Human skin retention and penetration of a copper tripeptide in vitro as function of skin layer towards anti-inflammatory therapy.
Hostynek. Jurij J JJ; Dreher. Frank F; Maibach. Howard I HI
Key Findings
- Permeability coefficient through dermatomed skin was 2.43 ± 0.51 × 10⁻⁴ cm/h.
- About 136 µg of copper per cm² crossed the skin over 48 hours.
- Approximately 82 µg of copper per cm² was retained in the skin as a depot.
Practical Outcomes
- Topical GHK‑Cu formulations can deliver copper into the skin at levels that could be biologically active for anti‑inflammatory purposes. Biohackers could consider low‑dose skin applications (e.g., creams or patches) as a way to experiment with copper‑based inflammation support, but exact dosing and long‑term safety still need human studies.
Summary
The study shows that a copper‑binding peptide (GHK‑Cu) can pass through human skin and stay in the skin layers when applied as a cream or patch, delivering measurable amounts of copper that might help reduce inflammation.
Abstract
The skin retention and penetration characteristics of copper applied as glycyl-L-histidyl-L-lysine cuprate diacetate were evaluated in vitro in order to assess the potential for its transdermal delivery as anti-inflammatory agent. Flow-through diffusion cells with 1 cm(2) exposure area were used under infinite dose conditions. 0.68% aq. Copper as a tripeptide was applied on isolated stratum corneum, on heat-separated epidermis and on dermatomed skin. Receptor fluid collected over 48 h in 4 h intervals was analyzed by inductively coupled plasma mass spectrometry for copper in tissues and receptor fluid. The permeability coefficient of the compound through dermatomed skin was 2.43 ± 0.51 × 10(-4) cm/h; 136.2 ± 17.5 μg/cm(2) copper permeated 1 cm(2) of that tissue over 48 h, while 82 ± 8.1 μg/cm(2) of copper were retained there as depot. Applied tansdermally as the tripeptide on human skin ex vivo, copper permeated the skin and was also retained in skin tissue in amounts potentially effective for the treatment of inflammatory diseases.
Study Information
pubmed
2010
2010-08-13T00:00:00.000Z
10.1007/s00011-010-0214-4
19
41