Acrivon Therapeutics outlines phase 2-ready ACR-525
Acrivon describes ACR-525 as Phase 2-ready, while its highlighted PKCθ inhibitor remains at the preclinical stage.
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Rhea-AI Filing Summary
Acrivon Therapeutics, Inc. outlined its new immunology and inflammation programs, led by ACR-525, an oral, selective JAK1 inhibitor it describes as Phase 2-ready for initial development in eosinophilic esophagitis (EoE). The company said Phase 1 healthy-volunteer studies showed dose-proportional pharmacokinetics, a dose-dependent reduction in CXCL10, and no serious adverse events; it reported an approximately 12-hour half-life.
Acrivon also described a preclinical PKCθ inhibitor program and potential combinations with ACR-525. It said AP3 profiling showed ACR-525’s JAK1 selectivity and suppression of non-SMAD TGFβ signaling. The company described ACR-525 as wholly owned, with CoM protection through 2038 and extension opportunities. It cited current U.S. EoE prevalence above 500,000.
8-K Event Classification
Key Figures
Key Terms
Acrivon Predictive Precision Proteomics (AP3) technical
phosphoproteomics technical
IC50 technical
fibrostenosis medical
Eosinophilic esophagitis (EoE) medical
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UNITED STATES
SECURITIES AND EXCHANGE COMMISSION
WASHINGTON, D.C. 20549
FORM 8-K
CURRENT REPORT
Pursuant to Section 13 or 15(d) of the Securities Exchange Act of 1934
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Indicate by check mark whether the registrant is an emerging growth company as defined in Rule 405 of the Securities Act of 1933 (§ 230.405 of this chapter) or Rule 12b-2 of the Securities Exchange Act of 1934 (§ 240.12b-2 of this chapter).
Emerging growth company
If an emerging growth company, indicate by check mark if the registrant has elected not to use the extended transition period for complying with any new or revised financial accounting standards provided pursuant to Section 13(a) of the Exchange Act.
Item 7.01 Regulation FD Disclosure.
On November 10, 2026, Acrivon Therapeutics, Inc. (the “Company”) hosted a webcast corporate R&D event with Eosinophilic esophagitis (EoE) Key Opinion Leaders to discuss Acrivon’s new immunology and inflammation (I&I) programs, acquired using its AI-driven AP3 platform. The webcast took place from approximately 4:00 p.m. to 5:00 p.m. ET.
The agenda featured a presentation by the Company’s leadership team introducing the ACR-525 and PKCθ inhibitor preclinical programs and initial development plans in EoE, followed by an overview of EoE epidemiology and unmet need by Dr. Arjan Bredenoord (principal investigator and professor, Gastroenterology and Hepatology, Amsterdam University Medical Center) , a review of EoE standard of care by Dr. Evan Dellon (professor, Department of Medicine, Division of Gastroenterology and Hepatology and Director, Center for Esophageal Diseases and Swallowing, School of Medicine, University of North Carolina at Chapel Hill), and an interactive Q&A session and discussion.
In connection with this event, the Company posted to the “Investors & Media” section of the Company’s website at ir.acrivon.com, the presentation used in the event (the “Presentation”).
A copy of the Presentation is attached hereto as Exhibit 99.1 and is incorporated by reference into this Item 7.01 of this Current Report on Form 8-K.
The information in this Item 7.01, including Exhibit 99.1 attached hereto, shall not be deemed “filed” for purposes of Section 18 of the Exchange Act, or otherwise subject to the liabilities of that section, nor shall it be deemed incorporated by reference in any filing under the Securities Act or the Exchange Act, except as expressly set forth by specific reference in such filing.
Item 9.01 Financial Statements and Exhibits.
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Acrivon Therapeutics, Inc., Presentation |
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SIGNATURES
Pursuant to the requirements of the Securities Exchange Act of 1934, the registrant has duly caused this report to be signed on its behalf by the undersigned hereunto duly authorized.
