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BeOne’s Innovative Pipeline Progress Investor R&D Day JUNE 26, 2025
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2 Forward-looking Statements Certain statements contained in this presentation and in the accompanying oral presentation, other than statements of fact th at are independently verifiable at the date hereof, constitute forward looking statements. Examples of such forward-looking statements include statements regarding the projected size of the oncology market and related sectors; BeOne’s research, discovery, pre-clinical and early-stage clinical programs and plans including proof of concept timing; the adv ancement of and anticipated clinical development and the conduct of late-stage clinical trials; expected data readouts and approvals; projected regulatory milestones and commerc ialization of BeOne’s medicines; the ability of BeOne’s assets to meaningfully outperform current medicines and address all lines of therapy; the potential for BeOne to have a significant market share in hematologic diseases; the ability for BeOne to become the most impactful global oncology company; and BeOne's future growth and financial performan ce. Actual results may differ materially from those indicated in the forward-looking statements as a result of various important factors, including BeOne's ability to demonstrate t he efficacy and safety of its drug candidates; the clinical results for its drug candidates, which may not support further development or marketing approval; actions of regulat ory agencies, which may affect the initiation, timing and progress of clinical trials and marketing approval; BeOne's ability to achieve commercial success for its marketed medicines and drug candidates, if approved; BeOne's ability to obtain and maintain protection of intellectual property for its medicines and technology; BeOne's reliance on third parties t o conduct drug development, manufacturing, commercialization and other services; BeOne’s limited experience in obtaining regulatory approvals and commercializing pharma ceutical products; BeOne’s ability to obtain additional funding for operations and to complete the development of its drug candidates and maintain profitability, as well as those risks more fully discussed in the section entitled “Risk Factors” in BeOne’s most recent periodic report filed with the U.S. Securities and Exchange Commission ("SEC") , as well as discussions of potential risks, uncertainties, and other important factors in BeOne's subsequent filings with the SEC. Except where otherwise noted, all information in this presentation is as of the date of this presentation, and BeOne undertakes no duty to update such information unless required by law. This presentation and the accompanying oral presentation contain data and information obtained from third-party studies and internal company analysis of such data and information. BeOne has not independently verified the data and information obtained from these sources. Forward -looking information obtained from these sources is subject to the same qualifications noted above. This presentation is intended for the investor community only; it is not intended to promote the products referenced herein o r otherwise influence healthcare prescribing decisions. All trademarks in this presentation are the property of their respective owners. Some of the clinical data in this presentation relating to BeOne’s investigational drug candidates is from pre -clinical studies or early phase, single-arm clinical trials. When such data or data from later stage trials are presented in relation to other investigational or marketed drug products, the presen tation and discussion are not based on head-to-head trials between BeOne’s investigational drug candidates and other products unless specified in the trial protocol. BeOne is st ill conducting pre-clinical studies and clinical trials and, as additional patients are enrolled and evaluated, data on BeOne’s investigational drug candidates may change. Definitive conclusions cannot be drawn from cross-trial comparisons or anticipated data as they may be confounded by various fac tors and should be interpreted with caution.
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3 Agenda Welcome, safe harbor, and agenda Liza Heapes, Senior Director, Investor Relations 01 Global oncology leadership John V. Oyler, Co-Founder, Chairman and CEO 02 R&D strategy and overview Lai Wang, PhD, Global Head of R&D 03 Hematology portfolio Lai Wang Remus Vezan, MD, PhD, VP, Hematology Clinical Development Jacob D. Soumerai, MD, Assistant Professor of Medicine, Harvard Medical School Hematologist / Oncologist, Mass General Hospital Cancer Center Amit Agarwal, MD, PhD, VP, Hematology Clinical Development 04 Solid tumor portfolio Mark Lanasa, MD, PhD, SVP, Chief Medical Officer, Solid Tumors Dr. Shom Goel, MBBS, PhD, Group Leader and Medical Oncologist, Peter MacCallum Cancer Centre 05 Summary Lai Wang 06 Q&A BeOne management team and key opinion leaders Moderator: Aaron Rosenberg, CFO 07 Closing John V. Oyler B R E A K
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4 Global oncology leadership John V. Oyler Co-Founder, Chairman and CEO
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5 is a global oncology company that was built differently to deliver innovative medicines faster, more equitably and affordably to patients around the world
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6 3,700+ global development and medical affairs team 6 continents, 40 offices, 11,000+ colleagues 1,200+ proven research team In-house manufacturing including $800M U.S. flagship facility in New Jersey Purpose built with sustainable competitive advantages Leading science Superior returnsGlobal access We have treated >1.7 million patients with our medicines globally
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7 BeOne is driven by purpose: Transform cancer care and transcend borders to enable more affordable access to more patients here, and all around the world Our commitment to business sustainability Operating responsibly Innovating sustainably Empowering our colleagues Advancing global health
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8 Updates and new programs What you will hear today – industry leadership in R&D Our unique R&D model is delivering • Proven quality, speed, cost, and technological advantages • Diversified modalities, proprietary combinations, and scientific leadership 01 Hematology - serial innovation to drive sustained leadership • Wholly-owned combinations of foundational assets BRUKINSA, sonrotoclax, and BTK CDAC to comprehensively address unmet needs in CLL • Broadening beyond CLL, lymphomas e.g., B cell malignancies, MM 02 Solid tumors – breadth and depth across areas of focus • Burgeoning franchises in breast, lung, and GI cancers each anchored by potentially best-in-class assets and combinations 03 CDAC – chimeric degradation activating compound, TCE - T-cell engager, ADC – antibody drug conjugate, TsAb – trispecific antibody Hematology BRUKINSA Sonrotoclax BTK CDAC TCEs Breast/Gyn CDK4i B7-H4 ADC CDK2i/CDAC KAT6A/B Lung PRMT5i MAT2Ai EGFR CDAC/TsAb GI PanKRASi/CDAC RAS(ON) FGFR2b ADC I&I IRAK4 CDAC
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9 R&D strategy and overview Lai Wang, PhD Global Head of R&D
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10 BeOne R&D stands at an inflection point Proven capabilities converging to create a unique R&D model Prolific research organization Global manufacturing and process development Time, cost, and quality advantaged clinical development infrastructure Global commercial access Superior R&D returns
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11 Preclinical program numbers Internally developed NMEs entered clinic 2013-18 2019 2020 2021 2022 2023 20242011-18 2019 2020 2021 2022 2023 2024 2025 Evolution of BeOne’s scaled research organization New era of prolific, quality scientific output based on diversified modalities 7* 20 56 34 6666 8277 *Average numbers per year; SM, Small Molecule; CDAC, Chimeric degradation activation compound; ADC, Antibody drug conjugate; Bs/Ts Ab: Bispecific/Trispecific Antibody CDACTraditional SM ADCBs/Ts AbmAb OthersCell Therapy TIGIT PD1 BTKi BCL2i PI3Kdi OX40 BRAFi TYK2i HPK1i BTK CDAC SMAC mimetics CEA x 4-1BB DGKζi CDK4i BCL2i 2G HPK1i 2G CCR8 KRASi EGFR CDAC Pro-IL15 IRAK4 CDAC MUC1 x CD16 a FGFR2b ADC GPC3 x 4-1BB B7-H3 ADC CEA ADC EGFRxMETxMET TsAb 10 5 3 2 4 1 1*
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12 More potent and selective design aiming to improve efficacy and safety, respectively Shorter half-life for ease of TLS* monitoring Sonrotoclax First-in-class, retain ligand binding to avoid on-target ocular toxicity induced by mAb FGFR2b ADC First-in-class, fast ternary complex formation to drive complete degradation No QT issue IRAK4 CDAC Successful innovation with the same approach as BRUKINSA and now in parallel across many programs Perform the critical experiment and only advance high-quality molecules to clinic Halt programs that don’t meet our high standard • Over the past 3.5 years, 60+ pre-clinical programs terminated We focus on delivering high-quality innovation Committed to designing superior molecules with exceptional profiles TLS, Tumor lysis syndrome
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13 Establish scientific leadership in protein degradation - CDAC Over 20 programs including degrader antibody conjugate (DAC) GI, Gastrointestinal; CDAC, Chimeric degradation activation compound; DAC, Degrader antibody conjugate; Cut -off date: MAY2025 INDDiscovery Clinical KRAS CDAC CDAC 9 CDAC 13 Gastrointestinal EGFR CDAC KRAS CDAC CDAC 13 CDAC 9 CDAC 14 CDAC 15 Lung CDK2 CDAC CDAC 9 CDAC 10 CDAC 12 CDAC 11 DAC 3 Breast / Gynecologic BTK CDAC CDAC 6 CDAC 7 CDAC 8 DAC 1 DAC 2 Hematology CDAC 18 IRAK4 CDAC CDAC 19 CDAC 20 Non-Oncology CDAC 16 CDAC 17 DAC 3 Other Tumors
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14 Address various challenges in drug discovery via our industry-leading CDAC platform CDAC A D V A N T A G E Spare tissue- specific toxicity Drug undruggable Destroy scaffold function Solve low potency issue Gain selectivity Reduce on-target resistance KRAS CDAC EGFR CDAC, CDK2 CDAC BTK CDAC, EGFR CDACBTK CDAC, IRAK4 CDAC Multiple targets Target X
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15 Emerging player in ADC field Robust dual-TAA and novel payload ADC pipeline to drive next waves of innovation ADC, Antibody drug conjugate; DAC, degrader antibody conjugate; mADC, monospecific ADC; BsADC, bispecific ADC; TsADC, trispecific ADC; TAA, tumor associated antigen Cut-off date: 2025 May Lung EGFRxMETxMET Bs/TsADC 3 Bs/TsADC 4 Bs/TsADC 5 Bs/TsADC 6 Bs/TsADC RAS (ON)i ADC Novel ADC 3 Novel ADC 4 Novel payload ADC B7-H3 ◆ CEA ◆ ADAM9 mADC 7 mADC 8 mADC ◆ Clinical stage l Breast / Gynecologic B7-H4xHER3 Bs/TsADC Novel ADC 3 Novel DAC 3 Novel payload ADC B7-H4 ◆ mADC l Gastrointestinal EGFRxMETxMET Bs/TsADC 3 Bs/TsADC 4 Bs/TsADC 7 Bs/TsADC 8 Bs/TsADC 9 Bs/TsADC 10 Bs/tsADC RAS (ON)i ADC Novel ADC 4 Novel payload ADC B7-H3 ◆ FGFR2b ◆ CEA ◆ mADC Hematology Novel DAC 1 Novel DAC 2 Novel ADC 2 Novel payload ADC mADC 6 mADC
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16 Technology platforms enable us to build disease franchise Our CLL franchise has been a great success Approval indicates first (anticipated) CLL approval in a major market (US, EU, JP, CN) FIH, First in human BRUKINSA 2012 Initiation 2014 FIH 2020 Approval Sonrotoclax 2017 Initiation 2020 FIH 2026 Approval BTK CDAC 2019 Initiation 2022 FIH 2027 Approval
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17 Now, we can scale success across our disease areas of focus much faster Build a deep pipeline by aiming to deliver 8-10 highly differentiated NMEs into clinic in each of the following disease areas in the next 3-6 years B-Cell Malignancies Lung Breast/ Gynecological Gastrointestinal Immunology and Inflammation (I&I) AML/MDS
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18 BRUKINSA Sonrotoclax EGFR CDAC EGFR x MET x MET TsAb MTA-cooperative PRMT5i MAT2Ai Deep pipeline enables unique and proprietary combinations TCE, T-cell engager; TsAb, trispecific antibody; Target(i): target inhibitor + + B-Cell malignancies Lung Gastrointestinal + + CD3 TCE T-cell booster KRASi/KRAS CDAC RAS (ON)i +
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19 Our philosophy, scale, and sense of urgency has led to an industry-leading pipeline Molecule Indication Phase BRUKINSA® Zanubrutinib (BTKi) TN CLL/SLL Approved R/R CLL/SLL Approved R/R WM and TN WM Approved R/R FL Approved R/R MCL Approved R/R MZL Approved TN MCL Phase 3 B-Cell Malignancies Phase 2 pMN Phase 3 TEVIMBRA® Tislelizumab (PD1 mAb) 1L ES-SCLC Approved IL NonSq NSCLC Approved 1L Sq NSCLC Approved 2/3L NSCLC Approved Neo/Adj NSCLC Approved IL ESCC Approved 2L ESCC Approved 1L GC/GEJC Approved 1L HCC Approved 2/3L HCC Approved R/R cHL Approved 1L NPC Approved Late Line MSI-H or dMMR Approved 2L UBC Approved 1L UBC Phase 3 SubQ Formulation Phase 1 Molecule Indication Phase Sonrotoclax (BCL2i) TN CLL/SLL Phase 3 R/R CLL/SLL Phase 3 R/R MCL Phase 3 R/R WM Phase 2 R/R MM with t(11;14) Phase 1 AML/MDS Phase 1 B-Cell Malignancies Phase 1 BGB-16673 (BTK CDAC) R/R CLL/SLL Phase 3 R/R MCL Phase 2 B-Cell Malignancies Phase 1 Chronic spontaneous urticaria Phase 1 IMDELLTRA® Tarlatamab (DLL3 x CD3 BITE®) 1 1L ES-SCLC Phase 3 2L ES-SCLC Phase 3 LS-SCLC Phase 3 3L+ ES-SCLC Phase 2 2L+ ES-SCLC SubQ Formulation Phase 1 ZIIHERA® Zanidatamab (HER2 BsAb) 2 2L+ HER2+ BTC Approved 1L HER2+ GEA Phase 3 BLINCYTO® Blinatumomab (CD3 x CD19 BITE®)1 R/R B-ALL SC Phase 2 PARTRUVIX® Pamiparib (PARPi) 3L+ PSOC & PROC/PSOC Approved BGB-43395 (CDK4i) BC and Solid Tumors Phase 1 BG-68501 (CK2i)3 BC and Solid Tumors Phase 1 BG-C9074 (B7-H4 ADC)4 BC and Solid Tumors Phase 1 BGB-B455 (CLDN6 x CD3 BsAb) Gyn and Solid Tumors Phase 1 1) Amgen collaboration, 2) Zymeworks/Jazz collaboration, 3) Ensem collaboration, 4) DualityBio collaboration, 5) CSPC collaboration Molecule Indication Phase BGB-21447 (BCL2i 2G) HR+/HER2- BC Phase 1 B-cell Malignancies Phase 1 BG-60366 (EGFR CDAC) Lung Cancers Phase 1 BG-T187 (EGFR x MET TsAb) Lung Cancers Phase 1 BGB-58067 (MTA Coop. PRMT5i) Lung Cancers Phase 1 GI Cancers Phase 1 BG-89894 (MAT2Ai)5 Lung Cancers Phase 1 GI Cancers Phase 1 BGB-53038 (PanKRASi) Lung Cancers Phase 1 GI Cancers Phase 1 BG-C477 (CEA ADC) Lung Cancers Phase 1 GI Cancers Phase 1 BGB-B3227 (MUC1 x CD16A BsAb) Lung Cancers Phase 1 GI Cancers Phase 1 BGB-2033 (GPC3 x 4-1BB BsAb) GI Cancers Phase 1 BG-C137 (FGFR2b ADC) GI Cancers Phase 1 BGB-A3055 (CCR8 mAb) Solid Tumors Phase 1 BGB-26808 (HPK1i) Solid Tumors Phase 1 BGB-C354 (B7-H3 ADC) Solid Tumors Phase 1 BGB-R046 (IL-15 Prodrug) Solid Tumors Phase 1 BGB-30813 (DGKζi) Solid Tumors Phase 1 Xaluritamig (STEAP1 x CD3 XmAb®)1 mCRPC Phase 1 BGB-45035 (IRAK4 CDAC) Immunology & Inflammation Phase 1 Approved Ph 3 Ph 1/2 Heme Breast / Gyn Other CancersLung GI I&I
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20 # of trials by TA # of trials by phase # of Phase 1 trials by modality 54 37 5 Solid Tumor Heme I&I 5 24 23 44 Ph4 Ph3 Ph2 Ph1 19 13 7 4 1 SM Antibody Degrader ADC Other Proliferation of trials across phases, modalities, and disease areas Ongoing trials as of 28MAY2025 includes trials with Start-up, Enrolling, Maintenance, Close -out status Planned submissions through 2H26 30 Assets with active clinical development 96 Ongoing clinical trials 154 (83 countries) Ongoing or planned submissions 225 (75 countries) Total approvals
