Acrivon Therapeutics, Inc. · NASDAQ:ACRV
Acrivon Therapeutics — Investor Presentation (September 2026)
50 slides from Acrivon Therapeutics's investor presentation, September 2026
Slide 1: Corporate Presentation September 2026
Acrivon Therapeutics ACRIVON PREDICTIVE PRECISION PROTEOMICS (AP3) N E X T G E N E RAT I O N P R E C I S I O N M E D I C I NE C O R P O R AT E P R E S E N TAT I O N SEPTEMBER 2026
Slide 2: Forward-Looking Statements
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 o
Slide 3: Next-Generation Precision Medicine Powered by AP3
NEXT-GENERATION PRECISION MEDICINE POWERED BY AP3 Current focus oncology, Acrivon Predictive Precision Proteomics (AP3) I&I next • AI-driven, proteomics-based rational drug design and DNA informed clinical development • AP3 enables an exact match between the disease- RNA driving, dysregulated pathwa
Slide 4: Acrivon Therapeutics Overview
ACRIVON THERAPEUTICS OVERVIEW Development Site (Boston) Precision Proteomics Site (Lund/Copenhagen) • Drug development and clinical biomarkers • Early drug discovery • Clinical leadership and trial oversight • BM identification and drug profiling • ML/AI-driven AP3 analyses • AP3 mass spectrometry H
Slide 5: Accomplished Leadership Team
ACCOMPLISHED LEADERSHIP TEAM Peter Blume-Jensen, M.D., Ph.D. Mansoor Raza Mirza, M.D. Kristina Masson, Ph.D., M.B.A Adam Levy, Ph.D., M.B.A. CEO, President, Co-Founder Chief Medical Officer Site Head Acrivon AB, Co-Founder Chief Financial Officer EVP Business Operations • Executive Serono, Merck & C
Slide 6: Acrivon AP3-Based Precision Medicine
ACRIVON AP3-BASED PRECISION MEDICINE A REITERATIVE ENGINE DEVELOPED FOR RAPID CLINICAL POC Novel Target Identification Activated druggable targets – diseased vs normal Clinical Biomarkers Drug Discovery SAR Predictive OncoSignature tests Optimized pathway effects Indication Finding Therapeutic Index
Slide 7: Our Pipeline
OUR PIPELINE Preclinical Phase 1 Phase 2 Phase 3 Single-arm trial based on OncoSignature biomarker prediction BM+ patients, ACR-368 single-agent · Breakthrough Device & Fast Track · Arm 1 registrational intent ACR-368 Single-arm trials without pretreatment biopsy or biomarker stratification Endometr
Slide 8: Upcoming Milestones
UPCOMING MILESTONES ACR-368 (Phase 2b) • Prespecified simultaneous interim analysis and data update from both all-comer (biopsy-independent) serous EC arms of the ACR-368 Phase 2b study in second half of 2026 • Initiate Phase 3 confirmatory trial for ACR-368 in first half of 2027 • Based on interim
Slide 9: Acrivon CLIA Laboratory
ACRIVON CLIA LABORATORY STRENGTHENING ACRIVON PRECISION MEDICINE CAPABILITIES – Newly licensed CLIA laboratory – Translates AP3-driven biomarker discoveries into actionable and proprietary CDx for our therapeutics – Initially focused on ACR-368 OncoSignature testing – Unique capabilities to support
Slide 10: ACR-368: A Potent Selective CHK1/2 Inhibitor
ACR-368: A POTENT SELECTIVE CHK1/2 INHIBITOR • Clinical efficacy and safety: Durable monotherapy activity across multiple cancers with favorable tolerability and absence of non-hematological, severe toxicities • AP3 Indication Finding: Endometrial cancer was identified as a tumor type predicted to b
Slide 11: OncoSignature: Drug Response Prediction in Individual Patients
