Compass Therapeutics Announces Its Poster Presentation Entitled "Enhanced Efficacy of CTX-471, A CD137 Agonist Antibody, In Models Of Immune Checkpoint Failure Via Simultaneous Blockade Of Neo-Angiogenesis" American Association For Cancer Research Annual Meeting, April 25–30, 2025 In Chicago, Illinois

• CTX-471 monotherapy demonstrated efficacy in multiple murine models, including models highly resistant to immune checkpoint inhibitors.
• Combining CTX-471 with tovecimig (CTX-009) markedly increased anti-tumor efficacy in these models.
• Tovecimig in combination with CTX-471 showed evidence of enhanced innate and adaptive anti-tumor immunity ranging from increased tumor cell killing to increased antigen presentation and interferon signaling.
• The combination of tovecimig and CTX-471 has the potential to be an effective therapeutic regimen in patients where checkpoint inhibitors have failed, including anti-PD-1 and anti-PD-L1 antibodies.

Compass Therapeutics, Inc. (NASDAQ:CMPX), a clinical-stage, oncology-focused biopharmaceutical company developing proprietary antibody-based therapeutics, today announced its poster presentation entitled "Enhanced Efficacy of CTX-471, A CD137 Agonist Antibody, In Models of Immune Checkpoint Failure Via Simultaneous Blockade of Neo-Angiogenesis" at the American Association for Cancer Research (AACR) Annual Meeting, from April 25–30, 2025, at the McCormick Place Convention Center in Chicago, IL.

"We are encouraged by the preclinical data shared at AACR, which demonstrated increases in the tumoral immune infiltrate in several mouse models following CTX-471 monotherapy," said Thomas Schuetz, M.D., Ph.D., Chief Executive Officer and Scientific Founder of Compass. "Our results also suggest that combining CTX-471 with a next-generation anti-angiogenic agent such as tovecimig might not only enhance therapeutic efficacy and duration of response to CTX-471, but may also provide clinical benefit to patients in whom checkpoint inhibitors have failed. We look forward to advancing our ongoing work in these programs, with potential application across multiple solid tumor types and patient populations."

Tovecimig in combination with CTX-471 demonstrated compelling activity in multiple murine models, including novel models highly resistant to immune checkpoint inhibitors:

• CT26B2m and MC38B2m knockout mouse tumor models, engineered to mimic HLA loss in patients (B2m: beta-2 microglobulin).
• Two novel models of immunotherapy resistance without the enhanced NK cell susceptibility bias conferred by complete or targeted MHC-I loss:
  • A murine model with CT26 cells containing an engineered deletion of the B2m gene that were passaged in tumor-experienced mice, establishing a line of CT26B2m-/- cells that escaped immune rejection (CT26 B2m knockout escapers, CT26B2m-/-E).
  • A murine model containing an H-2k1 MHC-I locus knockout in MC38 cells, resulting in targeted homozygous loss (with the expression of the other MHC-I alleles, and therefore natural resistance to NK cells).

The combination of CTX-471 with tovecimig was effective in these mouse models where conventional immune checkpoint inhibitors show reduced activity. Mechanistically, the combination appears to enhance inflammasome activation, pyroptosis, and interferon-mediated signaling, potentially providing clinical benefit to patients in whom checkpoint inhibitors have failed.