Acrivon Announces Late-Breaking Oral Plenary Presentation of Early Phase 1/2 Clinical Results in AP3-Predicted Tumors for its First-in-Class WEE1/PKMYT1 Inhibitor ACR-2316 at the 38th EORTC-NCI-AACR Symposium
Globe Newswire•29/10/2026•08:00 ET
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Key Highlights
- ➤ACR-2316 produced confirmed complete response in heavily pretreated squamous NSCLC
- ➤Several lung adenocarcinoma patients remained on ACR-2316 treatment over one year
- ➤Safety profile primarily limited to transient, asymptomatic neutropenia
- ➤Phase 1/2 study expanded to include pancreatic ductal adenocarcinoma
- ➤Strong synergy with immune checkpoint and TOPO1 inhibitors supports combination development
Expert Statements
Timothy A. Yap, MBBS, Ph.D., FRCP, Professor of Investigational Cancer Therapeutics, The University of Texas MD Anderson Cancer Center
“I’m looking forward to presenting these data at the EORTC-NCI-AACR Symposium. The activity of ACR-2316 in endometrial and lung cancers, including a confirmed complete response in a heavily pretreated patient with squamous NSCLC, stands out, as lung cancers have not been previously shown to be sensitive to existing WEE1 or PKMYT1 inhibitors. The durability we’ve seen is also impressive, with several patients remaining on treatment for more than one year, along with a favorable safety profile.”
Peter Blume-Jensen, M.D., Ph.D., Chief Executive Officer, President and Co-founder of Acrivon
“Our data speak to the differentiation of ACR-2316 and the power of AP3-based drug design and indication finding. The long-lasting clinical benefit observed already during dose escalation in subjects with AP3-predicted tumor types, including heavily pretreated lung cancers, is notable. Together with a safety profile primarily limited to asymptomatic neutropenia, this underscores the potential of ACR-2316 to address difficult-to-treat cancers. Given the strong synergy we have observed with PD-(L)1 and TOPO1 inhibitors, together with its oral dosing route and favorable safety profile, we see great potential for combination development across solid tumor types where ICI and ADCs are beneficial. Furthermore, reported synthetic lethality of WEE1 inhibition in K-Ras-driven, TP53-deficient tumors warrants further investigation of ACR-2316 in PDAC, both as monotherapy and combined with K-Ras inhibitors.”
Timothy A. Yap, MBBS, Ph.D., FRCP, of The University of Texas MD Anderson Cancer Center to present results from the dose escalation phase of the ACR-2316 Phase 1/2 trial on November 20, 2026
Durable clinical activity, including confirmed complete and partial responses (RECIST 1.1) with ACR-2316 monotherapy in heavily pretreated, AP3-predicted tumor types, including endometrial and lung cancers
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