Description

GHK-Cu – Technical Biochemical Mechanism Profile

(Copper-Binding Tripeptide; ECM Remodeling & Gene-Expression Modulator – Research Use Only)

GHK-Cu is a naturally occurring glycyl-L-histidyl-L-lysine tripeptide that forms a high-affinity complex with Cu²⁺, enabling copper delivery into extracellular and intracellular signaling systems.
In vitro experiments show modulation of MMP/TIMP balance, TGF-β/SMAD, integrin signaling, and oxidative stress response gene programs associated with extracellular matrix turnover and cellular repair pathways.

✅ 1. Primary Molecular Targets

GHK chelates Cu²⁺ with nanomolar affinity, forming GHK-Cu complexes that can deliver copper to enzymes requiring copper-dependent redox activity.

✅ 2. Core Biochemical Pathways

A. Matrix Regulation (MMP/TIMP Axis)

In cell culture systems:

• ↓ MMP-1, MMP-2, MMP-9 (matrix proteases)

• ↑ TIMP-1, TIMP-2 (MMP inhibitors)

• Enhances collagen (COL1A1), elastin (ELN), integrin gene expression

Key effect: shifts ECM turnover toward structural rebuilding.

B. TGF-β / SMAD Signaling

• GHK-Cu modulates TGF-β1 expression and receptor activation

• Alters SMAD2/3 phosphorylation

• Promotes transcription of ECM-related genes:

  • COL1A1, COL3A1, COL4A1

  • FN1 (fibronectin)

  • ITGB1 / ITGA5 (integrins)

C. Antioxidant & Metal-Dependent Enzymes

Copper delivery may influence:

Gene-level increases in SOD1, GPX, CAT have been reported in oxidative-stress models.

✅ 3. Signal Transduction Cascades

✅ 4. Gene-Level Targets Measured in Assays

More than 4,000 human genes have been reported to shift expression levels when exposed to GHK-Cu in gene-array studies.

✅ 5. Metal-Binding Chemistry

• Peptide sequence coordinates Cu²⁺ via histidine imidazole nitrogen and terminal amine groups

• Stabilizes copper in a redox-active yet transportable state

• Protects against unbound copper–mediated oxidative damage

✅ 6. Mechanistic Summary

• Tripeptide with high-affinity copper chelation

• Modulates ECM remodeling via MMP/TIMP shifts

• Influences TGF-β/SMAD, FAK/ERK, and Nrf2 pathways

• Alters gene transcription for collagen, elastin, antioxidant defense, and DNA repair

• Does not function as a hormone or receptor agonist—acts through metal delivery and signaling modulation

✅ Research-Only Classification

GHK-Cu is supplied exclusively for in-vitro laboratory research.
Not approved for human or animal use, injection, ingestion, topical application, or any biological administration.