ACRIVON PREDICTIVE PRECISION PROTEOMICS (AP3) OVERCOMING LIMITATIONS OF GENETICS-BASED PRECISION MEDICINE CORPORATE PRESENTATION JANUARY 2024 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-causing, dysregulated pathways with a drug’s mechanism of action (Acrivon meaning ≈ exact, accurate) Is broadly applicable in drug discovery and development (including SAR and optimal selectivity, uncovering resistance mechanisms, and patient responder identification) and being leveraged for our internal therapeutics pipeline DNA RNA Protein Dysregulated Protein Dysregulated Pathways + OncoSignature®

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

Acrivon: next generation precision oncology overcoming limitations of genetics-based precision medicine Experienced team focused on execution with cash runway into 2H 2025 ACR-368 (Phase 2) CHK1/2 inhibitor in registrational intent trials in multiple solid tumor types ACR-2316 (IND-enabling) Dual WEE1/PKMYT1 inhibitor with superior selectivity and single agent activity Preclinical Drug Discovery Additional AP3-enabled, co-crystallography-driven precision oncology programs Clinically Actionable Resistance Mechanisms Rational drug combinations OncoSignature Proprietary, drug-tailored patient responder identification tests Drug Discovery AP3-based SAR facilitated by co-crystallography Compelling Pipeline of Potential First-in-Class Innovation Acrivon Predictive Precision Proteomics (AP3)

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, large national cancer center and hospital 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 Rasmus Holm-Jorgensen Chief Financial Officer Novo Nordisk Finance and IR Synageva pipeline expansion and $9bn sale to Alexion Kiniksa founding team, IPO and commercial launch 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) Jean-Marie Cuillerot, M.D. Chief Medical Officer Chief Medical Officer, Agenus Global head of clinical development in immuno-oncology at EMD Serono Clinical development leadership roles at BMS and Novartis

Development Site (Boston) Drug and clinical biomarker assay development Clinical trials Market access pending approval Precision-Proteomics Site (Lund/Copenhagen) Early pipeline drug programs BM identification and drug profiling Mass spectrometry Acrivon therapeutics at a glance Peter Blume-Jensen CEO, President, Co-Founder Kristina Masson EVP, Bus Ops, Site Head and Co-Founder Jesper V. Olsen Academic Co-Founder. Novo-Nordisk Foundation Protein Center, Cph. 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)

Acrivon predictive precision proteomics, AP3 *Oncogenic Kinase Signaling: Blume-Jensen, P. and Hunter, T. Nature (2001) Synthetic lethality as an engine for cancer drug target discovery: Huang, A. et al. NatRevDrugDisc (2020) Genomic Biomarkers are useful for patient selection in the smaller subset of cancers (<10%) with single gene driver mutations or known synthetic lethal context* Drug DNA RNA Protein Dysregulated Protein Dysregulated Pathways CANCER IS CAUSED BY DYSREGULATED PROTEIN ACTIVITY CANCER P P Acrivon’s AP3 platform directly measure the disease-driving, dysregulated proteins and is designed to enable an exact match with the drug mechanism-of-action independent of genetic alterations (Acrivon meaning: “Exact, Accurate”)

AP3 Platform Addresses High Unmet Need Beyond NGS-BASED Precision Medicine Acrivon Positioned to Increase Precision Oncology Market Size Sources: Company Filings, ACS, CDC, NCI, Wall Street Research (2022) Precision Oncology 1.0 Predictive Precision Proteomics Aiming to make targeted therapeutic solutions available to broader group of cancer patients Approved indications: HER2+ Breast Cancer HER2+ Gastric Cancer Approved indications: CML (BCR-ABL) Ph+ ALL Solid Tumors (NTRK)) IDH mutation in AML NSCLC (NTRK) and CRC (ROS1, ALK) NSCLC (KRAS G12C) Bladder (FGFR3) Solid Tumors (NRG1) Class II and III BRAF kinase alterations: N/A Precision Oncology 2.0 1st Gen Precision Oncology Current Precision Oncology Approaches Only Scratching the Surface Currently Unaddressed 72 unique approvals 51 drugs 31 genomic indications 18 cancer types Only 5% of patients respond 95% of patients are currently unaddressed by traditional genetics-based precision oncology

