ACRIVON PREDICTIVE PRECISION PROTEOMICS (AP3) NEXT GENERATION PRECISION MEDICINE CORPORATE PRESENTATION SEPTEMBER 2025 Exhibit 99.1

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Acrivon Therapeutics – a next-generation precision medicine company Neurological Cancer Inflammatory Fibrosis Drug P Metabolic Acrivon Predictive Precision Proteomics (AP3) Enables an exact match between the disease-driving, dysregulated pathways with a drug’s mechanism of action (Acrivon meaning ≈ exact, accurate) Broadly applicable in R&D (biological SAR, resistance, patient responders); leveraged for internal pipeline DNA RNA Protein Dysregulated Protein Dysregulated Pathways + OncoSignature® Blume-Jensen, P & Hunter, T: Oncogenic kinase signaling Nature (2001) Olsen, JV et al: Global, in vivo, and site-specific phosphorylation dynamics in signaling networks Cell (2006); Andersen, JN et al: Pathway-based identification of biomarkers for targeted therapeutics: personalized oncology with PI3K pathway inhibitors Sci Transl Med (2010)

Development Site (Boston) Drug development and clinical biomarkers ML/AI-driven AP3 analyses Clinical leadership and trial oversight Precision-Proteomics Site (Lund/Copenhagen) Early pipeline drug discovery programs BM identification and drug profiling Mass spectrometry Acrivon therapeutics OVERVIEW Peter Blume-Jensen, MD, PhD CEO, President, Co-Founder Inventor of AP3 Kristina Masson PhD, MBA EVP, Bus Ops, Lund Site HeadCo-Founder Jesper V. Olsen PhD Novo-Nordisk Foundation Protein Center, Cph. Academic Co-Founder. HQ located in Boston - access to leading drug discovery, BIOTECH, and pharma proteomic hub located in Medicon Valley - Northern Europe`s leading life science cluster For more information, please visit https://acrivon.com Founded 2018, IPO November 2022 (NASDAQ: ACRV)

Accomplished leadership team Peter Blume-Jensen, M.D., Ph.D. CEO, President, Founder Eric Devroe, Ph.D. Chief Operating Officer Erick Gamelin, M.D., Ph.D. Chief Development Officer Executive Serono, Merck & Co., Daiichi Sankyo CSO Metamark - Marketed prostate proteomic test ProMark® Inventor Acrivon Predictive Precision Proteomics (AP3) Professor, CEO, national cancer center, appointed by French Minister of Health Executive Amgen, Pfizer, Dynavax, MacroGenics; CMO STEP Pharma >100 ph 1-3 oncology trials Founder and CEO, Opsonix Business executive MD Anderson Cancer Center and Metamark EIR Wyss Institute, Harvard Associate, Flagship Pioneering Mary-Alice Miller, J.D. Chief Legal Officer Over 20 years corporate legal experience Served as general counsel of 2 companies taken public Boston Business Journal “40 Under 40” Kristina Masson, Ph.D., M.B.A Site Head Acrivon AB, Co-Founder EVP Business Operations Cross-functional Leadership Merrimack Pharmaceuticals, MIT/BROAD Founder and CEO, OncoSignature AB (acquired by Acrivon Therapeutics) Mansoor Raza Mirza, M.D. Chief Medical Officer World-renowned oncology KOL Lead investigator for multiple guideline-changing regulatory approvals, including PARP inhibitors for ovarian cancer and new frontline therapy for endometrial cancer Adam Levy, Ph.D., M.B.A. Chief Financial Officer Zentalis Pharmaceuticals, Turning Point Therapeutics, Novartis Head of Corporate Strategy Gilead Sciences Engagement manager in pharma practice at McKinsey & Company

Acrivon Pipeline Anticipated Next Milestone Phase 3 Phase 2 Phase 1 Preclinical ACR-368 (CHK1/CHK2) Single-Arm Trials Based on OncoSignature Prediction Other Trials Ongoing/Under Consideration: HPV+ SCC (H&N*, Anal, Cervical), Sarcomas, MDS/MPN Initial Clin Data 2H 2025 Registrational Trial and Confirmatory Trial Design Update 2H 2025 Endometrial Cancer AP3-Identified Tumor Types Future Development Candidates Additional AP3-driven Programs: Auto-Immune/Inflammatory ACR-368 Monotherapy ACR-368 + ULDG Sensitization Registrational intent Phase 2 single arm trial based on predicted sensitivity to ACR-368 monotherapy in OncoSignature-positive patients Phase 1b/2 single arm trial of ACR-368 with ultra low dose gemcitabine, or ULDG as sensitizer, in OncoSignature-negative patients ACR-368 + ULDG Sensitization ACR-368 Monotherapy Breakthrough Device & Fast Track Designations ACR-2316 (WEE1/ PKMYT1) Early Discovery Dose Escalation and Expansion AP3-Identified Tumor Types Cell cycle program (undisclosed target) Development Candidate Nomination 2025 Discovery *Investigator-Initiated Trial (IIT) at Moffitt Cancer Center (Clinicaltrials.gov: NCT06597565) Single-Arm Trial without Pretreatment Biopsy or Biomarker Stratification ACR-368 + ULDG Sensitization Initial Clin Data mid-2026 ACR-368 + ULDG Sensitization Phase 2 single arm trial of ACR-368 with ULDG as sensitizer, in biomarker unselected (“all comer”) 2nd line population

