AZN ESMO 2025 Conference Presentation

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Pascal is Executive Director and Chief Executive Officer at AstraZeneca. He has been a member of the Board and CEO since October 2012. Pascal has a passion for science and medicine as well as a successful track record of managing change, executing strategy and leading a diverse organisation. Prior to AstraZeneca, Pascal served as COO of Roche’s pharmaceuticals division from 2010 to 2012 and previously as CEO of Genentech where he led its successful merger with Roche. Pascal joined the pharmaceutical industry in 1986 and has worked in senior roles in numerous major companies around the world. He is a Doctor of Veterinary Medicine and holds an MBA from HEC Paris. Pascal received a British knighthood for services to life sciences and leadership in the global response to the COVID pandemic in the Queen’s Birthday Honours 2022. He is also on the board of the Sustainable Markets Initiative and champions the Health Systems Task Force which aims to accelerate the delivery of net zero, sustainable healthcare. Pascal Soriot Chief Executive Officer

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Dave was appointed Executive Vice-President, Oncology Haematology Business Unit in October 2017 and is responsible for driving growth and maximising the global commercial performance of the AstraZeneca global Oncology portfolio. Previously, Dave served as President of AstraZeneca Japan and Vice-President, Specialty Care in the US. While in Japan, Dave also served as Vice Chairman of the European Federation of Pharmaceutical Industries and Associations Japan and was a Director of the Japan Pharmaceutical Manufacturers Association. Before joining AstraZeneca, Dave worked at Roche/Genentech, where he served in several functions and leadership positions. Prior to this, Dave worked at the Monitor Group, now Monitor Deloitte Group, a global strategy consultancy. Dave is a graduate of Georgetown University in Washington DC. Dave Fredrickson Executive Vice President, Oncology Haematology Business

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Susan was appointed as Executive Vice President, Oncology Haematology Research & Development in July 2021, with responsibility for transforming the productivity and scientific output from Oncology R&D. Over her career, Susan has helped develop 12 approved medicines. As a clinical oncologist, Susan studied medicine at Manchester and Cambridge Universities and has a PhD from the University of London. In recognition of her contributions to Oncology drug development, she has been awarded an honorary Doctorate of Medical Science from the Institute of Cancer Research, is a Fellow of the Academy of Medical Sciences and elected to the Academy of the American Association for Cancer Research. Susan is a member of the Cambridge Cancer Centre Executive Committee and the Scientific Advisory Board of the ICR. From 2021 to 2024, she also served on the Board of Directors of the AACR and currently serves on the European Association of Cancer Research Advisory Council. Susan Galbraith Executive Vice President, Oncology Haematology R&D

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As Senior Vice President of Late Development Oncology, Leora leads a global team dedicated to advancing innovative and novel therapies through late-stage clinical development and regulatory approval. Prior to her current role, Leora served as Head of Clinical Development, Late Oncology, leading the development and resourcing for the physicians and scientists responsible advancing studies from early signal seeking to Phase III registrational trials spanning multiple indications. She also served as a Clinical Strategy Head for AstraZeneca’s global research and development in lung cancer. Leora previously worked at Vanderbilt Ingram Cancer Center where she led the lung cancer program and participated as principal investigator on several national and global lung cancer trials and published over 175 papers and book chapters. Leora is an active member, and served on the scientific committees, of the American Society of Clinical Oncology, the European Society of Medical Oncology, the International Association for the Study of Lung Cancer, and the Royal College of Physicians and Surgeons of Canada. Leora Horn SVP , Late Development Oncology

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Sunil Verma is Global Head, Oncology Franchise in AstraZeneca. His leadership is focused on advancing the commercial execution of the Company’s transformative medicines in markets across the globe and leading the Oncology business unit strategy to help to lead and build the next wave of portfolio. Dr Verma is internationally recognised for his leadership in helping to transform the cancer paradigms with the development of pivotal medicines across multiple tumor types and settings. Before joining AstraZeneca in August 2019, Dr Verma was a Medical Oncologist, providing clinical care and expertise with a focus in breast and lung cancer and held several pivotal leadership and research roles in academic medicine over 15 years. He served as Professor and Head of the Department of Oncology at the University of Calgary and the Medical Director of the Tom Baker Cancer Centre from 2015-2019. He also served on faculty at the University of Toronto as Associate Professor and Medical Director of the Breast Cancer Centre at Sunnybrook, Toronto. Sunil Verma Senior Vice President, Global Head, Oncology Franchise

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Dr Rebecca Dent is the Chair of the Division of Medical Oncology and Senior Consultant at the National Cancer Center Singapore. Dr Dent received her medical degree from McMaster University in Hamilton, Canada, and her graduate degree in clinical epidemiology and biostatistics from the University of Toronto, Canada. She obtained her internal medicine and medical oncology training at the University of Toronto, Canada (Princess Margaret Hospital and the Sunnybrook Odette Cancer Cancer). Prior to moving to Singapore in 2011, Dr. Dent was a consultant and Head of Breast Cancer Clinical Trials at the Sunnybrook Odette Cancer Center. Dr Dent’s primary research interest is in the field of breast cancer, and she is the principal investigator for multiple local, regional and international clinical trials for the treatment breast cancer. She serves as the chair or co-chair of several scientific committees at ASCO, ESMO, ESMO Asia, ASCO Breakthrough Asia and is the founder and co-chair of the Asia-Pacific Breast Cancer Summit. Rebecca Dent Head of the Department of Medical Oncology, Chief of the Breast Medical Oncology Service at the National Cancer Center Singapore

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Nadia Harbeck, MD, PhD, is Director of the Breast Center, and the Center for Hereditary Breast and Ovarian Cancer and holds the chair for Conservative Oncology at the Dept. of OB&GYN, LMU University Hospital, Munich, Germany. Prof. Harbeck is currently ESMO Director of Education, and Subject Editor of the ESMO Breast Cancer Guidelines and a member of the ESMO Executive Board. She is member of the ASCO Annual Meeting Educational Committee and a member of the expert panel issuing the German AGO recommendations for breast cancer therapy as well as co-director of the West German Study Group. Prof. Harbeck is principal investigator or steering committee member of numerous breast cancer trials. Prof. Harbeck is one of the most frequently cited clinical researchers worldwide. She has authored more than 750 papers in peer-reviewed journals and is coordinating editor-in-chief of Breast Care as well as a panel member of several international breast cancer consensus conferences. Nadia Harbeck Director of the Breast Center, LMU University Hospital

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Neal Shore graduated from Duke University and Duke University Medical School. He completed his general surgery/urology residency at New York Hospital-Cornell Medical Center/Memorial Sloan Kettering Cancer Center. He serves as the Medical Director for the START-Carolina Urologic Research Center as well as the Global Director, GU Oncology START Cancer Research. Dr Shore has conducted >500 clinical trials, focusing mainly on genitourinary oncology, and has authored >400 peer-reviewed publications and numerous book chapters. He serves on the Society for Immunotherapy of Cancer Guidelines Committee for Bladder Cancer, as has served on the boards of the Bladder Cancer Advocacy Network, the APCCC Scientific Steering Committee, Maple Tree Cancer Alliance, and the Duke Global Health Institute. He is the Chair of both the Prostate Cancer Academy and the Bladder/Kidney Cancer Academy, and the co- chair of the annual AUA International Prostate Cancer Forum. He has served/serves on the editorial boards of Urology Times, Chemotherapy Advisor, OncLive, PLOS ONE, Urology Practice, JUOP, Everyday Urology Oncology and World Journal of Urology. He is the Editor-in-Chief of Reviews in Urology. Neal Shore Medical Director, START-Carolina Urologic Research Center

