Pancreatic cancer treatment
An anti-cancer agent that selectively acts on CDK1 among the cyclin-dependent kinases (CDKs) that regulate the cell cycle
BEY1107P induces apoptosis through cell suicide mechanism by synchronizing cell cycles to G2 / M phase of pancreatic cancer cells. In addition, BEY1107P suppresses the mobility and invasiveness of pancreatic cancer cells and inhibits the self renewal of cancer stem cells, demonstrating effectiveness as a monotherapy as well.
In particular, when combined with the cytotoxic anti-cancer drug Gemcitabine, BEY1107P is expected to overcome the resistance developed from Gemcitabine.
In breast cancer clinical trials, while anti-cancer drugs increased the average survival period by 3 months, CDK4/6 inhibitors prolonged it by 10 months. Therefore, BEY1107P, which has a similar function, is expected to have a better effect than other pancreatic cancer treatments.
Furthermore, BEY1107P is able to regulate cancer stem cells that cause resistance to cytotoxic anti-cancer drugs, making a big difference from CDK 4/6 target anti-cancer drugs.
Currently, BEY1107 is in phase I/II clinical trial.