AP3 Generative phosphoproteomics platform Proprietary computational pipeline Structured Standardized AI-enabled AP3 Interactome AP3 KSR Predictor AP3 Data Portal AP3 Chatbot MS-proteomics Genomics Internal Multi-modal AP3 MS-proteomics Proprietary Public Validate Design + Insight Proprietary Database Drug design and optimization Target ID / Indication Finding MoA / response prediction PD and predictive biomarkers Single cell p-proteomics Spatial p-proteomics Clinical p-proteomics

AP3-based drug discovery and clinical development in predicted sensitive subjects and tumor types Predicted Responder AP3 Clinical BiomarkersPredictive OncoSignature tests Indication FindingSensitive tumor types Resistance Mechanisms Rational drug combinations Drug Discovery SAR Optimal target selectivity PD Markers~40,000 per compound Informs in-licensingAP3 profiling of candidates Streamlined Clinical Development Predicted sensitive indications with informed dose optimization

Infectious, CNS, and other diseases Oncology Fibrotic and inflammatory Autoimmune DDR and Cell Cycle Therapeutic areas Therapeutic modalities Small molecule Bifunctional molecule Antibody ADC Oligo/RNA The AP3 Approach is modality and disease agnostic Current pipeline Next

Oncosignature: Drug response prediction in individual patients “Disease Pathway-Based Method to Generate Biomarker Panels Tailored to Specific Therapeutics for Individualized Treatments”: EP 2 229 589, issued June 10, 2015; US2017/0067877A9, pending. OncoSignature® is a Registered Trademark: US Reg. No. 5,718,472; Int. Cl. 5, 42. Intl. Reg. 1382289 \ PROPRIETARY WORKFLOW INTEGRATING PROVEN TECHNOLOGIES STEP 1 STEP 2 STEP 3 BIOMARKER IDENTIFICATION THERAPEUTIC PACKAGE Acrivon drug with predictive BM assay PATIENT RESPONDERS Optimal indications and combinations AP3 DRUG PROFILING Resistant Sensitive BIOMARKER VALIDATION HIGH RES PROTEOMICS BY MS CELL LINES, PDX, HUMAN TISSUE CLINICAL SIGNATURE ASSAY 3-6 BIOMARKERS PROSPECTIVE RESPONSE PREDICTION ON PRETREATMENT BIOPSY No benefit Benefit Predicted Non-responder Predicted Responder Patients without biomarkers critical for drug sensitivity efficiently excluded + OncoSignature® CLASS 1 BM CLASS 2 BM CLASS 3 BM AI-DRIVEN

ACR-368: a clinically active phase 2 CHK1/2 inhibitor ATP-competitive inhibitor of CHK1 (0.9 nM) and CHK2 (8 nM) Acrivon holds full, unencumbered global rights to the asset Exclusively in-licensed from Eli Lilly & Company (WW rights); originally discovered by Array (Pfizer) Balanced inhibition of both CHK1 and CHK2 believed important for RECIST monotherapy activity CoM patent exp. Oct. 2030; Salt-form exp. Apr. 2037 ACR-368 (MW): 365.4 Durable monotherapy activity: Endometrial cancer (ongoing reg. intent Phase 2), ovarian, SCCHN, and other tumors Strong synergy with anti-PD-(L)1: Preclinical in-house and external data; non-overlapping toxicities (incl. clinical data) Favorable safety profile: >1,000 patients treated (~50% mono, ~50% in combination) Ideal for AP3 method: Proven clinical activity, but genetics-based biomarkers insufficient for patient responder ID G1/S-defective cancers rely on CHK1-regulated cell cycle checkpoints CHK1 pauses cell cycle to enable DNA repair G2/M Checkpoint S Phase Checkpoint M G1 S Cancer Cell Cycle G2 CHK1/2 CHK1/2 Defective G1/S Checkpoint

ACR-368 oncosignature test: prospective patient stratification Pretreatment tumor biopsy test Compatible with 5 business days turn-around Offered by CDx partner under exclusive license from Acrivon Pretreatment tumor biopsy Treatment decision based on patient stratification OncoSignature-positive OncoSignature-negative Routine FFPE processing Biopsy in FFPE block Automated tumor Region-of-Interest biomarker scoring ACR-368 monotherapy ACR-368 + ULDG sensitization +