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Acrivon Therapeutics, Inc. |
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November 10, 2026 |
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/s/ Peter Blume-Jensen, M.D., Ph.D. |
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Name: Peter Blume-Jensen, M.D., Ph.D. |
CORPORATE R&D AND KOL EVENT ACRIVON’S NEW I&I PROGRAMS DIFFERENTIATED ASSETS IDENTIFIED WITH PROPRIETARY AP3 PLATFORM NOVEMBER 10, 2026 Exhibit 99.1
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 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 statements. You are cautioned not to place undue reliance on these forward-looking statements, which are made only as of the date of this presentation. We undertake no obligation to update any forward-looking statements or to reflect new information or the occurrence of unanticipated events, except as required by law. Note: Acrivon intends to use its website as a means of disclosing material non-public information and for complying with its disclosure obligations under Regulation FD. For more information, please visit www.acrivon.com and follow the company on LinkedIn.
Today’s agenda Today’s agenda Welcome Adam Levy, PhD, MBA, CFO Introduction and Overview Peter Blume-Jensen, MD, PhD, CEO EoE epidemiology and unmet need Arjan Bredenoord, MD, PhD EoE SOC (ACG Guidelines) Evan Dellon, MD, MPH Q&A and Discussion Mansoor Mirza, MD, CMO Adjourn Peter Blume-Jensen, MD, PhD, CEO
Today’s Participants Arjan Bredenoord, M.D., Ph.D. Professor, Gastroenterology and Hepatology, Amsterdam University Medical Center; Former President of the European Society of Eosinophilic Esophagitis EUREOS, a member of the UEG Scientific Committee Evan Dellon, M.D., M.P.H. Professor, Department of Medicine, Division of Gastroenterology and Hepatology; Director, Center for Esophageal Diseases and Swallowing, School of Medicine, University of North Carolina at Chapel Hill Mansoor Raza Mirza, M.D. Chief Medical Officer, Acrivon Therapeutics; Formerly Chief Oncologist at Copenhagen University Medical School; Lead PI for numerous guideline-changing regulatory approvals Peter Blume-Jensen, M.D., Ph.D. Chief Executive Officer, President and Co-Founder, Acrivon Therapeutics; Formerly Executive at Serono, Merck & Co., Daiichi Sankyo, Metamark Genetics; Inventor of the AP3 Platform Erick Gamelin, M.D., Ph.D. Chief Development Officer, Acrivon Therapeutics; Formerly CEO for national cancer center; Executive at Pfizer, AMGEN, Dynavax, Macrogenics; Chevalier in the National Order of Merit by the French Minister of Health
next-generation precision medicine powered by AP3 Drug P Acrivon Predictive Precision Proteomics (AP3) Generative AI-driven, proteomics-based rational drug design and informed clinical development AP3 enables an exact match between the disease-driving, dysregulated pathways with drug mechanism of action (Acrivon meaning ≈ exact, accurate) DNA RNA Protein Dysregulated Protein Dysregulated Pathways Proprietary tools Data portal Interactome Protein activity predictor I&I Cancer Fibrosis Disease focus
AP3 Generative AI phosphoproteomics platform Matching global drug effects with disease driving mechanisms Global MS Phosphoproteomic Profiling Biological Multimodal Data Patient responder prediction Indication Finding Drug combinations Target ID Drug Resistance Global PD markers Asset prioritization AP3 Deliverables Structured AI-enabled Comprehensive Profiling of Drug Effects AP3 Data Portal Acrivon Proprietary Generative AI-driven tools Streamlined Clinical Development
