CORPORATE R&D EVENT September 14, 2024 ACRIVON PREDICTIVE PRECISION PROTEOMICS (AP3) OVERCOMING LIMITATIONS OF GENETICS-BASED PRECISION MEDICINE Exhibit 99.2

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outline Acrivon Therapeutics and AP3 overview Data update on the prospective ACR-368 registrational intent Phase 2 trial in endometrial cancer Update on ACR-2316, an AP3-derived dual WEE1/PKMYT1 inhibitor cleared for Phase 1 Intro to AP3 Interactome v.2: Real-time actionable analyses of Acrivon proprietary AP3 data Live Q&A For a comprehensive corporate deck, please visit: https://Acrivon.com

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)

AP3 developed to overcome Critical challenges facing biopharma industry Discovering potent compounds suitable for clinical monotherapy Determining which patients will benefit from those drugs Preventing or reducing resistance to maximize response durability AP3 is a proprietary, machine learning-enabled internal R&D engine that effectively addresses these challenges, driving rapid advancement of our pipeline Challenge Acrivon Predictive Precision Proteomics (AP3) Optimal target/pathway selectivity for rapid generation of single agent active compounds Identification of drug-sensitive indications and patients for actionable precision medicine Ability to rapidly identify and overcome resistance mechanisms

Acrivon Pipeline Anticipated Next Milestone Phase 3 Phase 2 Phase 1 Preclinical ACR-368 (CHK1/CHK2) Single-Arm Trials Based on OncoSignature Prediction Option to Initiate Additional Trials in HPV+ SCC (H&N*, Anal, Cervical) and Sarcomas Trial Initiation Q4 2024 Multiple Program Updates Q3 (ESMO) and Q4 2024 Endometrial Cancer Bladder Cancer OncoSignature-Predicted Monotherapy Sensitive Tumors Future Development Candidates Additional AP3-driven co-crystallography programs ACR-368 Monotherapy LDG Combination Registrational intent Phase 2 single arm trials based on predicted sensitivity to ACR-368 monotherapy in OncoSignature-positive patients Exploratory Phase 1b/2 single arm trials of ACR-368 in combination with low dose gemcitabine, or LDG, in OncoSignature-negative patients LDG Combination ACR-368 Monotherapy Fast Track Designation ACR-368 Monotherapy LDG Combination ACR-2316 (WEE1/ PKMYT1) Phase 1 Activated OncoSignature-Predicted Monotherapy Sensitive Tumors Cell cycle program (undisclosed target) Development Candidate Nomination 2025 Discovery *Investigator-Initiated Trial (IIT) activated at Moffitt Cancer Center Platinum-Resistant Ovarian Cancer ACR-368 Monotherapy Breakthrough Device & Fast Track Designations LDG Combination

Newly disclosed ACR-368 clinical data ESMO 2024: Interim data from the registrational intent Phase 2 prospective clinical trial in endometrial cancer Data cut as of July 25, 2024 Poster available on Acrivon’s website: https://acrivon.com/science/#publications-posters

AP3-based drug discovery and clinical development in predicted sensitive subjects and tumor types Predicted Responder AP3 Clinical Biomarkers Predictive OncoSignature tests Indication Finding Sensitive tumor types Resistance Mechanisms Rational drug combinations Drug Discovery SAR Optimal target selectivity PD Markers ~6,000 per compound Informs in-licensing AP3 profiling of candidates Streamlined Clinical Development Predicted sensitive indications with informed dose optimization

AP3 platform: 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) Exclusively in-licensed from Eli Lilly & Company (WW rights); originally discovered by Array (Pfizer) CoM patent exp. Oct., 2030; Salt-form exp. Apr., 2037 Balanced inhibition of both CHK1 and CHK2 believed important for RECIST monotherapy activity ACR-368 (MW): 365.4 DRUG TARGET PROFILE AT TIME OF IN-LICENSING Durable monotherapy activity: Platinum-resistant ovarian and squamous cell cancers (Anal and H&N) Large safety database, favorable safety profile: >1,000 patients treated (~50% mono, ~50% in combination) Ideal for AP3 method: Proven clinical activity, but requires patient responder identification to achieve sufficient ORR 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

Endometrial cancer is an AP3-predicted ACR-368-Sensitive tumor 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