ACR-368-201 trial protocol A Phase 2 Study of ACR-368 Therapy in Subjects with Endometrial Cancer Subjects with endometrial cancer who have relapsed after prior platinum-based chemotherapy and one prior line of anti-PD-(L)1 therapy OncoSignature Stratified Cohort (Positive or Negative) Subjects with up to three lines of prior therapy OncoSignature Unselected Cohort (All-comers) Subjects with one line of prior therapy Arm 1 OncoSignature Positive N=71 Arm 2 OncoSignature Negative N= up to ~150 Arm 3 All-comers N= up to ~90 ACR-368 (105 mg/m2 q2w) With ULDG Sensitization (10 mg/mg2 q2w) ACR-368 (105 mg/m2 q2w) With ULDG Sensitization (10 mg/mg2 q2w) ACR-368 (105 mg/m2 q2w) Registrational intent

Endometrial cancer is an AP3-predicted tumor type ACR-368 OncoSignature-based indication finding prior to trial entry ACR-368 OncoSignature imaging demonstrates addiction to CHK1/2 DDR axis Confirmation of predicted sensitivity in genetically non-modified PDX models Confirmation of ACR-368 OncoSignature prediction in PDX tumor tissues pretreatment In >1,000 cancer patients treated with ACR-368 in Lilly-sponsored trials, endometrial cancer was not tested

Symptoms (i.e. bleeding, pain) Evolving Treatment Landscape for the Management of Advanced Stage or Recurrent Endometrial Cancer Diagnosis Surgical Staging Carboplatin + Paclitaxel + Immune Checkpoint Inhibition US FDA approval in dMMR and pMMR – C/P + Pembrolizumab (NRG GY018) - C/P + Dostarlimab (RUBY/ENGOT-EN6) NCCN Compendium Listed - C/P + trastuzumab (HER2+ serous and carcinosarcoma) - C/P alone MAINTENANCE Pembrolizumab Dostarlimab ------------ Trastuzumab Other Lines of Therapy and Clinical Trials Prior-IO US FDA approval of T-Dxd Only In HER2 3+ (~10% of patients) Progression Majority (85%) of 2L treated with chemotherapy: ORR 10-12%; mPFS 3 mo Potential alternate strategies: hormonal therapy, single agent IO, T-Dxd in HER 2 2+ (NCCN) Adapted from Dr. R. Eskander and Dr. M. R. Mirza Accelerated Single Agent Opportunity 2L (~27K pts per year US) Confirmatory Anti-PD-1/Anti-PD-L1 + ACR-368 Switch Maintenance Opportunity 1L (~30K+ pts per year US) 14x6 weeks Lenvatinib + Pembrolizumab (reduced with new 1L regimen) -------------- C/P + IO -------------- US FDA approval of T-Dxd In HER2 3+ (~10% of patients) No Prior-IO (New) 1st Line Therapy PFS 9-13 months in pMMR 2nd Line Therapy Post-Progression OS (12-18 months) Progression

Endometrial patient Demographics and baseline characteristics Subject Demographics BM+ N = 20 BM- N = 38 Median Age (range) 65.0 (54, 76) 67.5 (42, 80) Race, n (%) White 14 (70) 22 (58) Black/African American 4 (20) 9 (24) Asian 1 (5) 5 (13) Unknown/Other 1 (5) 2 (5) Stage, n (%) III 4 (20) 14 (37) IV 16 (80) 22 (58) Unknown 0 2 (5) Histology, n (%) Serous 12 (60) 15 (40) Clear-cell carcinoma 0 4 (10) Carcinosarcoma 3 (15) 4 (10) Endometroid, G3 4 (20) 11 (29) Other 1 (5) 4 (10) ECOG Status at Baseline, n (%) 0 10 (50) 18 (47) 1 10 (50) 20 (53) Subject Demographics BM+ N = 20 BM- N = 38 Median (Mean) Number of Prior Lines 2 (2.6) 3 (3) Best Overall Response to Last Prior Line Refractory* 12 (60) 19 (50) Relapsed disease 6 (30) 14 (37) Unknown 2 (10) 5 (13) MMR Status, n (%) pMMR 13 (65) 19 (50) dMMR 2 (10) 9 (24) Unknown 5 (25) 10 (26) TP53 Status, n (%) Mutant 11 (55) 12 (32) Wildtype 3 (15) 7 (18) Unknown 6 (30) 19 (50) Prior exposure to PD-1/PD-L1, n (%) Yes 20 (100) 36 (95) No 0 2 (5) Prior exposure to Pembro/Len, n (%) Yes 13 (65) 23 (61) No 7 (35) 15 (39) EDC data extract Feb 25, 2025. *Best overall response to last prior line = PD

Encouraging safety profile Treatment-Related Adverse Events, n (%) BM+ (N=26) BM- (N=51) All Grades Grades 3/4 All Grades Grades 3/4 Thrombocytopenia 14 (54) 4 (15) 30 (59) 18 (35) Anemia 13 (50) 7 (27) 29 (57) 23 (45) Neutropenia 8 (31) 7 (27) 14 (28) 12 (24) Leukopenia 5 (19) 3 (12) 11 (22) 10 (20) Lymphopenia 2 (8) 0 5 (10) 3 (6) Febrile neutropenia 1 (4) 1 (4) 4 (8) 4 (8) Acute kidney injury 2 (8) 2 (8) 0 0 TRAEs with Grades 3/4 percentages ≥5% for either group are included in this table. No fatal TRAE in either group. G-CSF is encouraged for ACR-368 monotherapy and mandated for ACR-368 + ULDG Limited, transient, reversible, mechanism-based hematological AEs, which typically occurred during the first 1-2 cycles of therapy Notable absence of GI toxicities, long-lasting myelosuppression or more severe non-hematological AEs commonly seen with ADCs and chemotherapy