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2 Forward-looking statements This document contains certain forward-looking statements with respect to the operations, performance and financial condition of the Group, including, among other things, statements about expected revenues, margins, earnings per share or other financial or other measures. Although the Group believes its expectations are based on reasonable assumptions, any forward-looking statements, by their very nature, involve risks and uncertainties and may be influenced by factors that could cause actual outcomes and results to be materially different from those predicted. The forward-looking statements reflect knowledge and information available at the date of preparation of this document and the Group undertakes no obligation to update these forward-looking statements. The Group identifies the forward-looking statements by using the words 'anticipates’, 'believes', 'expects', 'intends' and similar expressions in such statements. Important factors that could cause actual results to differ materially from those contained in forward-looking statements, certain of which are beyond the Group's control, include, among other things: the risk of failure or delay in delivery of pipeline or launch of new medicines; the risk of failure to meet regulatory or ethical requirements for medicine development or approval; the risk of failures or delays in the quality or execution of the Group's commercial strategies; the risk of pricing, affordability, access and competitive pressures; the risk of failure to maintain supply of compliant, quality medicines; the risk of illegal trade in the Group's medicines; the impact of reliance on third-party goods and services; the risk of failure in information technology or cybersecurity; the risk of failure of critical processes; the risk of failure to collect and manage data and artificial intelligence in line with legal and regulatory requirements and strategic objectives; the risk of failure to attract, develop, engage and retain a diverse, talented and capable workforce; the risk of failure to meet our sustainability targets, regulatory requirements and stakeholder expectations with respect to the environment; the risk of the safety and efficacy of marketed medicines being questioned; the risk of adverse outcome of litigation and/or governmental investigations; intellectual property risks related to the Group's products; the risk of failure to achieve strategic plans or meet targets or expectations; the risk of geopolitical and/or macroeconomic volatility disrupting the operation of our global business; the risk of failure in internal control, financial reporting or the occurrence of fraud; and the risk of unexpected deterioration in the Group's financial position. Nothing in this document, or any related presentation/webcast, should be construed as a profit forecast.

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3 AstraZeneca @ ESMO 2025 Furthering the AstraZeneca ambition Pascal Soriot, Chief Executive Officer Key Oncology themes at WCLC and ESMO Susan Galbraith, EVP , Oncology Haematology R&D Redefining the breast cancer landscape • DESTINY-Breast11, DESTINY-Breast05 • TROPION-Breast02 • Integrating into clinical practice • Q&A Prof. Nadia Harbeck, LMU University Hospital Prof. Rebecca Dent, National Cancer Center Singapore Sunil Verma, SVP, Global Head, Oncology Franchise Dave Fredrickson, EVP , Oncology Haematology Business Realising our ambition in GU cancers and beyond • POTOMAC • Integrating into clinical practice Dr Neal Shore, Carolina Urologic Research Center Dave Fredrickson, EVP , Oncology Haematology Business Closing Remarks and Q&A Session Dave Fredrickson, EVP , Oncology Haematology Business

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Note: Ambition to achieve $80bn in Total Revenue by 2030 is risk-adjusted, based on long-range plan as of AstraZeneca Investor Day May 2024. Medicines and assets listed reflect key contributors to 2030 Total Revenue ambition; however, this list is not exhaustive. Medicines and assets listed in alphabetical order and sorted by therapy area. Laroprovstat previously AZD0780. Collaboration partners: Daiichi Sankyo (Enhertu, Datroway), Amgen (Tezspire), Ionis (Wainua), Compugen (rilvegostomig), Merck & Co., Inc. (Lynparza). Appendix: Glossary. 5 Ambition – $80bn Total Revenue by 2030 & sustained 2030+ growth Working on “today, tomorrow and the day after" 2024 2030 $54.1bn IRA impact Loss of Exclusivity Existing portfolio Calquence Datroway Enhertu Imfinzi/Imjudo Tagrisso Truqap Airsupra Breztri Fasenra Lokelma Saphnelo Tezspire Wainua Ultomiris Launching key NMEs AZD0120 camizestrant rilvegostomig surovatamig saruparib volrustomig AZN ADCs AZD5004 baxdrostat dapa FDCs hMPV/RSV vaccine laroprovstat tozorakimab efzimfotase alfa gefurulimab eneboparatide $80bn ADCs and Radioconjugates Cell therapy and T-cell engagers Gene therapy Next-generation IO bispecifics Weight management and risk factors Beyond 2030 Brilinta Farxiga Lynparza Soliris Illustrative only, not to scale 2030 Total Revenue ambition not dependent upon future M&A

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1. Primary endpoint not met in overall patient population; highly clinically meaningful improvement demonstrated in a prespecified subgroup of patients. Key upcoming pipeline catalysts are defined by a threshold of non-risk adjusted global peak year revenue expectations as of 29 July 2025. Collaboration partners: Daiichi Sankyo (Enhertu, Datroway), Hutchmed (Orpathys), Ionis (Wainua), Compugen (rilvegostomig), Merck & Co., Inc. (Lynparza). Appendix: Glossary. 6 Unprecedented catalyst rich period with key Phase III readouts in 2025 and 2026 AVANZAR | Datroway + Imfinzi 1L NSQ/NSQ TROP2+ NSCLC DESTINY-Breast05 | Enhertu early HER2+ breast cancer VOLGA | Imfinzi muscle-invasive bladder cancer TROPION-Breast02 | Datroway 1L TNBC TROPION-Lung07 | Datroway 1L NSQ NSCLC TROPION-Lung15 | Datroway ± Tagrisso 2L EGFRm NSCLC SAFFRON | T agrisso + Orpathys EGFRm NSCLC SERENA-4 | camizestrant 1L HR+ HER2- met. breast cancer CLARITY-Gastric01 | sonesitatug vedotin 2L+ CLDN18.2+ gastric cancer IRIS | Saphnelo lupus nephritis DAISY | Saphnelo systemic sclerosis CARDIO-TTRansform | Wainua ATTR-CM OBERON/TITANIA | tozorakimab COPD MIRANDA | tozorakimab COPD TILIA | tozorakimab lower respiratory tract disease ARTEMIS | Ultomiris CSA-AKI EMERALD-2 | Imfinzi early HCC EMERALD-3 | Imfinzi locoregional HCC ICAN | Ultomiris IgAN DESTINY-Breast09 | Enhertu 1L HER2+ breast cancer DESTINY-Breast11 | Enhertu early-stage HER2+ breast MA TTERHORN | Imfinzi resectable GC/GEJC POTOMAC | Imfinzi non-muscle invasive bladder cancer SERENA-6 | camizestrant 1L ESR1m HR+ HER2- adv. breast cancer CALYPSO | eneboparatide hypoparathyroidism KALOS/LOGOS | Breztri uncontrolled asthma CAPItello280 | Truqap mCRPC LATIFY | ceralasertib + Imfinzi post-IO NSCLC RESOLUTE | Fasenra moderate to severe COPD TULIP-SC | Saphnelo moderate to severe SLE BaxHTN | baxdrostat uncontrolled hypertension TMA-313 | Ultomiris HSCT-TMA (adults) CARES1 | anselamimab light-chain amyloidosis HICKORY/CHESTNUT/MULBERRY | efzimfotase alfa hypophosphatasia MG-301 | gefurulimab generalised myasthenia gravis FLAURA2 OS | T agrisso 1L EGFRm NSCLC H1 2025 • H2 2025 • H1 2026 • H2 2026 •