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

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 IND Filing in Q4 2024 Clinical Data at Major Medical Conference 1H 2024 Platinum-Resistant Ovarian Cancer Endometrial Cancer Bladder Cancer OncoSignature-Predicted Monotherapy Sensitive Tumors Future Development Candidates Additional AP3-driven co-crystallography programs ACR-368 Monotherapy Breakthrough Device & Fast Track Designations LDG Combination ACR-368 Monotherapy LDG Combination Notes 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 ACR-368 Monotherapy Fast Track Designation LDG Combination ACR-368 Monotherapy LDG Combination ACR-2316 (WEE1/ PKMYT1) IND-Enabling Studies OncoSignature-Predicted Monotherapy Sensitive Tumors Undisclosed cell cycle program Development Candidate 2025 Discovery

ACR-368: a clinically active phase 2 CHK1/2 inhibitor ATP-competitive inhibitor of CHK1 (0.9 nM) and CHK2 (8 nM) Good ADME properties, minimal drug-drug interaction (DDI) potential Discovered by Array Biopharma, acquired by Eli Lilly & Company CoM patent exp. Oct., 2030; Salt-form exp. Apr., 2037 ACR-368 (MW): 365.4 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 M G1 S Cancer Cell Cycle G2 S Phase Checkpoint CHK1 CHK1 Defective G1/S Checkpoint

Clinical overview of ACR-368 monotherapy (past data) Dosing and Administration IV q14d (RP2D = 105 mg/m2) Safety summary Acceptable safety profile in >1,000 patients - No clinical or regulatory holds imposed across all clinical studies to date Primary adverse events ≥ grade 3 were hematological (manageable neutropenia and thrombocytopenia) Limited ≥ grade 3 non-hematological toxicities (≤7% for all AEs) Drug-related discontinuations <1-2% *High grade serous ovarian cancer; ^Updated post-publication; # Overall response rate; °Duration of Response Indication Trial ORR# (confirmed) Median DoR° Reference HGSOC* (BRCA wild type, primarily platinum-resistant) Phase 2 single center (NCI) 29% >10 months^ Lee et al, Lancet Oncology, 2018 HGSOC (BRCA wild type and mutant; platinum-resistant and refractory) Phase 2 multi-center (Lilly) 12.1% (platinum-resistant) 5.6 months Konstantinopoulos et al; Gynec. Oncol.: 2022 Squamous cell cancer (anal cancer, head & neck cancer [H&N]) Phase 1b multi-center (Lilly) 19% HPV+ H&N 15% anal cancer 7 months (HPV+ H&N) 12 months anal cancer Hong et al, CCR, 2018

past phase 2 trials in high grade serous ovarian cancer Lee et al; Lancet Oncology: 2018 Past trials suggest unenriched all-comer ORR in HGS ovarian cancer is ~15-20% Durable clinical activity in most responders No predictive biomarkers identified, need for alternative biomarker approach (ideal for AP3) N = 169 PATIENTS COHORT DESCRIPTION PERCENT CONFIRMED ORR (95 % C.I.) Cohort 1 (53) Plat resistant BRCA wt; ≥3 lines of prior therapy 11.3 (4.3 to 23.0) Cohort 2 (46) Plat resistant BRCA wt; < 3 lines of prior therapy 13.0 (4.9 to 26.3) Cohort 3 (41) Plat resistant BRCA mt, any line of therapy (must include prior PARPi ) 12.2 (4.1 to 26.2) Cohort 4 (29) Plat refractory, any BRCA, any line of therapy 6.9 (0.8 to 22.8) Konstantinopoulos et al; Gynec. Oncol.: 2022 NCI single-center Phase 2 study (N=28) Heavily pre-treated patients; median 5 prior lines Pretreatment tumor biopsies mandated RESULTS ORR 29%; mDoR >10 months (post-publication) No genetic correlation with p53mut, DDRmut, or CCNE1 Lilly-sponsored multi-center (46 center, 8 country) Phase 2 study (N=169) All lines of prior therapy, BRCA wt and mt, incl. prior PARPi Pretreatment tumor biopsies mandated RESULTS ORR 12.1% (excl. unconfirmed); mDoR =5.6 months No correlation with genetic alterations