Best overall response* – endometrial BM+ patients PD PD PD PD PD PD PD PD PD PD PD N = 20 Best Overall Response in last prior line of therapy: *BOR of either BICR or INV EDC data extract Feb 25, 2025 OncoSignature accurately predicts tumor drug sensitivity 80% of tumors shrink and 80% DCR in predicted responders Confirmed ORR >2x higher than in last prior line of therapy 35% cORR (95% CI,18 - 57) with ACR-368

RELAPSED REFRACTORY 17 4 11 7 6 14 10 8 18 2 3 1 19 15 12 16 5 OT OT OT OT BoR on Treatment CR PR SD PD NE ACR-368 activity in patients relapsed after last prior line 50% ORR mDoR > 10 mo (not reached) 100% DCR** DoT > 8.5 mo (not reached) ACR-368 activity in patients refractory to last prior line 33.3% ORR mDoR = ~3.4 mo 65% DCR** DoT = 3.9 mo (mean) NE 20 13 9 BOR last prior line (≥2nd line) 12.5% cORR (N=16)* BOR to ACR-368 37.5% cORR (N=16)* ACR-368 ORR compared to BOR in last prior line (≥2nd) On treatment BM+ Key Take Home Messages All patients have progressed on prior platinum-based chemo and prior anti-PD-1 Median/mean of prior lines = 2/2.6 66% of patients refractory to last prior line The cORR is 3x higher than BOR in last prior line (≥2nd line) ACR-368 is active even in refractory patients (33% cORR and 65% DCR) Long durability with ACR-368 in relapsed patients (4/6 still on treatment) ACR-368 may be optimally positioned in patients who were not refractory to last prior line of therapy *Patients (N=16) annotated for BOR in last prior line (≥2nd); 7/16 of these had pembrolizumab + lenvatinib in last prior line ^BOR to new 1st line therapy (chemo + ICI); **DCR = [SD ≥12 weeks + PR + CR] N=18 ^ ^

AP3-predicted sensitization to ACR-368 by UlDG correlates with OncoSignature upregulation BM2 BM3 Quantified BM scores Pre/Post ULDG Tumor from H&N IIT patient A427 human lung tumor xenograft BM1 Pre- LDG Post- LDG Preclinical data Clinical data

Screening Week 8 Week 12 Complete resolution of hepatic target lesions (-100%) (-100%) Deep, rapid responses in BM+ patients with aggressive endometrial tumors Screening Week 8 and 12 (-100%) Confirmed PR with complete disappearance of >10 additional hepatic metastases spanning both lobes ACR-368 single agent activity in multifocal hepatic disease, even in high-disease burden cases 67 y old patient with stage IV serous cancer, pMMR, p53-mutated; patient was refractory to last prior line, including anti-PD-1

Development path for ACR-368 in endometrial cancer Accelerated approval pathway Ongoing single arm registrational intent Phase 2 monotherapy in BM+ patients Single arm 2nd line all-comer study ACR-368 + ULDG in all-comer patients based on ULDG MOA and clinical data in 2nd line ULDG is confirmed to not have any activity on its own as aligned with the FDA Confirmatory trial strategy - front-line switch maintenance in pMMR population Randomization anti-PD-1 vs [anti-PD-1 + ACR-368] post [C/P + anti-PD-1] (hierarchical: BM-stratified sub-group analysis followed by all-comer)* *Based on current clinical data showing cPRs in patients progressing on prior anti-PD-1, clinical safety data on ACR-368 + anti-PD-L1, and strong rationale and preclinical data, including Acrivon data, demonstrating strong synergistic activity of ACR-368 and anti-PD-(L)1 (Refs: Do KT et al, Cancer Immunol Immunother, 2021; Iyer et al, Cancer Disc 2021; McGrail et al, Sci Transl Med 2021; Sen et al, Cancer Disc 2019; Acrivon preclinical data)

Potent synergy of ACR-368 with anti-PD-L1 displays immune Memory in 100% of Mice Complete tumor regression Immune memory Immune memory independent of CD8 Immune memory independent of CD4 Immune memory requires both CD4 + CD8 Legends:

ACR-368 with anti-pd-l1 is well tolerated consistent with non-overlapping toxicities Legends:

Confirmatory trial option: First line expansion as switch maintenance – a significant market potential Anti-PD-1 IV Q3W + CT (paclitaxel + carboplatin) 6 cycles pMMR patients (~80%) with measurable stage III/IVA, stage IVB, or recurrent endometrial cancer Anti-PD-1 IV Q6W up to 14 cycles Median PFS in pMMR ~ 13.1 mo Median PFS in pMMR after chemo ~ 8.8 mo (Anti-PD-1 or Anti-PD-L1) + ACR-368 Large addressable total annual market (TAM) opportunity (US only) OncoSignature+ patients: ~(30,000 EC x 80% pMMR x 30% BM+ x >10 months mPFS) All-comer patients: ~(30,000 EC x 80% pMMR x >10 months mPFS)

