Compass Therapeutics Presents Novel Mechanism of Action Data for CTX-10726 (PD-1 x VEGF-A Bispecific Antibody) at the SITC 2026 Annual Meeting
Key Highlights
- ➤CTX-10726 cleaves PD-1 from T cells only when VEGF-A is present
- ➤VEGF-A increased CTX-10726 potency approximately ten-fold, lowering EC50 to 0.2 nM
- ➤Phase 1 dose-escalation study is ongoing across four advanced solid-tumor cancers
- ➤CTX-10726 plus CTX-471 inhibited tumors more than either agent alone in mice
Expert Statements
Thomas Schuetz, Chief Executive Officer of Compass Therapeutics
“These data reveal a new and differentiated mechanism of action for CTX-10726, setting it apart in this exciting new class of therapeutics”
Thomas Schuetz, Chief Executive Officer of Compass Therapeutics
“We believe PD-1 receptor cleavage results in more potent and potentially more durable checkpoint inhibition, which supports and explains what we saw in our earlier studies.”
Thomas Schuetz, Chief Executive Officer of Compass Therapeutics
“The dependence of this mechanism on VEGF links a traditionally anti-angiogenic agent directly to checkpoint control and may enhance the activity of CTX-10726 within VEGF-A-rich tumor microenvironments.”
Thomas Schuetz, Chief Executive Officer of Compass Therapeutics
“We are also encouraged by the combination results with CTX-471 in checkpoint-resistant models, supporting further investigation of these complementary approaches.”
* CTX-10726, a PD-1 x VEGF-A bispecific antibody discovered and engineered at Compass, exhibits a unique mechanism of action that has not been previously reported in this class of drugs, characterized by VEGF-A-dependent cleavage of PD-1 receptors from T cells resulting in conversion of PD-1 positive T cells into PD-1 negative T cells. * PD-1 receptor cleavage by CTX-10726 was only observed in the presence of VEGF-A, suggesting targeted activity in the tumor microenvironment. * A Phase 1 dose-escalation study of CTX-10726 in patients in the post-checkpoint setting with advanced solid tumors, including renal cell, gastroesophageal, endometrial, and hepatocellular cancers, is ongoing. * In checkpoint inhibitor resistant preclinical mouse models, the combination of CTX-10726 and Compass’s CD137 agonist, CTX-471, inhibited tumor growth more than either agent alone. BOSTON, Nov. 06, 2026 (GLOBE NEWSWIRE) -- Compass Therapeutics, Inc. (Nasdaq: CMPX), a clinical-stage, oncology-focused biopharmaceutical company developing proprietary antibody-based therapeutics to treat multiple human diseases, will present data on the novel mechanism of action for CTX-10726 at the 41(st) Society for Immunotherapy of Cancer (SITC) Annual Meeting. CTX-10726 is currently in a Phase 1 dose-escalation study in patients in the post-checkpoint setting with multiple types of advanced solid tumors.
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