AMBIGUOUS RESULTS

Acrivon presents early ACR-2316 partial responses in WEE1-resistant tumor types

Data at AACR D3 show tumor shrinkage and tolerable safety in a small, dose-escalation slice of Acrivon's Phase 1 trial, a decision-grade readout still lies ahead.

Acrivon Therapeutics presented mechanistic and initial Phase 1 clinical data for ACR-2316, its WEE1/PKMYT1 inhibitor, at the AACR D3 conference, including partial responses in AP3-selected tumor types.

By AppliedXLJuly 21, 2026Trial NCT06667141

Executive Summary

Acrivon Therapeutics presented mechanistic and clinical data on its WEE1/PKMYT1 inhibitor at a cancer drug discovery conference, extending a Phase 1 dose-escalation disclosure the company had already made months earlier.
The company reported tumor shrinkage, including partial responses, in a handful of lung and endometrial cancer subtypes it says had not previously responded to other drugs in this same mechanistic class, alongside a tolerability profile limited mainly to reversible low blood-cell counts.
The results come from a small, immature slice of an ongoing, non-registrational Phase 1 trial that is still enrolling patients and has not reported a primary endpoint result, so the activity signal is not yet decision-grade.
No same-target competitor appears in the sourced -tumor trial landscape, so the conference data cannot yet be benchmarked against a direct rival's clinical results.

The presentation

Acrivon Therapeutics, Inc. delivered a poster on July 22 and an oral presentation on July 23, 2026, at the AACR Drug Discovery and Development conference in Boston, detailing how its Generative Phosphoproteomics AP3 platform guided the design of ACR-2316, a WEE1/PKMYT1 inhibitor. The company said AP3 uncovered a resistance mechanism in which WEE1 inhibition activates PKMYT1, and used that finding to design ACR-2316 to sustain activation of CDK1, CDK2, and PLK1 to drive tumor cell death. The trial behind the data, NCT06667141, is a Phase 1 study testing ACR-2316 in patients with advanced tumors selected by the AP3 platform, enrolling 100 patients across sites in the United States. Acrivon+1

Probability of Success

Endpoint Met75%

Completes93%

Clinical Significance2%

Regulatory88%

The reported activity

Acrivon said initial observations showed tumor shrinkage, including partial responses, and durable clinical benefit in patients with small cell lung cancer, squamous non-small cell lung cancer, and adenosarcoma non-small cell lung cancer, tumor types the company said had not previously shown sensitivity to other clinical WEE1 or PKMYT1 inhibitors. The company also reported a favorable tolerability profile, with adverse events largely limited to transient, mechanism-based neutropenia (low white blood cell counts) and no non-hematological toxicity. Kristina Masson, co-founder and EVP at Acrivon, said the AP3 platform moves "beyond traditional target-centric drug discovery by directly measuring drug-regulated pathway activity in intact cells". This activity signal builds on an earlier disclosure from April 2026, when Acrivon first reported partial responses in endometrial cancer, small cell lung cancer, and squamous non-small cell lung cancer alongside the same neutropenia-limited safety profile. Acrivon

Trial status and design

The trial is still Recruiting, with a primary completion date of August 12, 2026, and full completion targeted for December 12, 2026. It is open-label, non-randomized, and not designated registrational, structured across two experimental arms covering dose escalation and dose expansion. Enrollment grew from a 90-patient to a 100-patient target in a protocol update recorded in January 2026, a change that falls within the routine range for a Phase 1 trial and was not flagged by the underlying operational model. The trial has otherwise logged one enrollment amendment since its October 2024 start, a pace the registry-churn proxy labels stable. NCT06667141

What the data can and cannot establish

The results presented at AACR D3 come from an initial, subgroup-level readout of an ongoing dose-escalation cohort, not a completed primary endpoint analysis; the underlying disclosure carries flags for subgroup-only and immature data. A single-arm, open-label, dose-escalation study in a small number of AP3-selected tumor types is built to establish a maximum tolerated dose and generate hypothesis-level activity signals, not to prove efficacy against a comparator. The trial's own primary completion date, five months forward, is the point at which a fuller data set covering the dose-expansion phase would become available.

The competitive frame

The sourced -tumor competitive landscape contains no trial that shares ACR-2316's WEE1/PKMYT1 target; the closest entries identified, spanning KRAS G12C, HIF-2alpha, PD-1 and other mechanisms in Phase 1 through Phase 3 -tumor trials from sponsors including Merck, Roche, and ModernaTX, work through different biology entirely. Acrivon's own pipeline in the sourced trial data shows a single active study for ACR-2316, with the company separately advancing ACR-368 in a Phase 2 endometrial cancer program noted in the AACR materials. Without a same-mechanism comparator in the sourced landscape, the tumor-type-specific responses Acrivon is reporting cannot yet be benchmarked against a rival WEE1 or PKMYT1 program's clinical results. Acrivon

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