Exhibit 99.1

Acrivon Therapeutics Reports Third Quarter 2023 Financial Results and Business Highlights

WATERTOWN, Massachusetts, November 9, 2023 – Acrivon Therapeutics, Inc. (“Acrivon” or “Acrivon Therapeutics”) (Nasdaq: ACRV), a clinical stage biopharmaceutical company developing precision oncology medicines that it matches to patients whose tumors are predicted to be sensitive to each specific medicine by utilizing its proprietary proteomics-based patient responder identification platform, today reported financial results for the third quarter ended September 30, 2023 and provided business highlights.

“Acrivon remains committed to being science and data-driven as we continue advancing our clinical and preclinical pipeline of precision oncology medicines, enabled by our highly differentiated Acrivon Predictive Precision Proteomics (AP3) platform,” said Peter Blume-Jensen, M.D., Ph.D., chief executive officer, president, and founder of Acrivon. “Our recent presentations at the AACR-NCI-EORTC International Conference on Molecular Targets and Cancer Therapeutics further demonstrate the unique and broad capabilities of AP3 and our drug-specific OncoSignature assays. As part of our third quarter highlights, we are also pleased to provide initial clinical readouts for ACR-368 and plan to present more mature data at a major medical conference during the first half of 2024. We are also very excited about the advancement of our novel, internally-discovered development candidate ACR-2316, a dual WEE1/PKMYT1 inhibitor specifically designed by AP3 for superior, single agent activity, as demonstrated in preclinical studies compared to benchmark clinical compounds. We plan to submit an IND for ACR-2316 in the fourth quarter of 2024.”

Recent Highlights

Anticipated Upcoming Milestones

Third Quarter 2023 Financial Results

Net loss for the quarter ended September 30, 2023 was $14.5 million compared to a net loss of $9.2 million for the same period in 2022.

Research and development expenses were $10.3 million for the quarter ended September 30, 2023 compared to $7.9 million for the same period in 2022. The difference was primarily due to the continued development of ACR-368, inclusive of progression of the ongoing clinical trial, as well as increased personnel costs to support these development activities and costs associated with our preclinical programs, including ACR-2316.

General and administrative expenses were $5.9 million for the quarter ended September 30, 2023 compared to $1.6 million for the same period in 2022. The difference was primarily due to the increased cost of operating as a public company, inclusive of increased personnel costs and non-cash stock compensation expense.

As of September 30, 2023, the company had cash, cash equivalents and marketable securities of $142.1 million, which is expected to fund operations into the second half of 2025.

About Acrivon Therapeutics

Acrivon is a clinical stage biopharmaceutical company developing precision oncology medicines that it matches to patients whose tumors are predicted to be sensitive to each specific medicine by utilizing Acrivon’s proprietary proteomics-based patient responder identification platform, Acrivon Predictive Precision Proteomics, or AP3. The AP3 platform is engineered to measure compound-specific effects on the entire tumor cell protein signaling network and drug-induced resistance mechanisms in an unbiased manner. These distinctive capabilities enable AP3’s direct application for drug design optimization for monotherapy activity, the identification of rational drug combinations, and the creation of drug-specific proprietary OncoSignature companion diagnostics that are used to identify the patients most likely to benefit from Acrivon’s drug candidates. Acrivon is currently advancing its lead candidate, ACR-368, a selective small molecule inhibitor targeting CHK1 and CHK2 in a potentially registrational Phase 2 trial across multiple tumor types. The company has received Fast Track designation from the Food and Drug Administration, or FDA, for the investigation of ACR-368 as monotherapy based on OncoSignature-predicted sensitivity in patients with platinum-resistant ovarian or endometrial cancer. Acrivon’s ACR-368 OncoSignature test, which has not yet obtained regulatory approval, has been extensively evaluated in preclinical studies, including in two separate, blinded, prospectively-designed studies on pretreatment tumor biopsies collected from past third-party Phase 2 trials in patients with ovarian cancer treated with ACR-368. In addition to ACR-368, Acrivon is also leveraging its proprietary AP3 precision medicine platform for developing its internally-discovered preclinical stage pipeline programs, consisting of its development candidate, ACR-2316, a selective, dual WEE1/PKMYT1 inhibitor, and additional programs targeting these two critical nodes in the DNA Damage Response, or DDR, pathways.

Forward-Looking Statements

This press release includes certain disclosures that contain “forward-looking statements” within the meaning of the Private Securities Litigation Reform Act of 1995 about us and our industry that involve substantial risks and uncertainties. All statements other than statements of historical facts contained in this press release, including statements regarding our future results of operations or financial condition, business strategy and plans and objectives of management for future operations, are forward-looking statements. 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. Forward-looking statements are based on Acrivon’s current expectations and are subject to inherent uncertainties, risks and assumptions that are difficult to predict. Factors that could cause actual results to differ include, but are not limited to, risks and uncertainties that are described more fully in the section titled “Risk Factors” in our reports filed with the Securities and Exchange Commission. Forward-looking statements contained in this press release are made as of this date, and Acrivon undertakes no duty to update such information except as required under applicable law.

Investor and Media Contacts:

Adam D. Levy, Ph.D., M.B.A

alevy@acrivon.com

Alexandra Santos

asantos@wheelhouselsa.com

Acrivon Therapeutics, Inc.

Condensed Consolidated Statements of Operations and Comprehensive Loss

(unaudited, in thousands, except share and per share data)

Acrivon Therapeutics, Inc.

Condensed Consolidated Balance Sheets

(unaudited, in thousands)

Exhibit 99.2

Acrivon T h e r a p e u t i c s ACRIVON PREDICTIVE PRECISION PROTEOMICS (AP3) OV E R C O M I N G L I M I TAT I O N S O F G E N E T I C S—B A S E D P R E C I S I O N M E D I C I N E C O R P O R AT E P R E S E N TAT I O N N OV E M B E R 2 0 2 3

F O R W A R D—L O O K I N G S T A T E M E N T S Certain meaning of information the Privatecontained Securities in Litigation this presentation Reform Act includes of 1995 regarding forward-looking our future statements results of within operations the or some financial cases,condition, you can identify business forward-looking strategy and plans statements and objectives because of they management contain words for future such as operations. “anticipate,” In “believe,” “predict,” “project,” “contemplate,” “should,” “continue,” “target,”“could,” “will,” or “estimate,” “would” or “expect,” the negative “intend,” of these “may,” words “plan,” or other “potential,” similar terms and projections or expressions. about future Our forward-looking events and trends statements that we believe are based mayprimarily affect our on business, our current financial expectations condition subject and results to risks of operations. and uncertainties, The outcome includingof the the factors events described described in in our the filings forward-looking with the U.S. Securities statements and is Exchange us to predict Commission. all risks and New uncertainties risks and uncertainties that could emerge have anfrom impact time onto the time, forward-looking and it is not possible statements for contained statementsinmay this not presentation. be achieved Theor results, occur,events, and actual and circumstances results, events, reflected or circumstances in the forward-looking could differ materially from those described in the forward-looking statements. as You ofare thecautioned date of this not presentation. to place undue Wereliance undertake on no these obligation forward-looking to updatestatements, any forward-looking which arestatements made only or to reflect new information or the occurrence of unanticipated events, except as required by law. 2 A C R I V O N T H E R A P E U T I C S

A C R I V O N : N E X T G E N E R A T I O N P R E C I S I O N O N C O L O G Y O V E R C O M I N G L I M I T A T I O N S O F G E N E T I C S—B A S E D P R E C I S I O N M E D I C I N E Clinically Actionable ACR-368 (Phase 2) Resistance Mechanisms CHK 1/2 inhibitor in Rational drug combinations registrational intent trials in multiple solid tumor types OncoSignature ACR-2316 (IND-enabling) Proprietary, drug-tailored Dual WEE1/PKMYT1 inhibitor patient responder with superior selectivity and identification tests single agent activity Drug Discovery Preclinical Drug Discovery AP3 based SAR Additional AP3-enabled, facilitated by co- co-crystallography-driven crystallography precision oncology programs Experienced team focused on execution with cash runway into 2H 2025 3 A C R I V O N T H E R A P E U T I C S

