EX-99.2 3 acrv-ex99_2.htm EX-99.2

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ACRIVON PREDICTIVE PRECISION PROTEOMICS (AP3) NEXT GENERATION PRECISION MEDICINE CORPORATE PRESENTATION MARCH 2026 Exhibit 99.2

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Forward-looking statements Certain information contained in this presentation includes forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995 regarding our future results of operations or financial condition, business strategy and plans and objectives of management for future operations. In some cases, you can identify forward-looking statements because they contain words such as “anticipate,” “believe,” “contemplate,” “continue,” “could,” “estimate,” “expect,” “intend,” “may,” “plan,” “potential,” “predict,” “project,” “should,” “target,” “will,” or “would” or the negative of these words or other similar terms or expressions. Our forward-looking statements are based primarily on our current expectations and projections about future events and trends that we believe may affect our business, financial condition and results of operations. The outcome of the events described in the forward-looking statements is subject to risks and uncertainties, including the factors described in our filings with the U.S. Securities and Exchange Commission. New risks and uncertainties emerge from time to time, and it is not possible for us to predict all risks and uncertainties that could have an impact on the forward-looking statements contained in this presentation. The results, events, and circumstances reflected in the forward-looking statements may not be achieved or occur, and actual results, events, or circumstances could differ materially from those described in the forward-looking statements. You are cautioned not to place undue reliance on these forward-looking statements, which are made only as of the date of this presentation. We undertake no obligation to update any forward-looking statements or to reflect new information or the occurrence of unanticipated events, except as required by law.

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next-generation precision medicine powered by AP3 Drug P Acrivon Predictive Precision Proteomics (AP3) AI-driven, proteomics-based rational drug design and informed clinical development AP3 enables an exact match between the disease-driving, dysregulated pathways with drug mechanism of action (Acrivon meaning ≈ exact, accurate) DNA RNA Protein Dysregulated Protein Dysregulated Pathways Proprietary tools Data portal Interactome Protein activity predictor Inflammation Cancer Fibrosis Current focus oncology, I&I next

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Development Site (Boston) Drug development and clinical biomarkers Clinical leadership and trial oversight ML/AI-driven AP3 analyses Precision Proteomics Site (Lund/Copenhagen) Early drug discovery BM identification and drug profiling AP3 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 Head Co-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)

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Accomplished leadership team Peter Blume-Jensen, M.D., Ph.D. CEO, President, Co-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

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Acrivon Pipeline Anticipated Next Milestone Phase 3 Phase 2 Phase 1 Preclinical ACR-368 (CHK1/CHK2) Single-Arm Trial Based on OncoSignature Biomarker Prediction Clinical Data & Dose Expansion Start, 2026 Clinical Update Mid-2026 Endometrial Cancer AP3-Identified Tumor Types Future Development Candidates Auto-Immune/Inflammatory ACR-368 Monotherapy (Breakthrough Device & Fast Track Designations) ACR-2316 (WEE1/ PKMYT1) Early Discovery Dose Escalation and Expansion AP3-Identified Tumor Types ACR-6840 (CDK11) IND Filing, Q4 2026 IND-Enabling Single-Arm Trials without Pretreatment Biopsy or Biomarker Stratification ACR-368 + ULDG Sensitization Initial Clin Data, Mid-2026 BM+ patients, registrational intent Serous all-comer, registrational intent ACR-368 Monotherapy Serous all-comer, registrational intent Initiation, 1H 2026

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Acrivon AP3-based precision medicine AP3 Clinical Biomarkers Predictive OncoSignature tests Single agent activity Target/pathway addiction Resistance Mechanisms Rational drug combinations Drug Discovery SAR Optimized pathway effects PD Markers ~60,000 per compound Informed in-licensing AP3 profiling of candidates Indication Finding Sensitive tumor types Therapeutic Index Dial out AE liabilities Novel Target Identification Activated druggable targets – diseased vs normal Streamlined Clinical Development Predicted sensitive indications with informed dose optimization

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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

