Abstract
The greatest risk factor for skin cancer is exposure to ultraviolet (UV) rays of the sun. Among the 3 types of solar radiation (UVA, UVB, UVC), UVB rays are most commonly associated with skin cancer. UVB exposure promotes the formation of cyclobutane pyrimidine dimers (CPDs) in the DNA of cells in the epidermal skin layers, which can lead to mutations as DNA repair machinery attempts to repair the damage. These mutations can lead directly to skin carcinogenesis. Previous studies in animal and in human ex vivo skin models have shown that topical application of acyclothymidine dinucleosides protects DNA from UV-induced damage by preventing the formation of CPDs and helps initiate repair through the activation of DNA repair enzymes. Here we review the biological evidence leading to the development and formulation of ProteXidine™ (Topix Pharmaceuticals, Inc., Amityville, NY), as a UV protective agent for topical human application. We also provide clinical data pertaining to four ProteXidine™ formulations (test materials 1-4) tested for their abilities to reduce CPDs in an ex vivo human skin tissue model.
Original language | English (US) |
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Pages (from-to) | 953-956 |
Number of pages | 4 |
Journal | Journal of Drugs in Dermatology |
Volume | 23 |
Issue number | 11 |
DOIs | |
State | Published - Nov 2024 |
Bibliographical note
Publisher Copyright:Copyright © 2024.
PubMed: MeSH publication types
- Journal Article
- Review