High grade advanced stage endometrial cancer opportunity has opened for ≥ 2nd line (post anti-PD-1) ACR-368 Target Indication: High grade, locally advanced or metastatic, recurrent endometrial cancer Significant unmet need, attractive commercial potential Must have recurred after prior chemo and PD-1/PD-L1 inhibitor therapy1 Irrespective of molecular (MMR, p53, other) alterations and subtype (serous, endometrioid, clear cell, carcinosarcoma) SOC: ≥2nd line (post-PD-1 + chemo) ~14.7% ORR, mPFS 3.8 months2 ≥3rd line ~9% ORR, mPFS 2.8 months3 ACR-368 Target Product Profile: ≥25% ORR with CI lower bound >20%; mDoR ≥5.5 months 1Unless ineligible for PD-1/PD-L1 therapy 2Eskander R et al, NEJM, 2023; Mirza MR et al, NEJM, 2023; Makker V et al, NEJM, 2022 3Ray-Coquard I et al, BJC, 2013

ACR-368-201 Trial and enrollment in endometrial cancer April 2024 Corporate R&D Event1 ESMO 20242 Endometrial Cancer BM+ BM- Total BM+ BM- Total Safety-Evaluable (enrolled ≥1 dose) 7 11 18 12 23 35 Efficacy-Evaluable (≥1 on-treatment scan) 5 5 10 8 15 23 BM+% (enrolled BM+/Total) 38.9% 34.3% BM+ BM- https://clinicaltrials.gov/study/NCT05548296 1https://ir.acrivon.com/news-events/events-presentations 2https://acrivon.com/science/#publications-posters Enrollment in Endometrial Cancer ACR-368-201 Trial Ongoing enrollment in ovarian and bladder cancer cohorts with update planned for future date

Demographics and subject disposition (N=35) Subject Demographics BM+ N = 12 BM- N = 23 Median Age (range) 66 (60-76) 68 (42-78) Race (%) White 8 (67) 16 (70) Black/African American 3 (25) 3 (13) Asian 0 (0) 3 (13) Other 0 (0) 1 (4) Unknown 1 (8) 0 (0) Current Stage (%) III 3 (25) 12 (52) IV 9 (75) 10 (43) unk 0 (0) 1 (4) Histology (%) Serous 8 (67) 7 (30) Endometrioid 3 (25) 7 (30) Carcinosarcoma 1 (8) 3 (13) Clear Cell Carcinoma 0 (0) 2 (9) Other 0 (0) 4 (17) ECOG Status at Baseline (%) 0 5 (42) 10 (43) 1 7 (58) 13 (57)  Subject Disposition BM+ N = 12 BM- N = 23 Median Prior Lines (range) 2 (1-4) 3 (1-4) Prior PD-1/PD-L1 Therapy (%) Yes 12 (100) 22 (96) No 0 (0) 1 (4)* Discontinued Study Drug (%) 3 (25) 13 (57) Reason for Discontinuing Study Drug (%) PD 2 (17) 10 (43) PI Decision 1 (8) 0 (0) Unacceptable Tox 0 (0) 1 (4) Subject Decision 0 (0) 1 (4) Subject Withdrawal of Consent 0 (0) 1 (4) Survival Status (%) Alive^ 10 (83) 14 (61) Deceased 2 (17) 7 (30) Unknown 0 (0) 2 (9) *Subject deemed ineligible for anti-PD-1therapy. ^1 BM+ and 4 BM- subjects are still on study for follow-up, but no longer receiving study drug. Data current as of 25July2024 and includes all subjects enrolled with registrational intent BM- includes all subjects treated with ACR-368 + low dose gemcitabine (LDG) at RP2D (105 mg/m2 and 10 mg/m2, respectively).

