|Melbourne, Australia, 14 February 2022||ASX:
Level 1 ADR:
- Afamelanotide evaluated as skin DNA repair therapy in disease-free adults
- Study evaluates oxidative damage caused by UV radiation
- Focus on potency of the drug in reduction & extent of regeneration
of cellular DNA damage
- Parallel study CUV156 in xeroderma pigmentosum C (XP-C) patients
CLINUVEL today announced that the first disease-free subjects have received afamelanotide as part of the CUV151 mechanistic study to evaluate the impact of the drug on DNA damaged skin. The Company ¬commenced its innovative DNA Repair Program in 2020, evaluating afamelanotide in patients with xeroderma pigmentosum (XP). The reduction of DNA damage caused by ultraviolet (UV) and solar exposure is relevant for both patients and individuals, who are at high risk of contracting skin cancer(s).
“Data from CUV151 will give us insights into afamelanotide’s ability to safely protect skin from light, and restore DNA which has incurred damage from solar exposure. The findings of this study assist us to address much broader audiences using our expertise in melanocortins and other technologies.”
“Up to two billion individuals worldwide have deficient DNA repair mechanisms of the skin,” CLINUVEL’s VP of Scientific Affairs, Dr Tim Zhou said. “Our DNA Repair Program focuses on understanding and quantifying the role of afamelanotide as an interventional therapy to help those individuals who are at greatest risk.”
Relevance of DNA Skin Damage and Repair
UV and high energy visible (HEV) light penetrate unprotected human skin, and damage DNA found in the nucleus of skin cells. If left unrepaired, DNA “photoproducts” may cause mutations, leading to skin cancer, and premature ageing (photoaging). At limited capacity, under normal conditions, our body can eliminate photoproducts through processes known as nucleotide excision repair (NER) and base excision repair (BER), where the damage is removed and replaced to restore the DNA helix.
Due to inherited genetic defects, however, many individuals have deficient DNA repair mechanisms, increasing their risk of long-term damage, and skin cancer. Particularly, XP patients belong to a group known to have the highest rate of skin cancer, due to a deficiency in the NER mechanism.
Clinically, afamelanotide has been shown to reduce photoproducts. Further research has demonstrated the ability of afamelanotide and other melanocortin molecules to assist skin cells in DNA repair mechanisms (NER and BER) as well as protecting skin from UV damage.
DNA Repair Program – CUV151 study
The mechanistic CUV151 study, conducted at an expert photodermatology unit, will expose up to ten adult disease-free subjects to afamelanotide, seeking to quantify whether the treatment can reduce DNA photoproducts and increase DNA regeneration.
“Afamelanotide 16 mg has been shown to be effective as a systemic photoprotective agent and we are now expanding the use of the molecule in patients at highest risk of skin cancers, the XP group,” CLINUVEL’s Head of Clinical Operations, Dr Pilar Bilbao said. “This current study is part of our overall DNA Repair Program to determine the mechanisms of our drug’s effects in UV-damage prone subjects, and provides a parallel protocol to the ongoing CUV156 study in XP-C patients.
“Now that disease-free subjects are allowed back in a hospital environment, the CUV151 study can proceed,” Dr Bilbao said.