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ACR-368: a potent selective CHK1/2 inhibitor Balanced potent (nM) inhibition of CHK1 and CHK2 enabling monotherapy activity Protected by composition-of-matter and salt form patents through 2030 and 2037, ensuring exclusivity Acrivon holds full, unencumbered global rights Clinical efficacy and safety: Durable monotherapy activity across multiple cancers with favorable tolerability and absence of non-hematological, severe toxicities Synergy with Immunotherapy: Preclinical data showing complete tumor regression and immune memory G2/M Checkpoint S Phase Checkpoint M G1 S Cancer Cell Cycle G2 CHK1/2 CHK1/2 Defective G1/S Checkpoint

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Oncosignature: Drug response prediction in individual patients PROPRIETARY WORKFLOW 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

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ap3 indication finding identifies endometrial cancer as sensitive to ACR-368 ACR-368 OncoSignature-based indication finding prior to trial entry Functional validation in preclinical models BM1 BM2 BM3 ~30% ~70% Clinical validation in ongoing Phase 2 study Endometrial patient tumor samples Predicted Responder Predicted Non-Responder

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Acrivon CLIA Laboratory Strengthening acrivon precision medicine capabilities Newly licensed CLIA laboratory Translates AP3-driven biomarker discoveries into actionable and proprietary CDx for our therapeutics Initially focused on ACR-368 OncoSignature testing Unique capabilities to support internal pipelines and new BD/partnering opportunities

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BM-Stratified Cohorts with Prospective Response Prediction Subjects with high-grade EC ≤3 lines of prior therapy The ACR-368 OncoSignature™ is a tumor agnostic, functional Biomarker (BM) test designed to prospectively predict benefit from ACR-368 (prexasertib), a potent, selective CHK1/2 inhibitor. It is composed of 3 protein biomarkers that measure the tumor’s addiction to CHK1/2-mediated DNA repair independent of genetic alterations. Screening with Acrivon’s OncoSignature BM test across routine-processed (FFPE) human tumor types, predicted endometrial cancer (EC) to be particularly sensitive to ACR-368. Subjects relapsed after prior platinum-based chemotherapy and one prior line of anti-PD-(L)1 therapy Arm 1 (BM+) ACR-368 (105mg/m2 iv q14d) (N=71) Arm 2 (BM-) ACR-368 (105mg/m2 iv q14d) + ULDG* sensitization (10mg/m2 iv q14d) (N=~150) Primary endpoint ORR: RECIST 1.1 *ULDG = ultra low dose gemcitabine Exploratory Arm Study Rationale and initial trial Design Registrational intent

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* Best of BICR and/or PI # Unconfirmed PR Non QC’ed data based on EDC data extract as of 12/04/2025 # # ORR = 39% (95% CI, 24 - 56) n = 31 DCR: 80.6%, CBR (16 weeks): 61.3%​ BOR by RECIST 1.1 on study treatment* Best overall response (BOR) DCR: Disease Control Rate (CR+PR+SD) CBR: Clinical Benefit Rate [(CR+PR)+(SD >16 weeks)] Significant Response in Arm 1 (BM+) ITT Population Treated with ACR-368

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# # # n = 25 n = 35 ORR = 26% (95% CI, 14 - 42) ORR = 44% (95% CI, 27 - 63) Arm 1 (BM+)  ACR-368 ARM 2 (BM-) ACR-368 + ULDG BOR by RECIST 1.1 on study treatment* * Best of BICR and/or PI # Unconfirmed PR Non QC’ed data based on EDC data extract as of 12/04/2025 Better ORR Observed in Subjects with ≤2 Prior lines of Therapy OncoSignature BM levels and the BM+ fraction were noted to be significantly higher in serous

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# # # n = 23 n = 37 Serous (≤ 2 Prior Lines) Non-Serous (≤ 2 Prior Lines) ORR = 22% (95% CI, 11 - 37) ORR = 52% (95% CI, 33 - 71) DCR: 74%, CBR (16 weeks): 65%​ BOR by RECIST 1.1 on study treatment* * Best of BICR and/or PI # Unconfirmed PR Non QC’ed data based on EDC data extract as of 12/04/2025 Significant ORR in Serous All-Comer Population with ≤ 2 Prior Lines of Therapy

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Screening Week 8 Week 12 Complete resolution of hepatic target lesions (-100%) (-100%) Deep, rapid responses in patients with aggressive serous 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