our Pipeline Phase 3 Phase 2 Phase 1 Preclinical ACR-368 (CHK1/CHK2) Single-arm trial based on OncoSignature biomarker prediction Endometrial cancer AP3-identified tumor types ACR-525 (JAK1) ACR-368 single-agent · Breakthrough Device & Fast Track · Arm 1 ACR-2316 (WEE1/PKMYT1) Dose expansion AP3-identified tumor types ACR-7280 (CDK11) IND-enabling Single-arm trials without pretreatment biopsy or biomarker stratification ACR-368 + ULDG sensitization · Arm 3 BM+ patients, registrational intent Serous all-comer arms, registrational intent ACR-368 single-agent · Arm 4 Eosinophilic esophagitis (EoE) Phase 2 ready PKCθ AP3-identified indications Discovery Oncology I&I Today’s topic
FIRST AP3-based I&I PROGRAM: Phase 2-ready, oral, SELECTIVE jak1 INHIBITOR, ACR-525 (also known as AQ280) AP3 profiling Differentiated profile Phase 1 clinical data Extensive AP3 profiling against approved JAK inhibitors and dupilumab Desirable global phospho-proteomic pathway effects Highly JAK1-selective, oral Desirable suppression of TGFb signaling (anti-fibrotic) No obvious pro-apoptotic BAD activation (potential safety advantage) Broader anti-inflammatory effects beyond IL-4 and IL-13 signaling than dupilumab Clinical PD/PK data support once daily oral dosing based on preclinical PD/PK/efficacy studies Favorable initial safety and dose-dependent PD (CXCL10) decrease Development path Phase 2-ready Initial development in eosinophilic esophagitis (EoE), but broader I&I opportunity Strong combo rationale with IL-23i, TNFi, PKC-Θi Wholly-owned, no milestone or royalty obligations CoM protection: 2038 (with extension opportunities)
ACR-525 compares favorably to clinical benchmarks Clinical comparators Disease-relevant cellular models AP3 phosphoproteomics Generative AI-enabled pathway insights ACR-525 Upadacitinib Filgotinib Abrocitinib Tofacitinib Brepocitinib Londamocitinib Y IL-4Rα antibody Tight, robust, structured data Dupilumab IFNa-stimulated Th2-polarized (TCR, IL-4) AP3 pathway mapping shows differentiated, high selectivity against JAK2, JAK3, and TYK2 signaling, suggesting potential for improved efficacy and safety over existing JAK inhibitors ACR-525 potently reduces inflammatory cytokine signaling activity IL-4 stimulation - + ACR-525 pSTAT6 + + - -
Generative AI-driven AP3 analyses uncover TGFb pathway suppression by Acr-525, a potential antifibrotic mechanism ACR-525-regulated pathway activity states Suppression of Non-SMAD TGFb pathway JAK1 STAT3 TGFβR1 P Fibrotic target genes ACR-525 Dupilumab Upadacitinib Brepocitinib Londamocitinib Control AP3 reveals ACR-525-induced inhibition of non-SMAD TGFb signaling activity JAK1-regulated non-SMAD TGFb signaling is reported to drive fibrotic processes ACR-525 (and dupilumab), unlike other JAK inhibitors, inhibit STAT3 pS727, a marker of non-canonical TGFb pathway activity