A C C O M P L I S H E D L E A D E R S H I P T E A M Peter Blume-Jensen, M.D., Ph.D. Rasmus Holm-Jorgensen Kristina Masson, Ph.D., M.B.A Erick Gamelin, M.D., Ph.D. Eric Devroe, Ph.D. Mary-Alice Miller, J.D. CEO, President, Founder Chief Financial Officer Site Head Acrivon AB, Co-Founder Chief Medical Officer Chief Operating Officer Chief Legal Officer EVP Business Operations • Executive Serono, Merck & • Novo Nordisk Finance and • Cross-functional Leadership • Professor, CEO, large • Founder and CEO, Opsonix • Over 20 years corporate Co., Daiichi Sankyo IR Merrimack Pharmaceuticals, national cancer center and • Business executive MD legal experience • CSO Metamark—Marketed • Synageva pipeline expansion MIT/BROAD hospital Anderson Cancer Center • Served as general counsel prostate proteomic test and $9bn sale to Alexion • Founder and CEO, • Executive Amgen, Pfizer, and Metamark of 2 companies taken ProMark® • Kiniksa founding team, IPO OncoSignature AB (acquired Dynavax, MacroGenics; • EIR Wyss Institute, Harvard public • Inventor Acrivon Predictive and commercial launch by Acrivon Therapeutics) CMO STEP Pharma • Associate, Flagship • Boston Business Journal Precision Proteomics (AP3) • >100 ph 1-3 oncology trials Pioneering “40 Under 40” Adam Levy, Ph.D., M.B.A. Monica Phadnis John van Duzer, Ph.D. Joon Jung, Ph.D. Parvin Miah David Proia, Ph.D. SVP, Investor Relations SVP, Clinical SVP, CMC VP, Head, Data VP, Head, Human VP, Drug Discovery and and Corporate Affairs Operations Science Resources Biology Praveen Marapaka, Ph.D. Karl Hsu, M.D. Bruce Close, M.S. Rajshree Kandadai, M.A. Katie Peterson, C.P.A. Michail Shipitsin, Ph.D. SVP, Global Regulatory SVP, Clinical Development VP, Quality and VP, Business Development VP, Finance and VP, Biomarker Affairs Compliance Accounting Development 4 A C R I V O N T H E R A P E U T I C S

A C R I V O N T H E R A P E U T I C S A T A G L A N C E Development Site (Boston) Precision-Proteomics Site (Lund/Copenhagen) • Drug and clinical biomarker assay development • Early pipeline drug programs • Clinical trials • BM identification and drug profiling • Market access pending approval • Mass spectrometry Peter Blume-Jensen Kristina Masson Jesper V. Olsen CEO, President, EVP, Bus Ops, Academic Co-Founder. Co-Founder Site Head and Novo-Nordisk Foundation Co-Founder Protein Center, Cph. Founded 2018, IPO November 2022 (NASDAQ: ACRV) For more information, please visit https://acrivon.com

A C R I V O N P R E D I C T I V E P R E C I S I O N P R O T E O M I C S , A P 3 DNA Genomic Biomarkers are useful for patient selection in the smaller subset of cancers (<10%) with single gene driver mutations or known synthetic lethal context* RNA Protein P Dysregulated CANCER IS CAUSED BY DYSREGULATED PROTEIN ACTIVITY Protein P Drug 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 Dysregulated Pathways (Acrivon meaning: “Exact, Accurate”) CANCER *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) 6 A C R I V O N T H E R A P E U T I C S

A P 3 P L A T F O R M A D D R E S S E S H I G H U N M E T N E E D B E Y O N D N G S—B A S E D P R E C I S I O N M E D I C I N E Current Precision Oncology Approaches Only Scratching the Surface Acrivon Positioned to Increase Precision Oncology Market Size 72 unique approvals 51 drugs Precision Oncology 1.0 31 genomic indications Approved indications: Approved indications: 18 cancer types HER2+ Breast Cancer CML (BCR-ABL) st Only 5% of patients respond HER2+ Gastric Cancer Ph+ ALL 1 Gen Precision Oncology Currently Unaddressed Precision Oncology 2.0 Solid Tumors (NTRK)) IDH mutation in AML NSCLC (NTRK) and NSCLC (KRAS G12C) CRC (ROS1, ALK) 95% of patients are currently unaddressed by Bladder (FGFR3) Class II and III BRAF Solid Tumors (NRG1) traditional genetics-based precision oncology kinase alterations: N/A Predictive Precision Proteomics Aiming to make targeted therapeutic solutions available to broader group of cancer patients Sources: Company Filings, ACS, CDC, NCI, Wall Street Research (2022) 7 A C R I V O N T H E R A P E U T I C S

AP3 PLATFORM: DRUG RESPONSE PREDICTION IN INDIVIDUAL PATIENTS Predicted Predicted Non-responder Responder CLASS 1 BM CLASS 2 BM AI-DRIVEN CLASS 3 BM Patients without biomarkers critical for drug sensitivity efficiently excluded “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 \ 8 A C R I V O N T H E R A P E U T I C S

A C R I V O N P I P E L I N E Anticipated Preclinical Phase 1 Phase 2 Phase 3 Next Milestone Single-Arm Trials Based on OncoSignature Prediction Platinum-Resistant ACR-368 Monotherapy Fast-Track Designation Ovarian Cancer LDG Combination ACR-368 Monotherapy Fast-Track Designation Clinical Data at Major ACR-368 Endometrial Cancer Medical Conference (CHK1/CHK2) LDG Combination 1H 2024 ACR-368 Monotherapy Bladder Cancer LDG Combination Option to Initiate Additional Trials in HPV+ SCC (H&N, Anal, Cervical) and sarcomas OncoSignature- ACR-2316 IND-Enabling Predicted Monotherapy IND Filing in Q4 2024 (WEE1/ PKMYT1) Sensitive Tumors Studies AP3-driven co-crystallography Additional Development programs Candidates Notes ACR-368 Monotherapy Registrational intent Phase 2 single arm trials based on predicted sensitivity to ACR-368 monotherapy in OncoSignature-positive patients LDG Combination Exploratory Phase 1b/2 single arm trials of ACR-368 in combination with low dose gemcitabine, or LDG, in OncoSignature-negative patients 9 A C R I V O N T H E R A P E U T I C S

A C R—3 6 8 : A C L I N I C A L L Y A C T I V E P H A S E 2 C H K 1 / 2 I N H I B I T O R • 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 M G1 Defective G1/S G1/S-defective cancers Cancer rely on CHK1-regulated G2/M Checkpoint Checkpoint Cell Cycle cell cycle checkpoints CHK1 S Phase CHK1 pauses cell cycle to G2 S Checkpoint enable DNA repair CHK1 • 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 10 A C R I V O N T H E R A P E U T I C S

C L I N I C A L O V E R V I E W O F A C R—3 6 8 M O N O T H E R A P Y ( P A S T D A T A ) Indication Trial ORR# (confirmed) Median DoR° Reference HGSOC* (BRCA wild type, primarily Phase 2 single center 29% >10 months^ Lee et al, Lancet platinum-resistant) (NCI) Oncology, 2018 HGSOC (BRCA wild type and mutant; Phase 2 multi-center 12.1% (platinum-resistant) 5.6 months Konstantinopoulos platinum-resistant and refractory) (Lilly) et al; Gynec. Oncol.: 2022 Squamous cell cancer (anal cancer, Phase 1b multi-center 19% HPV+ H&N 7 months (HPV+ H&N) Hong et al, CCR, head & neck cancer [H&N]) (Lilly) 15% anal cancer 12 months anal cancer 2018 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 11 A C R I V O N T H E R A P E U T I C S