Development of AP3-based patient selection oncosignature tests Quantitative mapping >20,000 p-sites; 25% drug-related Drug-regulated phospho-sites and biological processes Literature and database mining P-proteomics Technical Validation (Intended use tissue) BM antibody validation by quantitative IF on human and PDX samples Prediction of drug sensitivity in cancer cell lines and PDX models Patient responder prediction on pre-treatment tumor biopsies Functional Validation (Intended use tissue) Initial biomarker candidates Target engagement, cell assays, imaging Dose response, knockdowns, drug combinations Cellular MOA Pathway visualization and reconstitution Final OncoSignature Assay Human cancer screening: ID of drug-sensitive cancers and proportions of responders

oncosignature tests: usage in the clinic 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 Predicted Responder Predicted Non-responder Sample processing Biopsy in FFPE block Automated tumor Region-of-Interest biomarker scoring

Consistent ACR-368 oncosignature performance across PRECLINICAL studies Prediction of treatment outcome in human PDX models ORR enrichment to ≥ 55%; AUC of 0.88 and 0.9 Two separate, prospectively designed, blinded studies of biopsies from past Phase 2 trials with ACR-368 in patients with platinum-resistant ovarian cancer ORR enrichment to 47% (NCI) and 58% (Lilly multi-center) Prediction of the fraction of human tumors sensitive to single agent ACR-368 Selection rate 30-40% across lead indications Identification of additional human tumor types predicted sensitive to single agent ACR-368 Endometrial and bladder cancer

ACR-368 OncoSignature prediction of drug sensitivity: Biomarker quantitation across human Cancer patient samples Predicted Responder Patient with drug target dependency Class 1 BM Class 2 BM Class 3 BM Patient High Predicted Non-Responder Patient with no drug target dependency efficiently excluded Class 1 BM Class 2 BM Class 3 BM Patient Low

Biopsy study 1: substantial response and PFS benefit in predicted responders (blinded, prospectively designed study) Available pretreatment tumor biopsies from past phase 2 trials at NCI with ACR-368 in platinum-resistant ovarian cancer were obtained OncoSignature scores were generated blinded to treatment outcome at Acrivon and analyzed by 3rd party biostatistician in prospectively designed study Result: ORR ~47%; mPFS = 7.9 months

Two additional high unmet need solid canceRS predicted ACR-368-sensitive through human tumor sample screening OncoSignature-positive = 30-50% OncoSignature-positive = 30-40% OncoSignature-positive = 0% (ORR in past trial: 0%) OncoSignature-positive = 30% (ORR in past trials: 12+% and 29%) HGS Ovarian Sq. NSCLC Bladder cancer Endometrial cancer

Two attractive ACR-368-sensitive cancer types identified Bladder cancer patient samples Endometrial patient samples Class 1 BM Class 2 BM Class 3 BM Predicted Non-Responders Predicted Responders Predicted Non-Responders Predicted Responders ACR-368 OncoSignature screening of human cancer samples Patient 1 LOW Patient 1 LOW Patient 2 HIGH Patient 2 HIGH

ACR-368-sensitive responders A subset of endometrial and bladder PDX models are highly sensitive to ACR-368 Endometrial PDX Bladder PDX BM1 BM2 BM3 PDX-L PDX-H Predicted Non-Responders Predicted Responders

G1/S CELL CYCLE Unsupervised Hierarchical Clustering T-test significant Proteins, FDR<0.05 Parental Resistant Upregulated in ACR-368 Resistant Cells Downregulated in ACR-368 Resistant Cells DNA DAMAGE REPAIR AP3 uncovers actionable ACR-368 resistance mechanisms unbiased and independent of genetic information Data suggest that gemcitabine might be a rational combination to overcome DDR suppression

low dose gemcitabine sensitizes ovarian cancer cell lines to ACR-368 Prexasertib Abs EC50 + 0 nM Gem: >10 uM + 0.53 nM Gem: 100 nM + 2.7 nM Gem: 6 nM Prexasertib Abs EC50 + 0 nM Gem: 15 nM + 0.53 nM Gem: 2.7 nM + 2.7 nM Gem: 0.2 nM Bliss Synergy score: <-10: Drug interaction is likely antagonistic -10 to 10: Drug interaction is likely additive >10: Drug interaction is likely synergistic Ovarian-Parental ACR-368 Log10 (M) Ovarian-Resistant ACR-368 Log10 (M)