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Serous endometrial cancer - a significant unmet need Disproportionate Mortality Accounts for ~40-50% of all endometrial cancer deaths.5 Limited Effective Treatment Options Only moderate benefit from immunotherapy Chemotherapy responses short-lived. Rapid resistance, early recurrence. HER2-targeting benefits smaller proportion, no TP53-directed therapies Almost all serous patients progress to ≥2nd line of therapy SOC in ≥2nd line post-IO/platinum ~15% ORR and ~3.4 months PFS (single agent chemotherapy)5, 6 Serous EC is characterized by high-grade aplasia and aggressive histological features Nakayama, K.; Nakayama, N.; Ishikawa, M.; Miyazaki, K. Cancers 2012, 4, 799-807. 1SEER database 2https://pmc.ncbi.nlm.nih.gov/articles/PMC9445918 3Concin, C. et al, ESGO–ESTRO–ESP 2025 Guidelines; Lian Y., Luo P. Annals of Global Health (2025). 4Based on internal estimates of approximately 2.4% serous in the prevalence pool given survival approximations 5Bogani et al, Gynecol Oncol. 2021 July ; 162(1): 226–234. doi:10.1016/j.ygyno.2021.04.029. 6Makker et al, NEJM; 2022; 386:437-48 7KOL estimates EC Mortality (US + EU) = ~44K1, 3 Serous EC Mortality 40-50% ~18-22K/year2, 3,7 EC Prevalence ~2.4M patients1, 3 ~58,800 serous EC4

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Treatment-Related Adverse Events N = number of subjects (%) Arm 1 (ACR-368) N=40 Grades 3/4 Arm 2 (ACR-368 + ULDG) N=48 Grades 3/4 Thrombocytopenia 9 (22) 17 (34) Anemia 11 (27) 22 (46) Leukopenia 6 (15) 11 (23) Neutropenia 10 (25) 16 (33) Febrile neutropenia 2 (5) 4 (8) Acute kidney injury 2 (5) 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, mechanism-based hematological AEs Notable Absence of GI toxicities, ILDs, stomatitis, ocular toxicity, peripheral neuropathy, etc. Data-cut of 01/13/2026 Favorable safety profile

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Endometrial patient Demographics and baseline characteristics Subject Demographics BM+ N = 40 BM- N = 48 Median Age (range) 66.0 (40, 77) 66.0 (49, 80) Race, n (%) White 29 (72.5) 29 (60.4) Black/African American 6 (15) 10 (20.8) Asian 1 (2.5) 4 (8.3) American Indian or Alaska Native 0 0 Native Hawaiian or other pacific islander 1 (2.5) 0 Other/Unknown 3 (7.5) 5 (10.4) Stage, n (%) III 10 (25) 18 (37.5) IV 30 (75) 29 (60.4) Unknown 0 1 (2.1) Histology, n (%) Serous 20 (50) 16 (33.3) Clear-cell carcinoma 2 (5) 4 (8.3) Carcinosarcoma 6 (15) 10 (20.8) Endometroid, G3 9 (22.5) 15 (31.3) Other 3 (7.5) 3 (6.3) ECOG Status at Baseline, n (%) 0 20 (50) 25 (52) 1 20 (50) 23 (48) Subject Demographics BM+ N = 40 BM- N = 48 Prior Lines of Therapy, Median (Mean) 2 (2) 2 (2) Best Overall Response to Last Prior Line Refractory 9 (22.5) 15 (31.3) Relapsed disease 31 (77.5) 33 (68.7) Unknown 0 (0) 0 (0) MMR Status, n (%) pMMR 28 (70) 29 (60.4) dMMR 1 (2.5) 6 (12.5) Unknown 11 (27.5) 13 (27.1) TP53 Status, n (%) Mutant 24 (60) 15 (31.3) Wildtype 6 (15) 11 (22.9) Unknown 10 (25) 22 (45.8) Prior exposure to PD-1/PD-L1, n (%) Yes 39 (97.5) 46 (95.8) No 1 (2.5) 2 (4.2) Prior exposure to Pembro/Len, n (%) Yes 19 (47.5) 20 (41.7) No 21 (52.5) 28 (58.3) Non QC’ed data based on EDC data extract as of 01/13/2026