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21 2013 2026+202320222017 2024 2025 It took substantial effort to build our global clinical development organization, but it is now firing on all cylinders Start clinical development Build global clinical development capability Streamline the process Leverage AI/automation to achieve optimal efficiency Today
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22 Our 3,700+ global clinical development team is complex and spans many functions CDx: Companion diagnostic; PV: Pharmacovigilance Regulatory Policy & Intelligence Portfolio Strategy and Management Regulatory CMC Labeling Clinical Operations Compliance Quality Management Operations Statistics Data Management y Country and Site Management yy Clinical Supply Chain Program and Study Management yClinical Development Regulatory Operations Safety Science and Epidemiology Safety Operations Global and Regional Regulatory Strategy Digital and AI Solutions R&D Sourcing International PV CO Digital Solutions Project and Portfolio System and Reporting Clinical Biomarker Science Clinical Bioinformatics Biomarker Operations Medical Writing CDx Development Medical Translation yScientific Programming Clinical Pharmacology and Pharmacometrics Medical Affairs
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23 Over 100 inspections by 15 different health authorities across 10+ countries with zero critical findings Tremendous speed all around the world, including in hard to access regions Lower cost trials by eliminating CRO with internal operating model Established strong direct site relationships to enable operational efficiency Leveraging internal global clinical capabilities to drive speed, cost, quality, and site access
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24 BeOne’s patient enrollment spans diverse regions, reflecting our commitment to global representation Data as of 27MAY2025 Global patient enrollment in 2025 Broad and diverse global enrollment across distinct regions Growing representation in emerging markets 1% 2% 4% 5% 5% 18% 19% 22% 25% Southeast Asia Middle East Eastern Europe Japan and Korea LATAM Australia and New Zealand Western Europe North America China
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25 Streamline drug development process toward perfection, delivering with rigor and speed Data represents FSE, dose escalation cohort, or Ph1 dose expansions initiated since 01JAN2024 Start of GLP tox study to first subject enrolled (FSE) in Phase 1a Time per dose escalation cohort Initiate dose expansion after recommended dose identified 3.6 weeks in average from draft tox report to protocol finalization 1.2 weeks from protocol finalization to EC submission in AUS 2.6 weeks from last piece of data to IND submission in U.S. Initiate CDP discussion ~9m prior to the predicted completion of dose escalation Completion of critical documents earlier (protocol amendment, IND/EC submission) for site readiness prior to identification of recommended dose for expansion Real-time data cleaning 2-4 days from last patient completing safety evaluation to next dose level decision (SMC meeting) Allow early patient screening ~2 weeks before SMC meetings 9.9 months (12 programs) 7.1 weeks (13 programs/88 cohorts) 4.4 weeks (3 programs)
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26 zzzz CDK4i and BTK CDAC examples illustrate how we interrogate every development step to maximize efficiency BTK CDAC (BGB-16673) Enrolled 600+ patients in the past 3 years Opened ~100 sites in 22 countries Effectively leveraging backfill and safety expansion cohorts to generate dose response data Efficient path to RP2D/RP3D with manageable risk • 4 weeks from recommended dose for expansion to initiating potentially pivotal Phase 2 • 2 months from submission of FDA RP2D briefing book to starting pivotal Phase 3 CDK4i (BGB-43395) Enrolled 300+ patients within ~18 months Opened 67 sites in 11 countries Evaluated 22 dose levels, including 10 mono and 12 combo cohorts Initiated 1L letrozole combo in CDK4/6i naïve patients 13 days after finishing DLT evaluation of this combo in 2L+ by strategically opening sites in regions with limited CDK4/6i availability (Brazil, Malaysia, Moldova, and Thailand) 02JUN2025 data cutoff
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27 50% time reduction from data-cutoff to database lock Our internal model enables use of AI/automation to further improve efficiency Note: All data comparisons are with BeOne-sponsored studies 1. Applied in 5200 serious adverse event (SAE) cases of 54 studies 90% efficiency increase in SAE review and summary1 200 - 400 hours / month 20 – 40 hours / month >99% faster in table/figure preparation for safety monitoring committee meeting 3 FTE savings per study in data analysis 5 FTE 2 FTE -60% 2-5 days 3-5 mins 35 days 17 days -50% No AI/automation Leveraging AI/automation
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28 BeOne R&D strategy to transform patients’ lives 1. Develop a deep and impactful portfolio in focused disease area 2. Execute fast-to-POC for value maximization 3. Initiate combination therapies early to win 4. Advance only transformative medicines to late-stage development B e O n e R&D O v e r a l l S t r a t e g y Maximizing clinical trial efficiency with CRO-free model, powered by automation and AI technologies 1,200+ researchers covering diverse modalities, advancing science with urgency and agility E N A B L E D B Y :
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29 Hematology portfolio Amit Agarwal, MD, PhD Vice President, Hematology Clinical Development Remus Vezan, MD, PhD Vice President, Hematology Clinical Development Lai Wang, PhD Global Head of R&D
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30 Global CLL market size ($M) Novel therapies have transformed the CLL treatment paradigm EvaluatePharma, accessed 27MAY2025 $- $2,000 $4,000 $6,000 $8,000 $10,000 $12,000 $14,000 2015 2016 2017 2018 2019 2020 2021 2022 2023 2024 2025 2026 2027 2028 2029 2030 CLL market global branded sales Consensus forecasts Key FDA approvals in CLL 2013: Gazyva 2014: Imbruvica 2016: Venclexta 2019: Calquence 2023: BRUKINSA 2023: Jaypirca
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31 R/R CLL epidemiology1 - 5 10 15 20 25 2019 2020 2021 2022 2023 2024 2025 2026 2027 2028 2029 2030 2031 2032 # Patients (Thousands) +25% Fixed duration Yet there is still substantial unmet need in the treatment of CLL Novel options are needed for the increasing number of patients who will relapse after 1L therapy Patients and physicians are interested in the prospect of time-limited therapy However, current first-generation venetoclax-based regimens fail to address this unmet need due to efficacy, safety and convenience challenges We believe that patients should not have to accept an unfavorable treatment outcome in exchange for time off treatment 1 DelveInsight, US + EU5 + JP
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32 BeOne is the only company with potentially best-in-class assets across three foundational CLL MOAs Key CLL mechanisms BTKi BCL2i BTK degrader ✓ ✓ ✓ ✓ Wholly-owned best-in-class/potentially best-in-class medicine Wholly-owned medicine Partnered medicine BTKi BRUKINSA Sustained CLL leadership
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33 Future BeOne treatment optionsBeOne today BeOne is well-positioned to address CLL unmet need with our wholly-owned portfolio 2L CLL 3L+ CLL 1L CLL BRUKINSA sonrotoclax + zanubrutinib BRUKINSA BTK CDAC sonrotoclax + BTK CDAC sonrotoclax + anti-CD20 BRUKINSA BTK CDAC sonrotoclax + anti-CD20 sonrotoclax + BTK CDAC Treatment to progression Fixed-duration treatment BRUKINSA BRUKINSA cBTKi-naive BRUKINSA cBTKi-naive
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34 BRUKINSA
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35 U.S. revenue leader The only BTKi to show PFS superiority over ibrutinib in head-to-head Phase 3 CLL trial Launched in Japan and now approved in 75 markets 11 new or expanded reimbursements, including in Japan, EU, and Brazil 200K+ patients treated globally A network meta-analysis of BTKis found zanubrutinib to be the most efficacious treatment for patients with high-risk R/R CLL. 1 BRUKINSA continues to drive value for patients globally 1. Shadman M, Brown JR, et al. Comparative efficacy of Bruton tyrosine kinase inhibitors in the treatment of relapsed/refractory chronic lymphocytic leukemia: A network meta -analysis. Blood Adv. 2025: 2024014523 2. Munir T et al., Efficacy of continuous zanubrutinib vs fixed -duration venetoclax in combination with obinutuzumab in treatment -naïve chronic lymphocytic leukemia: a matching -adjusted indirect comparison. ICML, 2025 3. Chanan-Khan A, Hanna K, Xue M, et al. Number needed to treat and associated cost analysis of zanubrutinib vs ibrutinib in chronic lymphocytic leukemia. J Manag Care Spec Pharm. 2025; 31(5): 482 -490 4. Fan F, Liu X, Su Z, et al. Comparative safety of ibrutinib versus zanubrutinib in patients with Chronic Lymphocytic Leukemia: A Prospective Cohort Study. Hematol Oncol. 2025; 43(2): e70041 Recent publications Support best-in-class profile and unmet needs Zanubrutinib demonstrated a more favorable safety profile than ibrutinib, with fewer severe adverse events. 4 Based on a hypothetical scenario of a clinical practice of 100 patients treated with zanubrutinib instead of ibrutinib, the model estimated that approximately 13 patients would avoid disease progression or death over 24 months.3 Overall, this study’s results suggest that zanubrutinib is a clinically effective and cost-saving alternative to ibrutinib for the treatment of patients with R/R CLL. 3 1 2 3 4 5 These analyses further support the benefits of zanubrutinib as a first-line treatment for patients with CLL regardless of del(17p) or IGHV status. 2
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36 Time post-dose (hours) BRUKINSA PK vs. IC 50 1 Time post-dose (hours) Ibrutinib PK vs. IC 50 3 Time post-dose (hours) Acalabrutinib PK vs. IC 50 2 BRUKINSA designed from inception to be best-in-class Hypothesis: complete and sustained BTK inhibition would result in best-in-class profile 1 Health Canada Product Monograph 2 Byrd et al., NEJM, 2015; Zhou et al., Pharmacometrics Syst. Pharmacol. (2019) 8, 489–499 3 Advani, et al., JCO 2013.; NDA Clinical Pharmacology Review {NDA 205552, ibrutinib} The clinical significance of complete inhibition has not been established. In the absence of head-to-head data, definitive conclusions regarding comparative safety and efficacy cannot be drawn Free fraction in Plasma (nM) Free fraction in Plasma (nM) Free fraction in Plasma (nM) Ibrutinib 560mg Ctrough/IC50 ~1/8-fold Ctrough/IC50 ~1/13-fold 320mg QD: Ctrough/IC50 ~2-fold 160mg BID: Ctrough/IC50 ~7-fold Acala BTK IC50 =5.1nM Ibr BTK IC50=1.5 nM Zanu BTK IC50=0.5 nM 0.1 1 10 100 0 6 12 18 24 0.1 1 10 100 0 6 12 18 24 0.1 1 10 100 0 6 12 18 24 Acalabrutinib 100mg BIDBRUKINSA 160mg BID BRUKINSA 320mg QD
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37 PFS in del(17p)/TP53 subset consistent with IIT patient population1 0.0 10.0 20.0 30.0 40.0 50.0 60.0 70.0 80.0 90.0 100.0 0 3 6 9 12 15 18 21 24 27 30 33 36 39 42 45 48 51 54 57 60 63 Zanubrutinib Ibrutinib # of events (%) 134 (41.0%) 160 (49.2%) HR (95% CI): 0.66 (0.52, 0.84) nominal p-value 0.0005 Months from randomization 0 3 6 9 12 15 18 21 24 27 30 33 36 39 42 45 48 51 54 57 60 63 No. subjects at risk Zanubrutinib 327 313 301 295 286 268 257 247 241 236 214 208 189 151 128 108 103 43 19 2 0 0 Ibrutinib 325 304 292 271 256 238 227 213 197 194 182 173 147 116 101 76 73 30 10 2 1 0 Progression-free survival probability BRUKINSA is the only BTKi to demonstrate PFS superiority over ibrutinib in head-to-head Phase 3 R/R CLL trial PFS superiority in all comer population1 Zanubrutinib Ibrutinib # of events (%) 36 (48.0%) 51 (68.0%) HR (95% CI): 0.48 (0.31, 0.75) nominal p-value 0.0019 0.0 10.0 20.0 30.0 40.0 50.0 60.0 70.0 80.0 90.0 100.0 0 3 6 9 12 15 18 21 24 27 30 33 36 39 42 45 48 51 54 57 60 Months from randomization 0 3 6 9 12 15 18 21 24 27 30 33 36 39 42 45 48 51 54 57 60 No. subjects at risk Zanubrutinib 75 71 68 66 64 59 55 52 51 49 44 43 39 31 25 20 19 8 5 1 0 Ibrutinib 75 70 68 59 52 48 45 42 38 36 30 29 23 13 11 6 6 4 0 0 0 Progression-free survival probability 63.7 (57.8, 68.9) 53.0 (47.0, 58.7) 59.0 (46.2, 69.7) 32.4 (21.2, 44.1)Zanubrutinib Ibrutinib Zanubrutinib Ibrutinib 1Brown et al., Blood, 2024; COVID adjusted
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38 PFS of del(17p) in Arm C1 vs. PFS of w/o del(17p) in Arm A2 0 10 20 30 40 50 60 70 80 90 100 0 3 6 9 12 15 18 21 24 27 30 33 36 39 42 45 48 51 54 57 60 63 66 69 BRUKINSA demonstrated impressive PFS in SEQUOIA study in treatment naïve CLL/SLL patients regardless of risk status 1 Tam et al., ASCO, 2025 2 Shadman et al., JCO, 2024 3 Wang et al. Blood Cancer J. 2021 CLL, chronic lymphocytic leukemia; OS, overall survival; PFS, progression-free survival; SLL, small lymphocytic lymphoma; TN, treatment -naïve Presence of del(17p) is associated with ~2-fold greater risk of death due to CLL3 SEQUOIA Arm C is largest prospective cohort of uniformly treated patients with del(17p) TN CLL/SLL 60-month PFS with zanubrutinib was 72.2% in TN CLL/SLL patients with del(17p), similar to 75.8% observed in patients without del(17p) Progression-free survival probability Number of subjects at risk: Arm A 241 238 234 230 228 224 219 214 208 205 201 200 195 192 190 183 178 164 153 89 81 19 19 2 Arm C 110 109 106 104 104 101 98 96 94 93 89 89 88 86 82 81 80 78 76 66 62 24 22 1 Arm A: w/o del(17p) Arm C: del(17p) Censored Months
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39 Designing the right molecule and conducting the right experiment ultimately leads to market leadership despite later entry $0 $200 $400 $600 $800 $1,000 $1,200 2021 2022 2023 2024 1Q25 Ibrutinib Acalabrutinib U.S. cBTKI quarterly revenue ($M) CLL FDA approval based on SEQUOIA and ALPINE 9 and 3 years behind ibrutinib and acalabrutinib, respectively
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40 Sonrotoclax, combinations, and fixed duration
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41 Measured by MRD at the time of discontinuation – need to be comfortable when stopping therapy Adding only minimal AEs over BTKi monotherapy continuous No TLS, and no death/OS detriment No required hospitalizations Fewer clinic visits and less monitoring during ramp-up Usable in the community oncology centers Ideal fixed-duration treatment regimen must meet the following criteria Sustained PFS Safety ConvenienceDeep response Comparable to BTKi continuous therapy Current venetoclax-based fixed-duration treatments for CLL are suboptimal
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42 Venetoclax ramp-up and monitoring HCPs often cite issues with venetoclax – there is clear need for a next-generation BCL2i 20mg 50mg 100mg 200mg 400mgHospitalization required Hospitalization considered Tests pre-dose, 4, 8, 12h Tests pre-dose, 6-8h (ven), 4-6h (sonro) 1 test pre-dose Source: Primary Market Research, NOV2023 Low/Medium TLS Risk Week 1 Week 2 Week 3 Week 4 Week 5 D1 D2 D1 D2 D1 D2 D1 D2 D1 D2 High TLS Risk 2 1 2 1 4 1 4 1 2 1 2 1 2 1 1 1 1 4 2 1 5-7 clinic visits 8 clinic visits including two overnight Longer post- administration monitoring means greater likelihood of hospitalization - U.S. Community HCP Monitoring [venetoclax] can be very annoying. You want a treatment that simplifies staff responsibilities – U.S. Community HCP Ven’s ramp-up is a little annoying, but it is only required because it is an effective Tx - U.S. Community HCP