Enrolling and dosing ACR-368 in three HIGH UNMET NEED indications: Ovarian, endometrial and Bladder Cancer OncoSignature+ Single Arm Simon 2 Stage Monotherapy Phase 2b with Registrational Intent Stage 1 (N= 23 per cohort) Stage 2 (N= 48 per cohort) Phase 1b (N= ~21) Phase 2 Expansion (N= 33 per cohort) Single Arm Phase 1b/2 Exploratory Combination with Low Dose Gemcitabine OncoSignature- RP2D of ACR-368 based on predicted sensitivity using our ACR-368 OncoSignature Assay run by our CDx partner 59 sites currently activated1 Key opinion leaders, some with extensive experience using ACR-368 from previous trials are actively participating 1https://clinicaltrials.gov/ct2/show/NCT05548296 FDA Fast Track Designation granted May 8, 2023 for ACR-368 monotherapy in OncoSignature-positive patients with Platinum-Resistant Ovarian Cancer and Endometrial Cancer FDA Breakthrough Device Designation granted November 16, 2023 for ACR-368 OncoSignature Assay for the identification of ovarian cancer patients who may benefit from treatment with ACR-368 Ovarian Endometrial Bladder

Encouraging Initial clinical observations Consistent with the extensive experience and tolerability profile from past trials, drug-related adverse events are primarily hematological, reversible, and manageable In the limited number of patients evaluated by imaging, preliminary evidence of clinical activity has been observed in OncoSignature-positive patients across all three tumor types treated with single agent ACR-368 at RP2D   Consistent with AP3-predicted tumor sensitivity, early imaging-based evidence of clinical activity across all three tumor types was also observed in OncoSignature-negative patients treated with ACR-368 at RP2D and LDG during the dose escalation phase  As disclosed in 10-Q filing November 9, 2023

Wee1 and PKMYT1 validated cancer targets: ideal for AP3 approach Ghelli Luserna di Rorà et al. J. Hematol Oncol, 2020 WEE1 and PKMYT1 regulate S and G2-M cell cycle checkpoints to ensure proper DNA replication and mitotic completion through phosphorylation and inhibition of CDK2 and CDK1 and CDK1, respectively WEE1 inhibition propagates genomic instability by premature DNA replication and cell cycle progression, resulting in mitotic catastrophe PKMYT1 inhibition results in premature mitotic entry and cell death Strong preclinical data and emerging clinical data: Adavosertib (AstraZeneca) Debio0123 (Debiopharm) Azenosertib (Zentalis Pharmaceuticals) SGR-3515 (preclinical, Schrödinger) Lunresertib (Repare Therapeutics) Single agent clinical activity (WEE1 and PKMYT1) Synergy identified with dual inhibition, potential for strong monotherapy clinical activity Correlation with genetic alterations challenging, CCNE1 association being explored by others Acrivon intends to leverage OncoSignature for optimal patient selection

Internal pipeline: advancing development candidate acr-2316 and other ddr programs - leveraging AP3 >40 high resolution co-crystals (1.5-3.1 Å) and AP3-driven SAR Novel WEE1- and PKMYT1-selective structural series and lead candidates Optimal selectivity profiles generated based on AP3 profiling ACR-2316 and other DDR programs High throughput AP3 profiling AP3 used for biologically relevant selectivity profiling Rationale Leveraging our AP3 patient selection platform for high clinical POS Potentially optimal profile for monotherapy clinical development ACR-2316 advancing in IND-enabling studies High resolution co-crystals with WEE1 and PKMYT1 Novel, potent dual inhibitor (single digit nM potency) Designed to overcome WEE1 and PKMYT1 single inhibitor resistance Potent, selective single agent activity

