ledger that flattened them would be useless. What that produces is an honest balance sheet rather than a sales page. The strongest entries — the Maquart 1988 collagen dose-response [1], the Pickart 2015 skin-regeneration review [3], the Lee 2016 hair-count trial [4], the Hostynek 2011 penetration study [5] — are real, dated and citable. The gaps — no validated human pharmacokinetics, a literature heavily weighted toward in-vitro and rodent work, a foundational body of mechanism papers from a single investigator group — are posted as line items too. The [What a GHK-Cu peptide does](/) question is answered in the next section; the [copper peptide side effects](/faq) and [is copper peptide safe](/faq) questions are answered on the FAQ. ## What does a GHK-Cu peptide do? ### What does a GHK-Cu peptide do? In research models GHK-Cu acts as a copper-binding tripeptide that stimulates fibroblast synthesis of collagen, elastin and glycosaminoglycans and rebalances matrix-remodeling enzymes toward controlled repair [1][6]. It also carries broad tissue-repair gene effects, shifting expression of about 31.2% of human genes at a 50%-or-greater threshold toward repair and antioxidant programs [2]. Effects are documented across skin, hair-follicle, vascular and wound models. ### What is GHK-Cu and how does it work? GHK-Cu is the glycyl-histidyl-lysine copper(II) complex; it works as a copper chaperone and a pleiotropic signaling molecule, directly stimulating matrix synthesis at picomolar-to-nanomolar concentrations in study models [1]. Collagen synthesis in human fibroblasts began between 10^-12 and 10^-11 M and peaked near 10^-9 M, independent of cell number [1]. The copper coordination is what enables cross-linking and antioxidant chemistry [6]. ### What is the difference between GHK and GHK-Cu? GHK is the free tripeptide (MW 340.38); GHK-Cu is its copper(II) chelate (MW 402.92) [3][6]. Copper coordination is required for most documented matrix-remodeling activity — the free peptide does not reproduce the complex's fibroblast effects [3]. Free GHK is also rapidly metabolized in plasma to the dipeptide histidyl-lysine, documented in a rat pharmacokinetic study [10]. --- A compliance-grade ledger of the GHK-Cu copper-tripeptide literature — every collagen study, skin trial and regulatory status posted as a line item and reconciled to its source, with no clinic behind the statement and nothing here for sale.