P A S T P H A S E 2 T R I A L S I N H I G H G R A D E S E R O U S O V A R I A N C A N C E R NCI single-center Phase 2 study (N=28) Lilly-sponsored multi-center (46 center, 8 country) Phase 2 study (N=169) • Heavily pre-treated patients; median 5 prior lines • All lines of prior therapy, BRCA wt and mt, incl. prior PARPi • Pretreatment tumor biopsies mandated • Pretreatment tumor biopsies mandated RESULTS RESULTS • ORR 29%; mDoR >10 months (post-publication) • ORR 12.1% (excl. unconfirmed); mDoR =5.6 months • No genetic correlation with p53mut, DDRmut, or CCNE1 • No correlation with genetic alterations 100 N = 169 PATIENTS COHORT DESCRIPTION PERCENT CONFIRMED ORR Best response (95 % C.I.) 50 (N = 24 evaluable patients) Cohort 1 (53) Plat resistant BRCA wt; ≥3 lines of 11.3 (4.3 to 23.0) ) (% prior therapy se n 0 Cohort 2 (46) Plat resistant BRCA wt; < 3 lines of 13.0 (4.9 to 26.3) po prior therapy e s r (50) Cohort 3 (41) Plat resistant BRCA mt, any line of 12.2 (4.1 to 26.2) Best therapy (must include prior PARPi ) (100) Cohort 4 (29) Plat refractory, any BRCA, any line of 6.9 (0.8 to 22.8) Platinum-sensitive Platinum-resistant Platinum-refractory Still on study therapy Study ID 10 14 36 48 7 42 5 46 6 24 35 38 33 Lee 23 et 47 al; 28 Lancet 17 41 Oncology: 4 31 1 37 2018 40 29 Konstantinopoulos et al; Gynec. Oncol.: 2022 Number of previous lines of therapy 2 5 5 2 5 1 2 3 5 5 6 3 5 6 3 4 4 5 2 13 1 6 5 4 PFS (months) 2.0 2.0 2.0 2.0 2.0 9.5 2.0 2.0 8.0 4.0 8.5 3.0 16.0 4.0 7.5 10.0 13.0 3.5 9.0 7.5 9.0 13.5 12.5 16.5 Mutations in DDR genes CCNE1 gene amplification ✓ Past trials suggest unenriched all-comer ORR in HGS ovarian cancer is ~15-20% CCNE1 mRNA upregulation ✓ Durable clinical activity in most responders CCNE1 protein overexpression* ✓ No predictive biomarkers identified, need for alternative biomarker approach (ideal for AP3) Positive Negative Amplification Copy number gain Upregulation 12 A C R I V O N T H E R A P E U T I C S

DEVELOPMENT OF AP3-BASED PATIENT SELECTION ONCOSIGNATURE TESTS Technical Validation Functional Validation P-proteomics Cellular MOA respons Human cancer screening: owns, ID of drug-sensitive inations cancers and proportions of responders inal DMSO 4NQO 4NQO+Prex ignat OVCAR3 ssay A2780 Pathway visualization Target engagement, s, imag A

ONCOSIGNATURE TESTS: USAGE IN THE CLINIC Pretreatment Treatment decision tumor biopsy based on patient stratification Predicted Predicted Sample processing Responder Non-responder Biopsy in Automated tumor FFPE Region-of-Interest block biomarker scoring Pretreatment tumor biopsy test • • Compatible with 5 business days turn-around • Offered by CDx partner under exclusive license from Acrivon 14 A C R I V O N T H E R A P E U T I C S

C O N S I S T E N T A C R—3 6 8 O N C O S I G N A T U R E P E R F O R M A N C E A C R O S S P R E C L I N I C A L S T U D I E S Tissue ID. BM1 BM2 BM3 Fov060265 0.69 0.79 0.73 Fov050855 0.94 0.71 0.67 Fov041300 0.89 0.23 0.55 Fov060380 0.95 0.62 0.51 Fov060050 0.85 0.23 0.51 Fov041285 0.69 0.19 0.5 Fov100142 0.47 0.76 0.47 Fov050764 0.82 0.22 0.47 Fov041267 0.4 0.36 0.36 Fov100146 0.84 0.57 0.26 Fov060382 0.44 0.45 0.22 Fov041269 0.37 0.21 0.2 Fov060302 0.29 0.22 0.15 Fov020067 0.89 0.38 0.09 Fov100003 0.9 0.89 0.08 Fov050700 0.17 0.17 0.07 • Prediction of the fraction of human tumors sensitive to Fov050139 0.63 0.66 0.05 Fov041138 0.36 0.11 0.05 Fov060152 0.24 0.3 0.03 Fov030062 0.57 0.14 0.02 Fov060133 0.94 0.43 0.01 Fov050666 0.93 0.38 0.01 Fov060371 0.88 0.93 0 Fov020497 0.61 0.43 0 Fov010706 0.54 0.14 0 single agent ACR-368 Fov020386 0.11 0.09 0.12 Fov050734 0.11 0.06 0.08 Fov040872 0.23 0.04 0.36 Fov050659 0.29 0.01 0.02 Fov060293 0.42 0 0 Fov060210 0.1 0.1 0 Fov050840 0.07 0.29 0.01 Fov040855 0.05 0 0.22 o Selection rate 30-40% across lead indications Fov050816 0.04 0.33 0.12 Fov060355 0.04 0.27 0 Fov010252 0.03 0.17 0.02 Fov010682 0.03 0.03 0 Fov060553 0.03 0.02 0.03 71768C3 0.02 0 0 Fov150230 0 0.36 0.12 Fov060308 0 0 0 • Identification of additional human tumor types predicted sensitive to single agent ACR-368 o Endometrial and bladder cancer • Prediction of treatment outcome in human PDX models o 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 o ORR enrichment to 47% (NCI) and 58% (Lilly multi-center) 15 A C R I V O N T H E R A P E U T I C S

A C R—3 6 8 O N C O S I G N A T U R E P R E D I C T I O N O F D R U G S E N S I T I V I T Y : B I O M A R K E R Q U A N T I T A T I O N A C R O S S H U M A N C A N C E R P A T I E N T S A M P L E S Class 1 BM Class 2 BM Class 3 BM Tissue ID. BM1 BM2 BM3 Fov060265 0.69 0.79 0.73 Fov050855 0.94 0.71 0.67 Fov041300 0.89 0.23 0.55 Fov060380 0.95 0.62 0.51 Patient Fov060050 0.85 0.23 0.51 Fov041285 0.69 0.19 0.5 High Fov100142 0.47 0.76 0.47 Fov050764 0.82 0.22 0.47 Fov041267 0.4 0.36 0.36 Fov100146 0.84 0.57 0.26 Fov060382 0.44 0.45 0.22 Fov041269 0.37 0.21 0.2 Fov060302 0.29 0.22 0.15 Predicted Responder Fov020067 0.89 0.38 0.09 Patient with drug target dependency Fov100003 0.9 0.89 0.08 Fov050700 0.17 0.17 0.07 Fov050139 0.63 0.66 0.05 Fov041138 0.36 0.11 0.05 Fov060152 0.24 0.3 0.03 Fov030062 0.57 0.14 0.02 Fov060133 0.94 0.43 0.01 Fov050666 0.93 0.38 0.01 Fov060371 0.88 0.93 0 Fov020497 0.61 0.43 0 Class 1 BM Class 2 BM Class 3 BM Fov010706 0.54 0.14 0 Fov020386 0.11 0.09 0.12 Fov050734 0.11 0.06 0.08 Fov040872 0.23 0.04 0.36 Fov050659 0.29 0.01 0.02 Fov060293 0.42 0 0 Patient Fov060210 0.1 0.1 0 Fov050840 0.07 0.29 0.01 Low Fov040855 0.05 0 0.22 Fov050816 0.04 0.33 0.12 Fov060355 0.04 0.27 0 Fov010252 0.03 0.17 0.02 Fov010682 0.03 0.03 0 Fov060553 0.03 0.02 0.03 Predicted Non-Responder 71768C3 0.02 0 0 Fov150230 0 0.36 0.12 Patient with no drug target dependency efficiently excluded Fov060308 0 0 0 16 A C R I V O N T H E R A P E U T I C S