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43 38 118 344 792 1,337 1,820 2,009 2,288 2,583 2,672 2,848 3,010 3,146 3,259 3,359 2016 2017 2018 2019 2020 2021 2022 2023 2024 2025 2026 2027 2028 2029 2030 Despite its substantial use limitations, venetoclax is a blockbuster product Sales Consensus forecasts Global venetoclax revenue ($M) EvaluatePharma, accessed 27MAY2025 CLL New Patient Starts (All Lines 4Q24)/Source: Symphony Health Claims (SHS Polaris) • Venetoclax-based regimens represent ~25% of new patient starts in CLL, yet the vast majority of use lies in the academic setting • We believe there is substantial opportunity for a next-gen BCL2i to unlock the full potential of this class
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44 Sonrotoclax is designed to be best-in-class on efficacy, with favorable safety and convenient handling Sonrotoclax Venetoclax Implication in clinic Potency (IC50) 0.014 nM 0.20 nM 14-fold more potent, deeper target inhibition to eliminate the most difficult to treat tumor cells Selectivity (vs. BCLxL) 2000X 325X 6-fold improved selectivity for potentially better tolerability T1/2 in clinic ~5 h 26 h Aiming for only one clinic visit for sonro ramp-up for most patients; no accumulation leading to ease of TLS monitoring during ramp-up The clinical significance of pre-clinical data has not been established. There are no head-to-head data comparing sonrotoclax and venetoclax
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45 Jacob D. Soumerai, MD Assistant Professor of Medicine, Harvard Medical School Hematologist/Oncologist, MGH Cancer Center Sonrotoclax Speaker introduction: Dr. Jacob Soumerai, key opinion leader in CLL and lymphomas Hematologist/oncologist and clinical investigator in lymphoma and CLL at the Massachusetts General Hospital Cancer Center Dr. Soumerai’s clinical trial and translational research efforts focus on the development of innovative therapeutic combinations in CLL and B-cell lymphomas A major theme running through his research relate to identifying novel biomarkers with potential to guide personalized therapy approaches Recipient of multiple awards, like NIH K08 Award, Lymphoma Research Foundation Career Development Award, Kraft Translational Research Award and others 50+ publications as first author, with recent publications in high-impact journals including Blood, JCO, Lancet Oncology, Lancet Haematology
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46 Besides anti-proliferation, BTKi also prevents CLL cells’ homing in lymphoid tissues/organs and promotes cell migration to peripheral blood Then, BCL2i can effectively kill CLL cells in peripheral blood Distinct and complementary MoA of BTKi and BCL2i brings synergistic effects MOA of the synergistic effect of BTK and BCL2 inhibitors Zygmunciak P, et al. Int J Mol Sci. (2025); Zhang J, et al. Biomark Res. (2022); Cervantes-Gomez F, et al. Clin Cancer Res. (2016) Peripheral blood Lymph node, bone marrow, spleen, liver BTKi Inhibit homing and proliferation BCL2i Induce apoptosis CLL cells
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47 BGB-11417-101 study is a Ph 1/2 study that evaluated sonrotoclax monotherapy or in combinations with zanubrutinib ± sonrotoclax ± obinutuzumab in multiple B-cell indications, at various dose levels BGB-11417-101: Phase 1/2, open-label, sonrotoclax dose-escalation/expansion study in B-cell malignancies CLL/SLL, chronic lymphocytic leukemia/small lymphocytic lymphoma; MCL, mantle cell lymphoma; MTD, maximum tolerated dose; R/R, relapsed/refractory; RP2D, recommended phase 2 dose; TN, treatment naive TN CLL/SLL, R/R CLL/SLL, R/R MCL Combination dose escalation Combination dose expansion 640mg 320mg 160mg 80mg 40mg TN CLL/SLL expansion 320mg RP2D RR CLL/SLL RR MCL S+Z S+O S+Z S+Z S+Z+O
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48 sonrotoclax 320mg + zanubrutinib (n=86) Median follow-up (range): 25.53 mo (3.1-36.0) TEAEs observed with sonrotoclax + zanubrutinib in TN CLL/SLL were mostly low grade and transient DCO: 01MAR2025 a Includes the combined preferred terms neutrophil count decreased and neutropenia No TLS (clinical or laboratory) Neutropenia was transient and did not lead to higher rates of grade ≥3 infections No AE of febrile neutropenia reported No new safety signals observed with longer follow-up No TEAE leading to death TEAEs in ≥25% of all patients 25.6 27.9 30.2 29.1 8.1 38.4 2.3 27.9 0 10 20 30 40 Rash Diarrhea URTI COVID-19 Neutropenia Contusion Patients % TN CLL/SLL Grade >3 Grade 1 - 2 a
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49 0% 25% 50% 75% 100% 0 6 12 18 24 30 Median (in months) IGHV unmut 7.1 IGHV mut 7.2 32 27 3 2 2 0 40 33 8 2 1 0 MRD negative Number at risk Monthsa 84% 92% 94% 91% 100% 92% 12% 8% 6% 9% 8% a From day 1 of Zanubrutinib monotherapy treatment b As measured by ERIC flow cytometry panel uMRD4 is defined as less than 1 CLL cell per 10,000 leukocytes (<10 -4); MRD is best reported within a 2-week window following the week 48 assessment c Number of weeks at target dose, following zanubrutinib monotherapy and sonrotoclax ramp-up to target dose, different from a DCO: 01MAR2025 Sonrotoclax + zanubrutinib achieved fast and deep response in TN CLL/SLL regardless of risk status uMRD by week 48a,b mFU: 160mg 25.0 months; 320mg 25.5 months sonro 320mg Not evaluable Missing MRD4+ uMRD4 4% TN CLL/SLL sonro sonro IGHV IGHV Del17p/ Del17p/ 160mg 320mg unmut mut TP53+ TP53- (n=51) (n=59) (n=31) (n=22) (n=8) (n=47) Time to blood uMRD sonro(320 mg)+zanu IGHV mut IGHV unmut
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50 No PFS events observed at 320mg dose No PFS events at 320mg dose and only one progression at 160mg dose Patients (n=35) who reached week 96 and elected to stop therapy* all in remission with a time off median of three months (range 1-12 months) * Patients had the option to electively discontinue therapy after 96 weeks of combination DCO: 01MAR2025 Sonrotoclax and Zanubrutinib high uMRD rate translates into impressive PFS in TN CLL/SLL 160mg 51 51 51 51 51 51 51 50 50 49 49 48 48 48 47 45 43 43 42 37 27 24 24 24 23 23 22 21 19 19 16 16 13 10 9 9 9 6 1 0 320mg 86 85 83 83 82 82 80 69 64 61 61 61 58 58 55 52 51 51 50 48 47 40 40 39 38 36 26 14 13 10 7 3 1 0 0 0 0 0 0 0 0% 10% 20% 30% 40% 50% 60% 70% 80% 90% 100% 0 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 Months after first dose Number at risk:Progression-free survival probability (%) 160mg 320mg TN CLL/SLL
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51 sonrotoclax 320mg + zanubrutinib (n=22) Median follow-up (range): 19.6 (13.2-39.7) months All cohorts (n=47) Median follow-up (range): 32.2 (10.2-48.6) months TEAEs in ≥25% of all patients and those treated at sonrotoclax RP2D of 320mga No clinical or laboratory TLS and no febrile neutropenia observed No dose reductions occurred due to diarrhea No TEAE leading to death TEAEs observed with sonrotoclax + zanubrutinib in R/R CLL/SLL were mostly low grade and transient Cheah, EHA, 2025 a Grade is listed as worst grade experienced by patient on any drug b Neutropenia combines preferred terms neutrophil count decreased and neutropenia c Thrombocytopenia combines preferred terms platelet count decreased and thrombocytopenia RP2D, recommended phase 2 dose; TEAE, treatment -emergent adverse event; TLS, tumor lysis syndrome; URTI, upper respiratory tract infection 23 30 30 4 34 34 32 34 2 28 2 2 0 10 20 30 40 50 COVID-19 URTI Contusion (bruising) Diarrhea Neutropeniab Cough Fatigue Nausea 23 23 27 23 32 36 41 5 5 5 46 0 10 20 30 40 50 Neutropeniab URTI Diarrhea Cough Constipation Contusion (bruising) COVID-19 Thrombocytopeniac R/R CLL/SLL Grade >3 Grade 1 - 2 Patients (%) Patients (%)
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52 Only two PFS events across dose levels 0% 10% 20% 30% 40% 50% 60% 70% 80% 90% 100% 0 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 uMRD by week 48a,b 56% 100% 80% 83%75% 44% 15%25% 5% 17% Sonro 40 mg (n=4) Sonro 80 mg (n=9) Sonro 160 mg (n=6) Sonro 320 mg (n=20) Sonro 640 mg (n=6) 13 patients elected to stop therapy*, all in remission at the time of DCO with a time off median of 4.5 months (range 1.8-12.3 months) Sonrotoclax + zanubrutinib demonstrated high uMRD rate with impressive PFS in R/R CLL Cheah, EHA, 2025 a As measured by ERIC flow cytometry panel uMRD4 is defined as less than 1 CLL cell per 10,000 leukocytes (<10 -4); MRD is best reported within a 2-week window following the week 48 assessment b Number of weeks at target dose, following zanu monotherapy and sonro ramp-up to target dose * Patients had the option to electively discontinue therapy after 96 weeks of combination mFU: 32.2 months (combined all dose levels) 320mg – 19.6 months All 47 47 47 47 46 46 46 46 4545 4545 45 42 41 38 36 34 32 32 30 27 25 25 25 25 25 24 24 24 24 22 21 19 17 16 15 11 7 6 5 5 5 3 3 2 2 1 1 0 Months after first dose Number at risk:Progression-free survival probability (%) All Not evaluable Missing MRD4+ uMRD4 R/R CLL/SLL SZ combo demonstrated high uMRD rate, with 80% uMRD at the RP2D (320mg) To date, only two PFS events occurred on the study across all dose levels, one at 40mg dose and one at 320mg dose
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53 sonrotoclax 320mg + zanubrutinib (n=27) TEAEs in ≥15% of patients and in those at the sonrotoclax RP2D (320mg) Safety profile was generally similar across all doses tested, with no clinical or laboratory TLS observed and no cases of atrial fibrillation MTD was not reached with sonrotoclax up to 640mg; 320mg was chosen as RP2D combination with zanubrutinib in MCL Sonrotoclax + zanubrutinib in R/R MCL was generally well tolerated and showed a safety profile similar to CLL Cordoba, EHA, 2025 a Pleural effusion (80mg; due to PD), pneumonia (160mg), abdominal sepsis (320mg) b Lymph node pain (160mg, due to PD), diarrhea (320mg), MDS (160mg), abdominal sepsis (320mg), pneumonia (160mg), diarrhea (80m g), cryptococcal meningoencephalitis (320mg), abdominal pain (320mg) c Pneumonia (160mg) Abbreviations: MDS, myelodysplastic syndrome; MTD, maximum tolerated dose; PD, progressive disease; RP2D, recommended phase 2 dose; sonro, sonrotoclax; TEAE, treatment-emergent adverse event; zanu, zanubrutinib R/R MCL Patients, n (%) sonro 320mg+ zanu (n=27) All (N=51) Any TEAEs 26 (96.3) 48 (94.1) Grade ≥3 14 (51.9) 28 (54.9) Serious TEAEs 7 (25.9) 15 (29.4) Leading to death 1 (3.7) 3 (5.9)a Leading to zanu discontinuation 4 (14.8) 8 (15.7)b Treated with sonro, n (%) 24 (88.9) 46 (90.2) Leading to death 0 1 (2.0)c Leading to sonro dose reduction 0 0 19 15 19 15 15 19 22 11 37 4 7 7 4 19 4 0 10 20 30 40 50 Fatigue Headache Nausea Thrombocytopenia Hypertension COVID-19 Contusion Neutropenia Diarrhea Patients % Grade >3 Grade 1 - 2
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54 Best overall response rate ORRa was 82% with CR rate of 67% in 320mg dose group Median DORb in all patients was not reached; DOR rate at 24 months was 84.0% with median follow-up of 17.7 months 16 of 18 patients who achieved CR remain in CR at a median follow-up of 13 months Cordoba, EHA, 2025 a Responses were assessed per Lugano 2014 criteria and percentage of responding patients who had at least one post-baseline tumor assessment after dosing with sonrotoclax unless treatment was discontinued due to clinical progression or de ath prior to tumor assessment b For all patients as treated (n=51) BOR, best overall response; BTK, Bruton tyrosine kinase; CR, complete response; ORR, overall response rate; PD, progressive d isease; PR, partial response; SD, stable disease sonro 320mg + zanu (n=27) mFUc 13.2 (0.7-31.6) All (n=51) 16.4 (0.7-42.4) Sonrotoclax + zanubrutinib demonstrated deep and durable responses in R/R MCL R/R MCL Median DORc in all patients was not reached DOR probability (%) Time since first response, months Number at risk: 80mg 160mg 320mg 640mg ORR 82% ORR 80% 67 65 15 16 4 6 15 14 0 20 40 60 80 100Patients, % PD SD PR CR 0% 20% 40% 60% 80% 100% 0 2 4 6 8 10 12 14 16 18 20 22 24 26 28 30 32 80mg 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 5 4 4 4 160mg 10 10 10 10 9 8 7 7 7 7 6 5 5 4 4 4 4 4 4 4 3 3 3 3 2 2 2 2 2 2 1 1 1 320mg 22 18 18 17 15 15 15 14 14 13 12 11 11 11 10 8 8 7 6 6 6 5 4 4 1 1 1 1 1 0 0 0 0 640mg 4 4 4 4 4 4 4 4 4 4 4 2 2 2 2 2 2 2 2 0 0 0 0 0 0 0 0 0 0 0 0 0 0
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55 Favorable safety profile with no case of TLS during sonrotoclax ramp up Quick and deep uMRD rate, 87% and 90% of evaluable patients achieved uMRD by week 36 and 60, respectivelya,b Only two PFS events up to the DCO Sonrotoclax + obinutuzumab* shows promising efficacy in TN CLL/SLL uMRD by week 36 uMRD by week 60 87% 90% 4% 9% 10% Sonro 320 mg (n=23) Sonro 320 mg (n=19) Median follow up – 13.5 months 14.3 37.2 25.7 42.9 31.4 31.4 22.9 28.6 14.3 25.7 22.9 45.7 17.1 25.7 2.9 5.7 8.6 0 10 20 30 40 50 60 70 Neutropenia IRR Thrombocytopenia Nausea Headache Diarrhea Pyrexia Fatigue COVID-19 URTI Cough TN CLL/SLL Grade >3 Grade 1 - 2 sonrotoclax 320mg + obinutuzumab (N=35) Not evaluable Missing MRD4+ uMRD4 a As measured by ERIC flow cytometry panel uMRD4 is defined as less than 1 CLL cell per 10,000 leukocytes (<10 -4); MRD is best reported within a 2-week window following the week 48 assessment b Number of weeks on therapy from first obinutuzumab dose c Neutropenia combines preferred terms neutrophil count decreased and neutropenia d Thrombocytopenia combines preferred terms platelet count decreased and thrombocytopenia *combination treatment consist of 6 cycles of obinutuzumab (C1-C6;) and 14 cycles (c2-c15) or 26 cycles of sonrotoclax (C2-C27)for MRD4+ at C16. 1 cycle=4 weeks DCO: 01MAR2025. IRR, infusion related reaction; URTI, upper respiratory tract infection c d Patients (%)
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56 All oral sonrotoclax + zanubrutinib has potential to be best in disease combination, including fixed-duration therapy Sonrotoclax + zanubrutinib combination: Demonstrates favorable safety profile in patients with CLL/SLL and MCL, including a more convenient ramp up with no cases of TLS in this combination Demonstrates impressive efficacy in TN/ RR CLL/SLL and R/R MCL with responses continuing to deepen over time and high uMRD rates observed in CLL regardless of risk factors Has the potential to become the new standard in CLL and MCL
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57 ZS has best-in-class potential vs. VO, IV, and AV on efficacy, safety, and convenience Precedent fixed duration ZS1 VO2 VO3 IV4 IV5 AV7 Population all comers unfit fit unfit all comers fit uMRD 91% 76% 87% 55% 77% 34% 36-mo PFS 100% 24 mo. PFS 82% 88% 77% 90%6 77% Grade ≥3 TEAEs 45% 80% 80% 75% NR 54% TEAE leading to death 0% 9% 4% 6.6% NR 5.5% 1. CELESTIAL 101 - Soumerai et al., ASH, 2024; 320mg cohort 2. CLL14 – Al-Sawaf, The Lancet, 2020 3. CLL13 - Eichorst et al., NEJM, 2023 4. GLOW - Niemann et al., Lancet, 2023, estimated PFS value for all patients 5. CAPTIVATE fixed duration - Tam et al., Blood, 2022 6. CAPTIVATE – Allan, CCR, 2023, estimated PFS value for all patients 7. AMPLIFY - Brown et al., NEJM 2025 In the absence of head-to-head data, definitive conclusions regarding comparative safety and efficacy cannot be drawn; estimated PFS values; NR = not reported We are optimizing ramp-up scheduling for sonrotoclax and are optimistic that for vast majority of patients (>90%), only one clinic visit is required for sonrotoclax ramp-up after zanubrutinib lead-in Not currently approved in U.S.