ONCOSIGNATURE: DRUG RESPONSE PREDICTION IN INDIVIDUAL PATIENTS PROPRIETARY WORKFLOW INTEGRATING PROVEN TECHNOLOGIES STEP 1 STEP 2 STEP 3 THERAPEUTIC PACKAGE PATIENT RESPONDERS BIOMARKER IDENTIFICATION Acrivon drug with predictive BM assay Optimal indications and combinations Predicted Predicted Non-
Slide 12: AP3 Indication Finding Identifies Endometrial Cancer as Sensitive to ACR-368
AP3 INDICATION FINDING IDENTIFIES ENDOMETRIAL CANCER AS A NEW TUMOR TYPE SENSITIVE TO ACR -368 ACR-368 OncoSignature-based Functional validation in Clinical validation in indication finding prior to trial entry preclinical models ongoing Phase 2b study ~30% ~70% Endometrial patient tumor samples BM1
Slide 13: Initial Trial Design
INITIAL TRIAL DESIGN Subjects relapsed after prior platinum-based chemotherapy • The ACR-368 OncoSignature is a and one prior line of anti-PD-(L)1 therapy tumor agnostic Biomarker (BM) test designed to prospectively predict benefit from ACR-368 (prexasertib), a BM-Stratified Cohorts with potent, sel
Slide 14: Favorable Safety Profile
FAVORABLE SAFETY PROFILE Treatment-Related Adverse Arm 1 Arm 2 Events (ACR-368) (ACR-368 + ULDG) N=40 N=48 N = number of subjects (%) Grades 3/4 Grades 3/4 • Limited, transient, mechanism- based hematological AEs Thrombocytopenia 9 (22) 17 (34) • Notable Absence of Anemia 11 (27) 22 (46) - GI toxici
Slide 15: Endometrial Patient Demographics and Baseline Characteristics
ENDOMETRIAL PATIENT DEMOGRAPHICS AND BASELINE CHARACTERISTICS Subject Demographics BM+ BM- Subject Demographics BM+ BM- N = 40 N = 48 N = 40 N = 48 Median Age (range) 66.0 66.0 Prior Lines of Therapy, Median (Mean) 2 (2) 2 (2) (40, 77) (49, 80) Best Overall Response to Last Prior Line Race, n (%) Wh
Slide 16: Better ORR Observed in Subjects with ≤2 Prior Lines of Therapy
BETTER ORR OBSERVED IN SUBJECTS WITH ≤2 PRIOR LINES OF THERAPY Arm 1 (BM+) ARM 2 (BM-) ACR-368 ACR-368 + ULDG ORR = 44% ORR = 26% BOR by RECIST 1.1 (95% CI, 27 - 63) (95% CI, 14 - 42) on study treatment* # # # n = 25 n = 35 * Best of BICR and/or PI # Unconfirmed PR OncoSignature BM levels and the BM
Slide 17: Serous Endometrial Cancer - A Significant Unmet Need
SEROUS ENDOMETRIAL CANCER - A SIGNIFICANT UNMET NEED Disproportionate Mortality EC Mortality EC Prevalence • Accounts for ~40-50% of all endometrial cancer deaths.5, 8 (US + EU) = ~44K1, 3 ~2.4M patients1, 3 Limited Effective Treatment Options ~58,800 • After frontline IO + chemotherapy, pem + len n
Slide 18: Serous EC All-Comer Population (KEYNOTE-775) PFS and OS
SEROUS EC ALL-COMER POPULATION (KEYNOTE-775) S H O W S 3 . 6 M O N T H S P F S A N D 1 0 M O N T H S O S I N 2 ND L I N E Control arm from KEYNOTE-775 study (N = 115) Lorusso et al, 2022 18 ACRIVON THERAPEUTICS
Slide 19: Serous EC All-Comer Population (KEYNOTE-775 Control Arm) Shows 13% ORR
SEROUS EC ALL-COMER POPULATION (KEYNOTE-775 CONTROL ARM) SHOWS 13% ORR Lorusso et al, 2022 19 ACRIVON THERAPEUTICS
Slide 20: Significant ORR in Serous All-Comer Population with ≤2 Prior Lines
SIGNIFICANT ORR IN SEROUS ALL-COMER POPULATION WITH ≤ 2 PRIOR LINES OF THERAPY Serous (≤ 2 Prior Lines) Non-Serous (≤ 2 Prior Lines) ORR = 52% ORR = 22% (95% CI, 33 - 71) (95% CI, 11 - 37) BOR by RECIST 1.1 on study treatment* # # # n = 23 n = 37 DCR: 74%, CBR (16 weeks): 65% * Best of BICR and/or P
Slide 21: ACR-368 Program Increasingly Focused on Serous Endometrial Cancer