ACR-525 does not activate pro-apoptotic BAD signaling, suggesting a potential safety advantage PAK1 BRAF BAD Apoptosis P S134 Th2 condition (TCR activation and IL4 stimulation) ACR-525 dupilumab Upadacitinib Brepocitinib Londamocitinib Control DMSO BAD_S134_M1 Log2 Intensity P Phosphorylation Differential JAK1 inhibitor regulation of BAD S134 phosphorylation Decreased BAD-S134 phosphorylation can lead to pro-apoptotic cell death ACR-525 Apoptosis pathways Brepocitinib JAK1 inhibitor engaged phospho-pathway network IL4-JAK1 pathways AP3 pathway reconstitution shows differential engagement of apoptosis pathways by brepocitinib and londamocitinib compared to ACR-525 Brepocitinib and londamocitinib uniquely suppress phosphorylation of BAD S134, releasing its pro-apoptotic function, a potential rhabdomyolytic liability MAPK pathways Cytokine, RTK signaling Cell cycle GTPases Ubiquitination Sumoylation
Molecule Relative potency (biochemical IC50) JAK1/JAK2 Relative potency (cellular IC50) JAK1/JAK2 (right panel) ACR-525 49× JAK1: 3.5 JAK2: 171 >120× IFNα ~24 GM-CSF >3,000 Abrocitinib 28× JAK1: 29.2 JAK2: 803 >90× IFNα ~34 GM-CSF >3,000 BMS-911543 0.01× JAK1: 75 JAK2: 1.1 0.40× IFNα ~1,300 GM-CSF ~540 Fedratinib 0.03× JAK1: 105 JAK2: 3 6× IFNα ~170 GM-CSF ~980 Filgotinib ~1x JAK1: 10–53 JAK2: 28–29 19× IFNα ~400 GM-CSF ~7,500 Tofacitinib 1.3× JAK1: 3.2 JAK2: 4.1 30× IFNα ~20 GM-CSF ~610 Upadacitinib 2.8× JAK1: 43 JAK2: 120 >4× IFNα <30 GM-CSF ~110 Brepocitinib* 4.6× JAK1: 16.8 JAK2: 76.6 24× IFNα 85 GM-CSF 1,995 Grey values in nM. Ratios >1 favor JAK1-selective inhibition. *Brepocitinib: Public data only ACR-525 is potent and highly selective for JAK1 comparing favorably to other jak inhibitors ACR-525 [ACR-525] nM JAK1 read-out (IFNα / pSTAT1 ) JAK2 read-out (GM-CSF / pSTAT5 ) Cellular pathway engagement [ACR-525] nM
ACR-525 dose-dependently reduces Th2-relevant disease markers in preclinical and clinical studies Log [ACR-525] (mM) Log [ACR-525] (mM) ACR-525 reduces the inflammation marker CXCL10 (Phase 1 MAD) ACR-525 reduces pSTAT3 in Th2 allergic inflammation in vivo mouse model ACR-525 reduces EoE Th2 inflammation markers (ex vivo stimulated human donor whole blood) Summary of Phase 1 healthy volunteer studies PD biomarker changes consistent with JAK1-selective inhibition Limited effect on reticulocytes (consistent with minimal JAK2 inhibition) Dose-proportional, predictable PK (T1/2 ~12h) Safe and tolerable – no SAEs Preclinical Clinical ACR-525 Abrocitinib Tofacitinib Dose-proportional PK (Phase 1)
Kleuskens et al. DDW 2026 JAK1 plays a central role in EoE Key cytokines IL-4 and IL-13 signal via JAK1-STAT6 Several critical Single Nucleotide Polymorphisms (SNPs) within the JAK-STAT signaling pathway in EoE JAK inhibitors are effective for atopic dermatitis Case reports show efficacy of JAK inhibition in EoE Modified from: B.Underwood et.al, Annals of Allergy, Asthma & Immunology, January 2023
JAK1 is a key mediator of inflammatory signaling in EoE EoE, an attractive first indication for ACR-525 IL-13 IL-4 IL-15 OSM IL-9 IL-5 TSLP Esophageal epithelium Th2 inflammation Eosinophils Mast cells APCs Stromal / epithelial cells TSLP IL-7Rα / CRLF2 JAK1 IL-4 γc / IL-4Rα JAK1 IL-13 IL-4Rα / IL-13Rα1 JAK1 IL-5 IL-5Rα / βc JAK1 IL-9 IL-9Rα / γc JAK1 IL-15 IL-2/15Rβ / γc JAK1 OSM gp130 / OSMR or LIFR JAK1 ACR-525 Y Y dupilumab Y Y tezepelumab cendakimab Dupilumab (approved) targets only IL-4 and IL-13 Tezepelumab and cendakimab (Phase 3) target only TSLP and IL-13, respectively
ACR-525 Epithelium Th2 inflammation Eosinophils Mast cells APCs Stromal/ Epithelial cells dupilumab tezepelumab cendakimab ACR-525 prevents il-13 and OSM-induced epithelial barrier damage Broader activity than Dupilumab, which fails to prevent OSM damage Medium IL-13 DMSO + IL-13 ACR-525 + IL-13 Isotype + IL-13 Dupiliumab + IL-13 Medium IL-13 DMSO + IL-13 ACR-525 + IL-13 Isotype + IL-13 Dupiliumab + IL-13 Medium OSM DMSO + OSM ACR-525 + OSM Isotype + OSM Dupiliumab + OSM Medium OSM DMSO + OSM ACR-525 + OSM Isotype + OSM Dupiliumab + OSM IL-13 OSM Kleuskens et al. Digestive Diseases Week 2026 EoE model
