Last reviewed 2026-04-23 · How we verify

ASP1650

ASP1650 is a selective antagonist of the prostaglandin E receptor EP4, which reduces inflammatory signaling and immune suppression in the tumor microenvironment.

ASP1650 is a selective antagonist of the prostaglandin E receptor EP4, which reduces inflammatory signaling and immune suppression in the tumor microenvironment. Used for Advanced solid tumors (in combination with checkpoint inhibitors).

At a glance

Mechanism of action

EP4 antagonism blocks prostaglandin E2 (PGE2) signaling, a pathway that promotes immunosuppression and tumor growth. By inhibiting EP4, ASP1650 enhances anti-tumor immune responses and may restore T-cell function. This mechanism is being explored to enhance the efficacy of checkpoint inhibitors and other immunotherapies.

Approved indications

• Advanced solid tumors (in combination with checkpoint inhibitors)

Common side effects

• Diarrhea
• Fatigue
• Nausea

Key clinical trials

• Phase 1 Trial of IMAB027 in Patients With Recurrent Advanced Ovarian Cancer (OVAR) (PHASE1)
• A Study to Assess the Safety and Efficacy of ASP1650, a Monoclonal Antibody Targeting Claudin 6 (CLDN6), in Male Subjects With Incurable Platinum Refractory Germ Cell Tumors (PHASE2)

Primary sources

Every claim on this page is sourced from regulatory or scientific primary sources. See our editorial policy for full methodology.

Competitive intelligence

For the full competitive landscape — auto-detected comparators, recent regulatory actions across the set, upcoming PDUFA, patent timeline, sponsor landscape:

• ASP1650 CI brief — competitive landscape report
• ASP1650 updates RSS · CI watch RSS
• Astellas Pharma Global Development, Inc. portfolio CI