Executive summary: ACR-2316 development candidate Superior activity across human tumor cell lines and in mouse tumor models, vs clinical benchmark WEE1 and PKMYT1 inhibitors Favorable in vitro ADME, PK, and oral bioavailability with safety MTD/DRF studies consistent with predicted desirable human exposure Advancing rapidly in ongoing IND-enabling studies Discovered by AP3-based SAR facilitated by co-crystallography with WEE1 and PKMYT1 Unbiased detection of WEE1 inhibitor-induced resistance mechanisms, overcome by balanced PKMYT1 inhibition to achieve potent single agent activity ACR-2316 OncoSignature test being developed for indication finding and monotherapy clinical development AP3-Enabled Differentiation A selective dual WEE1/ PKMYT1 inhibitor optimized using AP3 for potent single agent activity On track for IND by Q4 2024 preparing for monotherapy clinical development Mechanism of Action Preclinical Data Single digit nM WEE1 inhibition with optimized ratio of PKMYT1 inhibition in cells Superior selectivity and potency compared to clinical benchmark WEE1 and PKMYT1 inhibitors Potent induction of CDK1/2 and PLK activity resulting in drastic induction of mitotic catastrophe

ACR-2316 ++++ ++ ++++ ++++ ++++ Adavosertib ++ - ++ +++ ++ Azenosertib ++ - +++ ++ ++ Debio0123 + - ++++ + + Lunresertib - +++ + + + WEE1 cellular drug target engagement PKMYT1 cellular drug target engagement In vivo efficacy Kinome selectivity Relative performance Human tumor cell viability Acr-2316 shows attractive profile in ongoing preclinical studies

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

ACR-2316 SHOWS SUPERIOR ACTIVITY VS BENCHMARKS across all human tumor cell lines tested Example: Ovarian human cancer cell lines 19 ovarian and other human tumor cell lines tested to date

ACR-2316 is highly potent across human tumor cell lines and patient-derived ex vivo tumor models Patient-derived ex vivo tumor models Human tumor cell lines ACR-2316 Azenosertib Lunresertib Adavosertib Debio 0123 CTG-0703 CTG-3383 CTG-2733 CTG-2884 CTG-1703 CTG-0956 CTG-1448 CTG-1498 CTG-3226 CTG-1692 CTG-1301 CTG-3522 CTG-2561 CTG-3718 Breast Lung Ovarian Prostate Renal Cell Line A Cell Line B Cell Line C Cell Line D Cell Line E Cell Line F Cell Line G Cell Line H Cell Line I Cell Line J Cell Line K Cell Line L Cell Line M Cell Line N Cell Line O Cell Line P Cell Line Q Cell Line R

Efficacy (5 ON / 2 OFF) Tolerability (5 ON / 2 OFF) ACR-2316 shows potent anti-tumor activity compared to clinical wee1 or pkmyt1 inhibitors

ACR-2316 shows deep regression in tumors progressing on a benchmark wee1 inhibitor Anti-tumor activity Tolerability

ACR-2316 emerging safety profile from preclinical animal studies appears promising Mice: ACR-2316 is well-tolerated at target doses up to ≤60 mg/kg daily oral dosing resulting in tumor regression in xenograft mouse models Reversible, mechanism-based hematological effects; moderate reticulopenia, monocytopenia, and lymphopenia based on initial studies Rat and dog MTD and preliminary DRF studies: Plasma PK exposure consistent with projected human exposure levels required for potential anti-tumor activity Reversible, mechanism-based hematological effects (white blood cells) Primary toxicities at MTD were decreased activity, food consumption, and soft stool

Streamlined AP3-based biological SAR OPTIMIZATION FOR SINGLE AGENT ACTIVITY OF PRECLINICAL PROGRAMS Peptide clean up Direct DIA analysis Drug treatment Proteolysis P-peptide enrichment Ultra high resolution P-proteomic profiling Week 0 Week2 Turnaround <2 weeks Quantitative mapping (>35,000 phospho-sites covering >4,500 proteins) Drug-regulated phospho-sites and biological process enrichment Drug-regulated pathway activity mapping and reconstitution P P Proprietary pipe for automated AP3 analyses with actionable results High resolution and throughput MS-based P-proteomics