ACR-368 potential in other high unmet tumor types Myelodysplastic Syndrome (MDS) and Myeloproliferative Neoplasms (MPN): Prevalent (~50%) mutations in splicing factor (SF) genes resulting in hyperactivated CHK1,2 Preclinical murine transplant studies of SF3B1-mutated human HSCs show potent ACR-368 single agent activity High unmet need and prevalence (>400K in the US), decades of blood transfusion dependency, fatal myelofibrosis Squamous Cell Cancer (SCC) and sarcomas: ACR-368 has also shown promising clinical activity in HPV+ SCC and sarcomas3 HPV+ SCC increasing incidence (~50K+/y/US); ~75% oropharyngeal H&N, ~20% of esophageal, ~90% of cervical, and 95% of anal cancers4 SCCHN: Dr. Chung, Moffitt Cancer Center has begun an IIT (ACR-368 + ULDG post anti-PD-1) 1Sarchi et al, Blood Cancer Discovery 2024; 2Malcovati et al, NEJM 2011 3Hong et al, CCR 2018, Slotkin et al, ASCO Annual Meeting 2022; 4CDC 2023; ICO/IARC Information Centre on HPV and Cancer 2023; Gribb et al, Dela J Public Health 2023, NCI 2023

ACR-368 combination opportunities in all-comer populations supported by strong rationale and data Anti-PD-(L)1 inhibitors ACR-368 is strongly synergistic with anti-PD-(L)1 and the two agents also have non-redundant activity Opportunity for frontline expansion in high unmet need tumors with significant market potential Entirely non-overlapping toxicities ADCs Moving towards frontline as backbone therapies in OB-GYN cancers and beyond – label expansion opportunity Main resistance mechanisms include upregulation of DDR, increasing sensitivity to CHK1/2 and WEE1/PKMYT1 inhibitors Largely non-overlapping toxicities ACR-368 + ACR-2316 Resistance to CHK1/2 inhibition is frequently through WEE1/PKMYT1 activation and vice versa Distinct dosing regimens and elimination t1/2 allows for combination despite overlapping mechanism-based hematological AEs CDK4/6 inhibitors Resistance to CDK4/6 inhibitors phenocopy G1 deficiency resulting in S /G2-M accumulation and DDR dependency ACR-368 and ACR-2316 (Acrivon’s superior single agent active WEE1/PKMYT1 inhibitor) ideal combinations or follow-on therapies to overcome resistance In-house studies ongoing supporting solid preclinical evidence and rationale K-Ras inhibitors DDR inhibitors, including ACR-368, have shown clinical activity in K-Ras mutant tumors in preclinical studies ACR-368-induced DNA damage and apoptosis is enhanced in K-Ras mutant settings Largely non-overlapping toxicities

Internal pipeline: AP3-based drug discovery potential first- and best in class candidates Streamlined AP3-based drug discovery AP3 used for biologically relevant selectivity profiling Program 2: Preclinical cell cycle program (undisclosed target) No known competitive programs Strong preclinical evidence and rationale for critical role in cancer Several almost identical protein isoforms, ideal for Generative Phosphoproteomics AP3 Lead optimization ongoing across several attractive lead series Anticipated development candidate nomination 2025 ACR-2316: Clinical stage, novel WEE1/PKMYT1 inhibitor Superior single agent activity and dosing regimen flexibility; highly differentiated Designed by AP3 to overcome drug resistance to achieve superior single agent activity and expanded therapeutic index Initial clinical activity (including cPR) observed during ongoing dose escalation Streamlined development: Internally discovered and advanced in 15 months from initial lead to first patient dosed in phase 1

Streamlined AP3-based drug design: integrated AI/ML-driven proteome-wide SAR Peptide clean up Direct DIA analysis Drug treatment Proteolysis P-peptide enrichment Ultra high resolution P-proteomic profiling Week 0 Week2 Turn-around <2 weeks Quantitative mapping (>150,000 phospho-sites covering >13,000 proteins) Drug-regulated phospho-sites and biological process enrichment Drug-regulated pathway activity mapping and reconstitution P P Proprietary Generative Phosphoproteomic AP3 analyses with actionable results High resolution and throughput MS-based P-proteomics Cellular material (~0.3 ng / human cell)

AP3: proprietary HIGH-RESOLUTION DATA for streamlined biological drug design and development Acrivon proprietary compound data (>150 million data points per experiment) Several hundred samples (quadruplicates) in each experiment; >100 compounds profiled Miniaturized, high throughput, scalable: <2 week turn-around, automated AI computational analyses in 1 day QC MS Data Data Clean Up QC Processed Data Volcano Plots Hierarchical Clustering Consensus Sequence Motif Kinase Inference Pathway Enrichment Functional Annotation Network Mapping Biomarkers Actionable AP3 results: Resistance mechanisms, rational combinations, indication finding, response prediction ~164,000 phosphosites ~50,000 phosphosites