B I O P S Y S T U D Y 1 : S U B S T A N T I A L R E S P O N S E A N D P F S B E N E F I T I N P R E D I C T E D R E S P O N D E R S ( B L I N D E D , P R O S P E C T I V E L Y D E S I G N E D S T U D Y ) • 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 OncoSignature Prediction: OncoSignature Prediction: PR Non-Responders Responders SD 1.2 PR SD PR 0.9 PR SD SD mPFS PR Predicted Responders e 0.6 g PR mPFS = 7.9 months (days) chan SD All Predicted R 238.0 0.3 SD All Predicted NR 66.5 SD SD in predicted R 238.0 PR PD SD in predicted NR 108.0 fractional 0.0 mPFS in R r SD (0.3) SD Tumo SD SD Predicted Non-Responders PD mPFS = 2.2 months (0.6) PD ORR = 0% ORR = 47% PD (0.9) PD mPFS in NR PD SD PD PD PD SD SD SD PD SD SD SD SD SD SD SD PR PR PR PR PR PR PR 0 100 200 300 400 500 600 700 Duration (days) Result: ORR ~47%; mPFS = 7.9 months 17 A C R I V O N T H E R A P E U T I C S

T W O A D D I T I O N A L H I G H U N M E T N E E D S O L I D C A N C E R S P R E D I C T E D A C R—3 6 8—S E N S I T I V E T H R O U G H H U M A N T U M O R S A M P L E S C R E E N I N G HGS Ovarian Sq. NSCLC Bladder cancer Endometrial cancer Tissue ID BM1 BM2 BM3 Tissue ID BM1 BM2 BM3 Tissue ID BM1 BM2 BM3 Tissue ID BM1 BM2 BM3 Fov010719 0.96 0.68 0.78 Rln020132 0.17 0.26 0.02 Fur021904 0.16 0.38 0.86 Ubd040512 0.99 0.48 0.65 Fov060075 0.54 0.51 0.38 Rln010099 0.08 0.06 0.01 Fur021989 0.86 0.17 0.71 Fov020069 0.31 0.30 0.38 Ubd040016 0.30 0.58 0.63 Fov010809 0.94 0.16 0.36 Rln020029 0.48 0.28 0.00 Fur021785 0.14 0.55 0.69 Fov030970 0.93 0.28 0.33 Fov010892 0.95 0.72 0.32 Rln020005 0.34 0.06 0.00 Ubd040039 0.43 0.33 0.54 Fur021984 0.87 0.62 0.63 Fov040102 0.98 0.23 0.29 Rln010095 0.28 0.02 0.00 Ubd030040 0.88 0.73 0.45 Fur021937 0.81 0.65 0.61 Fov050734 0.95 0.22 0.25 Rln020051 0.11 0.01 0.14 Fur022037 0.12 0.22 0.54 Fov040164 0.94 0.69 0.21 Rln010167 0.14 0.00 0.00 Ubd040287 0.63 0.34 0.40 Fur130035 0.55 0.48 0.50 Fov020776 0.60 0.18 0.19 Fov050764 0.77 0.35 0.17 Rln020284 0.09 0.00 0.00 Fur030113 0.90 0.65 0.31 Ubd040151 0.65 0.72 0.34 Fov060380 0.98 0.58 0.17 Fov010172 0.85 0.51 0.17 Rln020141 0.05 0.18 0.00 Fur020288 0.60 0.26 0.30 Rln020032 0.05 0.01 0.00 Ubd040225 0.76 0.64 0.33 Fov100051 0.92 0.21 0.16 Fur020281 0.21 0.57 0.27 Fov100142 0.58 0.82 0.14 Rln010199 0.05 0.06 0.03 Fov020160 0.58 0.30 0.14 Ubd040282 0.27 0.16 0.26 Fur130010 0.79 0.75 0.27 Rln020197 0.04 0.00 0.00 Fur021781 0.75 0.31 0.26 Fov010252 0.96 0.21 0.14 Ubd060279 0.29 0.13 0.16 Fov050617 0.61 0.76 0.14 Rln020250 0.04 0.00 0.00 Fur140135 0.72 0.35 0.25 Fov060302 0.24 0.29 0.13 Fov050836 0.79 0.28 0.13 Rln020190 0.04 0.00 0.00 Ubd030229 0.79 0.39 0.15 Fur150643 0.61 0.73 0.22 Fov060050 0.86 0.25 0.12 Rln020243 0.02 0.00 0.01 Fur021558 0.61 0.33 0.22 Ubd040104 0.84 0.58 0.15 Fov041285 0.50 0.15 0.11 Rln020012 0.02 0.41 0.07 Fur020131 0.73 0.57 0.18 Fov030109 0.97 0.39 0.10 Rln010148 0.02 0.05 0.06 Ubd040056 0.79 0.83 0.14 Fov020386 0.58 0.08 0.09 Fur021367 0.30 0.55 0.18 Fov020067 0.96 0.44 0.08 Rln020006 0.01 0.00 0.02 Fov110030 0.92 0.39 0.08 Ubd070017 0.62 0.40 0.14 Fur020506 0.94 0.68 0.17 Rln020296 0.01 0.00 0.00 Fov041267 0.44 0.39 0.06 Ubd040204 0.12 0.76 0.12 Fur020163 0.23 0.33 0.12 Fov100004 0.95 0.36 0.05 Rln020186 0.01 0.02 0.02 Fov060003 0.78 0.24 0.05 Fur130009 0.18 0.69 0.10 Rln020166 0.01 0.05 0.01 Ubd040131 0.95 0.81 0.10 Fov020061 0.87 0.20 0.05 Fur021197 0.35 0.70 0.09 Rln020208 0.01 0.01 0.00 Fov041269 0.70 0.38 0.04 Fur010587 0.18 0.34 0.08 Ubd040142 0.84 0.62 0.09 Fov010873 0.97 0.53 0.03 Rln020327 0.01 0.00 0.00 Fur140260 0.77 0.51 0.07 Fov041300 0.90 0.27 0.03 Fov060152 0.63 0.59 0.02 Rln020343 0.01 0.00 0.01 Ubd030138 0.54 0.11 0.09 Fur021980 0.30 0.70 0.06 Fov060265 0.48 0.38 0.02 Rln020233 0.01 0.04 0.06 Ubd040043 0.65 0.92 0.08 Fur020831 0.18 0.45 0.04 Fov100146 0.66 0.63 0.01 Rln020007 0.00 0.26 0.00 Fur020809 0.36 0.58 0.00 Fov060382 0.28 0.37 0.01 Rln020138 0.00 0.01 0.01 Ubd050077 0.72 0.46 0.08 Fov010706 0.87 0.70 0.01 Fur030068 0.41 0.63 0.00 Fov060133 0.93 0.69 0.01 Rln020321 0.00 0.00 0.01 Ubd020464 0.73 0.63 0.07 Fur030131 0.50 0.68 0.00 Fov020059 0.97 0.27 0.01 Fov010682 0.85 0.59 0.01 Rln020231 0.00 0.00 0.01 Fur021437 0.98 0.37 0.00 Rln020088 0.00 0.00 0.00 Ubd040177 0.89 0.84 0.04 Fov100220 0.69 0.18 0.00 Fur021620 0.41 0.10 0.33 Fov010750 0.98 0.81 0.00 Rln020169 0.00 0.16 0.00 Ubd040214 0.29 0.17 0.03 Fov060434 0.91 0.56 0.00 Rln020164 0.00 0.00 0.00 Fur020073 0.29 0.06 0.21 Fov050840 0.16 0.23 0.00 Fur020115 0.56 0.02 0.00 Ubd040128 0.77 0.29 0.03 Fov040044 0.81 0.54 0.00 Rln030301 0.00 0.18 0.00 Fur020107 0.68 0.00 0.17 Fov030062 0.10 0.17 0.00 Fov010563 0.71 0.58 0.00 Rln020083 0.00 0.00 0.00 Ubd050035 0.17 0.33 0.02 Fur020703 0.05 0.27 0.00 Fov010903 0.82 0.09 0.00 Rln020086 0.00 0.00 0.00 Ubd080024 0.18 0.28 0.01 Fur021233 0.05 0.66 0.00 Fov050139 0.40 0.57 0.00 Rln020160 0.00 0.00 0.00 Fov020262 0.91 0.09 0.00 Fur021561 0.04 0.01 0.14 Rln020096 0.00 0.00 0.00 Ubd040101 0.26 0.31 0.01 Fov060553 0.84 0.08 0.00 Fur020837 0.04 0.06 0.04 Fov050417 0.72 0.26 0.00 Rln020140 0.00 0.00 0.00 Ubd030151 0.79 0.61 0.00 Fov050855 0.92 0.61 0.00 Fur020266 0.04 0.40 0.03 Fov060371 0.81 0.82 0.00 Rln020302 0.00 0.00 0.00 Ubd040098 0.35 0.40 0.00 Fur020280 0.03 0.42 0.25 Fov040694 0.59 0.81 0.00 Rln020253 0.00 0.00 0.00 Fov030128 0.99 0.68 0.00 Fur030193 0.03 0.10 0.02 Fov020497 0.83 0.59 0.00 Rln020331 0.00 0.00 0.08 Ubd040008 0.75 0.90 0.00 Fur021641 0.02 0.30 0.01 Rln020002 0.00 0.00 0.00 Fov050700 0.37 0.25 0.00 Ubd040162 0.97 0.10 0.00 Fur020121 0.02 0.14 0.01 Fov060210 0.48 0.22 0.00 Rln020415 0.00 0.00 0.00 Fov020106 0.95 0.07 0.11 Fur030025 0.01 0.03 0.01 Fov041138 0.27 0.06 0.00 Rln020298 0.00 0.00 0.00 Ubd040341 0.19 0.09 0.03 0.00 0.00 0.00 Fur021248 0.01 0.32 0.05 Fov020002 0.57 0.06 0.08 Rln010086 Ubd070027 0.20 0.08 0.01 Fov020111 0.16 0.05 0.11 0.00 0.11 0.00 Fur021721 0.01 0.35 0.00 Fov040872 0.31 0.04 0.01 Rln020361 Fov050666 0.99 0.03 0.00 Rln020383 0.00 0.01 0.06 Ubd040030 0.95 0.07 0.01 Fur021423 0.01 0.35 0.04 Fov050659 0.81 0.03 0.00 Rln020386 0.00 0.03 0.00 Ubd040067 0.81 0.06 0.03 Fur020604 0.01 0.02 0.00 71768C3 0.44 0.03 0.05 Fur020155 0.01 0.09 0.07 Fov050555 0.20 0.02 0.01 Rln020248 0.00 0.00 0.00 Rln020221 0.00 0.00 0.00 Ubd040074 0.60 0.03 0.10 Fur020408 0.01 0.39 0.02 Fov020193 0.69 0.02 0.00 Fov031530 0.81 0.01 0.10 Rln020184 0.00 0.00 0.01 Fur020821 0.00 0.22 0.08 Ubd040213 0.85 0.02 0.15 Fov030763 0.59 0.01 0.29 Fov021215 0.52 0.01 0.07 Rln010119 0.00 0.00 0.05 Fur030114 0.00 0.73 0.00 Ubd040055 0.07 0.03 0.02 Fur021562 0.00 0.07 0.00 Fov040855 0.11 0.01 0.04 Rln020380 0.00 0.00 0.02 Fov050706 0.12 0.01 0.00 Fur020786 0.00 0.00 0.00 Fov030120 0.70 0.01 0.00 Rln020244 0.00 0.00 0.00 Ubd040050 0.06 0.58 0.00 Fov030286 0.10 0.00 0.00 Rln020324 0.00 0.00 0.00 Ubd020068 0.05 0.11 0.18 Fur021353 0.00 0.00 0.00 Fov020132 0.03 0.00 0.01 Rln010122 0.00 0.00 0.00 Fur021216 0.00 0.21 0.04 Fov020486 0.03 0.00 0.00 Rln010079 0.00 0.03 0.00 Ubd040144 0.03 0.57 0.00 Fur021372 0.00 0.08 0.40 Fov050816 0.03 0.25 0.00 Fov020263 0.01 0.29 0.06 Rln020282 0.00 0.00 0.00 Ubd040242 0.00 0.05 0.00 Fur021334 0.00 0.04 0.01 Fov050388 0.01 0.00 0.05 Fov010181 0.00 0.00 0.00 Rln020249 0.00 0.00 0.00 Fur021642 0.00 0.38 0.01 Rln020255 0.00 0.00 0.00 Ubd040256 0.00 0.17 0.01 Fur021075 0.00 0.19 0.07 Fov150230 0.00 0.06 0.19 OncoSignature-positive = 30% OncoSignature-positive = 0% OncoSignature-positive = 30-50% OncoSignature-positive = 30-40% (ORR in past trials: 12+% and 29%) (ORR in past trial: 0%) 18 A C R I V O N T H E R A P E U T I C S

