On November 6, 2026 Compass Therapeutics, Inc. (Nasdaq: CMPX), a clinical-stage, oncology-focused biopharmaceutical company developing proprietary antibody-based therapeutics to treat multiple human diseases, reported it will present data on the novel mechanism of action for CTX-10726 at the 41st Society for Immunotherapy of Cancer (SITC) (Free SITC Whitepaper) 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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Data highlights from the presentation include:

Novel PD-1 Cleavage Mechanism. In addition to the expected dual blockade of VEGF-A and PD-1, preclinical studies also revealed a novel mechanism of action for CTX-10726. Specifically, the multimerization of CTX-10726 facilitates the cleavage and removal of PD-1 from the surface of T cells, converting PD-1 positive T cells into PD-1 negative T cells and extending the mechanism beyond simply checkpoint blockade and angiogenesis inhibition.
VEGF-A Enhanced Potency. Adding VEGF-A increased the potency of CTX-10726 approximately ten-fold in a human immune-cell assay measuring interferon-gamma production, reducing the EC50 from 2.0 to 0.2 nM. In vitro studies showed PD-1 receptor cleavage by CTX-10726 in the presence of VEGF-A compared to PD-1 receptor internalization in the absence of VEGF-A. Neither pembrolizumab nor bevacizumab alone demonstrate comparable PD-1 cleavage. Two in vivo models further demonstrated the VEGF-A-dependent nature of PD-1 receptor cleavage by CTX-10726.
Combined Activity with CTX-471. A mouse surrogate of CTX-10726 combined with CTX-471 (CD137 agonist antibody) further enhanced anti-tumor activity in mouse models, accompanied by coordinated upregulation of chemokines, interferon-stimulated genes, and inflammatory cytokines. These changes were associated with increased immune cell recruitment and establishment of a more permissive tumor microenvironment.

"These data reveal a new and differentiated mechanism of action for CTX-10726, setting it apart in this exciting new class of therapeutics," said Thomas Schuetz, MD, PhD, Chief Executive Officer. "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. 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. We are also encouraged by the combination results with CTX-471 in checkpoint-resistant models, supporting further investigation of these complementary approaches."

The Phase 1 multiple ascending dose-escalation study of CTX-10726 includes four dosing cohorts (0.3, 1.0, 3.0, and 10.0 mg/kg) in a 3+3 format. The multi-center study is enrolling post-checkpoint patients with a prioritized set of locally advanced, unresectable or metastatic malignancies, including renal cell carcinoma, gastroesophageal cancer, hepatocellular carcinoma, and endometrial cancer, in whom standard of care therapies have failed.

Details of the presentation are as follows:

Title: VEGF-dependent cleavage of cell surface PD-1 mediated by CTX-10726, a novel PD-1×VEGF-A bispecific antibody
Date & Time: Saturday, November 7, 2026 from 10:00 AM–2:00 MT PM and 6:00–8:10 MT PM
Poster number: 678
Location: Phoenix Convention Center – North Building – Lower Level – Exhibition Halls 4-5

A copy of the presentation materials can be accessed on the Compass website at View Source once the presentation has concluded.

About CTX-10726
CTX-10726 is a tetravalent PD-1 x VEGF-A bispecific antibody discovered and engineered at Compass. CTX-10726 is designed to synergistically deliver VEGF-A blockade and checkpoint inhibition, potentially applicable to multiple solid tumor indications. The bispecific antibody demonstrates a highly stable structure with high affinity target binding. CTX-10726 exhibits more potent PD-1 suppression and a novel mechanism of action compared with data reported for other drugs in the class.

(Press release, Compass Therapeutics, NOV 6, 2026, View Source [SID1234674424])