Wee1 and PKMYT1 - critical cell cycle checkpoints in human cancer WEE1 and PKMYT1 regulate S and G2-M cell cycle checkpoints to ensure proper DNA replication and mitotic completion Defective DNA repair is highly prevalent in cancers, creating a dependency on checkpoint proteins Only known substrate for WEE1 is CDK-Y15 and for PKMYT1 is CDK-T14, both of which inhibit CDK activity Despite demonstrated clinical activity, the Therapeutic Index has been challenging AP3 was applied to design a molecule with potent single agent activity and exquisite selectivity to achieve an expanded Therapeutic Index

ACR-2316: uniquely enabled by AP3 to overcome limitations of benchmark wee1 and pkmyt1 inhibitors Drug Design by AP3-based SAR for desirable pathway effects and suppressing resistance mechanisms ACR-2316: Rationally designed, differentiated WEE1/PKMYT1 inhibitor for superior Therapeutic Index Complete tumor regression across all models High selectivity (co-crystallography) and short elimination T1/2 to ensure transient, mild AEs Potent WEE1 inhibition, balanced PKMYT1 inhibition, overcomes resistance and enables robust activation of CDK1, CDK2, and PLK1 for mitotic catastrophe Development ongoing in high unmet need solid tumor types predicted sensitive by AP3 Reciprocal quenching Potent mitotic catastrophe

Acr-2316 is a potentially best- and first-in-class agent designed using Acrivon’s ap3 platform Program Goals Demonstrated Results Superior single agent activity High selectivity and potency Streamlined clinical development Favorable ADME-PK, Therapeutic Index, and safety profile Broad preclinical therapeutic index and anti-tumor activity across all dosing regimens 5-20-fold more potent* in preclinical models than clinical benchmarks; complete tumor regression Potent tumor cell killing*, short elim.T1/2, and high selectivity at weekly on-off schedule; only transient AEs Superior anti-tumor activity* (robust CDK1, CDK2, and PLK1 activation; inhibition of PKMYT1 resistance AP3-Enabled SAR AP3-based Indication Finding and PD biomarkers 1 2 3 4 *Head-to-head preclinical studies against benchmarks with clinical data Significant drug target engagement observed in human PBMCs already at DL1 Confirmed PR at DL3 before projected RP2D and initial clinical activity in several solid tumors

Dual wee1/pkmyt1 inhibitor ACR-2316 demonstrates strong potency and selectivity DNA content 100 nM, 24 hour ACR-2316 exerts potent cell cycle effects with pronounced S-G2/M accumulation KinomeScan (468 kinases @ 1mM) DMSO Azenosertib Lunresertib ACR-2316 94% 41% 58% 50% ACR-2316 is highly selective (KinomeScan) WEE1 PKMYT1 WEE1 WEE1 PKMYT1 ACR-2316 Adavosertib Azenosertib Lunresertib ACR-2316 potently inhibits cancer cell viability

AACR 2025: Generative Phosphoproteomics AP3 uncovers robust tumor cell death through cdk1, cdk2, and plk1 Poster link here

Acr-2316 results in strong activation of cdk1 across cell lines Unbiased quantitation of ACR-2316-regulated CDK1 substrate p-sites (308) in intact cells based on CDK1 consensus recognition motif (Acrivon proprietary hybrid database approach) across multiple experiments Actionable insight into drivers of mitotic catastrophe and on-target CDK1-driven pathways CDK1 consensus substrates CDK1 consensus substrates CDK1 consensus substrates CDK1 consensus substrates CDK1 consensus substrates DMSO Res. Sens.

ACR-2316 is highly potent across human tumor cell lines and patient-derived ex vivo tumor models Patient-derived ex vivo ovarian tumor models Human tumor cell lines (not genetically selected) Breast Lung Ovarian Prostate Renal Medulloblastoma Glioblastoma Pancreatic WEE1i PKMYT1i

SUPERIOR ACTIVITY OF ACR-2316 oVER WRN INHIBITORS IN BOTH MSI HIGH AND MSS CELL LINES HRO761 is a noncovalent allosteric inhibitor of WRN (Novartis); VVD-133214/ RO7589831 is a covalent allosteric WRN inhibitor (Roche); ACR-2316 is more potent than both WRN inhibitors even in the optimal MSI high context, associated with strong dependency on WRN activity

ACR-2316 induces complete tumor regression across models and dosing regimens 5d on/2 d off Model 1 5d on/2 d off Model 2

Potent synergy of ACR-2316 with anti-PD-L1 displays immune Memory in 100% of Mice Legends: Complete tumor regression Immune memory Immune memory independent of CD8 Immune memory independent of CD4 Immune memory requires both CD4 + CD8

ACR-2316 with anti-pd-l1 is well tolerated consistent with non-overlapping toxicities Legends:

ACR-2316 phase 1 PATIENT enrollment and dosing ongoing ACR-2316-101: Phase 1 study of ACR-2316 in subjects with specific advanced solid tumors Aiming for streamlined clinical development: ACR-2316 advanced in 15 months from initial lead into Phase 1 uniquely enabled by AP3 AP3-based indication finding has identified commercially attractive indications Dose optimization guided by drug target engagement aligned with Project Optimus Dose Expansion RP2D determination in 2 selected tumor types Dose Escalation (N ≤ 42 patients) In selected solid tumor types DL1 DL2 DL3 DL4

ACR-2316 clinical trial status Dose level (DL) 1, DL2 and DL3 cleared without safety concerns or DLTs by the safety review committee Preliminary PK data indicate approximate dose proportionality in the first 2 DL cohorts Significant drug target engagement observed in human PBMCs at DL1 and even deeper at DL2 (as expected) using our proprietary AP3 MS PD method Development focused on selected high unmet need solid tumor types (beyond endometrial and ovarian cancer) predicted sensitive by AP3 Indication Finding Initial clinical activity observed during dose escalation in several solid tumor types, including an ongoing confirmed partial response in endometrial cancer Prior chemotherapy and anti-PD-1; 3 prior lines of therapy Baseline tumor burden: 3 index lesions each between 3 to 4.4 cm Significant decreased size of metastatic lesions throughout the chest, abdomen and pelvis Patient remains on therapy Currently enrolling patients in DL4

AP3 MS Pharmacodynamic (PD) PBMC Assay established to support ACR-2316 Phase 1 study Blood draw PBMC isolation LC-MS analysis Quantitative PD result PBMCs isolated from ACR-2316 Phase 1 trial patients Non-invasive liquid biopsy for pharmacodynamic biomarkers Exhaustive depth: ∼8,000 proteins and ∼ 20,000 phospho-sites Rapid turn-around: ∼ 1 week from sample shipment to data output Quantitative measurement of drug PD effects Plasma Gel plug Granulocytes & RBCs

significant drug target engagement observed in pBMCs already at dose level 1 CDK1 CDK2 CDK5 PLK1 AKT1 AKT2 Drug-regulated P-sites (paired t-test : p-value < 0.05) (xxxxxxxS/TPxK/RxxSx) (QxxxxxxS/TPxxKxxx) (xTxxxxxS/TPxxxxEx) (xxxxRxxS/TxSxxxxx) (xxxxLDxS/TxxExxxx) (xxRxRxxS/TxSxxxxx) N=32196 N=2229 Phosphosites identified from MS-proteomics Phosphosites measured in all samples (no imputation) Drug-regulated substrates of key kinases (consensus motifs) CDK1_substrate1 CDK2_substrate1 CDK5_substrate1 PLK1_substrate1 AKT1_substrate14 AKT2_substrate10 Pre-Dose vs Post-Dose of specific substrates N=125

Preclinical Cell Cycle program (Undisclosed Target) Potential for first- and best-in-class program Attractive cancer drug target, no/minimal competitor programs, well-suited for AP3 platform Strong mechanistic target rationale for critical role in oncogenesis DepMap data suggests target X is an essential gene for cancer cell viability Highly selective tool compound shows strong anti-tumor efficacy in rodent models AP3 profiling of benchmarks and lead compounds ongoing to enable MOA-based SAR Co-crystallography done for two promising lead series with compounds demonstrating oral bioavailability Tool compound (wt cells) Tool compound (target mutant cells) Lead compound series C (wt cells) Lead compound series C (target mutant cells) Series D Resol. : 2.64 Å Series C Resol. : 2.4 Å Tool compound is a selective target X inhibitor (originally believed to be inhibitor for another target) Development candidate 2025

AP3-predicted substrates and pathways Target is a protein Serine kinase Clusters of selected substrates for cell cycle drug target Protein domain and function Protein pathway and cell/tissue Pathway enrichment of key substrates GO:1903047, Mitotic cell cycle process, FDR: 2.66E-21 T: 12% Y: 0 S: 88% 528 significant 103 significant 38 significant 187 significant 63 significant 67 significant 56 significant 38 significant String enrichment GO:0003682, Chromatin binding, FDR: 4.77E-24 Phosphorylation residues Total: 3265 ESR1 TP53 AR EZH2 BAP1 TACC1 SMC5 BRCA2 BRCA1 FOXM1 CDKN1A TP53 CDK2 EXOC7 PDS5B

Data completeness Peptide IDs CV Pearson Correlation PCA Hierarchical Clustering DEPs Volcano Plots ANOVA Hierarchical clustering Consensus Sequence Motif Kinase Inference Pathway Enrichment Network Mapping Biomarkers Machine-Learning Filtering Batch effects Normalization Imputation ~164,000 phosphosites ~50,000 phosphosites Ap3 interactome: Proprietary Interactive Data analysis infrastructure for all Acrivon data and experiments Actionable data across all AP3 experiments accessible for all Acrivon scientists Fully scripted, algorithm-based machine learning-enabled pathway and biomarker analyses