T W O A T T R A C T I V E A C R—3 6 8—S E N S I T I V E C A N C E R T Y P E S I D E N T I F I E D Bladder cancer patient samples Endometrial patient samples Patient 1 LOW Patient 2 HIGH Patient 1 LOW Patient 2 HIGH Class 11 BM 2 Class 2 BM 3 Class 3E BM Predicted Predicted Predicted Predicted Non-Responders Responders Non-Responders Responders ACR-368 OncoSignature screening of human cancer samples A C R I V O N T H E R A P E U T I C S

A S U B S E T O F E N D O M E T R I A L A N D B L A D D E R P D X M O D E L S A R E H I G H L Y S E N S I T I V E T O A C R—3 6 8 Bladder PDX Endometrial PDX 2,000 BL001 2,000 BL002 1,500 Endo 1 2,000 Endo 2 mm3) mm3) r s rs ( 1,500 ( 1,500 e e e 1,000 mete ACR-368-sensitive um um imet i l l 1,000 i ll ill 1,000 1,000 M M Vo Vo r r bic 500 responders mo 500 mo 500 Cu Cubic Tu Tu 0 0 0 0 0 5 10 15 20 25 30 0 5 10 15 20 25 30 0 7 14 21 0 7 14 21 28 PDX-L PDX-H Study Days Study Days Day Day 2,500 BL003 3,000 BL004 2,000 Endo 3 1,500 Endo 4 (mm3) 2,000 (mm3) 2,250 1,000 BM1 1,500 olume olume 1,500 Millimeters 1,000 Millimeters V 1,000V 500 750 Tumor 500 Tumor Cubic Cubic 0 0 0 0 0 5 10 15 20 25 30 0 5 10 15 20 25 30 0 7 14 21 28 0 7 14 Study Days Study Days Day Day ) 3,000 BL005 ) 3,500 BL006 1,500 Endo 5 1,500 Endo 6 BM2 3 (mm (mm 3 2,250 2,625 ume ume m eters 1,000 1,000 Vo l 1,500 Vo l 1,750 Milli Millimeters 500 500 umor 750 umor 875 Cubic Cubic T T 0 0 0 0 0 5 10 15 20 25 30 0 5 10 15 20 25 30 0 7 14 0 7 14 21 BM3 Study Days Study Days Day Day 2,000 BL007 2,500 BL008 2,000 Endo 7 2,000 Endo 8 (mm3) (mm3) 2,000 1,500 1,500 1,000 1,000 1,000 Millimeters Millimeters Volume Volume 1,000 500 Tumor Tumor 500 Cubic Cubic Predicted Predicted 0 0 0 0 0 5 10 15 20 25 30 0 5 10 15 20 25 30 0 7 14 21 28 35 0 7 14 21 28 Non-Responders Responders Study Days Study Days Day Day 20 A C R I V O N T H E R A P E U T I C S

