GHK (Copper-Free)

GHK (Glycine-Histidine-Lysine, copper-free form) is the tripeptide backbone of GHK-Cu without the coordinated copper(II) ion. Providing GHK as a separate research compound alongside GHK-Cu enables mechanistic dissection of copper-dependent from copper-independent biological effects — an important research distinction given that GHK-Cu's broad biological activity profile may involve both the tripeptide sequence itself and the coordinated copper's chemistry.

GHK was first isolated from human plasma by Pickart in 1973. The free tripeptide (without copper) has been studied in its own right and shows measurable biological activity in fibroblast models — collagen synthesis stimulation, cell migration effects, and antioxidant gene expression changes — though typically at higher concentrations and with reduced potency compared to the copper complex. This activity profile suggests GHK has intrinsic receptor or chromatin interactions mediated by the amino acid sequence independently of copper coordination.

Structure-activity relationship research using GHK (copper-free) and GHK-Cu in parallel experiments enables: quantification of the copper contribution to biological activity (if GHK-Cu effect minus GHK effect is attributable to copper chemistry); identification of sequence-dependent activities common to both compounds; assessment of whether copper's contribution is primarily through ATCUN coordination chemistry or through non-specific copper delivery; and determination of concentration ranges where GHK (copper-free) achieves equivalent effects to GHK-Cu.

The free tripeptide also serves as a control for experiments where copper contamination would confound results — particularly in redox biology assays, mitochondrial function assays (where copper is an essential cofactor for cytochrome c oxidase), and assays examining copper homeostasis or cuproenzyme activity.

Experimental comparison design: run GHK (0.1-100 nM), GHK-Cu (0.1-100 nM), and CuSO4 alone (equivalent copper concentration) as three parallel treatment groups in the same assay. Any effect shared by GHK and GHK-Cu is sequence-dependent; any effect unique to GHK-Cu or CuSO4 is copper-dependent.

MW: 340.38 g/mol. CAS: 49557-75-7. Molecular formula: C14H26N6O4. Freely water-soluble. Reconstitute in bacteriostatic water at 1mg/mL. Store lyophilised at -20°C. For laboratory and analytical research purposes only.

GHK (copper-free) mechanistic dissection research: the most informative experimental design uses four treatment groups simultaneously — vehicle, GHK (copper-free), GHK-Cu (copper complex), and CuSO4 alone at the equivalent copper concentration present in the GHK-Cu treatment. This 2×2 factorial design (peptide present/absent × copper present/absent) allows direct attribution of biological effects. Effects shared by GHK and GHK-Cu but absent from CuSO4 are peptide sequence-dependent and copper-independent. Effects unique to GHK-Cu are copper-dependent. Effects shared by GHK-Cu and CuSO4 may be non-specifically copper-mediated.

Published research has suggested that GHK alone (without copper) can activate SP1 transcription factor and stimulate collagen synthesis in fibroblasts, though at higher concentrations than GHK-Cu. Testing GHK (copper-free) across a broad concentration range (0.1nM-10µM) in fibroblast collagen synthesis assays (PICP ELISA) and SP1 reporter assays (SP1-responsive luciferase construct) will characterise the intrinsic sequence-dependent activity independent of copper. Additionally, GHK (copper-free) is the appropriate control for confirming that GHK-Cu effects in assays involving redox-sensitive endpoints (MMP expression, antioxidant gene induction via Nrf2) are not confounded by copper-catalysed Fenton chemistry generating artefactual oxidative stress. MW: 340.38 g/mol. CAS: 49557-75-7. Reconstitute in bacteriostatic water at 1mg/mL. Store lyophilised at -20°C. For laboratory and analytical research purposes only.