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58 0% 25% 50% 75% 100% 0 6 12 18 24 30 36 42 48 54 60 66 72 78 0% 25% 50% 75% 100% 0 6 12 18 24 30 36 42 48 54 60 66 72 78 ZS combination had much faster kinetics with time to blood uMRD than IV combo regardless of IGHV status aInternal data, DCO: 01MAR2025 bTalha Munir, EHA 2025 Time to blood uMRD IV (FLAIR study)b Median (in months) IGHV mut 7.2 IGHV unmut 7.1 32 27 3 2 2 0 40 33 8 2 1 0 MRD negative Time to blood uMRD ZS (CELESTIAL 101)a IGHV mut IGHV unmut Number at risk Months Median (in months) IGHV mut 18.0 IGHV unmut 11.9 97 86 60 48 40 36 27 23 20 17 13 11 0 0 123 111 61 47 29 18 14 11 8 6 6 6 6 0 MRD negative Number at risk Months IGHV mut IGHV unmut
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59 CELESTIAL-TNCLL (301): fixed duration sonro+zanu vs. ven+obin Only global Phase 3 trial designed to demonstrate PFS superiority over current FD SOC Source: NCT06073821 Completed enrollment in February 2025 TN CLL • PFS • CRR • OS Primary endpoint Key secondary endpoints sonrotoclax + zanubrutinib 12 cycles after 3 cycles zanubrutinib alone venetoclax 12 cycles + obinutuzumab 6 cyclesArm B Arm A Randomize 1:1 Previously untreated CLL N = 698 Stratification factors: • Age (<65 years vs. ≥ 65 years) • IGHV (mutated vs. unmutated) • del(17p)/TP53
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60 CELESTIAL-RRMCL (302): sonrotoclax + zanubrutinib vs. zanu Phase 3 global study design Randomize 1:1 R/R MCL N = 300 Arm B Arm A zanubrutinib until progression / intolerance + sonrotoclax x 26 cycles zanubrutinib until progression / intolerance + placebo x 26 cycles Enrollment ongoing R/R MCL • PFS • OS Primary endpoint Key secondary endpoints Stratification factors: • Age (<70 years vs. ≥ 70 years) • Prior lines of therapy (1 vs. >1) • Geographic regions Source: NCT06742996
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61 CELESTIAL-RRCLL (303): sonro+anti-CD20 vs. ven+anti-CD20 A head-to-head trial to demonstrate superiority of sonrotoclax over venetoclax Source: NCT06943872 • PFS of SO vs. VR • PFS of SR vs. VR • uMRD • CRR • OS Primary endpoint Key secondary endpoints Stratification factors: • Refractory to prior BTKi • Del (17p)/TP53 mut • Prior BCL2i exposure First site initiated R/R CLL sonrotoclax plus obinutuzumab n=~180 venetoclax plus rituximab n=~180 sonrotoclax plus rituximab n=~180 sonrotoclax plus obinutuzumab with MRD guided therapy n=~90 Arm B Arm A Arm D Arm C Randomize 2:2:1:2 Active CLL/SLL, previously treated ≥ 1 line of therapy N = 630
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62 Sonrotoclax+dex shows promising efficacy 5.6 3.6 15.8 19.4 18.2 21.1 30.6 27.3 36.8 25.0 29.1 Sonro 320 mg + dex (n=19) Sonro 640 mg + dex (n=36) Total (N=55) Patients, (%) PR VGPR CR sCRVGPR or better 36.8% VGPR or better 55.6% VGPR or better 49.1% ORR 78.2% ORR 80.6%ORR 73.7% t(11;14) represents ~20% of the multiple myeloma population Sonrotoclax ORR compares favorably to previous study with venetoclax (ORR-62%a) Sonrotoclax+dara+dex dose escalation ongoing, without any new safety signals Pivotal phase 3 study in 2L+ MM for sonrotoclax triplet with the use of an intermediate endpoint for accelerated approval is being planned We are moving aggressively towards registration in multiple myeloma patients with t(11;14) a Mateos et al. Results from the randomized, open -label phase 3 CANOVA study of venetoclax -dexamethasone versus pomalidomide -dexamethasone in patients with t(11;14)-positive relapsed/refractory multiple myeloma. IMS Annual Meeting Sep 2023 CR, complete response; dex, dexamethasone; ORR, overall response rate; PR, partial response; sCR, stringent complete response; VGPR, very good partial response MM
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63 Sonrotoclax has broad development program with registrational plans in multiple indications AA, accelerated approval potential; COC, contribution of components; dara, daratumumab; dex, dexamethasone; *submitted in China, global filings anticipated in 2H25 Indication Regimen Study details Early clinical development Registrational trial TN CLL/SLL +zanubrutinib 108: ramp-up optimization 204: COC study CELESTIAL 301: vs. venetoclax+obinutuzumab R/R CLL/SLL Monotherapy CELESTIAL 202: ph2 for AA (CN) +anti-CD20 CELESTIAL 303: vs. venetoclax+rituximab R/R MCL Monotherapy CELESTIAL 201: ph2 for AA +zanubrutinib CELESTIAL 302: vs. zanubrutinib R/R WM Monotherapy CELESTIAL 203: ph2 for AA R/R MM +anti-CD38, dex 105: dose escalation/expansion TN, R/R AML +azacitidine 103: dose escalation/expansion Ongoing Ongoing Ongoing Filed Start-up Filed* Ongoing Ongoing Ongoing Ongoing OngoingUnder planning
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64 Sonrotoclax initial market filings started based on two Phase 2 single-arm monotherapy studies in R/R CLL and R/R MCL Indication Countries Target filing R/R CLL China only Filed in April 2025 in China R/R MCL Global Filed in May 2025 in China; Global filing 2H25 CDE granted Priority Review for both filings ▪ CLL filing was completed in 2.5 months from DCO Global filing in R/R MCL in 2H25
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65 BTK CDAC (BGB-16673)
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66 BGB-16673 designed to address unmet need in CLL and other B-cell malignancies 1 DelveInsight, US + EU5 + JP Unmet needs in CLL are evolving and while there have been improvements in outcomes in treatment-naïve CLL patients, there is an enduring unmet need especially in the relapsed setting Novel options are needed for the increasing number of patients who will relapse after 1L therapy BGB-16673 is potential first-in-class, orally available BTK degrader R/R CLL epidemiology1 - 5 10 15 20 25 2019 2020 2021 2022 2023 2024 2025 2026 2027 2028 2029 2030 2031 2032 # Patients (Thousands) +25%
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67 CDAC emerging as enhanced approach to target BTK pathway Degraders offer significant advantages over small molecule inhibitors 1 Yoon H. et al J Clin Invest. 2024;134(1):e175265 2 Feng X et al; Poster presented at EHA 2023; #P1239 3 Yuan et al J Biol Chem. 2022 Nov; 298(11) Catalytic activity1 Higher barrier to resistance2 Disrupts scaffold function3 Inhibitor CDAC Inhibitor CDAC Inhibitor CDAC Blocks one target protein Degrades multiple target proteins Mutations that weaken binding abolish activity Retains activity despite mutations that impair binding Active only against kinase-mediated signaling Nullifies all associated signaling … …… ... E3 ligaseWild-type BTK Mutant BTK Proteasome BTK CDAC Traditional BTK inhibitor Incomplete target inhibition Kinase-independent signal still active
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68 CaDAnCe 101: Phase 1/2, BGB-16673 monotherapy dose-escalation/expansion study in R/R B-cell malignancies BTK, Bruton tyrosine kinase; cBTKi, covalent Bruton tyrosine kinase inhibitor; CLL/SLL, chronic lymphocytic leukemia/small lymphocytic lymphoma; DLBCL, diffuse large B-cell lymphoma; ECOG PS, Eastern Cooperative Oncology Group performance status; FL, follicular lymphoma; GCB, germinal center B-cell; MCL, mantle cell lymphoma; MTD, maximum tolerated dose; MZL, marginal zone lymphoma; QD, once daily; RDFE, recommended dose for expansion; R/R, relapsed/refractory; RT, Richter transformation; WM, Waldenström macroglobulinemia Selected B-cell malignancies BTK naïve (CLL/SLL, MCL, WM, RT, MZL) Part 1f: expansion Phase 2 Phase 1 (except 1f) Pts (n) R/R CLL 66 R/R WM 36 R/R FL/MZL 46 Other B-cell malignancies 46 Phase 1 Cohort 1: Post BTKi/BCL2i R/R CLL/SLL Potential pivotal cohort with enrollment ongoing and >100 pts enrolled to date Cohort 2-7: B-cell malignancies Selected R/R B-cell malignancies (CLL/SLL, WM, MZL, FL, MCL, DLBCL, RT) Part 1: dose escalation and expansion
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69 Scarfo, EHA, 2025 DCO:: 03MAR2025 a Analyzed centrally by next-generation sequencing with limit of detection of 0.1% b The remaining seven patients discontinued prior BTK inhibitor due to toxicity (n=4), treatment completion (n=2), and other (n =1) Abbreviations: BCL2, B-cell lymphoma 2; BTK, Bruton tyrosine kinase; cBTK, covalent Bruton tyrosine kinase; CLL, chronic lymphocytic leukemia; ECOG PS, Eastern Cooperative Oncology Group performance status; ncBTK, noncovalent Bruton tyrosine kinase; PD, progressive disease; SLL, small lymphocytic lymphoma Patient characteristics Total (N=66) Mutation status, n/N (%) BTK mutation present 24/63 (38.1) PLCG2 mutation present 10/63 (15.9) No. of prior lines of therapy, median (range) 4 (2-10) Prior therapy, n (%) Chemotherapy 47 (71.2) cBTK inhibitor 62 (93.9) ncBTK inhibitor 14 (21.2) BCL2 inhibitor 54 (81.8) cBTK + BCL2 inhibitors 42 (63.6) cBTK + ncBTK + BCL2 inhibitors 12 (18.2) Discontinued prior BTK inhibitor due to PD, n/N (%)b 55/62 (88.7) Patient characteristics Total (N=66) Age, median (range), years 70 (47-91) CLL/SLL risk characteristics at study entry, n/N with known status (%) Binet stage C 29/62 (46.8) Unmutated IGHV 38/49 (77.6) del(17p) and/or TP53 mutationa 43/66 (65.2) Complex karyotype (≥3 abnormalities) 22/44 (50.0) R/R CLL patients from CaDAnCe-101 phase 1 study are heavily pretreated with high-risk features R/R CLL
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70 Common adverse events noted in Phase 1 n=148 The AE profile of BGB-16673 is consistent with the MOA and related to on target BTK degradation Treatment related AE leading to discontinuation occurring in <5% of these very late line patients Off target AEs associated with BTK inhibitors including arrythmia, hypertension have not been noted higher than the baseline rate in this population In large group of late line R/R B-cell malignancy patients, BGB-16673 has shown tolerable safety profile DCO:: 03MAR2025 10 9 12 10 12 13 10 15 13 24 24 27 5 1 2 4 5 24 Amylase Dyspnea Cough Lipase URTI COVID-19 Thrombocytopenia Pyrexia Anemia Fatigue Diarrhea Contusion Neutropenia > Grade 3 Grade 1 - 2
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71 In heavily pretreated R/R CLL patients, significant responses have been observed Scarfo, EHA, 2025 a Of 44 patients with PR, 12 achieved all nodes normalized b Includes best overall response of PR -L or better c Includes best overall response of SD or better d In patients with a best overall response of PR -L or better CR, complete response; CRi, complete response with incomplete marrow recovery; PD, progressive disease; PR, partial response; PR -L, partial response with lymphocytosis; SD, stable disease Response rates 200mg (n=16) Total (N=66) Best overall response, n (%) CR/CRi 1 (6.3) 3 (4.5) PRa 12 (75.0) 44 (66.7) PR-L 2 (12.5) 9 (13.6) SD 0 5 (7.6) PD 1 (6.3) 2 (3.0) Discontinued prior to first assessment 0 3 (4.5) Overall response rate, n (%)b 15 (93.8) 56 (84.8) Disease control rate, n (%)c 15 (93.8) 61 (92.4) Time to first response, median (range), monthsd 2.9 (2.6-8.3) 2.8 (2.0-19.4) Time to best response, median (range), months 3.4 (2.6-13.8) 3.4 (2.0-19.4) Duration of exposure, median (range), months 16.2 (2.9-24.6) 12.9 (0.2-29.6) Responses are seen in patients with high-risk features cBTKi+BCL2i exposure (n=42) 90.5% cBTKi+ncBTKi+BCL2i exposure (n=12) 75% BTK mutation (n=24) 75% PLCγ2 mutation (n=10) 90% R/R CLL
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72 BGB-16673: PFS by investigator1 Pirtobrutinib: PFS by IRC2 Emerging data for R/R CLL provides confidence to conduct H2H superiority trial vs. pirtobrutinib 1 Scarfo L. et all EHA 2025 2 Sharnan J. et al ASH 2024 CaDAnCe-101 (BTK CDAC) BRUIN321 (pirtobrutinib) Median prior lines of therapies 4 3 BTKi+BCL2i exposed 82% 50% Prior BTKi discontinuation due to PD 89% 71% BGB-16673 n=66 Median PFS, mo (95% CI) 22.8 Median follow-up, mo 15.6 100 90 80 70 60 50 40 30 20 10 0 0 2163 189 12 15 24 Progression-free survival probability 66 59 37 33 31 15 13 3 1 Number at risk 27 Pirtobrutinib n=119 Median PFS, mo (95% CI) 14.0 (11.2-16.6) Median follow-up, mo 19.4 119 113 100 84 79 69 54 44 36 19 12 10 4 3 3 3 2 0 Progression-free survival probability Time since randomization (months) 10 12 14 16 22 28 342 8 0 30 3220 2618 244 6 Number at risk 100 90 80 70 60 50 40 30 20 10 027 R/R CLL Time since randomization (months)
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73 CaDAnCe 304: BTK CDAC vs. pirtobrutinib Global phase 3 in R/R CLL/SLL post-cBTKi First patient expected in 2H 2025 CLL dose for Phase 3 agreed with FDA R/R CLL Randomize 1:1 R/R CLL/SLL N = 500 Arm B Arm A BTK CDAC 200mg PO QD pirtobrutinib 200mg PO QD Stratification factors: • Prior BCL2i • del(17p)/TP53 • Refractory to last cBTKi • PFS • OS Primary endpoint Key secondary endpoints
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74 Median PFS was not reached Responses were observed starting at the lowest dose (100mg; 10/10) and in patients with prior cBTK inhibitor (27/32) or ncBTK inhibitor (4/4) Frustaci, EHA, 2025 a Efficacy-evaluable population b Includes best overall response of MR or better c Includes best overall response of PR or VGPR d Includes best overall response of SD or better WM = Waldenström macroglobulinemia, cBTK, covalent BTK; MR, minor response; ncBTK, noncovalent BTK; PD, progressive disease; PR, partial response; SD, stable disease; VGPR, very good partial response Response rates Totala (N=32) Best overall response, n (%) VGPR 10 (31.3) PR 14 (43.8) MR 3 (9.4) SD 3 (9.4) PD 1 (3.1) Discontinued prior to first assessment 1 (3.1) ORR, n (%)b 27 (84.4) Major response rate, n (%)c 24 (75.0) Disease control rate (DCR), n (%)d 30 (93.8) R/R WM Median follow-up: 8.2 months (range, 0.6-30.6 months) 100% Progression-free survival probability (%) 90% 80% 70% 60% 50% 40% 30% 20% 10% 0% 0 36 3 25 6 22 9 11 12 7 15 4 18 3 21 2 24 2 27 0 Months No. at risk CaDAnCe 101: deep and durable responses seen in R/R WM Responses across all risk groups including with prior cBTKI and ncBTKI
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75 Responses by histology for R/R FL and MZL patients from CaDAnCe-101 study Zinzaini, ICML, 2025 a Includes best overall responses of PR or CR b Includes best overall responses of SD or better c In patients with best overall response better than SD Abbreviations: CR, complete response; NE, not estimable; ORR, overall response rate; PD, progressive disease; PR, partial res ponse; SD, stable disease FL, follicular lymphoma; MZL marginal zone lymphoma; TEAE, treatment -emergent adverse event Response rates FL (n=12) MZL (n=20) Best overall response, n (%) CR 1 (8.3) 3 (15.0) PR 4 (33.3) 7 (35.0) SD 3 (25.0) 5 (25.0) PD 3 (25.0) 3 (15.0) ORR, n (%)a 5 (41.7) 10 (50.0) Disease control rate, n (%)b 8 (66.7) 15 (75.0) Time to first response, median (range), monthsc 2.6 (2.3-3.3) 2.9 (2.6-9.9) Duration of response, median (95% CI), monthsc 9.5 (5.7-NE) 10.8 (2.8-NE) BGB-16673 had durable antitumor activity with short time to response in heavily pretreated patients with NHL, including those with BTK inhibitor–resistant disease ORR was 41.7% in patients with FL and 50% in those with MZL Four patients achieved CR (FL, n=1; MZL, n=3) R/R FL, MZL CaDAnCe 101: efficacy data in R/R FL and MZL In heavily pretreated patients, BGB-16673 has shown favorable risk-benefit profile
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76 69-year-old male Diagnosed with CLL in 2009 and treated with multiple treatments Diagnosed with Richters transformation in 2024 Progressed after initial therapy of R-CHOP for RT and enrolled in CaDAnCe-101 trial Responses have been observed in patients with Richters Transformation indicating the potential of the mechanism Cycle1 Day1
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77 69-year-old male Diagnosed with CLL in 2009 and treated with multiple treatments Diagnosed with Richters transformation in 2024 Progressed after initial therapy of R-CHOP for RT and enrolled in CaDAnCe-101 trial Responses have been observed in patients with Richters Transformation indicating the potential of the mechanism Cycle1 Day21 Cycle1 Day1 After only 3 weeks of treatment!
