Photoprotection
Protection of skin from UV radiation damage, achieved through external means (sunscreen, clothing) or biological mechanisms (increased melanin). Afamelanotide provides pharmacological photoprotection by stimulating the skin's natural melanin-based UV defence system through MC1R activation.
Technical Context
Biological photoprotection mechanisms: constitutive (baseline melanin content, SC thickness, urocanic acid in sweat — absorbing UV), inducible (tanning response — UV exposure → DNA damage → p53 activation → POMC/α-MSH production by keratinocytes → MC1R activation on melanocytes → melanogenesis; delayed tanning takes 3-5 days to develop), and enzymatic (DNA repair enzymes — nucleotide excision repair fixing UV-induced pyrimidine dimers). Afamelanotide provides pharmacological photoprotection by: directly stimulating melanogenesis without requiring UV-induced DNA damage (bypassing the need for the UV→p53→α-MSH cascade), achieving higher eumelanin levels than natural tanning in many individuals, and maintaining melanisation during periods of minimal sun exposure (the implant provides continuous MC1R stimulation for ~60 days). Complementary external photoprotection: broad-spectrum sunscreen (SPF ≥30), protective clothing, and behavioural UV avoidance. For EPP patients, afamelanotide supplements but does not replace external photoprotection measures.