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8 represents Plenary (WCLC) or Presidential (ESMO) session. All sessions except for FL 1. Plenary (WCLC) or Presidential (ESMO) session. 2. Data at WCLC 2025. All other listed datasets are at ESMO 2025. Appendix: Glossary. >160 abstract acceptances 98 poster presentations 35 oral presentations 4 plenary presentations1 – DESTINY-Breast11 (291O) – DESTINY-Breast05 (LBA1) – TROPION-Breast02 (LBA21) – rilvegostomig ex vivo data2 (OA03.03) – ARTEMIDE-01 (1853MO) – TROPION-PanTumor03 (3072MO) – FONTANA (1065MO) – PETRANHA (2384MO) Five presidential plenary presentations in the past three years at ESMO – POTOMAC (LBA108) – FLAURA2 final OS2 (PL02.06) – MATTERHORN final OS (LBA81) Transforming care today Establishing the pipeline for tomorrow at WCLC and ESMO 2025

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Focused strategy to redefine cancer care Collaboration partners: Daiichi Sankyo (Enhertu), Merck & Co., Inc. (Lynparza). Appendix: Glossary. 9 Novel ADCs and Radioconjugates Replace the backbone of chemotherapy and radiotherapy Novel IO Next wave of IO agents will segment the IO-sensitive space Cell therapy and T-cell engagers Scalable, accessible therapies in both liquid and solid tumours Powerful combinations Transform outcomes through new combinations including novel ADC, Radioconjugate and next-generation IO Early intervention Improve long-term outcomes by acting at the earliest stages of disease 2 3 4 5 1 DESTINY-Breast11 DESTINY-Breast05 TROPION-Breast02 TROPION- PanTumor03FONT ANA ARTEMIDE-01 TROPION- PanTumor03 TROPION- PanTumor03 POTOMAC MATTERHORN OS PETRANHA Significant progress at ESMO and WCLC 2025 QCS real world implementation FLAURA2 OS Upcoming data for surovatomig and AZD0120 ■ Phase III dataset ■ Early phase dataset

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10 All numbers are approximate. Illustrative settings and populations, not to scale. Breast Cancer map reflects Phase III/pivotal trials. Collaboration partners: Daiichi Sankyo (Enhertu, Datroway), Merck & Co., Inc. (Lynparza). Appendix: Glossary. RECURRENCE gBRCAm 5% of HR-positive 15% of TNBC HER2-positive 15-20% HR-positive 65-75% TNBC 10-15% Est. epi (G7, 2025) 540k 135k 100k 75k 60k 1st line 2nd line 3rd line 4th line + Early Neoadjuvant Adjuvant Metastatic CTx → Lynparza OlympiA Enhertu → THP DESTINY-Breast11 NST → residual disease → Datroway ± Imfinzi TROPION-Breast03 CTx → AI ± CDK4/6i 2-5 yrs → camizestrant CAMBRIA-1 Good outcomes with current SoC for low-risk patients CTx → camizestrant ± abemaciclib CAMBRIA-2 NST→ residual disease → Enhertu DESTINY-Breast05 PD-L1- 60% PD-L1+ 40%Datroway + Imfinzi TROPION-Breast04 Lynparza OlympiAD camizestrant + palbociclib SERENA-4 AI + CDK4/6i → camizestrant + CDK4/6i SERENA-6 ESR1m 35% Enhertu ± pertuzumab DESTINY-Breast09 Datroway TROPION-Breast02 Datroway + Imfinzi TROPION-Breast05 Truqap + Faslodex + CDK4/6i CAPItello292 saruparib + camizestrant EvoPAR-Breast01 tBRCAm, PALB2m 9% Enhertu DESTINY-Breast03 Enhertu DESTINY-Breast01/02 Datroway TROPION-Breast01 Enhertu DESTINY-Breast06 HER2-low (1+, 2+) 60% HER2-ultralow (0-1+) 25% Truqap + Faslodex CAPItello291 PIK3CA, AKT1, PTEN alt.40% HER2-low (1+, 2+) 35% PD-L1-inelig. 70% DESTINY-Breast04 HER2-low (1+, 2+) 35% Enhertu DESTINY-Breast04 HER2-low (1+, 2+) 60% PD-L1-eligib. 30% established SoC launched indication Leading development programme in breast cancer DXd ADC PARPiIO ngSERD AKTiKey: Darker boxes denote trials of focus for ESMO 2025

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DESTINY-Breast11: Advancing Enhertu into curative early breast cancer setting 12 Surgery R 1:1:1 ― Previously untreated HER2+ eBC ― HR+ or HR- ― High-risk defined as: • ≥cT3 and N0−3 or cT0–4 and N1−3 • Inflammatory BC Enhertu → THP 4 + 4 cycles ddAC → THP 4 + 4 cycles Enhertu 8 cycles N = 321 N = 320 N = 286 Stratification factors ― HR status: ER and/or PR–positive or negative ― HER2 status (IHC 3+ or ISH+ in the absence of IHC 3+ status) Primary endpoint: pCR (ypT0/is ypN0) (BICR) Secondary endpoints: ― pCR (ypT0 ypN0) (BICR) ― EFS, safety, PK and immunogenicity, IDFS, OS, HRQOL Additional outcome measures ― Residual cancer burden The Enhertu monotherapy alone arm closed following IDMC recommendation on 12 March 20242 Recommended post-neoadjuvant treatment per study protocol1 ypT0/is ypN0, absence of invasive cancer in the breast and axillary nodes; ypT0 ypN0, absence of invasive and in-situ cancer in the breast and axillary nodes. 1. pCR: radiotherapy and concomitant trastuzumab ± pertuzumab for up to 1 year; no pCR: radiotherapy and T-DM1 for up to 14 cycles; HR–positive: endocrine therapy. 2. The reasons for closure were multifactorial, including a lower pCR rate, low likelihood that Enhertu alone would be superior to ddAC-THP, and the timing of surgery. The recommendation was not based on new safety findings. Harbeck N et al. Abstract 291O presented at the European Society of Medical Oncology 2025. Collaboration partner: Daiichi Sankyo (Enhertu). Appendix: Glossary.

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Enhertu-THP ddAC-THP T-DXd-THP ddAC-THP T-DXd-THP ddAC-THP DESTINY-Breast11: Highest reported pCR rate in registrational neoadjuvant HER2+ eBC trial 13 HR–positive HR–negativeITT population (primary endpoint)2 pCR1 Δ16% (95% CI 3.0, 28.8) Δ9% (95% CI 0.2, 17.9) Δ11% (95% CI 4.0, 18.3; P=0.003) 67% (n=216/321) 56% (n=180/320) 61% (n=145/236) 52% (n=123/235) 83% (n=69/83) 67% (n=57/85) Enhertu-THP ddAC-THP Enhertu-THP ddAC-THP Enhertu-THP ddAC-THP 1. By blinded central review.2. pCR responders were defined as patients who only received randomised study treatment (at least one dose) and had pCR. Harbeck N et al. Abstract 291O presented at the European Society of Medical Oncology 2025. Collaboration partner: Daiichi Sankyo (Enhertu). Appendix: Glossary.