significant ACR-368 responder enrichment in efficacy-evaluable subjects1 (N=23) in registrational intent phase 2 trial Overall Response BM+ Monotherapy BM- LDG Combination Total N = 8  N = 15 N=23   N (%) N (%) N (%) CR 0 (0) 1 (7) 1 (4) cPR 5 (63) 0 (0) 5 (22) uPR 0 (0) 1 (7) 1 (4) SD 1 (13) 6 (40) 7 (30) PD 2 (25) 7 (47) 9 (39) cORR (95% CI) 62.5% (30.4, 86.5) 6.7% (0.84, 31.8) 26% (12.3,46.8) OncoSignature BM+ vs BM- Segregation P = 0.009 Prospective initial validation of the AP3-based ACR-368 OncoSignature now achieved for endometrial cancer (P = 0.009 vs P = 0.083) Confirmed ORR in BM+ subjects now 62.5% with the lower bound of 95% C.I. 30.4% (vs. 22.9%) Confirmed ACR-368 responders still on therapy; mDoR not yet reached (~6 months at time of data-cut vs ~2 months) 1Subjects with ≥1 on-treatment scan 2https://ir.acrivon.com/news-events/events-presentations Meaningful positive data maturation since April R&D Event2

Clinical activity in BM+ patients who have all progressed on prior anti-pd-1 therapy Data current as of 25July2024, includes all BM+ subjects Percent Change from Baseline (sum of diameters) cPR SD PD Still on Treatment Confirmed ORR = 62.5% 95% C.I. (30.4%, 86.5%) Significant disease control (75%) with most RECIST responses occurring early

Ongoing confirmed responses in BM+ subjects across subtypes Data current as of 25July2024 Months on Treatment 4 – BOR on last prior line 5 – BOR on ACR-368 1 – Subtype 2 – MMR Status mDOR not yet reached (~6 months at time of data cut-off) Durable responses in patients who all progressed on prior anti-PD-1 and whose BOR in last prior line was mostly PD Most patients are pMMR and p53 mutant, consistent with their prevalence in high grade endometrial cancer ACR-368 OncoSignature prediction is independent of molecular (incl. MMR) and histological subtype 3 – p53 Status 1 2 3 4 5

Confirmed responses in subjects who all progressed on prior anti-PD-1 Endometrial subtype # Prior Lines Last Prior Therapy (LPT) BOR on LPT BOR on ACR-368 Serous 3 Pembrolizumab/Lenvatinib PD cPR Serous 2 Pembrolizumab/Lenvatinib PD cPR Endometrioid 4 Cisplatin PD cPR Serous 1 Pembrolizumab SD cPR Carcinosarcoma 2 Pembrolizumab/Lenvatinib PR cPR Serous 4 Liposomal doxorubicin PD SD Serous 3 Pembrolizumab/Lenvatinib UNK PD Serous 3 Pembrolizumab/Lenvatinib NA PD BOR = Best Overall Response, UNK = unknown, NA = not applicable, NT = not tested Data shown current as of 25Jul2024 and includes all efficacy-evaluable (at least one scan on-treatment) BM+ subjects All confirmed responders progressed on prior PD-1 therapy and majority had BOR = PD on last prior line of therapy Only 1 RECIST response amongst 6 patients with BOR data from LPT

Deep, rapid responses seen in patients with large tumor lesions Screening Week 8 Week 16 Superior vaginal cuff Inferior vagina 0 mm 72-yo female with Stage III serous endometrial carcinoma (pMMR) PD on last prior line (pembrolizumab/lenvatinib) Confirmed PR at Week 16 73% overall decrease in sum of target lesions from baseline

Evidence of LDG sensitization in proportion of BM- subjects in exploratory phase 1b/2 trial Best Overall Response Initial disease control (1 cCR, 1 uPR, and 6 SD) observed in a proportion of BM- subjects LDG sensitization may potentially increase ORR across BM+ and BM- patients 1 2 3 4 Data current as of 25July2024, includes all BM- subjects enrolled at RP2D for LDG (10 mg/m2). 1– Histology; 2 – MMR; 3 – BOR on most recent prior line; 4 – BOR on ACR-368 + LDG PR SD PD Still on Treatment CR Confirmed Response Time on Treatment (Weeks) Percent Change from Baseline (sum of diameters) Percent Change from Baseline (sum of diameters) Months on Treatment