ACR-368 PROGRAM INCREASINGLY FOCUSED ON SEROUS ENDOMETRIAL CANCER Subjects relapsed after prior platinum- based chemotherapy • Serous EC shows particularly and one prior line of anti-PD-(L)1 therapy high ORR in both BM+ and BM- tumors BM-Stratified Cohorts with Biopsy-Independent Serous Cohorts Pros
Slide 22: Potent ACR-368 + Anti-PD-L1 Synergy with Complete Tumor Regression
POTENT ACR-368 + ANTI-PD-L1 SYNERGY WITH COMPLETE TUMOR REGRESSION AND IMMUNE MEMORY MEDIATED BY CD4+ AND CD8+ CELLS Part IV: Part l: Part Il: Part IlI: CD4, CD8 & NK Part V: ACR-368 + α-PD-L1 synergy Immune memory CD8 T-cell depletion cell depletion CD4 Depletion Tumor re-challenge Tumor re-challen
Slide 23: AACR 2026: ACR-368 Synergy with Checkpoint Inhibition
AACR 2026: ACR-368 SYNERGY WITH CHECKPOINT INHIBITION 23 ACRIVON THERAPEUTICS
Slide 24: AACR 2026: ACR-368 Synergy with Topoisomerase 1
AACR 2026: ACR-368 SYNERGY WITH TOPOISOMERASE 1 24 ACRIVON THERAPEUTICS
Slide 25: ACR-368 Offers Multiple Attractive Opportunities
ACR-368 OFFERS MULTIPLE ATTRACTIVE OPPORTUNITIES Broad Indication and Future Indications Combination Expansion Opportunities MDS/MPN, HPV+ SCC, H&N, GBM ACR-368-201 Arm 1 ACR-368-201 Biomarker-Positive Arm 3 All histopathologies Confirmatory Phase 3 Endometrial Biomarker Unselected optionality Serou
Slide 26: Internal Pipeline: AP3-Based Drug Discovery
INTERNAL PIPELINE: AP3-BASED DRUG DISCOVERY POTENTIAL FIRST- AND BEST IN CLASS CANDIDATES Streamlined AP3-based drug discovery ACR-2316: Clinical stage, novel WEE1/PKMYT1 inhibitor Global analysis Pairwise analysis > 10 k p-sites. ANOVA, HA, FDR=0.05 Volcanoplot, FDR=0.05 • Additional clinical data
Slide 27: WEE1 and PKMYT1 - Critical Cell Cycle Checkpoints in Human Cancer
WEE1 AND PKMYT1 - CRITICAL CELL CYCLE CHECKPOINTS IN HUMAN CANCER • WEE1 and PKMYT1 regulate S and G2-M cell cycle checkpoints to ensure proper DNA replication and mitotic completion • Defective DNA repair is highly prevalent in cancers, creating a dependency on checkpoint proteins • Demonstrated cl
Slide 28: ACR-2316 Is a Potentially Best- and First-in-Class Agent
ACR-2316 IS A POTENTIALLY BEST- AND FIRST-IN-CLASS AGENT – FIRST POC FOR AP3 PLATFORM Program Goals Demonstrated Results Superior single agent activity ▪ Superior anti-tumor activity* (robust CDK1, CDK2, and 1 PLK1 activation; inhibition of PKMYT1 resistance) ▪ 5-20-fold more potent* in preclinical
Slide 29: ACR-2316: Uniquely Designed by AP3 for Superior Therapeutic Index
ACR-2316: UNIQUELY DESIGNED BY AP3 FOR SUPERIOR THERAPEUTIC INDEX OVER WEE1 AND PKMYT1 INHIBITORS ACR-2316: Novel WEE1/PKMYT1 inhibitor Drug Design by AP3-based SAR for desirable pathway effects and suppressing resistance mechanisms with potent single agent activity ✓ Complete tumor regression acros
Slide 30: ACR-2316 Is Highly Potent Across Tumor Cell Lines and Ex Vivo Models
ACR-2316 IS HIGHLY POTENT ACROSS HUMAN TUMOR CELL LINES AND PATIENT-DERIVED EX VIVO TUMOR MODELS Human tumor cell lines Patient-derived ex vivo (not genetically selected) ovarian tumor models HCC38 Breast CTG-0703 T47D A172 CTG-3383 Glioblastoma LN229 T98G CTG-2733 Lung A427 Medulloblastoma DAOY CTG
Slide 31: Superior Activity of ACR-2316 Over WRN Inhibitors
SUPERIOR ACTIVITY OF ACR-2316 OVER WRN INHIBITORS IN BOTH MSI HIGH AND MSS CELL LINES TOV21G (Ovarian, MSI High) HCT116 (Colorectal, MSI High) 140 140 120 120 HRO761 IC50 > 10000 nM HRO761 IC50 = 166 nM 100 VVD-214 IC50 > 10000 nM 100 VVD-214 IC50 = 105 nM % Viability ACR-2316 IC50 = 291 nM % Viabil