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Subjects relapsed after prior platinum-based chemotherapy and one prior line of anti-PD-(L)1 therapy Arm 1 BM+ N=71 ACR-368 Arm 2 BM- N= up to ~150 ACR-368 with ULDG sensitization Biopsy-Independent Serous Cohorts (US + EU) Subjects with ≤2 lines of prior therapy Arm 3 Serous All-Comer N= up to ~90 ACR-368 w/ ULDG sensitization Enrollment completion Q4 2026 BM-Stratified Cohorts with Prospective Response Prediction (US only) Subjects with ≤3 lines of prior therapy Primary endpoint ORR by RECIST 1.1 Primary endpoint ORR by RECIST 1.1 Exploratory Arm Arm 4 Serous All-Comer N= up to ~90 ACR-368 Monotherapy ACR-368 program focused exclusively on registrational intent opportunities ✓ Arms 1, 3, and 4 are registrational intent Primary endpoint ORR by RECIST 1.1 Serous EC shows particularly high ORR in both BM+ and BM- tumors ACR-368 has a favorable safety profile Arm 3 and Arm 4 are evaluating ACR-368 + ULDG and ACR-368, respectively, in serous EC all-comer (biopsy-independent) subjects The study is being expanded to >20 EU sites Completed

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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 Co-mediated by CD4 + CD8 Legends:

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Development path for ACR-368 in endometrial cancer Registrational intent Phase 2 single arm study of ACR-368 monotherapy in all BM+ EC patients All endometrial subtypes Enrollment completion (N =71 BM+ subjects) anticipated 2027 Registrational intent Phase 2 single arm study of ACR-368 with ULDG as sensitizer in all-comer serous EC (no biopsy requirement) Enrollment completion (N ~90 subjects) anticipated Q4 2026 Alignment with the FDA that ULDG (10 mg/m2) has no activity of its own Registrational intent Phase 2 single arm study of monotherapy ACR-368 in all-comer serous EC (no biopsy requirement) Planned confirmatory Phase 3 trial - front-line switch maintenance in pMMR population Randomization anti-PD-1 vs [anti-PD-1 + ACR-368] post [C/P + anti-PD-1] Protocol submitted to the FDA November 12, 2025

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ACR-368 + Anti PD-1 confirmatory phase 3 trial Placebo Carboplatin AUC 5 mg/mL/min Paclitaxel 175 mg/m2 Q3W for 6 cycles ACR-368 Q2W plus Anti PD-1 Q6W Placebo plus Anti PD-1 Q6W Follow- up R1:1 Eligible patients Subjects with advanced stage (III, IVA, or IVB) or recurrent pMMR EC with measurable disease, all histopathologies eligible. Subjects must have completed at least 4 cycles of chemo + anti-PD-1 ≥6 weeks before first dose of study treatment ECOG PS 0-1 Adequate organ function Co-primary endpoints (hierarchical testing) PFS OS Planned Phase 2 safety run-in transitioning into Phase 3 Randomized, double-blinded, multicenter study of ACR-368 plus anti PD-1 versus placebo plus anti PD-1 in the ICI maintenance phase for patients with MMRp, primary advanced or recurrent EC

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Monotherapy ULDG Sensitization PD1 Combination PD1/VEGF Bispecific Combination ADC Combination Endometrial MDS/MPN, HPV+ SCC, H&N, GBM Future Indications Initial Focus Broad Indication and Combination Expansion Opportunities acr-368 offers multiple attractive opportunities ACR-368-201 Arm 1 Biomarker-Positive All histopathologies Arm 4 Serous all-comer ACR-368-201 Arm 3 Biomarker Unselected Serous all-comer Confirmatory Phase 3 Expansion Opportunities

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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 ACR-6840: Development candidate, novel CDK11 inhibitor Anticipated IND filing Q4 2026 Multiple equally promising back-up series being pursued in parallel ACR-2316: Clinical stage, novel WEE1/PKMYT1 inhibitor Additional clinical data and transition to dose expansion 2026 Additional AP3-based internal programs

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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 Demonstrated clinical activity, but the Therapeutic Index has been challenging AP3 was applied to design a molecule with potent single agent activity and exquisite selectivity to achieve expanded Therapeutic Index