Encouraging safety profile Limited, predominantly transient, reversible, mechanism-based hematological AEs, which typically occurred during the first 1-2 cycles of therapy Notable absence of long-lasting myelosuppression or the typical more severe non-hematological AEs commonly seen with ADCs and chemotherapy ACR-368 data current as of 25July2024 and includes the safety population of endometrial carcinoma subjects (any subject who has received at least one dose of ACR-368) enrolled (BM+ and BM-) and at the RP2D for LDG (BM-). Prophylactic G-CSF encouraged in BM+ and mandated in BM- subjects (compatible with q14d dosing regimen). Treatment-Related Adverse Events of Note ACR-368 (BM+) ACR-368 + LDG (BM-) N = 12  N = 23 All (%) Gr 3/4 (%) All (%) Gr 3/4 (%) Thrombocytopenia 6 (50) 2 (17) 12 (52) 8 (35) Anemia 4 (33) 3 (25) 12 (52) 9 (39) Neutropenia 3 (25) 3 (25) 7 (30) 7 (30) Febrile Neutropenia 0 0 3 (13) 3 (13) Fatigue 3 (25) 0 7 (30) 0 Vomiting 3 (25) 0 2 (9) 0 Diarrhea 2 (17) 0 2 (9) 0 Infusion Reaction 0 0 1 (4) 0 Hypertension 0 0 1 (4) 1 (4) Dyspnea 0 0 2 (9) 0

blinded KOL Market research underscores endometrial cancer represents significant opportunity for acr-368 Endometrial cancer (EC) projected to be the third most prevalent cancer and the fourth leading cause of cancer-related death among women by 20401 Incidence = 67,880, prevalence = 865,000 in the US (2023)*; Incidence increasing by 1-3% per year Mortality = 13,250 in the US (2023); 5-year survival ~ 80%* High grade EC accounts for majority of EC deaths each year Second line (2L) now represents a high unmet need New cases of high grade, recurrent EC (progressed on anti-PD-1 + chemo) ~30K patients/year 90% of cases believed to progress to 2L therapy Recent front-line approvals of anti-PD-1 plus chemo followed by anti-PD-1 only1,2 for high grade EC reduces/eliminates pembro + lenvatinib3 as viable 2L option for most patients Reported chemotherapy efficacy in 2L is ORR = 14.7% and mPFS = 3.8 months3 *SEER database 1Eskander et al, NEJM 2023; 2Mirza et al, NEJM 2023; 3Makker et al, NEJM 2022

Blinded Kol market research suggests acr-368 profile attractive to gynecologic oncologists Themes Implications Representative quotes Significant SOC gap and unmet need exists in 2L opportunity for ACR-368 Huge unmet need still exists in endometrial cancer treatment, especially pMMR ”People that develop recurrence almost invariably do not survive their endometrial cancer.” “That's really where there is the biggest opportunity is – in 2L.” “I would say that you would really want to see something with a response rates north of 30% to really get people excited about that but really the bar is above 20% and would be interesting.” “I know the FDA is very interested in companion diagnostics. I think that they really want to see that the work is being done to understand the responders.” Biomarker driven approach highly attractive and justified for high ORR “I believe that in pMMR the contribution of immune therapy is modest.” “If you had a 20% or 25% response rate, that would be pretty good” “If you could predict which patients would respond so that the patients that you chose would be higher, then I think you'd be in like Flynn.” “I think everybody's struggling with what to do for 2L therapy.” Clinicians eager to embrace new therapeutic options especially in challenging to treat molecular sub-groups “Those patients (pMMR) we know they don't have as robust as response as those patients that are mismatch repair deficient. Certainly, that's a big unmet need.” Recent changes to standard of care leaves opportunity for significant penetration with new 2L therapies That ACR-368 OncoSignature is independent of genetic background or histology further favorably differentiates the agent Source: Single blinded, proprietary third-party market research with endometrial KOLs conducted August-September 2024 “Over 60% ORR? I hope such a compound really exists!”

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 Approved in the dMMR and pMMR populations - C/P + Pembrolizumab (NRG GY018) - C/P + Dostarlimab (RUBY/GOG 3031) NCCN Compendium Listed - C/P + trastuzumab (HER2+ serous and carcinosarcoma) - C/P alone MAINTENANCE Pembrolizumab Dostarlimab ------------ Trastuzumab Progression-Free Survival (9-13 months in the pMMR EC population) Progression Lenvatinib + Pembrolizumab -------------- C/P + IO -------------- US FDA approval of T-Dxd In HER2 3+ Other Lines of Therapy and Clinical Trials Post-Progression Survival (12-18 months) No Prior-IO Prior-IO Single agent vs combination Chemotherapy -------------- US FDA approval of T-Dxd In HER2 3+ Progression With chemotherapy: ORR 15%; mPFS 3.8 mo Potential alternate strategies: hormonal therapy, single agent IO, T-Dxd in HER 2 2+ (NCCN) Courtesy Dr. R. Eskander

