GHK-Cu
preclinicalAlso known as: Copper peptide, Copper tripeptide-1
GHK-Cu (copper tripeptide-1) is a naturally occurring copper-binding tripeptide (glycyl-histidyl-lysine) that exerts its effects primarily through modulation of gene expression and extracellular matrix remodeling. Its mechanism involves chelating copper ions, which facilitates activation of matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs), thereby promoting balanced collagen turnover. GHK-Cu also upregulates genes associated with collagen synthesis (e.g., COL1A1, COL3A1), angiogenesis, and antioxidant defense, while downregulating pro-inflammatory cytokines. These actions collectively enhance wound healing, dermal regeneration, and tissue repair. Preclinical research (72 PubMed-indexed studies) demonstrates that GHK-Cu accelerates wound closure in animal models by increasing fibroblast proliferation, neovascularization, and re-epithelialization. In vitro, it stimulates synthesis of collagen I, III, and glycosaminoglycans, and reduces UV-induced DNA damage. Studies also show neuroprotective and anti-inflammatory properties, with potential applications in skin aging, hair growth, and bone repair. However, no human clinical trials have been published to date, limiting translational evidence. Clinically, GHK-Cu is widely used in topical cosmetic formulations for anti-aging and wound healing, though regulatory approval for therapeutic indications remains preclinical. Its safety profile appears favorable in animal studies, but efficacy claims lack robust human data. For research purposes only — not medical advice.
Key data
C14H21CuN6O4-Research & studies
BPC-157 showed potential in tendon and muscle repair but lacks validation in human trials.; TB-4 and TB-500 promoted angiogenesis in preclinical models, but human orthopaedic data are absent.; CJC-1295 with ipamorelin improved muscle tension in murine models, limited to animal studies.; No clinical evidence supports GHK-Cu or tesamorelin for musculoskeletal conditions.
GHK-Cu was successfully loaded onto hydroxyapatite microspheres by electrostatic adsorption.; GHK-Cu@CMHA gel exhibited sustained release of GHK-Cu for 7 days with good flowability and injectability.; In LPS-induced inflammation models, GHK-Cu@CMHA reduced inflammatory factors and ROS levels while increasing SOD activity.; H&E and Masson staining showed significant collagen deposition, confirming anti-inflammatory and antioxidant properties.
GHK-Cu reduced weight loss, DAI, colonic edema, and inflammatory damage in DSS-induced UC mice.; GHK-Cu upregulated ZO-1 and Occludin expression, promoting mucosal healing in a co-culture model.; GHK-Cu increased SIRT1 and decreased p-STAT3 expression; STAT3 silencing abolished its effects on healing and tight junction proteins.; GHK-Cu suppressed inflammatory cytokines and RORγt expression, indicating potential Th17 cell reduction.
GHK-Cu is a hydrophilic compound with limited permeation through the lipophilic stratum corneum.; Liposomes may improve GHK-Cu's skin permeation potential.; Literature shows little attention to transport of liposomes containing GHK-Cu.; This research gap drives need for new methods to evaluate liposome effects on GHK-Cu transportation.
GHK-Cu binds to peroxiredoxin 6 (PRDX6) to reduce lung inflammation and fibrosis in silicosis mice.; GHK-Cu inhibits crystalline silica-induced oxidative stress in alveolar macrophages.; No significant systemic toxicity was observed with GHK-Cu treatment.; GHK-Cu attenuates progression of pulmonary inflammation and fibrosis in silicosis.
GHK promotes tissue regeneration, collagen synthesis, and angiogenesis, supporting its anti-wrinkle potential.; GHK-Cu and Pal-GHK are widely used in cosmetics but lack sufficient clinical studies on their effectiveness.; Metal complexation and hydrophobic modification increase skin permeability of GHK derivatives.; Cell-penetrating peptides and microneedle pretreatment show promise for enhancing GHK skin permeation.
Phenothiazine-based sensor shows high selectivity for Cu(II) ions compared to other transition metals.; Lewis acidity of Cu(II) salt enhances sensing response in methanol solvent.; Optimal sensor-to-Cu(II) ratio for desired response is 1:1.
Frequently asked questions
What is GHK-Cu?
GHK-Cu (copper tripeptide-1) is a naturally occurring copper-binding tripeptide (glycyl-histidyl-lysine) that exerts its effects primarily through modulation of gene expression and extracellular matrix remodeling. Its mechanism involves chelating copper ions, which facilitates activation of matrix metalloproteinases (M
How does GHK-Cu work?
Copper-binding tripeptide that stimulates collagen synthesis, wound healing, and remodeling gene expression.
What is the research status of GHK-Cu?
GHK-Cu is currently classified as preclinical, with 74 research references on record. This is for research purposes only and is not medical advice.
What is the molecular weight of GHK-Cu?
GHK-Cu has a molecular weight of approximately 400.9 g/mol (formula C14H21CuN6O4-).
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