Our DNA is constantly subjected to damage by ultraviolet light (UV) and this DNA damage accumulates in replicating cells, giving rise to mutations that can lead to premature aging, cancer, and other diseases. The two main toxic photoproducts that occur during UV skin exposure are cyclobutane pyrimidine dimers (CPDs) and 6-4 photoproduct (6-4PPs) photolesions. CPDs are the major lesions that contribute to mutagenic events, and UV-induced carcinogenesis compared with 6-4PPs.
Normally, cells utilize a complex network SOS network called DNA damage response (DDR), which is responsible for detecting, repairing or stopping replication of damaged DNA cells. Individuals with XP either lack of the normal cellular repair mechanism or have defective repair pathways so that damage is not managed effectively.
Our lead drug development candidate, HB4208, is a DNA Damage Response (DDR) enzyme for topical treatment of the rare genetic disorder (orphan disease) Xeroderma Pigmentosum (XP). There is no cure or effective treatment for DNA damage in XP patients. HB4208 has shown positive results to modulate UV-induced DNA damage repair in animal model. The Company’s rare disease program is in early preclinical development.