Slide 32: ACR-2316 Induces Complete Tumor Regression Across Models and Dosing Regimens
ACR-2316 INDUCES COMPLETE TUMOR REGRESSION ACROSS MODELS AND DOSING REGIMENS 5d on/2 d off 5d on/2 d off Model 1 Model 2 32 ACRIVON THERAPEUTICS
Slide 33: ACR-2316 Dose Expansion in AP3-Defined Tumor Types
ACR-2316 DOSE EXPANSION IN AP3-DEFINED TUMOR TYPES Dose Escalation – 2 weekly oral regimens established (N = 35) Randomized Dose Expansion: 3d on / 4d off AP3-identified, 120 mg QD Cohort A 160 mg molecularly 30 mg 60 mg 120 mg 240 mg 200 mg 3on/4off defined tumor types 160 mg QD Cohort B 2on/5off 2
Slide 34: ACR-2316 Demonstrates Clinical Activity in Heavily Pretreated Lung Cancer
ACR-2316 DEMONSTRATES CLINICAL ACTIVITY IN HEAVILY PRETREATED LUNG CANCER PATIENTS Duration of Last Prior Therapy and Time on ACR-2316 by Patient 12 adNSCLC-01 66 9 adNSCLC-02 66 42 adNSCLC-03 7 sqNSCLC-01 26 60 • Durable single-agent activity, sqNSCLC-02 6 including tumor shrinkage 26 and PRs 21 sq
Slide 35: Differentiated, Favorable Safety Profile, Primarily Transient Neutropenia
DIFFERENTIATED, FAVORABLE SAFETY PROFILE, PRIMARILY LIMITED TO TRANSIENT NEUTROPENIA Established weekly dosing regimens; N = 22 Grade 3 Grade 4 Grade ≥3 Event n (%) n (%) n (%) Neutropenia 4 (18.2) 2 (9.1) 6 (27.3) Leukopenia 1 (4.5) 1 (4.5) 2 (9.1) TOTAL (unique subjects) 5 (22.7) 2 (9.1) 6 (27.3)
Slide 36: ACR-2316-101 Demographics and Baseline Characteristics
ACR-2316-101 DEMOGRAPHICS AND BASELINE CHARACTERISTICS Subject Demographics N = 35 Cancer Type, n (%) N = 35 ECOG Status at Baseline, n (%) Median Age, years (range) 63.0 (35–77) Endometrial 6 (17.1) 0 11 (31.4) Sex, n (%) Ovarian Carcinoma 5 (14.3) 1 24 (68.6) Breast 4 (11.4) Female 22 (62.9) Prior
Slide 37: Potent ACR-2316 + Anti-PD-L1 Synergy with Complete Tumor Regression
POTENT ACR-2316 + ANTI-PD-L1 SYNERGY WITH COMPLETE TUMOR Part I Part III Part IV REGRESSION AND IMMUNE MEMORY MEDIATED BY CD4+ AND CD8+ CELLS Vehicle a-PD-L1 (IP, Q3D) Control Naive Innoculation-2 Control Naive Control Naive Innoculation-3 Mice previously treated with ACR-2316 + a-PD-L1 → CD8 NAb (I
Slide 38: AACR 2026: ACR-2316 Synergy with Checkpoint Inhibition
AACR 2026: ACR-2316 SYNERGY WITH CHECKPOINT INHIBITION 38 ACRIVON THERAPEUTICS
Slide 39: Potential Development Paths for ACR-2316
POTENTIAL DEVELOPMENT PATHS FOR ACR -2316 • AP3-predicted solid tumor types of high unmet need, e.g. SCLC, sqNSCLC, HPV+ tumors, etc., in ≥2nd line – Single agent – Chemo combination (DDR stress sensitization) • ACR-2316 (oral) in combination with either anti-PD(L)1 or TOPO1 payload ADCs based on st
Slide 40: CDK11 Program Highlights
CDK11 PROGRAM HIGHLIGHTS • First-in-class opportunity: No known clinical-stage selective CDK11 inhibitors • Compelling oncology target: Broad role in cell cycle control and oncogenesis, including transcription, pre- mRNA processing and splicing of mitotic genes • AP3 fit: AP3-based cellular SAR and
Slide 41: AP3-Based Indication Finding Identifies AML for CDK11 Inhibition
AP3-BASED INDICATION FINDING IDENTIFIES AML AS ONE OF THE TOP INDICATIONS FOR CDK11 INHIBITION AP3 Indication Screening for CDK11 inhibitor Overlap of AML disease network with CDK11 inhibitor AP3 profile (>2000 diseases) Top 10 indications matching AP3 profile Disease Classification Rank T-cell non-
