DEVELOPMENT STAGE

Phase 1 — Ongoing in patients with solid tumors

AT A GLANCE

PGE2 signaling can promote tumor regrowth and immune suppression following anticancer therapy

Standard anticancer therapies can initially reduce tumor burden, but treatment-induced cell death may increase PGE2 production through the COX-2 pathway. Within the tumor microenvironment, PGE2 activates EP2 and EP4 receptors on tumor and immune cells, promoting the regrowth of surviving tumor cells and suppressing antitumor immune responses. This signaling may limit the durability of standard anticancer therapies and contribute to disease recurrence, providing a rationale for blocking PGE2 signaling through EP2 and EP4 to sustain treatment response.

Dual EP2/EP4 blockade enhances antitumor activity and response durability

OCT-598 is a small-molecule dual antagonist of the PGE2 receptors EP2 and EP4. Across multiple preclinical tumor models, OCT-598 demonstrated greater antitumor activity than EP4-selective inhibition alone, supporting the rationale for targeting both receptors.
In preclinical studies, combining OCT-598 with chemotherapy, immunotherapy or radiation produced durable tumor control. In selected models, these combinations induced complete tumor regression, with responses largely maintained after treatment discontinuation. These findings support further clinical evaluation of OCT-598 as a combination therapy with the potential to improve response durability and limit treatment resistance.

Publications & Presentations

Research on the OCT-598 EP2/EP4 dual antagonist program

PRECLINICAL RESEARCH

CIn-licensed from KANAPH Therapeutics

Exclusive global license · March 2022

Abbreviations — PGE2: prostaglandin E2 · EP2/EP4: prostaglandin E2 receptors 2/4 · COX-2: cyclooxygenase-2 · SoC: standard of care · IND: investigational new drug