AP3 reveals drug-regulated kinase activity in intact cells not detectable by standard methods Time : 60 minutes Dose : 20 nM KinomeScan @ 1mM ACR-2316 Drug-regulated kinase activity* in intact cells ACR-2743 (previous lead candidate) *Kinase activity based on substrate motif analysis using a proprietary PTM-SEA hybrid method ACR-2316 ACR-2743 MAPK3K4 PRKCE GAK PKMYT1 PLK1 PLK2 WEE2 PLK3 WEE1 YSK4 Traditional selectivity profiling AP3-based pathway profiling

Optimized dual inhibitors show desirable pathway effects Activity (NES) -5 0 5 Substrate motif-inferred kinase activities Kinase activity based on proprietary PTM-SEA-based hybrid workflow and analyses Optimized dual WEE1 and PKMYT1 inhibitors affect cell cycle and canonical MAPK pathways in desirable manner ACR-2743 ACR-2316 Benchmark* WEE1 + PKMYT1 Inhibitors in combination *Clinical-stage selective WEE1 and PKMYT1 inhibitors

AP3 Reciprocal quenching identifies PKMYT1 as a key wee1 inhibitor-induced resistance mechanism Induced Suppressed Enrichment Score (NES) 500 5 Protein set size Mitotic regulation Cell cycle and cancer DNA homology repair DNA damage responses Sensitive Resistant WEE1i PKMYT1i PKMYT1i WEE1i PUJANA_BRCA1_PCC_NETWORK PUJANA_CHEK2_PCC_NETWORK REACTOME_CELL_CYCLE REACTOME_SEPARATION_OF_SISTER_CHROMATIDS Protein set name EC75 Comprehensive annotation, weighted for protein set size

AP3 reciprocal quenching reveals optimal target potency profile for dual WEE1/PKMYT1 inhibitor PKMYT1i WEE1i PKMYT1i WEE1i Sensitive Resistant HCL, Euclidean 1043 p-sites from 298 proteins 4 -4 Centered log2FC (treated vs. DMSO) Target substrate of ACR-368 Target substrate of PKMYT1i Optimal potency ratio results in significant synergy WEE1i and ACR-368 WEE1i and PKMYT1i dual inhibition synergy Sensitive Resistant Target substrates Target substrates PKMYT1i WEE1i PKMYT1i WEE1i

Acr-2316 induces potent activation of pro-apoptotic mitotic kinases in sensitive tumor cells Robust activation of CDK1with ACR-2316 exemplified by enrichment of 206 upregulated substrates of CDK1 ACR-2316 @60min and 200nM in ACHN

Robust potent inhibition of CDK1 consensus substrate Y15 by ACR-2316 AP3 interactome enables real time quantitative computational analyses of proprietary AP3 drug profiling data across different conditions and experiments Comparison @60min and 200nM in ACHN Time-dependent comparison @ 200nM in ACHN Dose-dependent comparison @ 60min in ACHN ACR-2316 ACR-2316 3 -3 log2FC 3 -3 log2FC 3 -3 log2FC

AP3-based compound design in intact cells: optimal activation and inhibition of critical pathways CDK1, CDK2, and PLK1 top activated kinases critical for potent pro-apoptotic tumor cell death (mitotic catastrophe) Top inhibited kinases involved in resistance to WEE1 inhibitors

data driven execution and value creation Recent Accomplishments (Last 12 Months) Anticipated Next Milestones (2025) Positive ACR-368 data (ESMO 2024 and April 2025 Corporate R&D Event) in registrational intent endometrial cancer trial Dose level (DL) 1, DL2 and DL3 for ACR-2316 cleared without safety concerns; Initial clinical activity observed (incl cPR) in DL3 (Q1-2 2025) Presented data demonstrating AP3 driven mechanism of ACR-2316 delivering robust tumor cell death through CDK1, CDK2, and PLK1 activation (AACR Q2 2025) Development candidate nomination for novel cell cycle program with an undisclosed target 2025 Target/compound validation and indication finding for new program in autoimmune/inflammatory diseases leveraging AP3 Initial clinical data for ACR-2316 Phase 1 trial 2H 2025 Corporate R&D Events (Q2, Q3 2024 and Q1 2025) presenting positive clinical and preclinical pipeline data and Generative Phosphoproteomics IND clearance for ACR-2316 (Q3 2024) and first patient dosed in Q4 2024 (2 quarters ahead of schedule) with initial lead to Phase 1 initiation achieved in 15 months, uniquely enabled by AP3 Update on ACR-368 Phase 2 registrational intent trial and confirmatory trial design 2H 2025 Initiation of ACR-368 biomarker unselected (“all comer”) arm in 2L endometrial in ongoing Phase 2 trial

FINANCIAL HIGHLIGHTS Cash and Investments $147.6M Projected runway intoQ2 2027 Fully Diluted Shares Outstanding 45.2M Current operating plan, assuming no additional financing Balance sheet  30-Jun-2025 Shares, PFW, and equity grants outstanding 30-Jun-2025 Notes: Unaudited.