Development path for ACR-368 in endometrial cancer Accelerated approval pathway Ongoing single arm registrational intent Phase 2 monotherapy endometrial cancer trial represents the first potential approval opportunity for ACR-368 Confirmatory trial strategy Evaluating options to potentially move towards new front line setting Randomization anti-PD-1 vs anti-PD-1 + ACR-368 post C/P + anti-PD-1 (sub-group analysis; MMR status in all-comer)* Potential ≥2nd line options: ACR-368 + ULDG in all-comer patients *Based on current clinical data showing cPRs in patients progressing on prior anti-PD-1 together with a strong rationale for, and preclinical data demonstrating additive/synergistic activity of ACR-368 and anti-PD-1 (Refs: Lyer et al, Cancer Disc 2021; McGrail et al, Sci Transl Med 2021; Sen et al, Cancer Disc 2019)

ACR-368 potential in high unmet tumor types beyond endometrial, ovarian, and bladder cancer Enrollment is continuing in our ongoing multicenter phase 2 trials in ovarian and bladder cancer with planned update at a future date ACR-368 has also shown promising clinical activity in HPV+ squamous cell cancers (SCC), and sarcomas* HPV+ SCC are of increasing incidence (~50,000-60,000 new cases per year in the US) and includes ~70-80% of oropharyngeal H&N, ~20% of esophageal, ~90% of cervical, and 95% of anal cancers** SCCHN: Dr. C Chung, MD, Chair, Moffitt Cancer Center has begun an investigator-initiated trial with ACR-368 + ULDG in both HPV+ and HPV- SCCHN post anti-PD-1. IND cleared and site is activated HPV+ SCC represent tumor types of high unmet need and attractive option for next Acrivon-sponsored trial(s) with ACR-368 *Hong et al, CCR 2018, Slotkin et al, ASCO Annual Meeting 2022 **CDC 2023; ICO/IARC Information Centre on HPV and Cancer 2023; Gribb et al, Dela J Public Health 2023, NCI 2023

ACR-2316, a potent, novel, dual WEE1/PKMYT1 inhibitor optimized for superior single agent activity and therapeutic index IND CLEARED AND FIRST CLINICAL SITES ACTIVATED AHEAD OF SCHEDULE AP3-BASED DRUG DISCOVERY

Streamlined AP3-based design of compounds for superior single agent activity and therapeutic index Peptide clean up Direct DIA analysis Drug treatment Proteolysis P-peptide enrichment Ultra high resolution P-proteomic profiling Week 0 Week 2 Turnaround <2 weeks Quantitative mapping (>105,000 phospho-sites covering >10,000 proteins) Drug-regulated phospho-sites and biological process enrichment Drug-regulated pathway activity mapping and reconstitution P P AP3 enables pathway-based drug design for optimal drug properties High resolution and throughput MS-based P-proteomics

ACR-2316: uniquely enabled by AP3 to overcome limitations of current wee1 and pkmyt1 inhibitors Zhu et al, J. Med. Chem. (2017) Program goals (superior therapeutic index): Superior single agent activity (AP3) Potent activation of CDK1, CDK2, and PLK1 and quenching of resistance through balanced WEE1/PKMYT1 inhibition to ensure robust pro-apoptotic tumor death High selectivity for minimal AEs (co-crystallography) Structure-guided design to limit adverse events (AEs) to be strictly mechanism-based, transient, short-lived Streamlined clinical development (ACR-2316 OncoSignature) To identify/prioritize sensitive indications prior to clinical start and for drug target engagement-based dose optimization during Phase 1 AP3 used for pathway-based optimization to achieve superior single agent activity Co-crystallography for drug design and selectivity ACR-2316: Rationally designed WEE1/PKMYT1 inhibitor Superior anti-tumor efficacy with complete tumor regression across models High selectivity ensures transient, short-lived, mild AEs Potent WEE1 inhibition, balanced PKMYT1 inhibition, overcomes resistance and enables robust activation of CDK1, CDK2, and PLK1 for mitotic catastrophe