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DESTINY-Breast11: Consistent benefit for Enhertu-THP observed across subgroups 14 pCR rate, % (n/N) Enhertu-THP (n=321) ddAC-THP (n=320) ΔpCR, % (95% CI) All patients 67.3 (216/321) 56.3 (180/320) 11.2 (4.0, 18.3) Age at baseline <65 years 66.7 (188/282) 58.0 (167/288) 8.7 (0.7, 16.5) ≥65 years 71.8 (28/39) 40.6 (13/32) 31.2 (8.0, 51.4) Geographical region Asia 66.4 (101/152) 56.6 (86/152) 9.9 (−1.1, 20.6) Western Europe 75.4 (52/69) 62.3 (48/77) 13.0 (−2.2, 27.5) North America 74.4 (32/43) 36.6 (15/41) 37.8 (16.8, 55.7) Rest of world1 54.4 (31/57) 62.0 (31/50) −7.6 (−25.7, 11.2) Eastern Cooperative Oncology Group performance status score 0 68.7 (191/278) 55.7 (156/280) 13.0 (5.0, 20.9) 1 58.1 (25/43) 60.0 (24/40) −1.9 (−22.6, 19.1) Menopausal status Post 68.8 (86/125) 56.9 (87/153) 11.9 (0.5, 23.0) Pre 66.8 (123/184) 55.2 (90/163) 11.6 (1.4, 21.7) HER2 status IHC 3+ 71.1 (199/280) 61.5 (174/283) 9.6 (1.8, 17.3) Other 42.5 (17/40) 16.7 (6/36) 25.8 (5.2, 44.4) HR status Positive 61.4 (145/236) 52.3 (123/235) 9.1 (0.2, 17.9) Negative 83.1 (69/83) 67.1 (57/85) 16.1 (3.0, 28.8) American Joint Committee on Cancer clinical stage II–IIIA 65.7 (163/248) 56.4 (146/259) 9.4 (0.9, 17.7) IIIB–IIIC 72.2 (52/72) 55.7 (34/61) 16.5 (0.1, 32.3) Nodal status N0 57.7 (15/26) 57.1 (20/35) 0.6 (−24.2, 24.8) N+ 68.3 (196/287) 56.6 (159/281) 11.7 (3.8, 19.5) Favours ddAC-THPFavours Enhertu-THP −200204060 −40 Size of circle is proportional to the number of patients. 1. Brazil, Bulgaria, Peru, Poland, Russia, and Saudi Arabia. Harbeck N et al. Abstract 291O presented at the European Society of Medical Oncology 2025. Collaboration partner: Daiichi Sankyo (Enhertu). Appendix: Glossary.

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DESTINY-Breast11: Promising early EFS trend for Enhertu-THP 15 321 320 315 303 313 296 305 285 248 231 220 199 208 187 189 163 141 124 93 72 50 35 14 14 2 1 0 0 Enhertu-THP ddAC-THP No. at risk Time from randomisation (months) 96.9% (95% CI 93.5, 98.6) 93.1% (95% CI 88.7, 95.8) 1.0 393633302724211815129630 Probability of EFS 0.9 0.8 0 Enhertu-THP (N=321) ddAC-THP (N=320) EFS event rate 11 18 EFS HR (95% CI)1 0.56 (0.26, 1.17) The median duration of follow up was 24.3 months with Enhertu-THP and 23.6 months with ddAC-THP. 1. At data cutoff (March 12, 2025) EFS event maturity was 4.5%; at final cutoff, maturity is predicted to be ~10%. Harbeck N et al. Abstract 291O presented at the European Society of Medical Oncology 2025. Collaboration partner: Daiichi Sankyo (Enhertu). Appendix: Glossary.

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16 DESTINY-Breast11: Enhertu-THP demonstrates a favourable safety profile vs ddAC-THP Events, n (%) Enhertu-THP (n=320)1 ddAC-THP (n=312) 1 Any AE 314 (98.1) 308 (98.7) Grade ≥3 120 (37.5) 174 (55.8) Any serious AE 34 (10.6) 63 (20.2) AE leading to any dose reduction 58 (18.1) 60 (19.2) AE leading to any drug interruption 121 (37.8) 170 (54.5) AE leading to any treatment discontinuation 45 (14.1) 31 (9.9) Any AE with outcome of death1 2 (0.6) 2 (0.6) AE of special interest Drug-related adjudicated ILD/pneumonitis 14 (4.4) 16 (5.1) Grade ≥3 2 (0.6) 6 (1.9) Left ventricular dysfunction 4 (1.3) 19 (6.1) Grade ≥3 1 (0.3) 6 (1.9) AE leading to surgical delay2 11 (3.4) 8 (2.6) Median total treatment duration of whole regimen was 24.1 months (Enhertu-THP), and 21.0 months (ddAC-THP). 1. Safety analyses included all patients who received at least one dose of any study treatment; 1. Enhertu-THP arm: death of unknown cause (n=1), drug-related pneumonitis adjudicated by the Independent ILD Adjudication Committee (n=1); ddAC-THP arm: investigator-determined drug-related bacterial encephalitis (n=1), drug-related pneumonitis adjudicated by the ILD Adjudication Committee (n=1). 2. Defined as surgery not occurring within 3–6 weeks after the last cycle of neoadjuvant treatment. 3. Treatment-emergent AEs in at least 20% of patients in either arm. 4. Grouped term. Harbeck N et al. Abstract 291O presented at the European Society of Medical Oncology 2025. Collaboration partner: Daiichi Sankyo (Enhertu). Appendix: Glossary.

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DESTINY-Breast11: Enhertu-THP potential to be preferred regimen for patients with high-risk HER2+ eBC 18 Enhertu-THP has the potential to transform the neoadjuvant treatment landscape, underscoring the importance of bringing Enhertu into earlier stages of HER2+ disease ― Enhertu-THP showed a 67% pCR rate, the highest reported in a HER2+ eBC registrational study in the neoadjuvant setting, despite a high-risk, predominantly HR+ population ― Early positive trend in EFS was observed, favouring Enhertu-THP vs ddAC-THP (HR 0.56) ― Safety profile of Enhertu-THP was favourable vs ddAC-THP ― Lower rates of Grade ≥3 AEs, serious AEs, and AEs leading to dose reductions/interruptions ― Lower rates of haematological AEs, left -ventricular dysfunction, and fatigue ― Similar and low ILD rates between arms Harbeck N et al. Abstract 291O presented at the European Society of Medical Oncology 2025. Collaboration partner: Daiichi Sankyo (Enhertu). Appendix: Glossary.

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DESTINY-Breast05: Moving Enhertu into high-risk post-neoadjuvant setting 1. High risk is defined as clinical stages T4, N0-3, M0 or T1-3, N2-3, M0 at presentation (prior to NAT) or clinical stages T1-3, N0-1, M0, with axillary node-positive disease (ypN1-3) following NAT. Geyer C et al. Abstract LBA1 presented at the European Society of Medical Oncology 2025. Collaboration partner: Daiichi Sankyo (Enhertu). Appendix: Glossary. ― High-risk1 HER2+ eBC ― Residual disease after neoadjuvant chemotherapy and preoperative HER2-directed treatment ― ECOG PS 0 or 1 Primary endpoint: IDFS (inv) Key secondary endpoint: DFS (inv) Secondary endpoints: ― OS ― DRFI (inv) ― BMFI (inv) ― Safety Enhertu 14 cycles trastuzumab emtansine 14 cycles R 1:1 N = 818 N = 817 20 Stratification factors ― Extent of disease status at presentation ― HER2-targeted NAT (single, dual) ― Hormone receptor status ― Post-NAT pathologic nodal status