AP3: TIGHT, HIGH-RESOLUTION DATA WITH DEEP COVERAGE Acrivon proprietary compound data (~30 million data points per experiment); dozens of compounds profiled Miniaturized, high throughput, scalable: <2 weeks turn-around, automated AI computational analyses in 1 day Actionable results: Resistance mechanisms, rational combinations, drug-tailored OncoSignature patient selection 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 35388 p-sites 15733 p-sites

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-derived dual potency optimization to overcome wee1 inhibitor resistance: Reciprocal quenching 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

Expediting ACR-2316 towards clinical monotherapy development A novel, AP3-enabled, internally discovered dual WEE1 / PKMYT1 inhibitor Rational Design Demonstrated preclinical superiority vs. benchmark WEE1 and PKMYT1 compounds Stronger preclinical anti-tumor activity vs. benchmark WEE1 and PKMYT1 compounds Superior Profile Optimized via AP3 structure-activity relationship (SAR) AP3-enabled design with optimized WEE1 / PKMYT1 properties AP3-based optimization of functional target profile Streamlined Development Aiming for expedited monotherapy development Rapidly advancing towards IND (expected Q4 2024) OncoSignature test in development for indication finding and patient selection Dose optimization to be guided by drug target engagement (BM2)

AP3 is broadly applicable across drug discovery and development 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 Intellectual Property De novo exclusivity & protection against generics

FINANCIAL HIGHLIGHTS Cash and marketable securities $142.1M Projected runway into H2’25 Fully Diluted Shares Outstanding 27.6M Current operating plan, assuming no additional financing Balance sheet 30-Sept-2023 Shares and equity grants outstanding 30-Sept-2023

Acrivon Addressable markets (US & EU incidence) Prioritized indications for single agent ACR-368 All cancers US and Europe Est. >6.3M cases/year Potential additional indications (N = 634,000) US cancer stats are based on ACS 2022 publication and subtype estimation from literature; EU cancer stats are based on IARC 2020 publication and subtype estimation from literature. ~45% Cancers with DDR stress are estimated to be 67% which is calculated from MSK-IMPACT patient samples with DDR relevant mutations and CNVs, such as TP53, KRAS, CCNE1, etc. Potential additional indications for single agent ACR-368 0 100000 200000 300000 400000 500000 0 100000 200000 300000 Bladder Cancer Endometrial Cancer HPV+ SCC Ovarian cancer Sarcoma Colorectal Cancer Pancreatic Cancer ~30% (N = 223,000) of prioritized indications predicted sensitive to single agent ACR-368 WEE1 and/or PKMYT1 inhibitor combinations with ACR-368 might further expand addressable fraction within sensitive tumor types Prioritized indications (N=742,000) 12% 10% Other cancers predicted to have DDR stress * * * *Currently enrolling and dosing

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Team has pioneered outcome-predictive quantitative proteomic multiplex in situ test ProMark®: Marketed, automated in situ proteomic test for human outcome prediction included under NCCN guidelines Founding team: Has pioneered p-proteomics and quantitative multiplex imaging including double-blinded clinical validation* *Blume-Jensen et al: Development and clinical validation of an in situ biopsy-based multimarker assay for risk stratification in prostate cancer. Clinical Cancer Research (2015) Prostate cancer 8-marker biopsy test developed and launched by Founding team Ideal test Protein multiplex in situ test Current CDx tests Quantitative and automated ✓ (✓) Validated Abs and reagents ✓ (✓) Drug target and pathway activation context ✓ Biomarkers measured in relevant region on tumor biopsy ✓ Imaging algorithm (tissue pattern) ✓ Addresses tumor heterogeneity ✓ Double-blinded, prospective validation ✓ (✓)

(2015) Third-party blinded clinical validation, bioinformatic analysis (U. Montreal) Validation of locked ProMark™ test on single institution biopsy cases (N=274) Secondary validation on multi-center biopsy cohort (N=359) for clinical use indication Marketed test included under NCCN Guidelines and Medicare coverage Proof-of-Concept for Protein Biomarker Signature: marketed, Outcome-Predictive multiplex Cancer Test

pioneering phospho-Proteomics study identifies novel pi3’k pathway inhibitor biomarkers Sci Transl Med 2: 1-14 (2010) TOWARD CUSTOMIZING TUMOR TREATMENT Just as our view of Earth has become increasingly global, cells are now seen as complex networks of interacting and intersecting signaling pathways rather than a collection of regulated genes. Editorial Highlights: A discovery strategy for novel cancer biomarkers

