Despite the development of numerous anticancer drugs, most tumors still relapse after treatment, often becoming more malignant and resistant to conventional therapies. The current antitumor therapeutic paradigm focuses on maximizing tumor-selective cell killing. However, recent studies indicate that cancer cells actively adapt to these hostile environments through evolutionary mechanisms, such as the ploidy cycle, leading to treatment resistance. Prostaglandin E2 (PGE2) is well-known for its physiological role in promoting wound healing and tissue regeneration in normal tissues, and cancer cells leverage this mechanism to develop resistance to anticancer drugs. Cell death signals triggered by anticancer agents enhance PGE2 synthesis, while EP receptors on surrounding cancer and immune cells drive tumor regeneration and immune suppression, ultimately leading to the recurrence of drug-resistant tumors. As an antagonist targeting these EP receptors (EP2 and EP4), OCT-598 is expected to inhibit the role of PGE2, thereby preventing the expression of therapeutic resistance and suppressing tumor recurrence.
Target patient
Solid tumor patients, Combination therapy with standard treatment
Development stage
Planned IND submissions to FDA and MFDS (Korea) in 2025
OCT-598 is a small-molecule compound that targets both EP2 and EP4 receptors, mediating tumor promotion and immune suppression through PGE2 binding. It has demonstrated remarkable efficacy across various solid tumor animal models. In combination with standard therapies, OCT-598 not only inhibits tumor growth but also shows sustained efficacy in preventing recurrence. These findings suggest that OCT-598 has the potential to overcome therapeutic resistance when used alongside a range of standard treatments.
Indications