Huge increase in EoE over the past 25 years Dellon and Hirano, Gastroenterology 2018
EoE – a rapidly growing patient population of unmet need Growth Metric US Estimate Prevalence in 2009 28.3/100,000 Prevalence in 2022 163.1/100,000 Total increase over 13 years +477% Average annual growth ~14.4% Equivalent growth every 5 years ~96% Multiplication over 13 years 5.8× Annual Incidence (US): ~120,000 Current prevalence (US): >500,000 Greenhawt M, Bansal P, Goodwin B, et al. (2025) Journal of Allergy and Clinical Immunology Thel HL, Anderson C, Xue AZ, Jensen ET, Dellon ES. (2025)Clinical Gastroenterology and Hepatology.
EoE burden: symptoms and chronic therapy EoE leads to esophageal obstruction: inability to pass solid foods EoE leads to a profound loss in health-related quality of life EoE is chronic and leads to fibrostenosis Requires long-term treatment for symptom control and prevention of esophageal scarring Dellon & Hirano Gastroenterology 2018; Bredenoord et al. Am J Gastroenterol 2022 EGD Normal Histology EoE inflammation EoE inflammation + fibrosis EoE fibrosis
EoE treatment algorithm – ACG guidelines 2025 EoE diagnosis established Treat inflammation and assess for fibrostenosis in all patients Anti-inflammatory treatment Pharmacologic treatment Diet elimination treatment Shared decision-making PPI Topical steroids Empiric elimination Assess response Fibrostenosis reassessment Stricture or narrowing present Dilation Goal diameter of 16–18 mm Non-response Response Dupilumab Change or modify prior treatments Assess response Non-response Maintenance therapy and long-term monitoring Response Dellon et al; AJG; 2025
Unmet need in EoE – new treatments are still needed First line therapies: Suboptimal responses (>50% may be non-responders) Adherence difficulties (twice daily dosing; restrictive diets) Concern for side effects Loss of response is frequently observed Biologics Currently position as “step-up” and second line agents Require frequent injections There are no advanced small molecule orally-available medications at either the first or second line for EoE treatments A highly specific, oral JAK1 inhibitor, if proven to be safe and effective, would fill an important treatment gap and unmet need
Preclinical PKCθ program PKCθ plays critical role in T cell activation Key role in T-cell activation Induces NF-κB and AP-1 activation Strong evidence based on extensive preclinical studies Mouse colitis, allergic airway and human RA studies uncover key role of PKCθ in T cell-mediated inflammation Selected primary studies: Sun, Nature 2000. Marsland, J Exp Med 2004. Nagahama, Gastroenterology 2008. Zanin-Zhorov, Science 2010. Kong, Nat Immunol 2011. T cell signaling APC Cell–cell interface Effector T cell TCR CD28 PKCθ IKK NF-κB AP-1 Nucleus APC - T cell synapse APC Effector T cell PKCθ PKCθ recruited to immune synapse to mediate T cell activation SPAK ACR-525+PKCθi combination rationale JAK/STAT pathways converge with PKCθ for Th2/Th17 activation