OLSEN LAB-EXAMPLES OF DEEP PROTEOMICS DRUG PROFILING ONGOING (MULTICENTER): Profiling of DDR and core kinase pathway inhibitors (>45) ALK-i : LDK378, TAE684, crizotinib, lorlatinib. SHP2-i: SHP099 -allosteric inhibitor. CHK1-i: SCH900776, ATM-i: KU55933 CDK7-i: THZ-1 JNK p38a DNAPK ATM CHK1 ATR Science Signaling (2018) Cell Reports (2018) Cell Reports (2017) Cell Reports (2017) Cell Systems (2017) Deepest proteome resolution of a human cell to date Cell (2019) Functional mapping of differential signaling by RPTK mutants Nature Communications (2020) Highest throughput, sensitivity, and scalability to date Subcellular compartmental proteomics Nature Communications (2021) Clinically actionable resistance mechanisms Nature Communications (2021)

advisorS anD collaborators GU Pathologist; bladder cancer expert Expert on protein biomarkers and quantitative tissue imaging Academic lead on ProMark® David Berman, M.D., Ph.D. Professor, Director, Queen’s Cancer Res. Inst., Ontario Canada George Demetri, M.D., FACP, FASCO, FAACR Professor, Harvard Med. School, Dir. Dana-Farber Cancer Institute & Ludwig Center, Boston Leader in Precision Oncology Key contributor to development and rapid approvals of Gleevec, Sutent, Stivarga, Zelboraf, Votrient, and Yondelis Jung-Min Lee, M.D. NCI Collaborator Investigator, Lasker Clinical Research Scholar, NCI Expert on women’s cancers and DNA damage response (DDR) Lead and co-PI on numerous HGSOC &TNBC trials Lead PI on ACR-368 platinum-resistant ovarian trials Robert Abraham, Ph.D. EVP, Head Cancer Biology, Odyssey Therapeutics Adj. Prof. , Burnham Inst. Adj. Prof. UCSD Expert in signal transduction-based R&D Previously SVP and WW Head, Oncology R&D, Pfizer VP, Oncology Res., Wyeth Professor, Burnham Institute Professor, Duke University Timothy Yap, M.B.B.S., Ph.D., F.R.C.P. Associate Prof., MD Anderson Cancer Center, Medical Director, Inst. for Applied Cancer Science Expert on DDR accelerated clinical development and predictive biomarkers Previously oncologist Royal Marsden, London and Inst. Cancer Res, London Lead/P.I. on numerous DDR trials SAB Recognized pioneer and leading authority in phosphoproteomics and proteomic systems analyses Top 0.1% most cited scientist in protein sciences Jesper V. Olsen, Ph.D. Academic Co-Founder Professor, Novo-Nordisk Foundation Protein Center, Cph. University

AP3 is APPLICABLE across drug development stages Target ID Hit ID Lead Opt IND Enabling Early Clinical Late Clinical Approval & Commercialization Indication Finding: OncoSignature patient sample screening AP3 drug profiling: Unbiased drug target engagement & PD biomarkers OncoSignature patient responder identification Rational Combinations Resistance Mechanisms ID druggable driver targets AP3 is also applicable in preclinical phase

ACR-2316 meets pre-specified development candidate criteria Target ACR-2316 MOA AP3 phosphoproteomics-based, optimized MOA; selective, dual WEE1/PKMYT1 inhibition ü Potency In vitro kinase activity, IC50 ≤ 10 nM Potent in cell target engagement in optimized ratio Activity across sensitive human tumor cell lines, IC50 <20 nM ü ü ü Selectivity Kinase panel profiling – highly selective (kinome selectivity) AP3 profiling confirms desirable CDK and PLK activation for mitotic catastrophe/apoptosis ü ü ADME/PK Orally bioavailable T½ suitable for once/day dosing ü ü In vitro safety Low in vitro hERG (>10 µM) and CYP inhibition and induction (>1 µM) ü Solubility > 50 µM for active compounds  ü PPB < 90% ü In vivo efficacy Demonstrated potent target engagement intratumorally in vivo Potent single agent activity in CDX models ü ü