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78 We plan to file CaDAnCe 101 in CLL globally in 2026 for accelerated approval BGB-16673 has a broad development program with registrational plans in multiple indications AA, accelerated approval potential; * 303 is China -only study Indication Regimen Study details Early clinical development Registrational trial TN CLL/SLL Monotherapy CaDAnCe 101: dose escalation/expansion +zanubrutinib CaDAnCe 104: dose escalation/expansion +sonrotoclax R/R CLL/SLL Monotherapy CaDAnCe 101: phase 2 part for AA CaDAnCe 302, 303*: vs. investigator’s choice CaDAnCe 304: vs. pirtobrutinib +sonrotoclax CaDAnCe 104: dose escalation/expansion +anti-CD20 bispecifics B-cell malignancies including WM and NHL Monotherapy CaDAnCe 101: dose escalation/expansion +sonrotoclax CaDAnCe 104: dose escalation/expansion+zanubrutinib +anti-CD20 bispecifics Ongoing Under planning Ongoing Ongoing Ongoing Ongoing Ongoing Ongoing Ongoing Ongoing Ongoing Start-up WM under planning Ongoing
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79 Recap and looking ahead
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80 BeOne has comprehensive registrational program to address all CLL segments for treatment naïve and relapsed settings BR, bendamustine + rituximab; VO, venetoclax + obinutuzumab * China only; global filing for MCL anticipated in 2H25 ** Global filing anticipated in 2026 Indication Treatment Study details Phase 2 Phase 3 Approval TN CLL/SLL Continuous use Zanubrutinib monotherapy vs. BR Fixed duration Zanubrutinib + sonrotoclax vs. VO R/R CLL/SLL Continuous use Zanubrutinib vs. ibrutinib Sonrotoclax monotherapy (AA*) BGB-16673 monotherapy (AA**) BGB-16673 monotherapy vs. investigator’s choice BGB-16673 monotherapy vs. pirtobrutinib Fixed duration Sonrotoclax + anti-CD20 Sonrotoclax + BGB-16673 Approved Approved Ongoing Filed Start-up Ongoing Ongoing Start-up Under planning BTKi BCL2i BTK CDAC
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81 T-cell engager cluster Cell therapy cluster Macrophage engager Oncogenic signal cluster B-cell malignancy pipeline outlook – CLL and beyond Focus on immune cell-based modalities to develop practice-changing therapies B-cell malignancy Deliver greater patient impact by fully harnessing the killing function of immune cells Cornerstone assets established the franchise leadership BTKi BCL2i BTK CDAC Dual TAA x engager CD19 x CD20 x CD3 BAFFR x CD22 x CD3 CD79b x TAA 1 x CD3 CD20 x CD28 CD20 x 4-1BB CD19 iγδT TAA iT BTKi BCL2i BTK CDAC CD19 x CD20 x CD3 BAFFR x CD22 x CD3 CD20 x CD28 CD20 x 4-1BB CD19 iγδT Small molecule Protein degrader Cell TherapyBi/Tri-specific Discovery Investigational New Drug (IND) BCL2i 2G
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82 • Broader coverage and mitigation of antigen loss issue - CD19 and CD20 dual targeting covers ~95% B-NHL cells • Robust efficacy in all CD19 and CD20 positive cells • On track to enter clinic in 2026 Fully exploiting the killing potential of T-cells by CD3 T-cell engager and T-cell booster combinations TCE, T-cell engager; tsAb, Tri-specific antibody; BsAb, bispecific antibody; PCC, pre-clinical candidate; FPI, first patient in Biosimilar molecules of AZD486, CMG1A46, REGN5837 and RG6333 were used in studies; In the right panel, 5pM epcoritamab was used to induce the first T-cell activation signal CD19 x CD20 x CD3 TsAb CD20 x CD28 BsAb • CD20 selected due to higher tumor cell density than other TAAs • Strong CD28 affinity enables superior T-cell activity boosting • On track to enter clinic in early 2027 Better activity than leading competitors 0 4 8 12 16 20 24 28 32 36 0 400 800 1200 1600 Days Post tumor injection Mean Tumor Volume (mm 3 ± SEM) Vehicle AZD486 CD19 x CD3 2.5mpk CMG1A46 CD19 x CD20 x CD3 2.5mpk BeOne CD19 x CD20 x CD3 2.5mpk * * Stronger T-cell activation with combination of CD19 x CD20 x CD3 and CD20 x CD28 Superior T-cell activity enhancement versus leading competitors NALM6 model (CD19+) Ramos cell with comparable CD19/CD20/CD22 levels 1 10 100 1000 10000 0 2000 4000 6000 BsAb (pM) IL-2 (pg/ml) 0 BeOne CD20 x CD28 REGN5837 CD22 x CD28 RG6333 CD19 x CD28 hIgG control BeOne CD20 x CD28 (pM) BeOne CD19 x CD20 x CD3 (pM) 10000 100 BGB2801 IL-2 (pg/mL) BG-T0050 (pM) 0 pM 0 2000 4000 6000 IL-2 (pg/mL)
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83 Early exhaustion in tumor killing assay KO, knock-out; KI, knock-in Fresh tumor cells were added daily to assay without changing the iPSC-derived γδT cells to determine durability of tumor cell killing w/o IL2 and IL15 Despite impressive clinical outcomes, autologous cell therapies have limited adoption Our proprietary iPSC derived allogeneic γδT cell therapy platform: • Highly optimized for γδT differentiation (purity>99%) and expansion (>10M fold) • Integrates unique signal converter that synergizes with the additional proprietary genetic edits (>10) to enhance efficacy and persistence On track to enter clinic in 2026 Our first cell product, CD19-CAR iγδT, potentially provides a solution to persistence issues associated with allo-CAR-T 0 10 20 30 0 50 50 0 50 100 Cytotoxicity (%) Time (days) WT iγδT CD19-CAR engineered iγδT
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84 Prolonged tumor cell killing with signal converter KO, knock-out; KI, knock-in Study artificially stopped Fresh tumor cells were added daily to assay without changing the iPSC-derived γδT cells to determine durability of tumor cell killing w/o IL2 and IL15 Despite impressive clinical outcomes, autologous cell therapies have limited adoption Our proprietary iPSC derived allogeneic γδT cell therapy platform: • Highly optimized for γδT differentiation (purity>99%) and expansion (>10M fold) • Integrates unique signal converter that synergizes with the additional proprietary genetic edits (>10) to enhance efficacy and persistence On track to enter clinic in 2026 Our first cell product, CD19-CAR iγδT, potentially provides a solution to persistence issues associated with allo-CAR-T 0 10 20 30 0 50 50 0 50 100 Cytotoxicity (%) Time (days) WT iγδT CD19-CAR engineered iγδT CD19-CAR engineered iγδT w/SC
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85 Provide options for all CLL segments. A systematic development plan will help develop BeOne combinations across the disease spectrum Accelerate development with unparalleled speed from POC to multiple Phase 3 trial initiations planned for sonrotoclax and BTK CDAC Compelling continued innovation for B- cell malignancies beyond CLL with novel trispecific/bispecific TCEs and iPSC derived cell therapy platforms that have the potential to transform the field Brukinsa is just the start We are building a franchise
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86 10-minute break
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87 Solid tumor portfolio Mark Lanasa Senior Vice President, Chief Medical Officer, Solid Tumors
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88 Pan-tumor * Not yet in the clinic Target(i), target inhibitor; CDAC, chimeric degradation activating compound; ADC, antibody drug conjugate; BsADC, bispecific ADC; TsADC, trispecific ADC; BsAb, bispecific antibody; TsAb, trispecific antibody BeOne has global rights for CDK2i (Ensem partnership), B7 -H4 ADC (DualityBio partnership), MAT2Ai (CSPC Zhongqi Pharmaceutical T echnology) Our pipeline includes diverse modalities and mechanisms across disease franchises Gastrointestinal MTA Cooperative PRMT5i MUC1 x CD16A BsAb FGFR2b ADC GPC3 x 4-1BB BsAb CEA ADC PanKRASi MAT2Ai Breast/Gynecologic CDK4i CDK2i BCL2i 2G B7-H4 ADC Claudin6 x CD3 BsAb KAT6A/Bi* CDK2 CDAC* Lung Lung EGFR CDAC CEA ADC B7-H3 ADC PanKRASi EGFR x MET x MET TsAb MTA Cooperative PRMT5i MAT2Ai EGFR x MET x MET ADC* Small molecule Protein degrader ADCBi/Tri-specific Cytokine therapymAb HPK1i CCR8 mAb IL-15 prodrugDGKζi
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89 Breast and gynecologic cancers
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90 ADC Cluster ER Cluster Immune cell engagers Cell cycle cluster Establishing an innovative breast and gynecological franchise Breast / Gynecological CDK4i CDK2i BCL2i 2G B7-H4 ADC Claudin6 x CD3 BsAb KAT6A/Bi CDK2 CDAC2 Novel MOAs establish new paradigms Replace SOC CDK4/6 inhibition with selective CDK inhibitors CDK4i CDK2i CDK2 CDAC KAT6A/Bi B7-H4 ADC Claudin6 x CD3 BsAb BCL2i 2G Novel payload ADC B7-H4 x HER3 BsADC 1 Novel payload DAC Novel CDAC 1 MUC1 x CD16A BsAb Small molecule Protein degrader ADCBi/Tri-specific Discovery Investigational New Drug (IND) Target(i), target inhibitor; CDAC, chimeric degradation activating compound; ADC, antibody drug conjugate; BsADC, bispecific ADC; BsAb, bispecific antibody
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91 CDK4/6 inhibitors represent one of largest drug classes in solid tumors at ~$13B and growing EvaluatePharma, accessed 27MAY2025 CDK4/6i are blockbusters yet leave room for improvement Issues with CDK4/6i and what is unmet need Heme tox that drives dosing interruptions and holidays, and therefore suboptimal target coverage Safety concerns due to off-target inhibition Hypothesis: CDK4 selective inhibitor can ameliorate these issues and drive superior therapeutic benefit for patients Global CDK4/6i market is large, and still growing $0B $2B $4B $6B $8B $10B $12B $14B $16B $18B $20B CDK4/6i global branded sales Consensus forecasts
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92 BGB-43395 (CDK4 inhibitor) Thoughtfully designed to have superior potency and selectivity vs. atirmociclib CDK4/6=cyclin-dependent kinase 4/6, HER2=human epidermal growth factor receptor 2, HR=hormone receptor, HSC=hematopoietic stem cell MCF-7, breast cancer cell line, is a commonly used model of early -stage breast cancer that is estrogen receptor positive and non invasive Selective CDK4 inhibitor sparing CDK6 and off- target toxicities Closed time gap with atirmociclib (Pfizer) in 1L HR+ breast cancer Emerging best-in-class profile with low hematologic toxicity at active PD dose levels Clinical progress 300+ patients enrolled across dose escalation and expansion cohorts in HR+/HER2- MBC as of June 3, 2025 Favorable tolerability, PD and clinical responses in extensively pretreated patients Planning underway for Phase 3 studies in 1L and 2L HR+ breast cancer with 2L start as early as 4Q25 BeOne CDK4i presents the highest CDK4 potency and CDK6 selectivity CDK4i potency CDK4/CDK6 selectivity 356 639 326 544 126 1.3 7.7 16 21 38 Cellular CDK6 IC50 divided by cellular CDK4 IC50 to assess CDK6 selectivity: 1) CDK4 cellular IC50 measured by pRB in Jeko-1; 2) CDK6 cellular IC50 measured by pRB in Pfeiffer CDK4 KO cell MCF-7 proliferation assay to assess CDK4 potency
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93 Dr. Shom Goel, MBBS, PhD Group Leader and Medical Oncologist, Peter MacCallum Cancer Centre BGB-43395 (CDK4 inhibitor) Speaker introduction: Dr. Shom Goel, key opinion leader in breast cancer Associate Professor and Clinician-Scientist at the University of Melbourne and Peter MacCallum Cancer Centre Global PI / Translational PI for four randomized clinical trials in breast cancer Chair of the American Society of Clinical Oncology Education Committee (2023) Recent Snow Fellowship awardee and Era of Hope Scholar Award (U.S. Department of Defense) 60+ publications, with recent publications in high-impact journals including Nature, Cancer Cell, and Nature Cancer
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94 Ribociclib Neutropenia Neutropenia Neutropenia Low Low Diarrhea Inhibition of CDK6 Inhibition of CDK6 Off targeting of CDK9, GSK3β and CAMKIIs Heme toxicity GI toxicity Suspected cause of key toxicity CDK4/6 inhibitors block the CDK4/6 complex and prevent the phosphorylation of the RB protein This stops the tumor cycle from progressing past the G1 phase, inhibiting further tumor cell growth and causing tumor regression More potent inhibition of CDK4 prevents emergence of resistance BGB-43395 (CDK4 inhibitor) Three CDK4/6 inhibitors approved, all with toxicity issues and loss of efficacy over time Palbociclib Abemaciclib Palbociclib (Ibrance®, Pfizer), abemaciclib (Verzenio®, Eli Lilly), and ribociclib (Kisqali®, Novartis) are approved CDK4/6 inhibitors indicated for the treatment of HR+/HER2 – advanced or metastatic breast cancer
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95 BGB-43395 (CDK4 inhibitor): study design and enrollment 1 This data will enable subsequent development of this combo Dose optimization (target n=120) Fulvestrant combo 240mg, 400mg, 600mg BID n=62 Letrozole combo 240mg, 400mg, 600mg BID n=44 Completed In Progress Not Commenced Global dose escalation Monotherapy n=60 Fulvestrant combo Doses to 800mg BID n=64 Letrozole combo Doses to 800mg BID n=54 Elacestrant combo ER+/HER2- BC1 Cohort expansion (target n=80) Fulvestrant combo 2L HR+ BC Letrozole combo CDK4/6i Naïve BC Region Enrolled patients (as of 09JUN2025) France 79 United States 59 Brazil 39 Australia 38 China 22 Korea 19 Region Enrolled patients (as of 09JUN2025) Japan 12 Moldova 9 Malaysia 4 New Zealand 2 Thailand 1 Total study enrollment 284
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96 BGB-43395 exhibited rapid absorption and linear PK within available dose range Mean elimination half-life is 13 hours BGB-43395 exposures are not impacted by co-administration with either fulvestrant or letrozole No major differences in exposures observed between non-Asian and Asian populations Preliminary mean BGB-43395 plasma concentration-time profiles 10 100 1000 0 2 4 6 8 10 BGB-43395 (CDK4 inhibitor): pharmacokinetic data Linear PK with no major impact of race or co-meds (fulvestrant/letrozole) Caveat: Non-compartmental analysis (NCA) is performed using nominal time points DCO: 10MAR2025 Mean BGB-43395 (ng/mL) Time (h) 240mg BID (N=12) 400mg BID (N=9) 600mg BID (N=6) Dose normalized AUC across doses PK is dose proportional 0 5 10 15 0 240 400 600 700 Dose (mg) Dose normalized AUC0_8 (h*ng/mL/mg) n = 12 n = 9 n = 6