Preclinical PKCθ program PKCθ plays critical role in T cell activation Selected primary studies: Sun, Nature 2000. Marsland, J Exp Med 2004. Nagahama, Gastroenterology 2008. Zanin-Zhorov, Science 2010. Kong, Nat Immunol 2011. ACR-525 + PKC-θi rational combination Cytokine receptors TCR / CD28 JAK1 PKCθ ACR- 525 PKCϴi STAT NF-κB / AP-1 Inflammatory T-cell function Activated T cell Broad potential: UC, RA, psoriasis, atopic dermatitis, allergic asthma, SLE Potent PKCθ inhibition Potent activity in human immune cells High selectivity over PKCδ Low clearance in human hepatocytes ✓ ✓ ✓ ✓ Promising PKCθ inhibitor lead series
AP3 ACR-525 profiled H:H against 6 approved JAK inhibitors and dupilumab Broader indication potential JAK1-selectivity + distinct TGFβ pathway suppression Benchmark differentiation Selectivity, oral availability, and desirable pathway potency Safety-related profiling No pro-apoptotic BAD phosphorylation Phase 2-ready ACR-525 is highly differentiated and compares favorably to approved jak inhibitors EoE targeted as a first indication for ACR-525
Q&A and Discussion
appendix
AP3 generative AI-driven phosphoproteomics profiling global, cellular drug pathway effects and compound differentiation AP3 Generative AI-driven phosphoproteomics analytics Drug-regulated pathway perturbation Drug-regulated kinase activity Drug-regulated phosphosites Drug treatment LC-MS/MS profiling ADC Bispecific Small molecule Cells or tissue samples
Infectious, CNS, and other diseases Oncology Fibrotic and inflammatory Autoimmune DDR and Cell Cycle Therapeutic areas Therapeutic modalities Small molecule Bifunctional molecule Antibody ADC Oligo/RNA The AP3 Approach is modality and disease agnostic AP3 Oncology programs AP3 I&I programs
Preclinical PKCθ program PKCθ plays critical role in T cell activation Critical role in T-cell activation Supports NF-κB and AP-1 activation and cooperates with calcium/NFAT signaling. Effector–regulatory balance Convergence with JAK/STAT mediated Th2/Th17 pathways Strong rationale based on extensive preclinical studies Mouse colitis, allergic airway and human RA Treg studies suggest PKCθ exterts a critical role in T cell-mediated inflammation Selected primary studies: Sun, Nature 2000. Marsland, J Exp Med 2004. Nagahama, Gastroenterology 2008. Zanin-Zhorov, Science 2010. Kong, Nat Immunol 2011. T-cell signaling APC Peptide–MHC CD80/CD86 (B7) Cell–cell interface Effector T cell TCR CD28 PKCθ Synaptic recruitment CBM complex CARD11/CARMA1 BCL10–MALT1 IKK Ca²⁺ / calcineurin Context-dependent NFAT NF-κB AP-1 Nucleus Gene transcription Synapse localization APC Effector T cell Immunological synapse PKCθ PKCθ recruitment to the effector T-cell synapse
Development opportunities: AP3-DEFINED RATIONAL COMBINATIONS WITH ACR-525 ACR-525 + PKC-θi ACR-525 + IL-23i Cytokine receptors TCR / CD28 JAK1 PKCθ ACR- 525 PKCϴi STAT NF-κB / AP-1 Inflammatory T-cell function IL-23 Tremfya IFNγ / IL-6 IL-23R JAK2 / TYK2–STAT3 JAK1 ACR- 525 IL-23-responsive Th17 / ILC3 STAT responses in immune, stromal / epithelial cells Mucosal inflammation Activated T cell Myeloid cells (DCs / macrophages) ACR-525 + TNFi Immune, epithelial and stromal cells TNF IFNγ / IL-6 TNFi TNFR JAK1 ACR- 525 NF-κB / MAPK STAT Inflammation + epithelial injury Indication potential: UC, RA, psoriasis, atopic dermatitis, allergic asthma, SLE Indication potential: Crohn’s, UC, psoriatic arthritis, plaque psoriasis, uveitis Indication potential: Candidate indications: IBD, RA, AS High selectivity and oral availability of ACR-525 provides for broad combination potential