A P 3 U N C O V E R S A C T I O N A B L E A C R—3 6 8 R E S I S T A N C E M E C H A N I S M S U N B I A S E D A N D I N D E P E N D E N T O F G E N E T I C I N F O R M A T I O N T-test significant Proteins, FDR<0.05 Unsupervised Hierarchical Clustering Resistant Parental G1/S CELL CYCLE Upregulated in ACR-368 Resistant Cells Downregulated in ACR- 368 Resistant Cells DNA DAMAGE REPAIR Data suggest that gemcitabine might be a rational combination to overcome DDR suppression 21 A C R I V O N T H E R A P E U T I C S

L O W D O S E G E M C I T A B I N E S E N S I T I Z E S O V A R I A N C A N C E R C E L L L I N E S T O A C R—3 6 8 Ovarian-Parental Ovarian-Resistant 150 No Gem 150 No Gem 0.53 nM Gem 0.53 nM Gem MSO 2.7 nM Gem O MS 2.7 nM Gem D D to to 100 100 tive ltiv e al a e r Prexasertib Abs EC50 e Prexasertib Abs EC50 ity + 0 nM Gem: 15 nMr + 0 nM Gem: >10 uM l i + 0.53 nM Gem: 2.7 nM ility + 0.53 nM Gem: 100 nM b a + 2.7 nM Gem: 0.2 nM b + 2.7 nM Gem: 6 nM 50 a 50 vi vi l Cel l %Cel % 0 0 -10 -8 -6 -4 -10 -8 -6 -4 ACR-368 Log10 (M) ACR-368 Log10 (M) Bliss Synergy score: o <-10: Drug interaction is likely antagonistic o -10 to 10: Drug interaction is likely additive o >10: Drug interaction is likely synergistic 22 A C R I V O N T H E R A P E U T I C S

E N R O L L I N G A N D D O S I N G A C R—3 6 8 I N T H R E E H I G H U N M E T N E E D I N D I C A T I O N S : O V A R I A N , E N D O M E T R I A L A N D B L A D D E R C A N C E R • RP2D of ACR-368 based on predicted sensitivity using our OncoSignature+ Single Arm Simon 2 Stage Monotherapy Phase 2b with Registrational Intent ACR-368 OncoSignature Assay run by our CDx partner Stage 1 Stage 2 Ovarian (N= 23 per cohort) (N= 48 per cohort) • 58 sites currently activated1 Endometrial Bladder OncoSignature- Single Arm Phase 1b/2 Exploratory • Key opinion leaders, some with Combination with Low Dose Gemcitabine extensive experience using Phase 1b Phase 2 Expansion ACR-368 from previous trials (N= ~21) (N= 33 per cohort) are actively participating FDA Fast Track Designation granted May 8, 2023 for ACR-368 monotherapy in OncoSignature-positive patients with Platinum-Resistant Ovarian Cancer and Endometrial Cancer 1https://clinicaltrials.gov/ct2/show/NCT05548296 23 A C R I V O N T H E R A P E U T I C S

E N C O U R A G I N G I N I T I A L C L I N I C A L O B S E R V A T I O N S • 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 of November 3, 2023 24 A C R I V O N T H E R A P E U T I C S

W E E 1 A N D P K M Y T 1 V A L I D A T E D C A N C E R T A R G E T S : I D E A L F O R A P 3 A P P R O A C H • proper WEE1 and DNA PKMYT1 replication regulate and mitotic S and G2 completion -M cell cycle through checkpoints phosphorylation to ensure and inhibition of CDK2 and CDK1 and CDK1, respectively • WEE1 replication inhibition and cell propagates cycle progression, genomic instability resulting in by mitotic premature catastrophe DNA • 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) Ghelli Luserna di Rorà et al. J. Hematol Oncol, 2020 – 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 25 A C R I V O N T H E R A P E U T I C S

I N T E R N A L P I P E L I N E : A D V A N C I N G D E V E L O P M E N T C A N D I D A T E A C R—2 3 1 6 A N D O T H E R D D R P R O G R A M S—L E V E R A G I N G A P 3 Rationale • Leveraging our AP3 patient selection platform for high clinical POS High throughput AP3 profiling • Potentially optimal profile for monotherapy clinical development Global analysis Pairwise analysis > 10 k p-sites. ANOVA, HA, FDR=0.05 Volcanoplot, FDR=0.05 ACR-2316 and other DDR programs • >40 high resolution co-crystals (1.5-3.1 Å) and AP3-driven SAR EE1- and PKMY ructural series and lead candidates selectivity pr based on AP3 profiling Activity analysis Causal networks Motifs ACR-2316 advancing in IND-enabling studies Kinase score • High resolution co-crystals with WEE1 and PKMYT1 GSEA • Novel, potent dual inhibitor (single digit nM potency) • Designed to overcome WEE1 and PKMYT1 single inhibitor resistance • Potent, selective single agent activity AP3 used for biologically relevant selectivity profiling A C R I V O N T H E R A P E U T I C S

E X E C U T I V E S U M M A R Y : A C R—2 3 1 6 D E V E L O P M E N T C A N D I D A T E A selective dual WEE1/ PKMYT1 inhibitor optimized using AP3 for potent single agent activity Accelerating IND-enabling studies and planning for monotherapy clinical development • AP3-based SAR optimization facilitated by co-crystallography with WEE1 and PKMYT1 – Quantitative visualization of drug-regulated global protein activity in cells not possible with standard methods – Unbiased detection of WEE1 inhibitor-induced resistance mechanisms overcome by balanced PKMYT1 inhibition • Single digit nM WEE1 inhibition with carefully optimized ratio of PKMYT1 inhibition in cells • Superior target selectivity and cell growth inhibition across human tumor cell lines vs clinical benchmark WEE1 and PKMYT1 inhibitors • Superior preclinical anti-tumor activity in tumor-bearing mice, including tumor regression, surpassing that of clinical benchmark molecules • In vitro ADME, PK, and oral bioavailability profiles meet pre-specified development candidate criteria • On track for Q4 2024 IND with safety observed in MTD studies consistent with predicted desirable human exposure • Generating ACR-2316-OncoSignature test for indication finding and to guide monotherapy clinical development 27 A C R I V O N T H E R A P E U T I C S

D U A L W E E 1 / P K M Y T 1 I N H I B I T O R A C R—2 3 1 6 D E M O N S T R A T E S S T R O N G P O T E N C Y A N D S E L E C T I V I T Y KinomeScan (106 kinases @ 1000 nM) Benchmark WEE1 inhibitor WEE1 Benchmark PKMYT1 inhibitor Dual inhibitor show potent cell cycle effects with pronounced S-G2/M accumulation PKMYT1 DMSO WEE1 Inhibitor PKMYT1 Inhibitor ACR-2316 58% 41% 94% 100 nM, 24 hour 50% Dual inhibitor ACR-2316 PKMYT1 WEE1 DNA content 28 A C R I V O N T H E R A P E U T I C S

A C R—2 3 1 6 S H O W S S U P E R I O R A C T I V I T Y VS B E N C H M A R K S A C R O S S A L L H U M A N T U M O R C E L L L I N E S T E S T E D Example: Ovarian human cancer cell lines 19 ovarian and other human tumor cell lines tested to date 29 A C R I V O N T H E R A P E U T I C S

A C R—2 3 1 6 I S H I G H L Y P O T E N T A C R O S S H U M A N T U M O R C E L L L I N E S A N D P A T I E N T—D E R I V E D O V A R I A N T U M O R O R G A N O I D S Human tumor cell lines Patient-derived tumor organoids CTG-1703 CTG-2884 CTG-3718 CTG-0956 CTG-3383 ACR-2316 CTG-2733 CTG-1448 WEE1i CTG-1498 PKMYT1i CTG-3226 CTG-1692 CTG-1301 CTG-0703 CTG-2561 CTG-3522 1 100 10000 IC50, nM 30 A C R I V O N T H E R A P E U T I C S

A C R—2 3 1 6 D E M O N S T R A T E S P O T E N T M O N O T H E R A P Y A N T I -T U M O R A C T I V I T Y I N T U M O R—B E A R I N G M I C E ACR-2316 anti-tumor activity (QDx7; PO) ACR-2316 anti-tumor activity (5d on/2d off; PO) ACR-2316 demonstrates potent anti-tumor activity, including tumor regression, compared to benchmark WEE1 and PKMYT1 inhibitors 31 A C R I V O N T H E R A P E U T I C S