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97 Plasma TK1 activity change post BGB-43395 +fulvestrant treatment (Dose-escalation, BC-only) ctDNA mVAF change post BGB-43395 +fulvestrant treatment (Dose-escalation, BC-only) 0 20 40 60 80 100 120 140 160 180 200 C1D1 C1D15 C2D1 0 100 200 300 Below 240 mg BID 240 mg BID 400 mg BID 600 mg BID Dose-dependent and durable PD biomarker modulation in blood (TK1 activity) was observed across dose levels Clinically meaningful PD effects were achieved at doses 240mg BID and above in fulvestrant combo cohort Early (C2D1) ctDNA decrease was observed starting from 240mg BID in fulvestrant combo BGB-43395 (CDK4 inhibitor): pharmacodynamic data Both TK1 and ctDNA data suggest 240mg BID doses and above are biologically active Plot: median with 95% CI DCO: 12MAY2025 **TK1 (Thymidine kinase1) reduction to 20% defined as goal, since several published datasets indicate an 80% TK1 reduction le vel from baseline, when CDK4/6 inhibitors used at full dose plus ET in the metastatic setting. Yap T et al ASCO Annual meeting 2023 ( atirmociclib), Malorni L et al EJC 2023 (ribociclib) mVAF- Mean variant allele fraction represents the average proportion of mutant DNA sequences within a sample, reflecting the overal l tumor burden % TK1 of baseline C2D1/C1D1 mVAF ratio (%) Dose levelVisit (predose) 0 20 40 60 80 100 120 140 160 180 200 C1D1 C1D15 C2D1 240mg BID (n=17) 400mg BID (n=13) Below 240mg BID (n=11) 600mg BID (n=10) 100 100 100 100 63 39 31 31 63 29 27 27 101 60 25 58
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98 BGB-43395 (CDK4 inhibitor): safety data Well-tolerated in combination with fulvestrant, with improved hematological tolerability 1 Patients included those who were randomized by DCO : 26MAY2025 98 n (%) CDK4i + fulvestrant (240 – 600mg BID) Dose escalation (N=37) Dose optimization (n=61)1 Patient with any TEAE 36 (97.3%) 54 (88.5%) Related TEAE 35 (94.6%) 51 (83.6%) ≥ G3 TEAE 19 (51.4%) 14 (23%) ≥ G3 Related TEAE 10 (20.7%) 12 (19.7%) TRAE leading to discontinuation 1 (2.7%) 1 (1.6%) Key AEs All Grade TEAE Gr3+ TEAE All Grade TEAE Gr3+ TEAE Diarrhea 83.8% 5.4% 65.6% 8.2% Anemia 13.5% 0% 11.5% 1.6% Neutrophil count decreased 21.6% 16.2% 29.5% 8.2% Platelet count decreased 5.4% 2.7% 6.6% 1.6% Well-tolerated safety profile across range of doses under consideration for future study Diarrhea is low grade and readily manageable with no associated treatment discontinuations due to diarrhea Potential best-in-class hematologic safety profile
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99 -100 -90 -80 -70 -60 -50 -40 -30 -20 -10 0 10 20 30 40 50 60 70 Breast cancer patients with ‘bone only’ metastatic disease are eligible for dose escalation but are not response evaluable (19 of 29 response evaluable) BGB-43395 (CDK4 inhibitor): combination with fulvestrant Preliminary anti-tumor activity in extensively pretreated dose escalation patients *Breast, endometrial, and ovarian cancer. Waterfall plot includes data from 27 response evaluable patients in BGB -43395 + fulvestrant dose escalation by DCO: 26MAY2025 # Unconfirmed ORR among the response-evaluable patients Tumor burden change from baseline (%) Patients Best overall response • Partial response • Stable disease • Progressive disease 240mg BID + Fulvestrant 400mg BID + Fulvestrant 600mg BID + Fulvestrant Investigator-assessed best change from baseline in target lesion sum of diameters* 53 22 30 50 14 0 -5 -10 -15 -28 9 -24 32 55 34 -6 -8 -12 -12 -24 -32 -51 -100 -100 -8 0 BGB-43395 + Fulvestrant Dose escalation N=29; Breast Cancer N=37; Total* Number of prior lines of therapy in metastatic setting • Median (range) • >= 3 Lines 4 (0-11) 90% 4 (0-11) 73% Prior chemotherapy (including ADC) 100% 100% Prior endocrine therapy 100% 84% Prior CDK4/6 inhibitor(s) 93% 76% Median follow-up (months) 3.0 2.7 Objective response rate# 11% (2 of 19) 15% (4 of 27)
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100 Strong pharmacodynamic effect across range of well-tolerated doses Potential best-in-class hematologic safety profile; diarrhea is low grade and readily manageable Emerging evidence of clinical efficacy in extensively pretreated, post-CDK4/6 patients at doses with pharmacodynamic activity Clear path to registration-enabling studies in next 6–12 months BGB-43395 (CDK4 inhibitor) BeOne’s CDK i pre-clinical differentiation translates to meaningful clinical results Key findings Next steps Read-out of dose-optimization randomized expansions informs both dose selection and final proof-of-concept for registrational intent studies Elacestrant combination enables broader development with different ET backbones, such as oral SERDs in future Target(i), target inhibitor; ET, endocrine therapy; SERD, selective estrogen receptor degrader
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101 BG-C9074* (B7-H4 ADC) Potential first-in-class ADC for patients with B7-H4 expressing tumors Target expressed in breast and gynecologic tumors with limited expression in normal tissues Demonstrated dose-dependent in vivo efficacy good internalization, and bystander killing Clinical Progress 95 patients enrolled in mono dose escalation and safety expansion as of June 2, 2025 Responses noted across multiple tumor types and at various dose levels with manageable toxicity Tumor-specific expansion cohorts to begin enrollment 3Q25 First data disclosure at ASCO 2025 with clinical updates today Robust and clinically validated drug linker design differentiates our molecule • Non-P-gp substrate# TOP1i payload • Strong bystander effect • DAR6 to balance efficacy and toxicity * BG-9074 in licensed from Duality named DB -1312. † Clin Cancer Res. 2023 Mar 1 ;29(6):1086-1101 #P-glycoprotein (P-gp) is a protein that can cause multidrug resistance (MDR) in cancer cells by preventing the uptake of many drugs (substrates), including anticancer drugs. Not being a P -gp substrate reduces drug resistance Normal Breast Epithelium Breast Ductal Adenocarcinoma Normal Ovary Follicle Ovarian Serous Adenocarcinoma Normal Endometrium Endometrial Carcinoma High B7-H4 expression in tumor tissue of breast, endometrial, ovarian cancer †
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102 BG-C9074 (B7-H4 ADC): early clinical data Well-tolerated monotherapy across clinically relevant dose levels *Include response evaluable patients in BC and Gyn cancers DCO: 02JUN 2025 TEAE, treatment emergent adverse events; DLT, dose limiting toxicities Most common TEAEs: nausea (low grade), neutropenia, and fatigue Most common Gr≥3 TEAE: neutropenia and thrombocytopenia Six DLTs: • Fatigue (n=1) • Neutropenia (n=1) • Febrile neutropenia (n=2) • Platelet count decreased (n=2) No adverse events leading to drug discontinuation or death n (%) Safety profile at selected monotherapy dose levels 4mg/kg (n=23) 5mg/kg (n=7) 6mg/kg (n=26) 6.5mg/kg (n=12) Total* (n=68) Patients With Any TEAE 22 (95.7%) 7 (100%) 25 (96.2%) 12 (100%) 66 (97.1%) Related 21 (91.3%) 7 (100%) 24 (92.3%) 11 (91.7%) 63 (92.6%) Related >= Grade 3 2 (8.7%) 0 (0%) 10 (38.5%) 5 (41.7%) 17 (25%) Related Serious 1 (4.3%) 1 (14.3%) 3 (11.5%) 2 (16.7%) 7 (10.3%) Related Leading to Dose Modification 1 (4.3%) 0 (0%) 9 (34.6%) 3 (25%) 13 (19.1%) Selected AE ≥Grade 3 Neutropenia 1 (4.3) 0 (0.0) 7 (26.9) 5 (41.6) 13 (19.1) Thrombocytopenia 0 (0.0) 0 (0.0) 4 (15.3) 2 (16.7) 6 (8.8) Leukopenia 0 (0.0) 0 (0.0) 2 (7.6) 1 (8.3) 3 (4.4) Nausea 0 (0.0) 0 (0.0) 2 (7.7) 0 (0.0) 2 (2.9)
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103 71 48 -51 15 -4-6 -34 36 23 20 13 12 8 2 0 0 -3 -5-5-6 -12 -17 -29-31-31 -35 -55 -59 1 0 -20-21 -45 -100 16 8 6 -8 -11-12 -25-25-27-29-30 -36 -39 -43 -50 -53-54 -64 -74 -100 40 24 1 -12 -17-18-19 -24-25 -19 -100 -90 -80 -70 -60 -50 -40 -30 -20 -10 0 10 20 30 40 50 60 70 80 BG-C9074 (B7-H4 ADC): early clinical data Compelling early antitumor activity observed in Breast and Gynecological Cancers BG-9074 in licensed from Duality named DB -1312. * 83 patients enrolled with Breast and gynecological cancers DCO: 02JUN2025 95 patients treated at 9 dose levels 6 enrolled tumor types; median 4 prior lines of therapy Emerging dose-response relationship in breast, ovarian, and endometrial cancers*: Confirmed ORR 24%, unconfirmed ORR 29% among 68 efficacy evaluable patients 14 of 20 responses ongoing as of June 2, 2025 Activity at 6mg/kg Q3W: confirmed ORR 43%, unconfirmed ORR 48% Investigator-assessed best change from baseline in target lesion sum of diameters (BC and GYN) 1 mg/kg Q3W 2 mg/kg Q3W 4mg/kg Q3W 6mg/kg Q3W 6.5mg/kg Q3W 7mg/kg Q3W 5mg/kg Q3W Best overall response • Partial response • Stable disease • Progressive disease
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104 BG-C9074 (B7-H4 ADC): biomarker data Greater response rates in patients with higher levels of B7-H4 expression Efficacy observed across a range of tumor types: Selecting patients with higher level B7-H4 expression enriches ORR Favorable safety profile at doses with strong early response rates Tumor specific expansion cohorts in breast and gynecological malignancies to open in 3Q25 Planning underway for registrational intent studies BG-C9074 Breast and Gynecological N 68 33 Dose level ≥1mg/kg ≥1mg/kg B7-H4 expression cutoff# None High uORR* 29.4% 42.4% Stronger efficacy in B7-H4 biomarker enriched patients * Unconfirmed; DCO: 02JUN2025
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105 BG-68501 (CDK2 inhibitor) Potent and selective - manageable safety and early signs of monotherapy activity in BC Joshi et al ASCO Annual Meeting 2025, Abstract 3115 Differentiated CDK2i vs. competitors with better potency, selectivity, CDK family kinome selectivity Potential synergy with CDK4i in solid tumors, including CDK4/6i-resistant breast cancer First data disclosure at ASCO 2025 49 patients with pre-treated solid tumors received ascending doses of BG-68501 Preliminary safety: No DLTs; Most common AEs include Nausea and vomiting (61%), and fatigue (25%). GI toxicity improved with scheduled anti-emetics Preliminary efficacy: 2 uPR (6%) (both BC), 15 (39%) SD in 33 patients (mFU of 2.9 months) Investigator-assessed best change from baseline in target lesion sum of diameters Response is unconfirmed. aThis plot shows post-baseline tumor assessments excluding patients without target lesions up to the initiation of new anti- cancer therapy or the first PD in the efficacy-evaluable population. Abbreviations: BC, breast cancer; BID, twice per day; End_C, endometrial cancer; Eso_C, esophageal cancer; HER2, human epidermal growth factor receptor 2; HR, hormone receptor; O, other: fallopian tube high grade serous; PCA, prostate cancer; PROC, platinum refractory or resistant ovarian cancer; SCLC, small cell lung cancer; TNBC, triple-negative breast cancer. -50 -40 -30 -20 -10 0 10 20 30 40 50 60 10mg BID 25mg BID 50mg BID 100mg BID 200mg BID Tumor burden change from baseline (%) Patients Best overall response • Partial response • Stable disease • Progressive disease • Not evaluated / not assessed
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106 Our breast cancer franchise is further extended by new and differentiated molecules 1 Mukohara T. et. Al Nature Medicine 2024 CDK2 CDAC - potential for superior potency and improved toxicity profile compared to small molecule CDK2 inhibitors KAT6A/B inhibitor - encouraging preclinical activity for both monotherapy and in combination with fulvestrant when compared to a leading competitor, PF-07248144 (Pfizer)1
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107 BG-75098 (CDK2 CDAC) Potential first-in-class CDK2 degrader with improved potency, selectivity, and PK *Study was carried out in a variety of CDK2-dependent and independent cell lines **Anti-proliferation assay in CDK2-dependent OVCAR3 and CDK1 -dependent TOV21G cell lines Catalytic MoA to elicit superior target inhibition over small molecule inhibitors Much improved CDK1 selectivity compared to small molecule inhibitors due to additional selectivity provided by tertiary complex formation with E3 ligase Long predicted T1/2 to support QD dosing and better target coverage with flat PK at steady state On track to enter clinic by YE 2025 BG-75098 presents exceptional potency and selectivity profile CDAC gains selectivity via unique interaction between CDK2 and E3 CDK2CDK1 Predicted E3 and CDK1/2 interaction region CDK1 specific region CDK2 specific region Selectivity comes from using rigid linkers that directs E3 binding to CDK2 specific regions, enabling stable interactions with CDK2 but not CDK1 Anti-proliferation assay** CDK2 cellular IC50 (nM) CDK1/2 selectivity (fold) Pfizer CDK2i 380 6 Incyte CDK2i 156 5 BeOne CDK2 CDAC 14 > 714 Degradation assay* CDK2 DC50 (nM) CDK1 DC50 (nM) BeOne CDK2 CDAC 1-13 > 10,000
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108 BG-75202 (KAT6A/B inhibitor) Potential best-in-class with opportunity to achieve better efficacy and safety PF-07248144 is KAT6A/B inhibitor from Pfizer; *** P<0.001 Greater potency in HR+ HER2- breast cancer cell lines (pIC50) 8 9 10 ZR75-1 T-47D CAMA1 HCC1428MCF7 BT-483 HCC1500 PF-07248144 BG-75202 Stronger efficacy in combo with fulvestrant Treatment Days Tumor Volume in T47D model (mm 3 ± SEM) 0 7 14 21 28 0 200 400 600 800 1000 Vehicle BG-75202 0.5 mpk + Fulvestrant 2 mg PF-07248144 0.5 mpk + Fulvestrant 2 mg *** PF-07248144 0.5mpk QD in mouse study is the clinically equivalent dose Improved efficacy in both monotherapy and combination setting in preclinical models, comparing to PF-07248144 Over 10-fold higher selectivity against KAT7 comparing to PF-07248144, potentially lowering hematology tox Prioritize development in HR+HER2-BC in combination with endocrine therapy, with and without BG-43395 On track to enter clinic by YE 2025