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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 tolerability 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; only transient AEs Superior anti-tumor activity* (robust CDK1, CDK2, and PLK1 activation; inhibition of PKMYT1 resistance) AP3-Enabled SAR AP3-based Indication Finding 1 2 3 4 *Head-to-head preclinical studies against benchmarks with clinical data AP3 MS-based PD assay developed for human PBMCs Clinical activity observed in AP3-predicted solid tumor types, including endometrial, SCLC, and sqNSCLC Advanced from lead to oral dosing in clinic in ≤15 month Two weekly oral dosing regimens established

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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

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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

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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

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Phase 1 Dose Escalation and Expansion Design Cohort A 3on/4off Cohort B 2on/5off Dose Level 1 Dose Level 2 Select tumor types Dose Escalation 30 mg 200 mg 240 mg 120 mg 60 mg 240 mg Cohort C 2on/12off 360 mg TBD 280 mg 160 mg Dose Expansion ✅ ✅ Two weekly oral regimens (3d on/4d off and 2d on/5d off) established with encouraging tolerability profile (N = 33) Bi-weekly (2d on/12d off) oral regimen being established based on ACR-2316 mechanism of action and limited, transient heme AEs Ongoing

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ACR-2316 shows promising clinical activity in lung cancer during dose escalation Non-QC’ed EDC data extract 3/3/2026 Two weekly oral dosing schedules established; Clinical activity observed at ≥120 mg DCR (Target lesion) across all tumor types 79% Initial clinical activity and DCR (6/7) observed in lung cancer (median 3 prior lines therapy, incl. ICI and chemo) adNSCLC-03 sqNSCLC-02 adNSCLC-01 adNSCLC-02 SqNSCLC-01 SCLC-02 SCLC-01 On treatment SCLC Sq. NSCLC Ad. NSCLC

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Favorable tolerability profile summary of ≥ grade 3 TRAEs # Subjects; % Total Gr. 3 N=20 Total Gr. 4 N=20 Total Gr 3/4 N=20 Neutropenia/neutrophil count decreased 4; 20% 1; 5% 5 25% Leukopenia/white blood cell count decreased 1; 5% 1; 5% 2; 10% Anaemia 1; 5% 0 1; 5% Lymphocyte count decreased 0 0 0 Alanine aminotransferase increased 1; 5% 0 1; 5% TOTAL 6 1 7 Non QC’ed EDC extract 2/23/2026 TRAEs with Grades 3/4 percentages ≥5% are included. No fatal TRAEs. Patients counted once at the maximum grade TRAEs in subjects treated up to or at established weekly dosing regimens Transient, mechanism-based hematological AEs, primarily neutropenia No other types of toxicities observed above (N = 13) tolerated weekly doses Notable absence of GI toxicities, long-lasting myelosuppression or more severe non-hematological AEs commonly seen with ADCs and chemotherapy

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Demographics AND BASELINE CHARACTERISTICS Non QC’ed data based on EDC data extract as of 12/22/2025 Subject Demographics N = 33 ECOG Status at Baseline, n (%) 0 10 (30) 1 23(70) Prior Lines of Therapy, n (%) 1 1 (3) 2 5 (15) 3 14 (42) 4 7 (21) 5 2 (6) 6 2 (6) 7 1(3) 8 1(3) Prior exposure to IO therapy, n (%) Yes 24 (73) No 9 (27) Subject Demographics N = 33 Median Age (range) 63 Race, n (%) White 26 (79) Black/African American 3 (9) Asian 1 (3) Native Hawaiian/Pacific Islander 1 (3) Unknown/Other 2 (6) Sex, n (%) Female 20 (61) Male 13 (39) Cancer Type, n (%) Bladder 1 (3) Breast 4 (12) Cervical 1(3) Colorectal 3 (9) Endometrial 5 (15) Head Neck Squamous Cell Carcinomas 3 (9) Small Cell Lung Cancer 2 (6) Squamous - Non Small Cell Lung Cancer 3 (9) Adenocarcinoma - Non Small Cell Lung Cancer 3 (9) Ovarian Carcinoma 4 (12) Pancreatic Cancer 2 (6) Prostate Cancer (Neuroendocrine) 2 (6)

