Acrivon Therapeutics, Inc. · NASDAQ:ACRV
Acrivon Therapeutics — Technical Presentation (July 2026)
15 slides from Acrivon Therapeutics's technical presentation, July 2026
Slide 1: Acrivon Predictive Precision Proteomics (AP3)
ACRIVON PREDICTIVE PRECISION PROTEOMICS (AP3) NEXT GENERATION PRECISION MEDICINE FOR PHOSPHOPROTEOMICS-GUIDED DRUG DISCOVERY Lei Shi, PhD Acrivon Therapeutics Inc. Watertown, MA Acrivon Therapeutics
Slide 2: Disclosure Information
Disclosure Information Lei Shi I have the following relevant financial relationships to disclose: Employee of: Acrivon Therapeutics Inc. Stockholder in: Acrivon Therapeutics Inc.
Slide 3: Next-generation precision medicine powered by AP3
Next-generation precision medicine powered by AP3 Current focus oncology, Acrivon Predictive Precision Proteomics (AP3) I&I next DNA • AI-driven, proteomics-based rational drug design and informed clinical development RNA • AP3 enables an exact match between the disease-driving, dysregulated pathway
Slide 4: Acrivon Therapeutics overview
Acrivon Therapeutics overview Development Site (Boston) Precision Proteomics Site (Lund/Copenhagen) • Drug development and clinical biomarkers • Early drug discovery • Clinical leadership and trial oversight • BM identification and drug profiling • ML/AI-driven AP3 analyses • AP3 mass spectrometry H
Slide 5: Acrivon pipeline
Acrivon pipeline Anticipated Preclinical Phase 1 Phase 2 Phase 3 Next Milestone Single-Arm Trial Based on OncoSignature Biomarker Prediction BM+ patients, ACR-368 Monotherapy Breakthrough Device & Fast Track Designations Arm 1 Clinical Update Mid-2026 registrational intent ACR-368 Endometrial Cancer
Slide 6: Acrivon AP3-based precision medicine
Acrivon AP3-based precision medicine Novel Target Identification Activated druggable targets – diseased vs normal Clinical Biomarkers Drug Discovery SAR Predictive OncoSignature tests Optimized pathway effects Indication Finding Therapeutic Index Tissue ID BM1 BM2 BM3 Fov010719 0.96 0.68 0.78 Fov060
Slide 7: AP3 reveals suboptimal mitotic pathway regulation by clinical WEE1/PKMYT1 inhibitors
AP3 reveals suboptimal mitotic pathway regulation by clinical WEE1/PKMYT1 inhibitors and guides discovery of ACR-2316 WEE1/PKMYT1 kinases are critical cell WEE1/PKMYT1 regulates compensatory CDK1 signaling A CDK1 substrate A PLK1 substrate cycle checkpoints in cancer efective hec oint ntra hase hec
Slide 8: AP3 biological SAR: phosphoproteomic pathway signatures guide prioritization of ACR-2316
AP3 biological SAR: phosphoproteomic pathway signatures guide prioritization of ACR-2316 AP3 defines the mechanistic therapeutic index derived AP3 profiles phosphoproteomic signaling across internal development candidates, from the combination WEE1/PKMYT1 inhibition enabling compound prioritization
Slide 9: ACR-2316: uniquely designed by AP3 for superior single-agent activity
ACR-2316: uniquely designed by AP3 for superior single-agent activity over WEE1 and PKMYT1 inhibitors ACR-2316 designed to quench dominant resistance ACR-2316 designed using AP3-based generative AI mechanisms originating from PKMYT1 identified by AP3 to potently activate both CDK1/2 and PLK1 ensurin
Slide 10: ACR-2316 is highly potent across human tumor cell lines and induces complete tumor regression
ACR-2316 is highly potent across human tumor cell lines and induces complete tumor regression Human tumor cell lines (not genetically selected) A human lung tumor HCC38 cell derived xenograft Breast T47D A172 Glioblastoma LN229 T98G Lung A427 DAOY A2780 CAOV3 MCAS OV7 OV90 OVCAR3 OVCAR8 OVISE PEO1 R
Slide 11: ACR-2316 demonstrates durable clinical activity in heavily pretreated patients with lung cancer
ACR-2316 demonstrates durable clinical activity in heavily pretreated patients with lung cancer % Change in Target Lesions from Baseline 40 20 0 SCLC Sq. NSCLC -20 Ad. NSCLC -40 -60 RECIST 1.1: PR -80 On treatment SD as of May 1 PD -100 0 10 20 30 40 50 Weeks on Treatment • Two w k o dosi g gim s st
Slide 12: ACR-2316 demonstrates a favorable clinical safety profile
ACR-2316 demonstrates a favorable clinical safety profile limited to transient, mechanism-based hematologic toxicity Summ of ≥ G d 3 TRAEs Subjects treated up to or at established weekly dosing regimens · N = 20 · bar length = number of grade 3/4 total events Grade 3 Grade 4 TOTAL r ≥3 1 (5%) Anemia
Slide 13: Summary
Summary AP3 enabled rational compound design ✓ Identified adaptive resistance mechanism induced by WEE1 inhibition ✓ Validated dual WEE1/PKMYT1 inhibition to quench resistance ✓ Selected lead candidates based on desirable signaling pathway activity, including potent PLK1 activation ACR-2316: novel W
Slide 14: Acknowledgement
Acknowledgement A sincere thank you to our talented colleagues at Acrivon, partners, clinical collaborators, patients and their families who participated in our trials.
Slide 15: AACR Drug Discovery and Development (AACR D3)
‘American Association for Cancer Research’ DO NOT POST AACR DRUG DISCOVERY AND DEVELOPMENT (AACR D3) DO NOT POST
Acrivon Therapeutics — Technical Presentation (July 2026) on 6ix