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109 CDK4i: emerging data supports differentiated and potentially BIC profile; progressing towards Phase 3 B7-H4 ADC: very promising efficacy and manageable toxicity; subsequent studies in OC, EC and BC in planning BCL2i: Phase 1b study ongoing to evaluate differentiated HR+ BC development opportunity CDK2i: manageable toxicity and early evidence of efficacy in advanced BC as monotherapy CDK2 CDAC and KAT6A/Bi: potentially differentiated based on improved selectivity and potency Tremendous progress in first 18 months since establishing breast/gynecologic cancer franchise Highly promising pipeline including several modalities (small molecule, CDAC and ADCs) with rapidly evolving dose-defining and POC data generation with potential for first pivotal study by YE (CDK4i) Target(i), target inhibitor; CDAC, chimeric degradation activating compound; ADC, antibody drug conjugate; BsADC, bispecific ADC;; BsAb, bispecific antibody
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110 Lung cancer franchise
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111 KRASm Cluster EGFRm Cluster MTAP-del Cluster ADC Cluster Building an industry-leading lung cancer franchise Broad and deep pipeline with proprietary, innovative and intentionally designed molecules Target(i), target inhibitor; CDAC, chimeric degradation activating compound; ADC, antibody drug conjugate; BsADC, bispecific ADC; TsADC, trispecific ADC; BsAb, bispecific antibody; TsAb, trispecific antibody Lung EGFR CDAC B7-H3 ADC EGFR x MET x MET TsADC PanKRASi EGFR x MET x MET TsAb MTA Cooperative PRMT5i MAT2Ai CEA ADC EGFRxMETxMET TsADC CEA ADC ADAM9 ADC Novel payload ADC 1-2 MTA Cooperative PRMT5i MAT2Ai EGFR CDAC EGFRxMETxMET TsAb EGFRxMETxMET TsADC mADC 1 -2 B7-H3 ADC Novel Bs/TsADC 1-4 KRAS CDAC RAS (ON) G12Di RAS (On)i RAS (ON) ADC panKRASi Small molecule Protein degrader ADCBi/Tri-specific Discovery Investigational New Drug (IND)
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112 BGB-58067 (PRMT5i) and BG-89894 (MAT2Ai) Synergistic combination between MTA-cooperative PRMT5 inhibitor and MAT2A inhibitor Only company with both clinical stage PRMT5i and MAT2Ai Potential best-in-class PRMT5i with superior potency, selectivity, and brain penetration Clinical progress Both programs in monotherapy dose escalation PRMT5i shows better than expected, dose dependent PK profile Favorable safety and tolerability profile with no DLT observed Early responses observed at the second dose level BeOne PRMT5i shows higher potency and selectivity BeOne PRMT5i MRTX-1719 TNG-462 TNG-908 AMG-193 1 10 100 1000 Relative EC50 (nM) 9 27 20 321 130 MTA-cooperative PRMT5i killing activity 1 BeOne PRMT5i MRTX-1719 TNG-462 TNG-908 AMG-193 0 20 40 60 80 100 66 52 35 9 22 Mean EC50 Fold Change MTA-cooperative PRMT5i killing selectivity 2 0 5 10 15 20 0 200 400 600 800 1000 Treatment days Tumor volume (mm 3 ±SEM) in H838 model Vehicle BeOne MAT2Ai BeOne PRMT5i BeOne PRMT5i + MAT2Ai 18 **** **** BeOne PRMT5i + MAT2Ai induce robust efficacy in animal model BeOne PRMT5i and MAT2Ai are highly brain penetrative Compound BGB- 58067 BG- 89894 Kpuu, CSF3 55% 102% 1Different dots in the “Tumor Cells” panel indicate different tumor cell lines. Del, deletion; 2Mean EC50 fold change of cell killing in 7 MTAP DEL and 2 MTAPWT cell lines; **** p＜0.0001 3Kpuu,CSF represents a measurement of how well a drug moves from the bloodstream into the CSF in cynomolgus monkeys, used for assessment of blood-brain penetration
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113 BGB-58067 (PRMT5i): pharmacodynamic data Target engagement is confirmed by rapid SDMA reduction in tumor and plasma SDMA – (symmetrical dimethylization) – reduced levels particularly in MTAP -deleted cells can be associated with increased protein stability, potentially promoting tumor growth and metastasis Baseline C2D1 H&E (100x) SDMA (400x) Isotype control (400x) Tumor Cell SDMA H-score Stromal cell SDMA+ percentage Baseline 300 100% C2D1 0 90% Rapid plasma SDMA reduction observed at dose level 1 (n=2) Target engagement with MTAP-del vs. normal cells in the tumor tissue of MTAP-del ESCC patient (dose level 1; paired lung biopsy ) -100 -75 -50 -25 0 C0D1 C1D1 C1D8 C1D15 C2D1 086081-005 086182-015 Plasma SDMA reduction (% change from baseline)
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114 BGB-58067 (PRMT5i): clinical safety and efficacy data Favorable safety profile with early efficacy signals DCO: 29MAY2025 * Responses - 1 confirmed, 2 unconfirmed, all ongoing Safety Favorable safety profile observed in 27 enrolled patients across four dose levels • Most common TRAEs were nausea (18.5%) and anemia (11.1%) • No significant hematological toxicity • No DLTs, ≥ Gr3 treatment-related AEs, serious treatment-related AEs, or TRAEs leading to discontinuation/modification Efficacy Target efficacious range achieved at second dose level due to better than anticipated clinical PK Three objective responses* in histologically distinct tumor types at second dose level
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115 Clinical stage BeOne Amgen BMS IDEAYA AstraZeneca PRMT5i ✓ ✓ ✓ X ✓ MAT2Ai ✓ X X ✓ X Phase 1 study is enrolling in China and will expand to U.S. and AUS in 2H 2025 4Q24 2025 2026 MAT2Ai PRMT5i + SOC PRMT5i + MAT2Ai BGB-58067 (PRMT5i) and BG-89894 (MAT2Ai) BeOne is only company with both PRMT5i and MAT2Ai in the clinic The bars represent phase 1 study timelines; the start of the bar represents the first patient in for the cohort(s) PRMT5i
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116 BG-60366 (EGFR CDAC) Truly differentiated MoA to completely, selectively abolish EGFR signaling WT, wild-type; LR, L858R; D19, exon 19 deletion; DT, exon 19 deletion/T790M; LT, L858R/T790M; DC, exon 19 deletion/C797S; LC, L8 58R/C797S; DTC, exon 19 deletion/T790M/C797S; LTC, L858R /T790M/C797S Highly potent against all typical EGFR mutations and major resistant forms Sparing wild-type EGFR and good proteomic selectivity Deep target degradation and strong efficacy in animal models Clinical progress In mono dose escalation Encouraging PK profile with good oral absorption (Tmax=~4 hours), high exposure and long elimination (T1/2 ~4.8 days) BG-60366+3G TKI combo planned to start in 2H25 Broadest EGFR mutation coverage w/o hitting WT EGFR Robust efficacy in both osimertinib-sensitive and resistant models IC50 >1000 nM IC50 =30~1000 nM IC50 =1~30 nM IC50 <1 nM WT LR D19 LT DT LC DC LTC DTC Osimertinib (3G TKI) BG-60366 Gefitinib (1G TKI) Address osimertinib resistance 0 4 8 12 16 20 0 400 800 1200 1600 2000 2400 Mean Tumor Volume in H1975 L858R/C797S model (mm 3 ± SEM) Vehicle QD Osimertinib 25mpk QD BG-60366 10mpk QD Treatment Days 0 7 14 21 28 0 100 200 500 1000 1500 2000 Mean tumor volume in exon 19 deletion model (mm 3 ± SEM) Vehicle QD Osimertinib 25mpk QD BG-60366 + Osimertinib 300 BG-60366 30mpk QD 300 p<0.01* Treatment days Deeper response when combined with osimertinib
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117 BG-T187 (EGFRxMETXMET TsAb) Best-in-class potential EGFRxMETxMET dual targeting TsAb with unique antibody design TsAb, trispecific antibody; 1We used HEKn, primary human epidermal keratinocytes isolated from neonatal foreskin, in the cellular study; 2Biosimilars of competitors’ EGFR x MET antibodies were used; 3Osimertinib-resistant model, MET IHC 3+; EGFR L858R; ; ***, p<0.001, ****, p<0.000; The clinical significance of pre -clinical data has not been established Superior and optimal MET inhibition with biparatopic MET antibody construct Pre-clinical data suggest stronger efficacy than amivantamab in MET-driven models Potential lower EGFR on-target skin toxicity due to weaker killing activity of primary keratinocyte1 than amivantamab Clinical progress In mono dose escalation Subcutaneous formulation planned to enter clinic in 3Q25 Superior efficacy in MET-driven and TKI resistant xenograft models Best-in-class cellular profile among EGFR x MET dual targeting Ab2 0 7 14 21 28 0 300 600 900 1200 1500 1800 Treatment days Tumor volume in LD1-0025-200730 3 PDX model (mm 3 ± SEM) Vehicle Amivantamab 30 mpk BG-T187 10mpk 0 1000 2000 3000 Treatment days Tumor volume in Hs-746T METamp & Exon14 skipping model (mm 3 ± SEM) Vehicle Amivantamab 10mpk 0 5 8 12 BG-T187 10mpk 15 19 *** 0 5 10 15 20 25 0 500 1000 1500 2000 Treatment days Tumor volume in EBC1 METamp model (mm 3 ± SEM) 1 BG-T187 10mpk Vehicle Amivantamab 10mpk **** EGFR x MET dual targeting Ab BG-T187 Amivantamab Strong EGFR signaling inhibition ✓ ✓ Strong MET signaling inhibition ✓ X Weak primary keratinocyte killing ✓ X
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118 EGFR TKI-responsive model EGFR TKI-resistant model BG-60366 (EGFR CDAC) and BG-T187 (EGFRxMETxMET TsAb) Combination generates durable response in both EGFR TKI-sensitive and resistant models TKI, tyrosine kinase inhibitor 0 14 28 42 56 70 84 98 0 500 1000 1500 Treatment days Mean tumor volume in H1975 (EGFR L858R T790M) model (mm 3 ± SEM) 160 Vehicle BG-60366 30mpk BG-T187 20mpk BG-60366 30mpk + BG-T187 20mpk 160 0 14 28 42 56 70 0 50 100 150 200 500 1000 1500 Treatment days Mean tumor volume in HCC 827 erlotinib resistant model (mm 3 ± SEM) Vehicle BG-60366 10mpk Lazertinib 10mpk BG-T187 10mpk Amivantamab 10mpk BG-60366 10mpk + BG-T187 10mpk Lazertinib 10mpk + Amivantamab 10mpk 200
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119 Broad and deep lung cancer portfolio with diverse and differentiated assets MTAP-del cluster: PRMT5i and MAT2Ai are foundational molecules for MTAP-del NSCLC and other MTAP-del tumors. Early data support differentiated and best- in-class profiles EGFR Cluster: differentiated and FIC molecules provide opportunity for substantial patient impact via in-portfolio combination and in combination with 3rd generation TKI Novel ADCs: multi-specific ADCs have potential to both broaden eligible population and improve therapeutic window. Novel payloads will further advance tumor- selective targeting Target(i), target inhibitor; CDAC, chimeric degradation activating compound; ADC, antibody drug conjugate; BsADC, bispecific ADC; TsADC, trispecific ADC; BsAb, bispecific antibody; TsAb, trispecific antibody
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120 Gastrointestinal cancer franchise
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121 KRAS Cluster PanKRASi EGFR Cluster MTAP-del Cluster ADC Cluster Immune Cell Engager Designing and delivering innovation in GI oncology Gastrointestinal MTA Cooperative PRMT5i MUC1 x CD16A BsAb FGFR2b ADC GPC3 x 4-1BB BsAb CEA ADC KRASi MAT2Ai FGFR2b ADCCEA ADC GPC3 x 4-1BB BsAb MAT2Ai MTA Cooperative PRMT5i EGFRxMETxMET TsAb MUC1 x CD16A BsAb B7-H3 ADC EGFRxMETxMET ADC Novel Bs/Ts ADC 1-6 Novel Payload ADC KRAS CDAC RAS (ON) G12Di RAS (On)i RAS (ON) ADC Small molecule Protein degrader ADCBi/Tri-specific Discovery Investigational New Drug (IND) Target(i), target inhibitor; CDAC, chimeric degradation activating compound; ADC, antibody drug conjugate; BsADC, bispecific ADC; TsADC, trispecific ADC; BsAb, bispecific antibody; TsAb, trispecific antibody
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122 RAS-GDP complex Targeting KRAS biology to maximize clinical benefit OFF Combinations to generate greater therapeutic benefits Clinical IND Discovery 1G KRASi 2G Improve potencyKRAS CDAC RAS-GTP complex ON 1G RAS(ON)i 2G Mitigate on-target toxicity RAS(ON) ADC RAS(ON) G12Di
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123 KRAS CDAC • Highly potent and selective, broad spectrum for KRAS mutations • Good pharmacological property, supporting daily dosing • Near complete target degradation at efficacious dose • Expected to enter clinic 2H26 Brain-penetrant RAS(ON)i • High brain penetration, 39% Kpuu1 in mice • Significantly lower anticipated efficacious dose enabled by better potency and PK properties • Expected to enter clinic by 2H26 New molecules for KRAS pathway poised to deliver greater patient impact 1Kpuu,CSF represents a measurement of how well a drug moves from the bloodstream into the CSF in cynomolgus monkeys, used for assessment of blood-brain penetration KRAS CDAC exhibits superior potency and selectivity over RAS(ON)i Marked increase of potency upon KRAS CDAC and RAS (ON)i combination BeOne RAS (ON)i produces robust efficacy at a much lower dose level 0 7 14 21 0 500 1000 1500 2000 2500 SW620 (KRAS G12V ) Treatment Days Mean Tumor Volume (mm 3 ± SEM) Vehicle RMC-6236 25mpk TGI(%) at Day21 100 102BeOne RAS(ON)i 1mpk Cell Viability IC50 >1000 nM Mutation KRAS G12V KRAS G12D KRAS G12C KRAS G13D KRAS Amp KRAS Q61H KRAS G12A KRAS G12S NRAS G12D HRAS G12V BeOne KRAS CDAC RMC-6236 1~10 nM10~100 nM <1 nM Cellular combo study in AsPC-1 (KRAS G12D) cell - 3 0 0 3 0 BeOne KRAS CDAC (nM) BeOne RAS(ON)I (nM) 100 16 Synergistic Score
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124 BG-C137 (FGFR2b ADC) Potential first-in-class with best-in-modality design 1Bemarituzumab is FGFR2b mAb from Amgen, whose combo with chemotherapy has shown Phase 2 efficacy in gastric cancer but 26% rate of treatment discontinuat ion due to on-target corneal toxicity; 2BG-C137 was dosed once, bemarituzumab was dosed BIW; 3 No ocular adverse findings in monkey GLP TOX study Superior efficacy over bemarituzumab1 in animal models with heterogeneous FGFR2b expression Spares corneal toxicity via unique epitope with weaker ligand blockade Clinical progress In 4th dose level cohort of monotherapy dose escalation Objective responses observed with no corneal or ocular AEs reported to date BG-C137 produces stronger efficacy in xenograft models2 1 3 5 7 9 11 13 15 17 19 0 200 400 600 800 1000 1200 1400 1600 Treatment Days Tumor Volume in FGFR2b low PDX model (mm 3 ± SEM) Vehicle BG-C137 8mpk BG-C137 3mpk Bemarituzumab 10mpk **** * 1 3 5 7 9 11 13 15 17 19 21 23 25 0 500 1000 1500 2000 Treatment Days Tumor Volume in FGFR2b medium PDX model (mm 3 ± SEM) Vehicle BG-C137 3mpk Bemarituzumab 10mpk **** Molecule Block FGF7- FGFR2b Block FGF10- FGFR2b BG-C137 Weak NO Bemaritu zumab Strong Strong 0 20 40 60 Mouse cornea Thickness(um) ns ✱✱✱✱ Vehicle BG-C137 10 mpk, Q2W x 2 Bemarituzumab 10 mpk, BIW x 8 BG-C137 has lower FGFR2b ligand blocking activity and does NOT induce corneal tox in animal studies3
