ACR-368, a CHK1/2 inhibitor in a registrational-intent Phase 2b study, showed potent preclinical synergy with Topoisomerase 1 (Topo 1) inhibitors, commonly used payloads in antibody-drug conjugates (ADCs) 

ACR-2316, a WEE1/PKMYT1 inhibitor currently in Phase 1, demonstrated complete and durable tumor regression in immunocompetent, syngeneic tumor mouse models in combination with anti-PD-L1 checkpoint inhibition

WATERTOWN, Mass., March 17, 2026 (GLOBE NEWSWIRE) -- Acrivon Therapeutics, Inc. ("Acrivon" or "Acrivon Therapeutics") (NASDAQ:ACRV), a clinical stage biotechnology company discovering and developing precision medicines utilizing its proprietary Generative Phosphoproteomics AP3 (Acrivon Predictive Precision Proteomics) platform deployed for rational drug design and predictive clinical development, today announced three poster presentations, including one late-breaking presentation, at the upcoming American Association for Cancer Research (AACR) Annual Meeting being held in San Diego, CA from April 17-22, 2026.

"These data further demonstrate our differentiated approach leveraging our AP3 platform to identify therapeutic candidates and combinations with the greatest potential for clinical impact," said Peter Blume-Jensen, M.D., Ph.D., chief executive officer, president, and co-founder of Acrivon. "Our data show that a key resistance mechanism to Topo1 inhibitors, the most common ADC payload, is the activation of the CHK1/2 DNA damage repair response, which can be overcome by ACR-368 treatment resulting in synergistic tumor cell killing. We also found that ACR-2316 induced mitochondrial and nuclear genomic damage resulting in activation of the innate and adaptive immune system, leading to complete tumor regression and lasting immune protection in mice when combined with immune checkpoint inhibition."