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DESTINY-Breast05: Enhertu reduced the risk of invasive disease recurrence or death by 53% vs T-DM1 21 818 788 781 776 771 768 758 753 731 684 634 544 440 380 370 275 218 212 129 92 90 46 14 14 0 0 0 0 817 781 769 760 745 734 719 708 687 632 599 527 417 355 337 233 186 177 120 84 79 38 14 13 4 1 1 0 No. at risk: T-DM1 Enhertu Invasive Disease-Free Survival1 0 2 4 6 8 10 12 14 16 18 20 22 24 26 28 30 32 34 36 38 40 42 44 46 48 50 52 54 0.0 0.6 0.8 1.0 Time, months 92.4% 83.7% Efficacy stopping boundary, P = 0.0183. 1. IDFS is defined as the time from randomization until the date of first occurrence of one of the following events: recurrence of ipsilateral invasive breast tumor, recurrence of ipsilateral locoregional invasive breast cancer, contralateral invasive breast cancer, a distant disease recurrence, or death from any cause. 2. Two-sided P value from stratified log-rank test. Hazard ratio and 95% CI from stratified Cox proportional hazards model with stratification factor of operative status at disease presentation. Geyer C et al. Abstract LBA1 presented at the European Society of Medical Oncology 2025. Collaboration partners: Daiichi Sankyo (Enhertu). Appendix: Glossary. Consistent benefit across all pre-specified subgroups including extent of disease status at presentation, HR status, post-NAT pathologic nodal status, and HER2-targeted NAT approach Enhertu (N=818) T-DM1 (N=817) IDFS event rate 51 (6.2) 102 (12.5) IDFS HR (95% CI) 0.47 (0.34-0.66), P < 0.00012

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DESTINY-Breast05: Secondary endpoints supportive of Enhertu benefit vs T-DM1 22 Consistent benefit across DRFI, BMFI and early trend to OS improvement (HR 0.61) at 2.9% maturity 1. DFS defined as the time between randomization and the date of the first occurrence of an IDFS event per STEEP criteria, including second primary non-breast cancer event or contralateral or ipsilateral ductal carcinoma in situ. 2. Two-sided P value from stratified log-rank test. Hazard ratio and 95% CI from stratified Cox proportional hazards model with stratification factor of operative status at disease presentation. Geyer C et al. Abstract LBA1 presented at the European Society of Medical Oncology 2025. Collaboration partners: Daiichi Sankyo (Enhertu). Appendix: Glossary. 0 2 4 6 8 10 12 14 16 18 20 22 24 26 28 30 32 34 36 38 40 42 44 46 48 50 52 54 0.0 0.6 0.8 1.0 818 788 781 776 771 768 758 753 731 683 633 543 440 380 370 275 218 212 129 92 90 46 14 14 0 0 0 0 817 779 767 757 743 733 718 707 686 631 598 526 416 354 336 233 186 177 120 84 79 38 14 13 4 1 1 0 Disease-Free Survival 1 Time, months No. at risk: Enhertu T-DM1 Enhertu (N=818) T-DM1 (N=817) DFS event rate 52 (6.4) 103 (12.6) DFS HR (95% CI) 0.47 (0.34-0.66), P < 0.00012 92.3% 83.5%

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DESTINY-Breast05: Generally manageable AE profile consistent with prior trials of Enhertu 23 TEAEs, n (%) Enhertu n=8061 T-DM1 n=8011 Any-grade 802 (99.5) 788 (98.4) Grade ≥3 408 (50.6) 416 (51.9) Serious 140 (17.4) 109 (13.6) Associated with drug discontinuation 144 (17.9) 103 (12.9) Related to drug-related ILD 30 (3.7) 8 (1.0) Associated with drug interruptions 400 (49.6) 329 (41.1) Associated with dose reductions 213 (26.4) 213 (26.6) Associated with deaths 3 (0.4) 5 (0.6) 1. All patients who received at least 1 dose of study treatment. 2. TEAEs in ≥20% of patients (either arm). Geyer C et al. Abstract LBA1 presented at the European Society of Medical Oncology 2025. Collaboration partners: Daiichi Sankyo (Enhertu). Appendix: Glossary.

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DESTINY-Breast05: Post-neoadjuvant Enhertu potential new standard-of-care in high-risk HER2+ eBC 25 Opportunity to transform clinical practice in the post-neoadjuvant setting for patients with high-risk disease ― Enhertu showed a statistically significant and clinically meaningful IDFS and DFS benefit versus T-DM1 in patients with HER2+ eBC with residual invasive disease and high risk of recurrence after neoadjuvant therapy ― Efficacy benefit was consistent across all prespecified subgroups ― Clinically meaningful benefit was observed in additional secondary endpoints ― The overall safety profiles of Enhertu and T-DM1 were generally manageable with no new safety signals Geyer C et al. Abstract LBA1 presented at the European Society of Medical Oncology 2025. Collaboration partners: Daiichi Sankyo (Enhertu). Appendix: Glossary.

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Please ensure you have added the correct confidentiality statement. Type the correct statement: ‘Company Restricted’ or ‘Strictly Confidential’ . No statement is needed for public information. ! TROPION-Breast02 Prof. Rebecca Dent HEAD OF DEPARTMENT OF MEDICAL ONCOLOGY, CHIEF OF BREAST MEDICAL ONCOLOGY, NATIONAL CANCER CENTER SINGAPORE

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TROPION-Breast02: Establishing Datroway in 1L TNBC with positive overall survival data ― Locally recurrent inoperable or metastatic TNBC ― No prior chemotherapy or targeted systemic therapy in the locally recurrent inoperable or metastatic setting ― Immunotherapy not an option1 ― ECOG PS 0 or 1 ― No minimum DFI Dual primary endpoints: PFS (BICR), OS Secondary endpoints included: ― ORR, DoR ― PFS (inv) ― Safety Datroway Investigator’s choice chemotherapy 2 R 1:1 N = 323 N = 321 27 1. Including patients with PD-L1 low tumours, or patients with PD-L1 high tumours with (a) disease relapse after prior PD-(L)1 inhibitor therapy for early-stage breast cancer, (b) comorbidities precluding PD-(L)1 inhibitor therapy, or (c) no regulatory access to PD- (L)1 inhibitor therapy. 2. If no prior taxane, or prior taxane in the (neo)adjuvant setting and DFI >12 months: paclitaxel 80 mg/m2 IV, D1, 8, 15, Q3W, or nab-paclitaxel 100mg/m2 IV, D1, 8, 15, Q4W; if prior taxane and DFI 0–12 months: capecitabine 1000 or 1250 mg/m2 orally twice daily, D1–14, Q3W (dose determined by standard institutional practice), or eribulin mesylate 1.4 mg/m2 / eribulin 1.23 mg/m2 IV, Day 1, 8, Q3W, or carboplatin AUC6 IV, D1, Q3W. Dent R et al. Abstract LBA21 presented at the European Society of Medical Oncology 2025. Collaboration partners: Daiichi Sankyo (Datroway). Appendix: Glossary. Stratification factors ― Geographic region (US/Canada/Europe vs other geographic regions) ― DFI history (de novo vs prior DFI 0-12 months vs prior DFI >12 months) ― PD-L1 status (high [CPS ≥10] vs low [CPS <10])

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TROPION-Breast02: Datroway reduced the risk of progression or death by 43% vs chemotherapy Dent R et al. Abstract LBA21 presented at the European Society of Medical Oncology 2025. Collaboration partners: Daiichi Sankyo (Datroway). Appendix: Glossary. 28 PFS by investigator assessment was consistent with PFS by BICR Datroway ICC PFS events, n (%) 199 (62) 209 (65) mPFS, mo 10.8 5.6 HR (95% CI) P-value 0.57 (0.47–0.69) <0.0001 0 3 6 9 12 15 18 21 24 27 30 33 36 39 Time from randomisation (months) Probability of PFS 323 265 191 150 116 84 56 41 24 20 10 5 1 0 321 191 107 64 46 29 19 16 8 6 1 0 0 0ICC Datroway No. at risk 0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1.0 12-mo rate: 45.6% 25.6% 18-mo rate: 32.7% 16.8%