A C R—2 3 1 6 E M E R G I N G S A F E T Y P R O F I L E F R O M P R E C L I N I C A L A N I M A L S T U D I E S A P P E A R S P R O M I S I N G 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 • No obvious anemia, neutropenia, or thrombocytopenia, moderate reticulopenia, monocytopenia, and lymphopenia Rat and dog MTD: • 30 mg/kg ≤ MTD in both species • Plasma PK exposure consistent with projected human exposure levels required for potential anti-tumor activity • Reversible hematological effects (white blood cells), no thrombocytopenia 32 A C R I V O N T H E R A P E U T I C S

S T R E A M L I N E D A P 3—B A S E D B I O L O G I C A L S A R O P T I M I Z A T I O N F O R S I N G L E A G E N T A C T I V I T Y O F P R E C L I N I C A L P R O G R A M S Quantitative mapping (>35,000 phospho-sites covering >4,500 proteins) Week 0 OVCAR3 A2780 Non-synchronized OVCAR3 A2780 OVCAR3 Synchronized A2780 synchronized synchronized es and biological process enrichment Turnaround <2 weeks activity mapping and reconstitution Week2 High resolution and throughput MS-based P-proteomics Proprietary pipe for automated AP3 analyses with actionable results A C R I V O N T H E R A P E U T I C S

A P 3 : T I G H T , H I G H—R E S O L U T I O N D A T A W I T H D E E P C O V E R A G E 35388 p-sites 15733 p-sites QC Consensus Data Clean Volcano Hierarchical Kinase Pathway Functional Network QC MS Data Processed Sequence Biomarkers Up Plots Clustering Inference Enrichment Annotation Mapping Data Motif ✓ 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 34 A C R I V O N T H E R A P E U T I C S

A P 3 R E V E A L S D R U G—R E G U L A T E D K I N A S E A C T I V I T Y I N I N T A C T C E L L S N O T D E T E C T A B L E B Y S T A N D A R D M E T H O D S KinomeScan @ 1mM Drug-regulated kinase activity* in intact cells ACR-2316 ACR-2316 Traditional AP3-based selectivity pathway profiling profiling ACR-2743 (previous lead candidate) ACR-2743 *Kinase activity based on substrate motif analysis using a proprietary PTM-SEA hybrid method A C R I V O N T H E R A P E U T I C S

O P T I M I Z E D D U A L I N H I B I T O R S S H O W D E S I R A B L E P A T H W A Y E F F E C T S Optimized dual WEE1 and PKMYT1 inhibitors affect cell cycle and canonical MAPK pathways in desirable manner Substrate motif-inferred Benchmark* WEE1 + PKMYT1 ACR-2316 ACR-2743 kinase activities Inhibitors in combination PTM- SEA-based hybrid workflow and analyses -5 0 5 *Clinical-stage selective WEE1 and PKMYT1 inhibitors 36 A C R I V O N T H E R A P E U T I C S

A P 3—D E R I V E D D U A L P O T E N C Y O P T I M I Z A T I O N T O O V E R C O M E W E E 1 I N H I B I T O R R E S I S T A N C E : R E C I P R O C A L Q U E N C H I N G Cell cycle and cancer Protein set name PUJANA_CHEK2_PCC_NETWORK DNA DNA damage homology responses Sensitive Resistant repair PKMYT1i WEE1i Mitotic regulation PUJANA_BRCA1_PCC_NETWORK WEE1i PKMYT1i REACTOME_CELL_CYCLE REACTOME_SEPARATION_OF_SIST Protein set size ER_CHROMATIDS 500 5 EC75 Enrichment Score (NES) Comprehensive annotation, Induced Suppressed weighted for protein set size 37 A C R I V O N T H E R A P E U T I C S

A P 3 R E C I P R O C A L Q U E N C H I N G R E V E A L S O P T I M A L T A R G E T P O T E N C Y P R O F I L E F O R D U A L W E E 1 / P K M Y T 1 I N H I B I T O R Sensitive Resistant Sensitive Resistant PKMYT1i PKMYT1i PKMYT1i WEE1i PKMYT1i WEE1i WEE1i and PKMYT1i dual inhibition synergy WEE1i WEE1i Target substrates Target substrate of ACR-368 Target substrate of PKMYT1i Target substrates Euclidean Optimal potency ratio results in significant synergy HCL, Centered log2FC (treated vs. DMSO) 4 -4 p-sites from 298 proteins 38 A C R I V O N T H E R A P E U T I C S

A C R—2 3 1 6 M E E T S P R E—S P E C I F I E D D E V E L O P M E N T C A N D I D A T E C R I T E R I A Target ACR-2316 MOA • AP3 phosphoproteomics-based, optimized MOA; selective, dual WEE1/PKMYT1 inhibition ✓ 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 ✓ Selectivity • Kinase panel profiling – highly selective (kinome selectivity) ✓ • AP3 profiling confirms desirable CDK and PLK activation for mitotic catastrophe/apoptosis ✓ ADME/PK • Orally bioavailable ✓ • T¹⁄₂ suitable for once/day dosing ✓ In vitro safety • Low in vitro hERG (>10 µM) and CYP inhibition and induction (>1 µM) ✓ Solubility • > 50 µM for active compounds ✓ PPB • < 90% ✓ In vivo efficacy • Demonstrated potent target engagement intratumorally in vivo ✓ • Potent single agent activity in CDX models ✓ 39 A C R I V O N T H E R A P E U T I C S

E X P E D I T I N G A C R—2 3 1 6 T O W A R D S C L I N I C A L M O N O T H E R A P Y D E V E L O P M E N T A novel, AP3-enabled, internally discovered dual WEE1 / PKMYT1 inhibitor Rational Design Superior Profile Streamlined Development • Co-crystallography-driven • Demonstrated preclinical • Aiming for expedited programs specifically superiority in target monotherapy development optimized via AP3 SAR selectivity / potency and vs. (clinically validated targets) • AP3-enabled design with benchmark WEE1 and • Rapidly advancing towards optimized WEE1 / PKMYT1 PKMYT1 compounds IND (expected Q4 2024) target engagement • Stronger anti-tumor activity • OncoSignature test in properties and ratio in tumor bearing mouse development for indication • AP3-based optimization of models vs. benchmark WEE1 finding and patient selection functional target profile and PKMYT1 compounds • Dose optimization (Project ensuring PLK and CDK1/2-Optimus) to be guided by drug driven mitotic catastrophe target engagement (BM2) 40 A C R I V O N T H E R A P E U T I C S

A P 3 : B R O A D A P P L I C A B I L I T Y A N D U N T A P P E D P O T E N T I A L DELIVERABLES Patient responder Indication Rational drug Resistance Pharmacodynamic (PD) identification finding combinations mechanisms biomarkers AP3 Patient selection for Rational drug design SAR Patient selection for novel Continued in-licensing broadly applicable drugs (druggable drivers, drug MOA, targets and drugs (active drugs, no patient (CDK4/6, K-RAS, ADCs) rational drug combinations (CRISPR, degraders, epigenetic) selection path) APPLICATIONS 41 A C R I V O N T H E R A P E U T I C S

A P 3 I S B R O A D L Y A P P L I C A B L E A C R O S S D R U G D I S C O V E R Y A N D D E V E L O P M E N T Clinical Biomarkers Indication Finding Predictive OncoSignature tests Sensitive tumor types Drug Discovery SAR Informs in-licensing Optimal target selectivity AP3 AP3 profiling of candidates Intellectual Property Resistance Mechanisms De novo exclusivity & Rational drug combinations protection against generics Predicted Responder PD Markers ~6,000 per compound 42 A C R I V O N T H E R A P E U T I C S

T H E A P 3 A P P R O A C H I S M O D A L I T Y A N D D I S E A S E A G N O S T I C Therapeutic modalities Antibody ADC Bifunctional Oligo/RNA molecule Small molecule Cancers with DDR stress Oncology Therapeutic areas Fibrotic and inflammatory Autoimmune Current focus Infectious, CNS, and other diseases 43 A C R I V O N T H E R A P E U T I C S

