Ingredient or product comparison
GHK-Cu Pharmacology Studies: Comparison Across Research Contexts
Wound healing (fibroblast proliferation) 1 nM – 10 µM Cell migration rate, collagen deposition Maximal effect at 1 µM; saturates above 10 µM Effective at low nanomolar concentrations; dose-response curve plateaus early Gene expression (microarray) 1 µM for 24
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- Wound healing (fibroblast proliferation)
- 1 nM – 10 µM
- Cell migration rate, collagen deposition
- Maximal effect at 1 µM; saturates above 10 µM
- Effective at low nanomolar concentrations; dose-response curve plateaus early
- Gene expression (microarray)
- 1 µM for 24 hours
- Genome-wide transcription
- Altered 31.2% of genes measured; upregulated repair pathways, downregulated inflammation
- Broad transcriptional modulator. Impacts extracellular matrix, inflammation, and senescence markers
- Neuroprotection (Alzheimer's models)
- 10 µM in vitro; 5 mg/kg in vivo
- Amyloid-β aggregation, oxidative markers
- Reduced Aβ plaque formation by 42% vs control; decreased lipid peroxidation
- Copper chelation may sequester metals that catalyze Aβ aggregation
- Skin remodeling (photoaging models)
- 0.1% – 2% topical formulation
- Dermal thickness, elastin content
- Increased dermal thickness by 18% after 12 weeks; improved elastin fiber density
- Clinical translation supported by histological endpoints
- Angiogenesis (VEGF-independent)
- 10 nM – 1 µM
- Endothelial tube formation assay
- Promoted capillary-like structures independent of VEGF receptor signaling
- Operates through distinct pathway from classical angiogenic growth factors