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125 Exciting GI cancer portfolio with deep focus on targeting RAS Pathway KRAS: deep commitment to developing differentiated RAS pathway targeting therapies via comprehensive multi- modality approach MTAP-del: exciting combination opportunity with PRMT5i and MAT2Ai for MTAP-deleted pancreatic cancer ADCs: multiple first-in-class (FIC) and/or best-in-class opportunities (BIC). FGFR2b ADC emerging profile indicates superior safety profile with FIC potential in gastric cancer Target(i), target inhibitor; CDAC, chimeric degradation activating compound; ADC, antibody drug conjugate; BsADC, bispecific ADC; TsADC, trispecific ADC; BsAb, bispecific antibody; TsAb, trispecific antibody
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126 Completely reshaped clinical-stage solid tumor portfolio in only two years enabling in-portfolio combinations across three disease areas Compelling continued innovation with two to three additional clinical-stage molecules in each disease area every year Accelerate development with unparalleled speed to POC with multiple Phase 3 trial initiations planned in 2026 for CDK4i and B7-H4 ADC, and possibly PRMT5i and FGFR2b ADC From innovation to impact: executing a strategic and rapidly progressing solid tumor portfolio to help more patients
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127 Summary Lai Wang Global Head of R&D
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128 BGB-45035 (IRAK4 CDAC) First-in-class with deep and sustained IRAK4 degradation MAD, multiple ascending dose; SAD, single ascending dose Designed with best-in-class properties: • Faster and deeper IRAK4 degradation with stronger cytokine inhibition compared to KT474 in preclinical models • No QT prolongation Clinical progress SAD and MAD completed Phase 1b in prurigo nodularis (PN)/atopic dermatitis initiated (AD) Long half-life in human (60-96 hours) Complete and sustained IRAK4 degradation in peripheral blood up to 7 days after a single dose of BGB-45035 Phase 2 to start in 2H25; POC for tissue IRAK4 degradation expected before YE 2025 IRAK4 degradation in blood SAD MAD 0 2 4 6 8 10 12 14 16 18 20 22 24 -100 -80 -60 -40 -20 0 20 40 60 80 100 120 Time (days) % IRAK4 Change from Baseline Placebo (n=8) MAD DL1 (n=6) MAD DL2 (n=6) MAD DL3 (n=6) MAD DL4 (n=6) BGB-45035 treatment 0 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 -100 -80 -60 -40 -20 0 20 Time (days) % IRAK4 Change from Baseline Placebo (n=12) SAD DL1 (n=6) SAD DL2 (n=6) SAD DL3 (n=6) SAD DL4 (n=6) SAD DL5 (n=6) SAD DL6 (n=6) BGB-45035
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129 Our sheer research output and number of clinical catalysts are unprecedented; we are at an inflection point that our capabilities are coming together to create a unique R&D model; we are pioneering first-in-class and best-in-class therapies BRUKINSA is just the start. We have thoughtfully considered all permutations of how the CLL field will evolve and have designed for the best solution regardless with sonrotoclax and BTK-CDAC We are approaching our priority solid tumor histologies, breast/gynecological cancer, lung cancer and GI cancers, with the same mindset of serial innovation as we did in hematology Industry leadership in R&D We have demonstrated the potential for BeOne’s innovative oncology pipeline to impact patient lives 02 01 03
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130 Key late-stage catalysts in 2025 and 2026 Asset Catalyst H1 2025 H2 2025 2026 BRUKINSA MANGROVE TN MCL Ph3 PFS interim analysis Sonrotoclax CELESTIAL-TNCLL (301) Ph3 enrollment completion (+BRUKINSA) ✓ CELESTIAL-RRMCL (302) Ph3 initiation (+BRUKINSA) ✓ CELESTIAL-RRCLL (303) Ph3 initiation (+anti-CD20) R/R MCL Ph2 data readout and AA submission if data support* ✓ R/R CLL Ph2 data readout and CN AA submission ✓ BTK CDAC (BTK CDAC) CaDAnCe-302 R/R CLL vs Investigator's Choice (IR/BR/VR) Ph3 initiation ✓ CaDAnCe-304 R/R CLL H2H vs pirtobrutinib Ph3 initiation CaDAnCe-101 R/R CLL Ph2 data readout - potentially pivotal TEVIMBRA 1L ESCC U.S. approval ✓ 1L ESCC and 2L ESCC JP approval ✓ 1L SCLC EU approval ✓ 1L NPC EU approval Neo/adj NSCLC EU approval 1L GC subcutaneous formulation Ph3 initiation 1L GC JP approval Zanidatamaba + TEVIMBRA HERIZON-301 1L HER2+ GEA Ph3 readout IMDELLTRA® (Tarlatamab)b 2L SCLC Ph3 readout ✓ 3L SCLC Ph2 readout ✓ ✓ achieved planned a Zymeworks/Jazz collaboration, b Amgen collaboration * CN submission in H1 2025 complete, global submission in H2 2025 planned
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131 Key early-stage catalysts in 2025 and 2026 Asset Catalyst H1 2025 H2 2025 2026 CDK4i POC Data ✓ 2L HR+/HER2- mBC Ph3 initiation B7-H4 ADCa POC Data ✓ Ph3 initiation PanKRASi POC Data EGFR CDAC POC Data CDK2ib POC Data B7-H3 ADC POC Data CEA ADC POC Data FGFR2b ADC POC Data IRAK4 CDAC POC Data* PRMT5i POC Data PRMT5i + MAT2Aic combination POC Data EGFRxMETxMET TsAb POC Data ✓ achieved planned a DualityBio collaboration, b Ensem collaboration, c CSPC collaboration * Tissue PD Note: Catalyst external data presentation subject to conference calendar
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132 Q&A BeOne management team and guest speakers
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133 Closing John V. Oyler Co-Founder, Chairman and CEO
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134 Our pipeline is at an inflection point 20 Registrational data readouts / potential approvals: • Sonrotoclax (R/R CLL and R/R MCL Phase 2 AA*) • BTK CDAC (R/R CLL Phase 2 readout - potentially registrational) 10+ POC data readouts across pipeline Pivotal trial initiations: • BTK CDAC vs. pirtobrutinib • CDK4i and B7-H4 ADC Near-term milestones in the next 18 months, including: What you should take away from today Our pipeline is at an inflection point *AA – accelerated approval
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Thank You 55 Cambridge Parkway Suite 700W Cambridge, MA 02142 1 (877) 828-5568 BeOneMedicines.com
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136 Appendix
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137 BeOne clinical pipeline (snapshot of our entire pipeline) Accepted submissions shown for major markets US, CN, EU, JP 1) DualityBio collaboration, 2) CSPC collaboration, 3) Ensem collaboration, 4) Amgen collaboration, 5) Zymeworks/Jazz collaboration. Please refer to our most recent 10-K filing for a full list of our commercial products, including in -licensed products, as well as commercial rights and collaboration details ** Trial is listed on clinicaltrials.gov, but may not have subjects enrolled Updated: 22 June 2025 BGB-16673 BTK CDAC 101 B-cell malignancies 102 B-cell malignancies 104 B-cell malignancies 107 Chronic spontaneous urticaria** BGB-21447 BCL2i 2G 101 B-cell malignancies 102 Metastatic breast cancer Xaluritamig4 STEAP1 x CD3 XmAb® 20180146 mCRPC BGB-R046 IL-15 prodrug 101 Solid tumors BGB-B2033 GPC3 x 4-1BB BsAb 101 Solid tumors BGB-B3227 MUC1 x CD16A BsAb 101 Solid tumors BGB-26808 HPK1i 101 Solid tumors BGB-30813 DGKζi 101 Solid tumors BGB-A3055 CCR8 mAb 101 Solid tumors Tislelizumab PD1 mAb 103 SubQ formulation BGB-B455 CLDN6 x CD3 BsAb 101 Solid tumors Tarlatamab4 DLL3 x CD3 BiTE ® 20240124 2L+ SCLC** 20230298 2L+ SCLC** Zanubrutinib BTKi 114 Tablet formulation (EU) Sonrotoclax BCL2i 201 R/R MCL (CN) 202 R/R CLL (CN) Tislelizumab PD1 mAb 315 Neo/adj NSCLC (EU) 309 1L NPC (EU) Alternate dosing Q6W (US, CN) Zanidatamab5 HER2 BsAb 203 HER2+ 2L BTC (CN) Zanubrutinib BTKi 215 B-cell malignancies BGB-16673 BTK CDAC 101 R/R CLL 102 R/R CLL Sonrotoclax BCL2i 203 R/R WM 204 TN CLL/SLL Blinatumomab4 CD3 x CD19 BiTE ® 20190359 R/R BP-ALL Tarlatamab4 DLL3 x CD3 BiTE ® 20230273 3L SCLC 20240092 2L+ SCLC** Sonrotoclax BCL2i 101 B-cell malignancies 102 B-cell malignancies 103 AML/MDS 105 R/R MM t(11;14) 108 Dose ramp-up BGB-43395 CDK4i 101/102 BC & Solid tumors BGB-53038 PanKRASi 101 Solid tumors BG-C90741 B7-H4 ADC 101 Solid tumors BG-60366 EGFR CDAC 101 Solid tumors BG-58067 MTA Coop. PRMT5i 101 Solid tumors BG-898942 MAT2Ai 101 Solid tumors BGB-45035 IRAK4 CDAC 101 Immunology & Inflammation BG-685013 CDK2i 101 BC & Solid tumors BG-C354 B7-H3 ADC 101 Solid tumors BG-C477 CEA ADC 101 Solid tumors BG-C137 FGFR2b ADC 101 Solid tumors BG-T187 EGFR x MET TsAb 101 Solid tumors Zanubrutinib BTKi 306 TN MCL 308 R/R MZL, R/R FL 309 pMN BGB-16673 BTK CDAC 302 R/R CLL 303 R/R CLL/SLL 304 R/R CLL/SLL** Sonrotoclax BCL2i 301 TN CLL 302 R/R MCL 303 R/R CLL/SLL** Tislelizumab PD1 mAb 310 1L UBC 314 R/R cHL Pamiparib PARPi 302 2L MTx gBRCAm PSOC Zanidatamab5 HER2 BsAb 301 1L HER2+ GEA Tarlatamab4 DLL3 x CD3 BiTE ® 20210004 2L SCLC 20200041 1L ES-SCLC 20230016 LS-SCLC Phase 2 Accepted Submissions Major marketsPhase 3Phase 1 GI Breast / GynHeme Lung I&I Other Cancers
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138 Acronyms (1 of 2) 1L 1st-line 2G 2nd generation 2L 2nd-line 3L 3rd-line AA Accelerated approval ADC Antibody drug conjugate AI Artificial intelligence AML Acute myeloid leukemia APAC Asia Pacific ASCO American Society of Clinical Oncology ASH American Society of Hematology AV Acalabrutinib + venetoclax AVO Acalabrutinib + venetoclax + obinutuzumab B-Cell B lymphocytes B7-H3 Tumor associated antigen B7-H4 Tumor associated antigen BCL2 B-cell lymphoma 2 BD Business development BIC Best-in-class BID Twice daily BiTE Bi-specific T-cell engager BP-ALL B-precursor acute lymphoblastic leukemia BR Bendamustine + rituximab BRCA "Breast Cancer" gene BsAb Bispecific antibody BTK Bruton's tyrosine kinase CCR8 C-C motif chemokine receptor 8 CD19 Cluster of differentiation 19 CD3 Cluster of differentiation 3 CDAC Chimeric Degradation Activation Compound CDK2 Cyclin-dependent kinase 2 CDK4 Cyclin-dependent kinase 4 CEA Carcinoembryonic antigen cHL Classical hodgkins lymphoma CI Confidence Interval CIT Chemoimmunotherapy CLDN6 Claudin6 CLL Chronic lymphocytic leukemia CMR CMR/Clarivate CN China COVID-19 Coronavirus Disease 2019 CRC Colorectal cancer CRO Contract research organization CSPC (Collaboration) CSPC Zhongqi Pharmaceutical Technology del(11q) Deletion of part of chromosome 11 del(17p) Deletion of part of chromosome 17 DGKζ Diacylglycerol kinase zeta DLBCL Diffuse large B-cell lymphoma DLL3 Delta-like canonical notch ligand 3 DNA-PK DNA-dependent protein kinase EGFR Epidermal growth factor receptor EGFRmut / EGFRm EGFR mutation EOT End of treatment EMEA Europe, the Middle East and Africa ES-SCLC Extensive-stage small-cell lung cancer ESCC Esophagea squamous cell carcinoma EU European Union FCR Fludarabine, cyclophosphamide, rituximab FDA U.S. Food and Drug Administration FGFR2b Fibroblast growth factor receptor 2 isoform IIIb FIC First-in-class FIH First-in-human FL Follicular lymphoma FMI Foundation Medicine, Inc FTE Full-time employee FULV Fulvestrant FY Full year GAAP Generally accepted accounting principles gBRCAm Germline BRCA mutation GC Gastric cancer GEA Gastroesophageal adenocarcinoma GI Gastrointestinal GLP Good laboratory practice GPC3 Glypican-3 GYN Gynecological H1 1st half H2 2nd half H2H Head-to-had HEME Hematology HER2 Human epidermal growth factor receptor 2 HNSCC Head & neck squamous cell carcinoma hPBMC Human peripheral blood mononuclear Cells HPK1 Hematopoietic progenitor kinase 1 HR Hazard ratio HSPC Human hematopoietic stem/progenitor cell i Inhibitor I&I Immunology & Inflammation IC50 Half maximal inhibitory concentration IL-15 Interleukin-15 IO Immuno-oncology IRA Inflation Reduction Act IRAK4 Interleukin-1 receptor-associated kinase 4 IRC Independent review committee ITT Intent-to-Treat JCO Journal of Clinical Oncology JP Japan KRAS Kirsten rat sarcoma viral oncogene homolog
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139 Acronyms (2 of 2) LATAM Latin America LC Lung cancer LoE Loss of exclusivity LS-SCLC Limited-stage small-cell lung cancer mAb Monoclonal antibody MAD Multiple ascending dose MAT2A Methionine adenosyltransferase 2A mBC Metastatic breast cancer MCL Mantle cell lymphoma mCRPC Metastatic castration resistant prostate cancer MDS Myelodysplastic syndromes MET Mesenchymal epithelial transition factor Mg Milligrams MM Multiple myeloma MoA Mechanism of action mRNA Messenger RNA MSS-CRC Microsatellite stable colorectal cancer MTA Cooperative PRMT5 Methylthioadenosine cooperative protein arginine methyltransferase 5 MTx Maintenance therapy MUC1 Mucin 1 MZL Marginal zone lymphoma NDA New drug application NEJM New England Journal of Medicine Neo/adj Neoadjuvant/adjuvant NME New molecular entity NPC Nasopharyngeal carcinoma NPS New patient share NSCLC Non small-cell lung cancer ONC Oncology OS Overall survival PanKRAS Molecule that targets all KRAS mutations PARP Poly(ADP-ribose) polymerases PBMC Peripheral blood mononuclear cells PD Progressive disease PD1 Programmed cell death protein 1 PFS Progression-free survival Ph1 Phase 1 Ph2 Phase 2 Ph3 Phase 3 Pirto Pirtobrutinib pMN Primary membranous nephropathy POC Proof of concept PSOC Platinum-sensitive ovarian cancer Q1 First quarter Q2 Second quarter Q3 Third quarter Q4 Fourth quarter Q6W Every 6-week dosing QD Once daily dosing R&D Research and development ROI Return on Investment ROW Rest of world R/R Relapsed / refractory SAD Single ascending dose SAE Serious adverse event SCLC Small-cell lung cancer SLL Small lymphocytic lymphoma SMAC Second mitochondrial activator of caspase SoC Standard of care ST Solid tumor STEAP1 Six-transmembrane epithelial antigen of prostate 1 SubQ Subcutaneous formulation t(11;14) Chromosomal translocation 11-14 TA Therapeutic area TCE T-cell engager TCR T-cell receptor TLR Toll like receptor TLS Tumor lysis syndrome TOX Toxicity TN Treatment naïve TP53 Tumor suppressor gene TsAb Trispecific antibody UBC Urinary / bladder cancer uIGHV Unmutated immunoglobulin heavy chain variable region uMRD Undetectable minimal residual disease U.S. United States of America VEN Venetoclax VI Venetoclax + ibrutinib VO Venetoclax + obinutuzumab WDs Working days WM Waldenström’s macroglobulinemia XmAb® XmAb® is a registered trademark of Xencor, Inc. Z Zanubrutinib ZS Zanubrutinib + sonrotoclax