Forward-looking statements Certain information contained in this presentation includes forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995 regarding our future results of

ACRIVON PREDICTIVE PRECISION

PROTEOMICS (AP3) OVERCOMING LIMITATIONS OF GENETICS-BASED PRECISION MEDICINE CORPORATE PRESENTATION JANUARY 2024 Exhibit 99.1

Forward-looking statements Certain

information contained in this presentation includes forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995 regarding our future results of operations or financial condition, business strategy and plans

and objectives of management for future operations. In some cases, you can identify forward-looking statements because they contain words such as "anticipate," "believe," "contemplate," "continue,"

"could," "estimate," "expect," "intend," "may," "plan," "potential," "predict," "project," "should," "target,"

"will," or "would" or the negative of these words or other similar terms or expressions. Our forward-looking statements are based primarily on our current expectations and projections about future events and trends that we

believe may affect our business, financial condition and results of operations. The outcome of the events described in the forward-looking statements is subject to risks and uncertainties, including the factors described in our filings with the U.S.

Securities and Exchange Commission. New risks and uncertainties emerge from time to time, and it is not possible for us to predict all risks and uncertainties that could have an impact on the forward-looking statements contained in this

presentation. The results, events, and circumstances reflected in the forward-looking statements may not be achieved or occur, and actual results, events, or circumstances could differ materially from those described in the forward-looking

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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

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

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

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