GHK-Cu 50mg
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GHK-Cu 50mg

Copper Peptide GHK-Cu

CAS: 49557-75-7

Copper Peptide GHK-Cu — naturally occurring tripeptide modulating 4,000+ genes. Collagen I +70%, elastin upregulation, and antioxidant enzyme expression in fibroblast models.

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$50.00

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HPLC verified · third-party tested · research use only

Specifications

Chemical NameCopper Peptide GHK-Cu
CAS Number49557-75-7
Vial Size50mg
FormLyophilized powder
Purity≥98% (HPLC verified)
Reconstitution10mL BAC water → 5mg/mL
Storage−20°C unreconstituted / 2–8°C up to 28 days reconstituted

4,000+ Gene Modulation — Collagen, Elastin, and Antioxidant Pathways

GHK-Cu (Glycyl-L-histidyl-L-lysine copper complex) operates as a global tissue repair signal — a biological property confirmed by the 2012 Broad Institute genomic analysis showing modulation of 4,000+ human genes. The directional pattern is consistent: upregulated genes include collagen I (+70% in fibroblast models), collagen III (+50%), elastin, glycosaminoglycans, and antioxidant enzymes (superoxide dismutase, catalase). Downregulated genes include those associated with inflammation, cellular senescence, and destructive matrix metalloproteinases. This bidirectional genomic signature makes GHK-Cu unique in the aesthetic peptide landscape — it simultaneously builds structural proteins and suppresses the processes that degrade them.

Collagen I +70% in Fibroblast Models

In fibroblast culture studies, GHK-Cu increased collagen I synthesis by 70% and collagen III by 50%. Collagen I is the primary structural protein of skin, tendons, and bone — its decline with age is the principal cause of visible skin thinning and reduced elasticity. GHK-Cu plasma levels decline 60% between age 20 and 60, temporally tracking this structural loss.

Broad Institute Genomic Data

The 2012 Broad Institute analysis identified 4,000+ genes modulated by GHK-Cu — one of the largest gene expression signatures documented for any tripeptide. The upregulation of skin repair genes while simultaneously downregulating senescence and inflammation genes produces an unusually broad anti-aging biological profile.

Wound Healing and Angiogenesis

Beyond cosmetic applications, GHK-Cu has documented wound healing evidence: keratinocyte migration, angiogenesis, and anti-inflammatory effects in dermal wound models. This dual aesthetic + wound healing profile makes it relevant for both looksmaxxing protocols and recovery applications.

Frequently Asked Questions

What does GHK-Cu do for skin?

GHK-Cu upregulates collagen I (+70%), collagen III (+50%), elastin, and antioxidant enzymes while downregulating inflammation and senescence genes. This dual profile — building structural proteins while suppressing their degradation — makes it the foundational skin quality compound in most aesthetic research protocols.

Why does GHK-Cu decline with age?

GHK-Cu is naturally present in plasma, saliva, and urine, where it acts as a tissue repair signal. Plasma concentrations decline from ~200 ng/mL at age 20 to ~80 ng/mL by age 60 — a 60% decline. This reduction correlates temporally with measurable loss of collagen, elastin, and wound healing capacity.

Can GHK-Cu be combined with SNAP-8 and Melanotan II?

Yes — the three compounds work through entirely different mechanisms. GHK-Cu targets systemic skin quality via gene regulation. SNAP-8 targets SNARE-mediated expression lines. Melanotan II targets MC1R for melanogenesis. None compete mechanistically and all three are commonly run as a layered aesthetic stack.

What is the reconstitution protocol for GHK-Cu 50mg?

Add 10mL bacteriostatic water to the 50mg vial for a 5mg/mL concentration. Inject slowly along the vial wall. Swirl gently — do not shake. Store at 2–8°C for up to 28 days. For lower concentrations, scale proportionally (e.g., 25mL water → 2mg/mL).

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