Slide 42: CDK11 Inhibition May Provide Broad AML Opportunity
CDK11 INHIBITION MAY PROVIDE BROAD AML OPPORTUNITY Beyond mutation-defined therapies in a fragmented, high-need disease AML is broad and Current therapies CDK11i fits a fragmented leave open space convergence point Venetoclax/HMA: broad ~22.7k ~11.5k Targets shared transcription / new US cases/year
Slide 43: T-Cell Lymphomas: High Unmet Need and CDK11 Opportunity
T-CELL LYMPHOMAS: HIGH UNMET NEED AND CDK11 OPPORTUNITY Peripheral T-cell lymphoma Cutaneous T-cell lymphoma T-ALL ~75K WW / ~11K US incidence ~20K WW / ~3K US incidence ~13K WW / ~2K US incidence ~40K US prevalence ~16K US prevalence ~20K US prevalence DISEASE LANDSCAPE & UNMET NEED WHY CDK11 IS CO
Slide 44: CDK11 Inhibitor Lead Series Shows Complete AML Tumor Regression
CDK11 INHIBITOR LEAD SERIES SHOWS COMPLETE AML TUMOR REGRESSION AND FAVORABLE TOLERABILITY Multiple Lead Compounds Complete Regression In Vivo Favorable Safety Profile ACR-C1 ACR-C4 Vehicle ACR-C2 ACR-C5 ACR-C1 (30 mg/kg, PO QD) 100 ACR-C6 ACR-C5 (10 mg/kg, PO QD) 20 Body Weight Change (%) % Viabili
Slide 45: CDK11 Inhibitor Activity Alone and with BCL-2 Family Inhibitors
CDK11 INHIBITOR ACTIVITY ALONE AND IN COMBINATION WITH BCL -2 FAMILY INHIBITORS IN HEMATOLOGICAL MALIGNANCIES ACR CDK11 inhibitors reduce Rationale: CDK11 inhibition sensitizes levels of anti-apoptotic MCL1 tumors to BCL-2 family inhibitors ( AP3 global proteomics analysis) through MCL1 downregulati
Slide 46: ACR-C2 Downregulates MCL-1 and Induces Cell Death
ACR-C2 DOWNREGULATES ANTI-APOPTOTIC MCL-1 PROTEIN AND INDUCES CELL DEATH AFTER 6H TREATMENT Pan MCL-1 levels % Cleaved caspase-3 positive cells at 6h - flow cytometry 4h DMSO ACR-C2 6h DMSO 100nM ACR-C2 caspase-3 Cleaved FSC [10-1000] Cleaved caspase-3 40 6h MV411 MV411 MOLM13 HL60 KG1 30 MOLM13 % S
Slide 47: AP3 Generative Phosphoproteomics Platform
AP3 GENERATIVE PHOSPHOPROTEOMICS PLATFORM AP3 AP3 AP3 Interactome KSR Predictor PSR Predictor AP3 AP3 Insight Chatbot MS-proteomics • Single cell p-proteomics • Spatial p-proteomics • Clinical p-proteomics AP3 Drug Design & Opt. Proprietary AP3 Data Portal Validate Internal Proprietary 150 Multi-mod
Slide 48: AP3 Interactome: Proprietary Data Analysis Infrastructure
AP3 INTERACTOME: PROPRIETARY INTERACTIVE DATA ANALYSIS INFRASTRUCTURE FOR ALL ACRIVON DATA AND EXPERIMENTS Actionable data across all AP3 experiments accessible for all Acrivon scientists Fully scripted, algorithm-based machine learning-enabled pathway and biomarker analyses ~164,000 phosphosites ~5
Slide 49: Data Driven Execution and Value Creation
DATA DRIVEN EXECUTION AND VALUE CREATION Recent Accomplishments (Last 12 Months) Anticipated Next Milestones ACR-368 (Phase 2b) Continued positive ACR-368 data in ongoing registrational intent EC trial (April 2025 and January 2026 Corporate R&D Events) • Prespecified simultaneous interim analysis an
Slide 50: Financial Highlights
FINANCIAL HIGHLIGHTS Cash and Investments Projected runway into Fully Diluted Shares Outstanding $90.0M Q4 2027 52.0M Balance sheet Current operating plan, assuming Shares and equity grants 30-Jun-2026 no additional financing outstanding 30-Jun-2026 Note: unaudited 50 ACRIVON THERAPEUTICS
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