Overview
GHK-Cu (copper glycyl-L-histidyl-L-lysine) is a small endogenous tripeptide–copper complex in which the peptide GHK coordinates with a Cu²⁺ ion. First identified in human plasma, it has been investigated in research settings as a copper-binding and copper-transport–associated molecule capable of influencing multiple molecular pathways.
Within laboratory environments, GHK-Cu is studied for its association with transcriptional regulation, extracellular matrix signaling, oxidative balance, and inflammatory-response pathways. Because copper functions as a redox-active cofactor in numerous enzymatic systems, its coordination with peptides such as GHK provides a useful model for examining copper-dependent signaling and gene-expression dynamics under defined in-vitro and preclinical conditions.
Experimental designs frequently include peptide-alone and copper-alone controls to distinguish effects attributable specifically to metal complexation.
Biochemical Characteristics
- Amino Acid Sequence: Gly-His-Lys (Cu²⁺ complex)
- Molecular Formula: C₁₆H₂₈CuN₆O₆²⁻
- Molecular Weight: 463.98 g/mol
- PubChem CID: 156588903
- CAS Number: 49557-75-7
- Synonyms: Copper glycyl-histidyl-lysine, Lamin
GHK coordinates Cu²⁺ through nitrogen- and oxygen-donor atoms contributed by the glycine N-terminus, histidine imidazole ring, and lysine-associated functional groups, resulting in a stable yet exchange-capable complex in aqueous systems. This coordination chemistry is leveraged in laboratory research to study copper partitioning between ligands, proteins, and cellular compartments, as well as copper-dependent catalytic and redox processes under controlled experimental conditions.
Research Applications
GHK-Cu is evaluated in cell-based systems and controlled preclinical models to measure molecular and cellular markers relative to appropriate controls.
Common experimental endpoints include:
- Extracellular matrix–associated gene targets (including collagen and elastin)
- Angiogenesis-related signaling markers
- Cytokine profiles, including IL-6 and TNF-related pathways
- Oxidative stress biomarkers and reactive oxygen species–associated gene expression
- DNA-repair–associated transcriptional markers
- Proteasome pathway components
- NF-κB–linked transcriptional activity
Transcriptomic analyses have reported broad shifts in gene-expression patterns following exposure under defined laboratory conditions. In injury-model research, investigators may measure histological remodeling markers, vascularization indicators, and inflammatory cell markers compared with untreated or vehicle-treated controls.
All findings are interpreted strictly within the framework of the model system used and remain confined to preclinical research settings.
Pathway & Mechanistic Context
GHK-Cu is studied as a copper-buffering and copper-delivery complex capable of influencing copper-dependent enzymes and signaling networks.
Preclinical literature describes:
- Modulation of oxidative stress pathways through altered redox-active copper availability
- Regulation of antioxidant defense–associated gene expression
- Changes in inflammatory signaling nodes, including NF-κB–associated transcriptional programs
- Transcriptional shifts in genes related to DNA repair, proteostasis, and extracellular matrix organization
In protein-aggregation research, copper is a key variable in redox chemistry and aggregation kinetics for certain amyloidogenic proteins. Laboratory investigations assess whether copper sequestration by GHK modifies copper-catalyzed oxidative reactions and aggregation behavior under defined experimental conditions. These observations are framed strictly as mechanistic evaluations of metal-ion contributions to cellular stress responses and protein chemistry in research systems.
Preclinical Research Summary
Preclinical studies include in-vitro investigations across fibroblast, endothelial, epithelial, and immune-relevant cell models, as well as in-vivo animal studies quantifying injury-responsive endpoints.
Reported findings commonly describe:
- Modulation of extracellular matrix–associated transcriptional and protein markers
- Alterations in inflammatory cytokine signaling pathways
- Engagement of antioxidant response networks
- Changes in angiogenesis-associated markers in tissue remodeling paradigms
- Broad transcriptomic shifts following exposure in controlled cell systems
These summaries refer exclusively to controlled laboratory investigations and are provided to support experimental design, mechanistic hypothesis development, and pathway mapping in research environments.
Form & Analytical Testing
GHK-Cu is supplied as a research-grade peptide–metal complex. Identity and composition are commonly assessed using:
- HPLC — purity profiling
- Mass Spectrometry — molecular confirmation
- ICP-MS / ICP-OES — copper content and stoichiometry verification
- UV-Vis Spectroscopy — copper coordination characterization in solution
Researchers should handle peptide–metal complexes using standard laboratory practices appropriate for synthetic peptides and transition-metal coordination compounds, including appropriate controls for metal contamination, chelator compatibility, and buffer composition effects on copper speciation.
Purity & Quality
- ≥99% Purity — HPLC Verified
- Independently tested by accredited third-party laboratory
- Certificate of Analysis (CoA) available for every batch
Research Use Only (RUO) Notice
All products are furnished strictly for in-vitro laboratory research use only. "In-vitro" refers to studies conducted outside of a living organism in controlled laboratory conditions. These materials are not medicines or drugs and have not been evaluated or approved by the U.S. Food and Drug Administration (FDA) to diagnose, treat, cure, or prevent any disease or medical condition. Introduction into humans or animals is strictly prohibited. Not for human, medical, diagnostic, or veterinary use.
