Product focus
Oncology
Infectious disease
DEBIO 0123
Wee1 kinase inhibitor
Debio 0123 is a Wee1 kinase inhibitor currently in phase I research in refractory solid tumors. The compound is being developed based on the deepened understanding of the DNA damage response (DDR) of cancer cells. Inhibition of WEE1 prevents cells to arrest or repair DNA damages and force them to prematurely continue through the cell cycle, therefore accumulating unrepaired DNA damages ultimately leading to cell death. The compound is being developed in light of the need to improve cancer patients’ treatment response and to overcome treatment resistance to current therapies. Pre-clinical models have shown anti-tumor activity both as a single agent and in combination with carboplatin. The advancement of Debio 0123 into clinical studies will assess the therapeutic results for cancer patients in various tumor types.
Focus on Debio 0123 Mode of Action
Wee1 is a key regulator of the G2/M and S phase checkpoints, activated in response to DNA damage, that allow cells to repair their DNA before resuming the cell cycle. Inhibition of Wee1, particularly in combination with DNA damaging agents, induces an overload of arrests in the DNA damage response process. Also, in conjunction with the failure of other checkpoints, such as G1 controlled by p53, Wee1 inhibition pushes the cells through their cycle before DNA repair, promoting mitotic catastrophe and inducing apoptosis of cancer cells. The resulting impairment of the G2-M checkpoint prevents cancer cells from repairing DNA damage, favoring the enhancement of the effect of the DNA damaging therapy and potentially improving therapeutic outcomes.
Focus on DNA Damage Response
DNA damage response consists of all proteins and processes that ensure that the cell cycle does not progress with damaged DNA. Replication is a highly regulated process that guarantees the faithful duplication of the genome once per cell cycle, and any condition that compromises it is referred to as replication stress. Replication stress, characterized by DNA synthesis slow down and or replication fork stalling, is a major cause of genome instability and is linked to the development of tumor cells. Replication is not present in normal cells and as such targeting DDR offers new opportunities for drug development.
DEBIO 4126 & 4127
Long-acting octreotide
We are currently developing sustained-release formulations designed to improve the performance and the convenience of cancer treatments.
DEBIO 1450
FabI inhibitor
Our first-in-class FabI Inhibitor antibiotic class specifically targets selected pathogens while preserving intestinal microbiota and meet all four WHO 2020 innovation criteria:
- new chemical class
- new target
- new mode of action
- no cross-resistance to other antibiotic classes