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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 co-mediated by CD4 + CD8

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Potential development paths for ACR-2316 AP3-predicted solid tumor types of high unmet need, e.g. SCLC, sqNSCLC, HPV+ tumors, etc. Single agent 2nd/3rd line Chemo combination (DDR stress sensitization in earlier lines) Weekly and bi-weekly dosing regimens provide flexibility for combinations, including potential frontline with both anti-PD(L)1 and TOPO1 payload ADCs (both strong synergy with ACR-2316) ACR-2316 + anti-PD-L1 therapy results in complete regression and permanent CD4 + CD8-mediated immune memory in preclinical models ACR-2316 + TOPO1 isomerase inhibitors (main backbone in ADCs) shows strong synergy in preclinical models Max synergy score = 34 Strong synergy with IO Potential for strong synergy with ADCs

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New preclinical cell cycle development candidate ACR-6840: potential first-in-class CDK11 inhibitor No clinical-stage competitors Attractive cancer cell cycle drug target, well-suited for AP3 platform, multiple protein isoforms Broad role in cell cycle control and oncogenesis; CDK11 controls transcription, pre-mRNA processing and splicing of mitotic genes, and is encoded by an essential gene for cancer cell viability (DepMap) AP3 profiling (benchmarks/leads) for MOA-based SAR and lead optimization Development candidate: ACR-6840 Small molecule CDK11 inhibitor, highly selective (kinome scan), orally available, potent (3 nM cellular target engagement; ~30 nM EC50 viability), preclinical antitumor activity Several equally promising back-up series Series D Resol. : 2.64 Å Series C Resol. : 2.4 Å AP3-based screening funnel guides intracellular protein SAR Series E  Resol. : 2.69 Å All AP3-driven programs deploy co-crystallography

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

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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

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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

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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

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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

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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

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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

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

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data driven execution and value creation Recent Accomplishments (Last 12 Months) Anticipated Next Milestones (2026) Continued positive ACR-368 data in ongoing registrational intent EC trial (April 2025 and January 2026 Corporate R&D Events) Two weekly oral dosing regimens for ACR-2316; promising clinical activity observed in AP3-prioritized tumor types, including lung cancer (Q3-4 2025) 4 presentations showcasing expanded AP3 capabilities and compelling ACR-2316 preclinical data (AACR Q2 2025 and AACR-NCI-EORTC Q4 2025) Achieve CTA approval in EU for the ongoing (US) registrational intent serous EC all-comer Arm 3 (ACR-368 + ULDG) by Q1 2026 Initial clinical data from Arm 3 and additional update on Arm 1 of the ACR-368 Phase 2b trial in mid-2026 Initiate enrollment for the registrational intent serous EC all-comer Arm 4 (ACR-368) in the US in first half of 2026 Achieve readiness for Phase 3 confirmatory trial for ACR-368 in combination with PD-1 therapy by mid-2026 Complete enrollment (up to N = 90 subjects) in the registrational intent serous EC all-comer Arm 3 (ACR-368 + ULDG) in Q4 2026 Additional ACR-2316 Phase 1 clinical data for weekly and bi-weekly dosing regimens and transition into dose expansion in AP3-identified tumor types in 2026 Submit IND filing to the FDA for ACR-6840 in Q4 2026 Initiate additional internal programs utilizing the AP3 platform in 2026 Development candidate nomination for ACR-6840, a potential first-in-class CDK11 inhibitor (Q4 2025) Initiation of additional registrational intent serous EC all-comer (biopsy independent) Arm 3 in ongoing Phase 2b trial (Q4 2025) Strong enthusiasm for promising ACR-368 clinical data at 2026 ESGO late breaking oral presentation and corporate live KOL expert panel (Q1 2026) cORR of 52% observed in serous EC, a high unmet need disease w/ limited treatment options contributing to ~50% of all EC mortality

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FINANCIAL HIGHLIGHTS Approximate Cash and Investments $118.6M Projected runway into Q2 2027 Approximate Fully Diluted Shares Outstanding 45.1M Current operating plan, assuming no additional financing Balance sheet 31-Dec-2025 Shares, pre-funded warrants, and equity grants outstanding 31-Dec-2025 Note: Unaudited