CU50 - GHK-CU - 50 MG - Research Use Only

Product definition

What is GHK-Cu?

GHK-Cu (Copper tripeptide-1) is a naturally occurring tripeptide-copper complex studied in preclinical models for collagen synthesis, wound healing, hair follicle activation, and skin repair.

GHK-Cu (Glycyl-L-histidyl-L-lysine copper(II)) is a tripeptide-copper complex that occurs naturally in human plasma, liver tissue, and saliva. Originally isolated by Loren Pickart in the 1970s during investigation of plasma factors affecting liver cell growth, the compound has since developed a broad research profile spanning dermatology, wound healing, and aging biology. The copper binding is integral to the molecule's proposed mechanism: GHK acts as a carrier that delivers copper to tissue sites where it serves as a cofactor for lysyl oxidase — the enzyme responsible for cross-linking collagen and elastin fibers in the extracellular matrix. Beyond copper delivery, GHK-Cu has been shown to modulate gene expression across hundreds of genes in cell culture models, including upregulation of tissue repair genes and downregulation of inflammatory signaling genes. The research base spans Pickart's foundational work through contemporary studies in cosmetic dermatology and regenerative medicine preclinical research.

Research context

What does the preclinical literature say about GHK-Cu?

GHK-Cu was originally characterized by Loren Pickart while studying the effect of albumin-derived fractions on liver cell regeneration. The finding that a tripeptide-copper complex — present in plasma at concentrations that decline with aging — could stimulate tissue repair processes set the foundation for subsequent research across multiple biological systems. In dermal wound healing research, GHK-Cu has been studied across in vitro fibroblast and keratinocyte models and in vivo rodent wound models. Consistently documented effects include accelerated wound closure, increased dermal collagen deposition, and enhanced angiogenesis in wound beds. These effects have been associated with TGF-β1 upregulation and VEGF promotion in experimental systems. In hair biology research, the compound has been studied in mouse and rat models for its effect on telogen-to-anagen transition and hair follicle size. Some rodent studies document increased hair count and follicle density in treated versus control areas. The proposed mechanism involves DHT pathway modulation and direct growth factor stimulation at the follicular level. GHK-Cu also has a substantial transcriptomic research footprint: Pickart's group published analyses of GHK-Cu effects on gene expression suggesting broad anti-inflammatory, pro-survival, and tissue-remodeling gene expression patterns across multiple cell types.