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TROPION-Breast02: Datroway improved overall survival by 5 months vs chemotherapy Dent R et al. Abstract LBA21 presented at the European Society of Medical Oncology 2025. Collaboration partners: Daiichi Sankyo (Datroway). Appendix: Glossary. 29 Datroway ICC OS events, n (%) 168 (52) 181 (56) mOS, mo 23.7 18.7 HR (95% CI) P-value 0.79 (0.64–0.98) 0.0291 0 3 6 9 12 15 18 21 24 27 30 33 36 39 Time from randomisation (months) 0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1.0 Probability of OS 323 311 291 272 235 201 157 122 86 64 37 14 3 0 321 290 268 231 199 158 122 93 70 48 27 12 4 0ICC Datroway No. at risk 12-mo rate: 75.2% 67.8% 18-mo rate: 61.2% 51.3%

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TROPION-Breast02: Datroway improved objective response rate by 33% vs chemotherapy Dent R et al. Abstract LBA21 presented at the European Society of Medical Oncology 2025. Collaboration partners: Daiichi Sankyo (Datroway). Appendix: Glossary. 30 Datroway (n=323) ICC (n=321) Confirmed ORR, n (%) 202 (62.5) 94 (29.3) Odds ratio (95% CI) 4.24 (3.03–5.95) Best confirmed objective response, n (%) Complete response 29 (9.0) 8 (2.5) Partial response 173 (53.6) 86 (26.8) Stable disease 87 (26.9) 151 (47.0) Progressive disease 27 (8.4) 52 (16.2) Not evaluable 7 (2.2) 24 (7.5) PR PR CR ORR 62.5% ORR 29.3% CR Δ 33.2% Datroway (n=323) ICC (n=321)

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TROPION-Breast02: Manageable and tolerable safety profile throughout longer duration of therapy 1. Most common treatment-related AEs (≥15% of patients). 2. In the Datroway arm only, ophthalmologic assessments were required every 3 cycles while on therapy; this was not required in the ICC arm. For all patients in both arms, ophthalmologic assessments were required at baseline, as clinically indicated, and at end of therapy. 3. Grouped term. Dent R et al. Abstract LBA21 presented at the European Society of Medical Oncology 2025. Collaboration partners: Daiichi Sankyo (Datroway). Appendix: Glossary. 31 Datroway (n=319) ICC (n=309) Median total treatment duration, mo (range) 8.5 (0.7–38.0) 4.1 (0.1–32.0) Total exposure >12 months, % 35.1 9.4 Treatment-related AEs, n (%) Any grade TRAEs 296 (93) 257 (83) Grade ≥3 TRAEs 105 (33) 89 (29) Serious TRAEs 29 (9) 26 (8) TRAEs associated with discontinuation 14 (4) 23 (7) TRAEs associated with death 0 0 Treatment-related AEs1, n (%) Datroway (n=319) ICC (n=309) Any Grade Grade ≥3 Any Grade Grade ≥3 Dry eye2 76 (24) 4 (1) 9 (3) 0 Stomatitis 182 (57) 27 (8) 27 (9) 0 Nausea 142 (45) 2 (<1) 53 (17) 2 (<1) Constipation 72 (23) 1 (<1) 31 (10) 0 Vomiting 65 (20) 4 (1) 23 ( 7) 1 (<3) Decreased appetite 49 (15) 1 (<1) 20 (6) 1 (<1) Neutropenia3 39 (12) 10 (3) 90 (29) 40 (13) Anaemia3 48 (15) 6 (2) 64 (21) 10 (3) Leukopenia3 27 (8) 3 (<1) 55 (18) 13 (4) Peripheral neuropathy3 14 (4) 0 75 (24) 5 (2) Alopecia 130 (41) 0 96 (31) 1 (<3)ǁ Fatigue3 101 (32) 8 (3) 86 (28) 9 (3)

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TROPION-Breast02: Datroway to be potential new 1L SoC for patients with TNBC for whom IO is not an option 32 Datroway is the first and only therapy to significantly improve overall survival vs CTx in this patient population ― TROPION-Breast02 met both dual primary endpoints: first-line Datroway demonstrated statistically significant and clinically meaningful improvement in OS and PFS over CTx ― 5 mo improvement in mOS, HR 0.79 ― ≥5 mo improvement in mPFS by BICR, HR 0.57 ― Despite more than double the duration of treatment in the Datroway arm, rates of Grade ≥3 TRAEs were similar, and discontinuations were lower with Datroway vs CTx Dent R et al. Abstract LBA21 presented at the European Society of Medical Oncology 2025. Collaboration partners: Daiichi Sankyo (Datroway). Appendix: Glossary.

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Moving Enhertu into early HER2+ disease increasing probability of cure 34 1. Estimated epidemiology for drug-treated patients in G7 in 2024. Appendix: Glossary. Potential new early breast cancer treatment paradigm DESTINY-Breast11 and DESTINY-Breast05 combined blockbuster opportunity across the Alliance DESTINY-Breast11 34k patients in G7 | neoadj. HER2+ eBC1 80% | high-risk disease (prior to neoadjuvant Tx) DESTINY-Breast11 4 cycles Enhertu → 4 cycles THP DESTINY-Breast05 34k patients in G7 | neoadj. HER2+ eBC1 50% | residual disease after neoadjuvant Tx (Enhertu-naïve) DESTINY-Breast05 14 cycles Enhertu 55% | high-risk characteristics

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RECURRENCE Enhertu opportunity to span continuum of HER2+ breast cancer 35 Enhertu → THP DESTINY-Breast11 high-risk early-stage disease neoadjuvant systemic Tx → residual disease → Enhertu DESTINY-Breast05 post-neoadjuvant, residual disease Enhertu DESTINY-Breast03 Enhertu DESTINY-Breast01/02 Enhertu + pertuzumab DESTINY-Breast09 ApprovedRegulatory decision H1’26 To be shared with regulatory authorities Regulatory decision H1’26 Approved Early Metastatic 3rd line +Neoadjuvant Post-neoadjuvant 1st line 2nd line 34k 23k 17k 11kEst. epi (G7, 2024) Epidemiology in the G7 countries (US, Europe 5, Japan). All consider epidemiology for drug-treated patients. Appendix: Glossary.

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Datroway redefining treatment in high unmet need TNBC population 36 Broadening Datroway impact in TNBC with Imfinzi combinations 1. Dent R et al. Abstract LBA21 presented at the European Society of Medical Oncology 2025. 2.n=46/62, from Schmid P et al. Abstract #555MO presented at the European Society of Medical Oncology 2025. Collaboration partner: Daiichi Sankyo (Datroway). Appendix: Glossary. TROPION-Breast02 | First and only therapy to significantly improve overall survival vs CTx in TNBC where IO is not an option1 24k patients in G7 | 1L TNBC, drug treated 70% | not candidates for IO TROPION-Breast02 Efficacy including OS as well as safety demonstrate clear differentiation from other possible treatment regimens BEGONIA Phase Ib/II data drive confidence in combinations Neoadjuvant + adjuvant Tx Residual disease post- neoadjuvant Tx 1L metastatic candidates for IO TROPION-Breast04TROPION-Breast03 TROPION-Breast05 Early disease Metastatic Ongoing Phase III programme | >2026 79% ORR in adv./ metastatic TNBC2

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37 Opportunity for Q&A on breast cancer Prof. Nadia Harbeck BREA S T C EN TER DIREC TO R, L MU UN IVERS ITY HOS P IT AL, MUN IC H Dr Rebecca Dent HEA D O F DEP ART MENT O F ME DIC A L O NC O LOG Y, C HIEF O F BREA S T ME DIC A L O NC O LO GY, N ATIO NA L C AN C ER C EN TER S ING AP ORE Key External Experts Pascal Soriot C HIEF EX EC UT IV E O F F ICE R Dave Fredrickson EV P, O NC O LO GY HA EMA TOL OGY BUS INE SS Sunil Verma S VP , GLO BA L HEA D, O NC O LOG Y F RA NC HISE Susan Galbraith EV P, O NC O LO GY HA EMA TOL OGY R&D Leora Horn S VP , LA TE DEVELO P MENT O NC O LOG Y AstraZeneca Leadership