Key data: ACR-2316 versus benchmarks Assay ACR-2316 Adavosertib Azenosertib Debio123 Lunresertib Biochemical Wee1 Binding IC50  1 nM 1 nM 2 nM 1 nM 31 nM PKMYT1 Binding IC50  27 nM 155 nM 337 nM 2 µM 10 nM Cellular Target Engagement WEE1 EC50 (Y15) 2 nM 19 nM 16 nM 109 nM >10 µM PKMYT1 EC50 (T14 AlphaLISA) 145 nM 4 µM 2 µM >10 µM 11 nM In Vitro Cancer Cell Viability Human cancer cell viability IC50  11 nM (cell line 1) 17 nM (cell line 2) 21 nM (cell line 3) 52 nM (cell line 1) 127 nM (cell line 2) 96 nM (cell line 3) 48 nM (cell line 1) 111 nM (cell line 2) 128 nM (cell line 3) 165 nM (cell line 1) 338 nM (cell line 2) 94 nM (cell line 3) 372 nM (cell line 1) 400 nM (cell line 2) 173 nM (cell line 3) Human PDX (CTG-3226) viability IC50  0.011 µM N/A 0.209 µM N/A 3.69 µM Selectivity Kinome selectivity: S(35) / S(10) 0.091 / 0.071 0.172 / 0.101 0.101 / 0.071 0.062 / 0.03 0.121 / 0.101 In Vivo Efficacy CDX model 1 efficacy [T/C (%) / dose mg/kg (frequency)] 0.6 % /  45 mg/kg (QD) 23 % / 60 mg/kg (QD) 26.8 % / 100 mg/kg (QD) 66.4 % / 30 mg/kg (QD) 33 % / 20 mg/kg (BID) CDX model 2 efficacy [T/C (%) / dose mg/kg (frequency)] 1.7 % / 60 mg/kg (QD) N/A 41 % / 100 mg/kg (QD) 87 % / 30 mg/kg (QD) 36 % /  20 mg/kg (BID) Ovarian PDX model Efficacy [T/C (%) / dose mg/kg (frequency)] 20 % / 45 mg/kg (QD) N/A 116 % / 60 mg/kg (QD) N/A 122 % / 18 mg/kg (BID)

AP3 analysis: ACR-2316 regulates cell cycle and mitosis more potently than benchmark wee1 inhibitor Resistant WEE1 inhibitor ACR-2316 Sensitive 60min 200nM Induced Suppressed Enrichment Score (NES) Significant Not significant p value Cell cycle RTK-MAPK HDR Mitotic pathways SREBP GTPases Mitotic pathways Cell cycle Tight junction Autophagy Post-synaptic transmission

AP3 analysis: ACR-2316 regulates cell cycle and mitosis more potently than benchmark pkmyt1 inhibitor Induced Suppressed Enrichment Score (NES) Significant Not significant p value Cell cycle RTK-MAPK HDR Mitotic pathways SREBP GTPases Tight junction Autophagy Post-synaptic transmission

Comprehensive kinome selectivity profiling ACR-2316 468 kinases @ 1mM Adavosertib Azenosertib Lunresertib Debio0123 WEE1 PKMYT1 WEE1 WEE1 WEE1 PKMYT1 KinomeScan

Cell Reports, August 9, 2022 Using spatial phosphoproteomics (Nat. Commun., 2021) Acrivon’s AP3 platform can uncover single agent sensitivity and rational drug combinations for targets with complicated mechanism of action AP3 reveals single agent sensitivity context and rational drug combinations independent of genetic information

Eli Lilly ACR-368 high level license terms In-licensing completed 27 January 2021 WW exclusive rights with rights to sub-license $5M up front and low single digit percentage equity subject to ordinary dilution going forward Aggregate development and commercial milestone payments of up to $168M, of which $5M is due prior to NDA Tiered percentage royalty on annual net sales ranging from low single-digit up to a maximum of 10% subject to certain specified reductions Drug product as well as drug substance sufficient to treat several hundred patients Limited right of first negotiation expiring 45 days upon completion of certain clinical milestones