F I N A N C I A L H I G H L I G H T S A S O F Q 3 2 0 2 3 Cash and marketable securities Projected runway into Fully Diluted Shares Outstanding $142.1M H2’25 27.6M Balance sheet Current operating plan, assuming Shares and equity grants 30-Sept-2023 no additional financing outstanding 30-Sept-2023 Unaudited. 44 A C R I V O N T H E R A P E U T I C S

A C R I V O N A D D R E S S A B L E M A R K E T S ( U S & E U I N C I D E N C E ) Prioritized indications for single agent ACR-368 Prioritized indications Bladder Cancer * (N=742,000) Endometrial Cancer * HPV+ SCC Potential additional indications 12% Ovarian cancer * *Currently enrolling Sarcoma and dosing (N = 634,000) 10% 0 100000 200000 300000 Other cancers Potential additional indications for single agent ACR-368 predicted to have ~45% DDR stress Colorectal Cancer Pancreatic Cancer All cancers US and Europe 0 100000 200000 300000 400000 500000 Est. >6.3M cases/year • ~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 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. 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. 45 A C R I V O N T H E R A P E U T I C S

A P P E N D I X 46 A C R I V O N T H E R A P E U T I C S

T E A M H A S P I O N E E R E D O U T C O M E—P R E D I C T I V E A T I M I C X I N psy test unding tea Raw Image Epithelium Classified Nuclei Classified ROI: Malignant Epithelium A B C D Protein Current Ideal test multiplex CDx in situ test tests Channel 1 Channel 2 Channel 3 Quantitative and automated ✓ (✓) ROI 2: Sub-cellular Validated Abs and reagents ✓ (✓) G. BM 3 Analysis F. BM 2 Analysis E. BM 1 Analysis Tumor Compartment G F E Drug target and pathway H ✓ activation context Biomarkers measured in relevant region on tumor ✓ biopsy Channel 6 Channel 5 Channel 4 Imaging algorithm (tissue ✓ pattern) autom for Addresses tumor ✓ edictio uidelines heterogeneity pioneer e luding tion* Double-blinded, prospective ✓ (✓) validation nt and cli timarker ass Clinical C R I V

P R O O F—OF—C O N C E P T F O R P R O T E I N B I O M A R K E R S I G N A T U R E : M A R K E T E D , O U T C O M E—P R E D I C T I V E M U L T I P L E X C A N C E R T E S T (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 48 A C R I V O N T H E R A P E U T I C S

P I O N E E R I N G P H O S P H O—P R O T E O M I C S S T U D Y I D E N T I F I E S N O V E L P I 3 ’ K P A T H W A Y I N H I B I T O R B I O M A R K E R S Sci Transl Med 2: 1-14 (2010) Editorial Highlights: 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. A discovery strategy for novel cancer biomarkers 49 A C R I V O N T H E R A P E U T I C S

O L S E N L A B—E X A M P L E S O F D E E P P R O T E O M I C S D R U G P R O F I L I N G Science Signaling (2018) Cell Systems (2017) Nature Communications (2020) ALK-i : LDK378, TAE684, crizotinib, lorlatinib. Deepest proteome resolution of a human cell to date Highest throughput, sensitivity, and scalability to date Cell Reports (2018) Nature Communications (2021) SHP2-i: SHP099 -allosteric inhibitor. Subcellular compartmental proteomics Cell (2019) Functional mapping of differential signaling by RPTK mutants Cell Reports (2017) Nature Communications (2021) CHK1-i: SCH900776, ATM-i: KU55933 Clinically actionable resistance mechanisms Cell Reports (2017) ONGOING (MULTICENTER): Profiling of DDR and core kinase pathway inhibitors (>45) CDK7-i: THZ-1 ATR CHK1 ATM DNAPK p38a JNK 50 A C R I V O N T H E R A P E U T I C S

A D V I S O R S A N D C O L L A B O R A T O R S SAB George Demetri, M.D., Robert Abraham, Ph.D. Timothy Yap, M.B.B.S., David Berman, M.D., Ph.D. FACP, FASCO, FAACR EVP, Head Cancer Biology, Ph.D., F.R.C.P. Professor, Director, Professor, Harvard Med. Queen’s Cancer Res. Inst., Odyssey Therapeutics Associate Prof., MD Ontario Canada School, Dir. Dana-Farber Anderson Cancer Center, Adj. Prof. , Burnham Inst. Medical Director, Inst. for Cancer Institute & Ludwig Adj. Prof. UCSD Applied Cancer Science Center, Boston • Leader in Precision Oncology • Expert in signal transduction- • Expert on DDR accelerated • GU Pathologist; bladder cancer • Key contributor to based R&D clinical development and expert development and rapid • Previously SVP and WW Head, predictive biomarkers • Expert on protein biomarkers approvals of Gleevec, Sutent, Oncology R&D, Pfizer • Previously oncologist Royal and quantitative tissue imaging Stivarga, Zelboraf, Votrient, • VP, Oncology Res., Wyeth Marsden, London and Inst. • Academic lead on ProMark® and Yondelis • Professor, Burnham Institute Cancer Res, London • Professor, Duke University • Lead/P.I. on numerous DDR trials Jesper V. Olsen, Ph.D. Jung-Min Lee, M.D. Academic Co-Founder NCI Collaborator Professor, Novo-Nordisk Investigator, Lasker Foundation Protein Clinical Research Center, Cph. University Scholar, NCI • Recognized pioneer and • Expert on women’s cancers and leading authority in DNA damage response (DDR) phosphoproteomics and • Lead and co-PI on numerous proteomic systems analyses HGSOC &TNBC trials • Top 0.1% most cited scientist • Lead PI on ACR-368 platinum-in protein sciences resistant ovarian trials 51 A C R I V O N T H E R A P E U T I C S

A P 3 I S A P P L I C A B L E A C R O S S D R U G D E V E L O P M E N T S T A G E S Approval & Target ID Hit ID Lead Opt IND Enabling Early Clinical Late Clinical Commercialization ID druggable AP3 drug profiling: AP3 is also applicable in preclinical phase driver targets Unbiased drug target engagement & PD biomarkers Resistance Mechanisms Rational Combinations Indication Finding: OncoSignature patient sample screening OncoSignature patient responder identification 52 A C R I V O N T H E R A P E U T I C S

A P 3 A N A L Y S I S : A C R—2 3 1 6 R E G U L A T E S C E L L C Y C L E A N D M I T O S I S M O R E P O T E N T L Y T H A N B E N C H M A R K W E E 1 I N H I B I T O R 60min WEE1 inhibitor ACR-2316 200nM Tight junction Post-synaptic transmission Autophagy GTPases Sensitive RTK-MAPK Mitotic pathways HDR Mitotic pathways Cell cycle Resistant p value SREBP Significant Not significant Cell cycle Enrichment Score (NES) Induced Suppressed 53 A C R I V O N T H E R A P E U T I C S

A P 3 A N A L Y S I S : A C R—2 3 1 6 R E G U L A T E S C E L L C Y C L E A N D M I T O S I S M O R E P O T E N T L Y T H A N B E N C H M A R K P K M Y T 1 I N H I B I T O R Tight junction Post-synaptic transmission Autophagy GTPases RTK-MAPK Mitotic pathways HDR p value SREBP Significant Not Cell cycle Enrichment Sco Induced 54 A C R I V O N T H E R A P E U T I C S

A P 3 R E V E A L S S I N G L E A G E N T S E N S I T I V I T Y C O N T E X T A N D R A T I O N A L D R U G C O M B I N A T I O N S I N D E P E N D E N T O F G E N E T I C I N F O R M A T I O N 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 Cell Reports, August 9, 2022 55 A C R I V O N T H E R A P E U T I C S

E L I L I L L Y A C R—3 6 8 H I G H L E V E L L I C E N S E T E R M S • 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 56 A C R I V O N T H E R A P E U T I C S