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POTOMAC: Transforming patient outcomes in a curative intent setting 39 Primary endpoint: DFS: I+BCG (I+M) vs BCG (I+M) Key secondary endpoints: ― DFS: I+BCG (I only) vs BCG (I+M) ― DFS at 24 months ― CRR at 6 months R 1:1:1 ― NMIBC ― BCG-naïve ― High-risk tumour defined as any of the following: • T1 • High-grade/G3 • CIS • Multiple and recurrent and large (≥3 cm) Stratification factors ― Higher-risk papillary disease (yes vs no)1 ― CIS (yes vs no) 1. Defined as T1G3/T1 high-grade or multiple and recurrent and large tumours (those with a diameter of ≥3 cm). 2. Weekly for 6 weeks. 3. 3 weekly doses at 3 mo, 6 mo, 12 mo, 18 mo and 24 mo. De Santis M et al. Abstract LBA108 presented at the European Society of Medical Oncology 2025. Appendix: Glossary. BCG induction 2 Imfinzi (13 cycles) BCG maintenance 3 Imfinzi (13 cycles) BCG induction 2 BCG induction 2 BCG maintenance 3 I+BCG (I+M) N=339 I+BCG (I only) N=339 BCG (I+M) N=340

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POTOMAC: Imfinzi + BCG (I+M) reduced the risk of a DFS event by 32%, with an early and sustained benefit 0 3 6 9 12 15 18 21 24 27 30 33 36 39 42 45 48 51 54 7875726966636057 81 Time from randomisation (months) 1.0 0.8 0.6 0.4 0.2 0 Probability of DFS 87% 82% 82% 77% 92% 87% I+BCG (I+M) N=339 BCG (I+M) N=340 DFS events, n (%) 67 (20) 98 (29) mDFS, mo NR NR HR (95% CI) P-value 0.68 (0.50–0.93) 0.0154 Median follow-up 60.7 months; DFS maturity 24%. De Santis M et al. Abstract LBA108 presented at the European Society of Medical Oncology 2025. Appendix: Glossary. No. at risk: I+BCG (I+M) 339 321 304 292 289 283 278 273 262 257 250 245 235 229 226 222 220 204 195 156 145 108 94 57 26 9 1 0 BCG (I+M) 340 322 303 292 283 276 271 265 258 254 249 244 237 235 231 227 225 209 196 160 150 101 86 50 20 8 0 0

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POTOMAC: Generally consistent DFS benefit across subgroups for Imfinzi + BCG (I+M) 41 1. With or without papillary disease as recorded per interactive voice response system. 2. Defined as T1G3/T1 high-grade or multiple and recurrent and large tumours (those with a diameter of ≥3 cm). 3. Assessed with the investigational VENTANA PD-L1 (SP263) Assay; high PD-L1 expression was defined as any of the following: ≥25% of TC exhibit membrane staining; or ICP >1% and IC+ ≥25%; or ICP=1% and IC+=100%. Data cutoff 03 April 2025. De Santis M et al. Abstract LBA108 presented at the European Society of Medical Oncology 2025. Appendix: Glossary.

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POTOMAC: No evidence of OS detriment with Imfinzi + BCG (I+M) 42 Median follow-up 65.6 mo in the I+BCG (I+M) arm and 65.9 mo in the BCG (I+M) arm; OS maturity 14%. De Santis M et al. Abstract LBA108 presented at the European Society of Medical Oncology 2025. Appendix: Glossary. I+BCG (I+M) N=339 BCG (I+M) N=340 Deaths, n (%) 41 (12) 52 (15) mOS, mo NR NR HR (95% CI) 0.80 (0.53–1.20) 0 3 9 12 15 21 24 27 30 36 42 45 48 51 7269636057 84 Time from randomisation (months) 1.0 0.8 0.6 0.4 0.2 0 Probability of OS 75 816 18 33 39 54 66 79 No. at risk: I+BCG (I+M) 339 336 328 325 323 319 318 314 313 310 305 302 297 295 292 289 289 285 282 246 222 184 144 115 73 34 14 1 0 BCG (I+M) 340 338 336 333 330 328 326 323 318 315 315 315 311 307 303 297 294 289 285 249 228 195 147 111 71 33 12 0 0

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POTOMAC: AE profile was tolerable and manageable, and consistent with known profiles of individual therapies 43 Events, n (%) I+BCG (I+M) n=336 BCG (I+M) n=339 TRAEs of any cause 325 (97) 307 (91) Maximum Grade 3 or 4 TRAE 71 (21) 13 (4) Serious TRAEs 45 (13) 13 (4) TRAEs leading to death 0 0 AEs leading to discontinuation of study treatment 105 (31) 68 (20) Possibly related to Imfinzi 54 (16) 1 (0.3)1 Possibly related to BCG 55 (16) 55 (16) Any grade immune-mediated AEs 91 (27) 4 (1) Maximum grade 3 or 4 27 (8) 1 (0.3) Leading to death 0 0 The safety population includes all patients who received treatment. Causality per investigator assessment. 1. Patient assigned to the BCG (I+M) arm due to a data entry error. 2. All-causality AEs reported for ≥10% of patients in the safety population for either arm. Data cutoff 03 April 2025. De Santis M et al. Abstract LBA108 presented at the European Society of Medical Oncology 2025. Appendix: Glossary. Hypothyroidism

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POTOMAC: Imfinzi + BCG potential to change the course of high-risk non-muscle-invasive bladder cancer 45 POTOMAC supports 1 year of Imfinzi in combination with BCG induction and maintenance as a new treatment option for patients with BCG-naïve, high-risk NMIBC ― Imfinzi in combination with BCG induction and maintenance resulted in a statistically significant and clinically meaningful improvement in DFS vs BCG induction and maintenance alone in patients with BCG-naïve, high-risk NMIBC at a median of 5 years follow-up ― 32% reduction in risk of a DFS event ― Early and sustained DFS benefit with Imfinzi (starting at <4 months) ― Descriptive OS analysis showed no negative impact on OS with the addition of Imfinzi (HR 0.80 at 14% maturity) ― Imfinzi plus BCG induction and maintenance had a tolerable and manageable safety profile that was consistent with the known safety profiles of the individual agents De Santis M et al. Abstract LBA108 presented at the European Society of Medical Oncology 2025. Appendix: Glossary.