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

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

ACR-2316 - favorable preclinical safety profile Mice: ACR-2316 was well-tolerated, resulting in tumor regression in xenograft mouse models at multiple dosing regimens (qw, 2qw, 3d on/4d off, 5d on/2d off, and qd) Transient, reversible, mechanism-based hematological adverse events Rat and dog MTD, DRF, and GLP tox studies: GLP tox studies (31 days) completed in rat and dog with the planned human dosing regimen achieving exposure required for tumor regression Adverse events were mechanism-based, short-lived, reversible and limited to dividing myeloid progenitors and gastrointestinal tract We believe the broad therapeutic index observed across all our preclinical studies conducted with the planned dosing regimen is consistent with the target human exposure required for anti-tumor activity and anticipated reversibility of mechanism-based AEs

ACR-2316 IND cleared and initial clinical sites activated ACR-2316-101: Phase 1 study of ACR-2316 in subjects with advanced solid tumors Aiming for streamlined clinical development: Multiple sites currently activated and screening, first dosing expected shortly AP3-based indication finding and OncoSignature development ongoing Dose optimization to be 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

Acr-2316 is a potentially best-in-class agent rationally designed using Acrivon’s ap3 platform Program Goals Demonstrated Preclinical Results Superior single agent activity High selectivity and potency Streamlined clinical development Favorable safety profile Broad preclinical therapeutic index and anti-tumor activity across dosing regimens 5-20-fold more potent* in preclinical models than clinical benchmarks High selectivity results in adverse events limited to transient, short-lived, mechanism-based, reversible Superior* single agent anti-tumor activity through robust CDK1, CDK2, and PLK1 activation and elimination of dominant resistance mechanisms through balanced WEE1 and PKMYT1 inhibition AP3-Enabled SAR AP3-based identification of PD biomarkers and prioritization of promising indications 1 2 3 4 *Head-to-head preclinical studies against benchmarks with clinical data

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 Filtering Batch effects Normalization Imputation ~150,000 phosphosites ~50,000 phosphosites Ap3 interactome v.2: Proprietary Interactive Data analysis infrastructure Actionable data across all AP3 experiments accessible for all Acrivon scientists Fully scripted, algorithm-based machine learning-enabled pathway and biomarker analyses

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

Robust potent inhibition of CDK1 consensus substrate Y15 by ACR-2316 vs comparators 60min and 200nM in ACHN 3 -3 log2FC

Robust potent inhibition of CDK1 consensus substrate Y15 by ACR-2316 vs comparators Dose-dependent comparison @ 60min in ACHN 3 -3 log2FC

Robust potent inhibition of CDK1 consensus substrate Y15 by ACR-2316 vs comparators Time-dependent comparison @ 200 nM in ACHN 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

FINANCIAL HIGHLIGHTS Cash and marketable securities $220.4M Projected runway into H2’26 Fully Diluted Shares Outstanding 43.9M Balance sheet 30-June-2024 Current operating plan, assuming no additional financing Including shares, pre-funded warrants and equity grants outstanding 30-June-2024

Key take aways Significant clinical advancements and continued prospective validation of our AP3 platform since last R&D update in April Interim registrational intent Phase 2 clinical data for ACR-368 endometrial cancer cohort*, with confirmed ORR (63%) and lower bound of confidence interval (~30%), solidifying endometrial cancer as likely first indication for potential approval Statistically significant segregation of responders in BM+ vs BM- subgroups based on prospective OncoSignature patient selection (p-value = 0.009) ACR-368 endometrial cohort data maturing with all responders still on therapy; mDoR not yet reached (~6 months at time of data-cut) IND clearance of ACR-2316, a potential best-in-class, dual WEE1/PKMYT1 inhibitor rationally designed using AP3; clinical sites activated and screening patients for enrollment in a Ph1b study AP3 Interactome generating proprietary, actionable insights, leveraging in-house data and delivering fully scripted, algorithm-based machine learning-enabled pathway and biomarker analyses 1 2 3 4 5 Cash and marketable securities ~$220M with runway projected into second half of 2026 6 * Data cut as of July 25, 2024 Actively evaluating potential confirmatory trial designs for a potential future label expansion 7

Infectious, CNS, and other diseases Oncology Fibrotic and inflammatory Autoimmune Cancers with DDR stress Therapeutic areas Therapeutic modalities Small molecule Bifunctional molecule Antibody ADC Oligo/RNA The AP3 Approach is modality and disease agnostic Current focus

Q&A session