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Building Imfinzi as a backbone in bladder cancer 47 1. Porten SP et al. Curr Opin Urol. 2012 Sep;22(5):385-9. 2. Estimated epidemiology in G7 (2024). All numbers are approximate. Illustrative settings and populations, not to scale. 3. Peak Year Revenue, non-risk adjusted. Appendix: Glossary. 96k Drug-treated patients with high-risk NMIBC across G7 Imfinzi CDP covers key stages of bladder cancer Imfinzi bladder cancer programme combined blockbuster opportunity3 High unmet need | Up to 80%1 will have disease recurrence with current SoC within 5y High-risk NMIBC MIBC 1L mUC 96k2 68k2 46k2 POTOMAC Imfinzi + BCG induction and maintenance NIAGARA Neoadj. Imfinzi + CTx → adj. Imfinzi VOLGA Neoadj. Imfinzi + EV ± Imjudo → adj. Imfinzi ± Imjudo NILE Imfinzi + CTx ± Imjudo POTOMAC | Moving Imfinzi into earlier stages of bladder cancer ~50% cis-eligible ~50% cis-ineligible/ refusal

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AstraZeneca commercial strategy to transform patient outcomes 48 Collaboration partners: Daiichi Sankyo (Enhertu, Datroway); Merck & Co., Inc. (Lynparza). Appendix: Glossary. Medicines that matter Leveraging scale Transforming patient care Precision diagnostics Patient experience Early detection Guideline-based treatment Lung Breast Gastrointestinal GYN/GU Haematology Building transformative brands Tumour area leadership Closing the care gap

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49 Opportunity for Q&A Prof. Neal Shore ME DIC A L DIREC TO R, S TA RT - C ARO LINA U ROL OGIC RES EARC H C ENT ER Key External Expert Pascal Soriot C HIEF EX EC UT IV E O F F ICE R Dave Fredrickson EV P, O NC O LO GY HA EMA TOL OGY BUS INE SS Sunil Verma S VP , GLO BA L HEA D, O NC O LOG Y F RA NC HISE Susan Galbraith EV P, O NC O LO GY HA EMA TOL OGY R&D Leora Horn S VP , LA TE DEVELO P MENT O NC O LOG Y AstraZeneca Leadership

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(a)BTC (advanced) biliary tract cancer 1L, 2L, 3L first-, second-, third-line a/mBC advanced/metastatic breast cancer ADC antibody conjugate adj. adjuvant AE adverse event AI aromatase inhibitor AKT1 AKT serine/threonine kinase 1 ALT alanine aminotransferase ASCO American Society of Clinical Oncology AST aspartate aminotransferase AZN AstraZeneca BCMA B-cell maturation antigen BICR blinded independent central review BMFI brain metastasis–free interval BTD Breakthrough Designation CAR-T chimeric antigen receptor T-cells CD19 Cluster of differentiation 19 CD3 Cluster of differentiation 3 CDK4/6i cyclin-dependent kinase 4/6 inhibitor CFS combined positive score CI confidence interval CLDN18.2 Claudin-18.2 COPD chronic obstructive pulmonary disease CRT chemoradiotherapy ctDNA circulating tumour DNA CTx chemotherapy CVRM Cardiovascular, Renal and Metabolism DB04 DESTINY-Breast04 DCO data cut-off ddAC dose-dense doxorubicin-cyclophosphamide DFI disease-free interval DFS disease-free survival DOR duration of response DRFI distant recurrence–free interval DXd deruxtecan eBC early breast cancer ECOG Eastern Cooperative Oncology Group EFS event-free survival EGFRm epidermal growth factor receptor-mutant ER+ estrogen receptor-positive ERoW Established Rest of World ESMO European Society for Medical Oncology ESR1m estrogen receptor alpha-mutated FL follicular lymphoma FLOT luorouracil, leucovorin, oxaliplatin and docetaxel FP fluoropyrimidine G7 US, Japan, EU5 gBRCAm germline BRCA-mutant ORR objective response rate OS overall survival P pertuzumab PALB2m partner and localizer of BRCA2 pCR pathologic complete response PD-(L)1/PD-L1 programmed cell death-(ligand) 1 PFS progression free survival PFS2 second progression-free survival PIK3CA(m) phosphatidylinositol-4,5-biphosphate 3-kinase catalytic subunit (mutated) PK pharmacokinetics PS performance status PSMA prostate-specific membrane antigen PTEN phosphatase and TENsin homolog deleted on chromosome 10 PTX paclitaxel PYR peak year revenue Q2W every 2 weeks Q4W every 4 weeks QoL quality of life R randomised R&D Research & Development R&I Respiratory & Immunology RAM ramucirumab RC radioconjugate RECIST v1.1 Response Evaluation Criteria in Solid Tumors v1.1 SARA selective amylin receptor agonist SBRT stereotactic brain radiotherapy SERD selective estrogen receptor degrader SoC standard-of-care SQ squamous Stg. stage T-DM1 trastuzumab emtansine TAP tumour area positivity tBRCAm tumor BRCA mutation TEAE treatment-emergent adverse event THP docetaxel, trastuzumab and pertuzumab TIGIT T-cell immunoreceptor with immunoglobulin and ITIM domains TKI tyrosine kinase inhibitor TNBC triple negative breast cancer TRAE treatment-related adverse event TROP2 trophoblast cell surface antigen 2 TTD time-to-treatment discontinuation Tx treatment V&I Vaccines & Immune Therapies WBC white blood cells WCLC World Conference on Lung Cancer ypT0 ypN0 absence of invasive and in-situ cancer in the breast and axillary nodes ypT0/is ypN0 absence of invasive cancer in the breast and axillary nodes GC gastric cancer GEJ(A) gastroesophageal junction (adenocarcinoma) gMG generalised myasthenia gravis HER2 human epidermal growth factor receptor 2 HER2-/negative human epidermal growth factor receptor 2-negative HER2- low/ultralow human epidermal growth factor receptor 2-low/ultralow HER2+/positive human epidermal growth factor receptor 2-positive HER2m human epidermal growth factor receptor 2-mutant HLR high-level results HPP hypophosphatasia HR hazard ratio HR-/negative hormone receptor-negative HR+/positive hormone receptor-positive HRQOL health-related quality of life HSCT-TMA hematopoietic stem cell transplantation-associated thrombotic microangiopathy ICC investigator’s choice of chemotherapy IDFS invasive disease–free survival IDMC Independent Data Monitoring Committee ILD interstitial lung disease INV invasive inv investigator assessment IO immuno-oncology IRA Inflation Reduction Act ITT intention-to-treat m(PFS/OS ) median (PFS/OS) M&A mergers & acquisitions mBC metastatic breast cancer mCRPC metastatic castration-resistant prostate cancer mDOR median duration of response mg milligram MIBC muscle invasive bladder cancer mo month mono monotherapy mOS median overall survival MPR major pathological response NAT neoadjuvant therapy NC non-calculable NEJM New England Journal of Medicine neoadj. Neoadjuvant NMIBC non-muscle invasive bladder cancer NMR normalised membrane ratio no. Number NSCLC non-small cell lung cancer NSQ non-squamous NST neoadjuvant systemic treatment oGLP-1 oral glucagon-like peptide-1 oPCSK9 oral protein convertase subtilisin/kexin type 9 OR odds ratio Glossary •

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Confidentiality Notice This file is private and may contain confidential and proprietary information. If you have received this file in error, please notify us and remove it from your system and note that you must not copy, distribute or take any action in reliance on it. Any unauthorized use or disclosure of the contents of this file is not permitted and may be unlawful. AstraZeneca PLC, 1 Francis Crick Avenue, Cambridge Biomedical Campus, Cambridge, CB2 0AA, UK +44(0)203 749 5000 www.astrazeneca.com 51

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All numbers are approximate. Illustrative settings and populations, not to scale. Lung Cancer map reflects Phase III/pivotal trials. Collaboration partners: Daiichi Sankyo (Enhertu, Datroway), Hutchmed (Orpathys), Compugen (rilvegostomig). Appendix: Glossary. 53 Tagrisso ADAURA EGFRm ~16-19% IO sensitive ~70% Stg. I Metastatic 1L 2L Est. epi (G7, 2025) ~150K ~310K ~190K HER2m ~2% Other tumour drivers ~12% ~50K ~100K Stg. I-II Stg. III UnresectableResectable Imfinzi AEGEAN Tagrisso neoADAURA rilvegostomig ± Datroway TROPION-Lung12 SBRT → Imfinzi / Tagrisso PACIFIC-4 Imfinzi combos PACIFIC-8, -9 improvements across PD-L1 spectrum CRT → Tagrisso LAURA CRT → Imfinzi PACIFIC CRT → Imfinzi PACIFIC Enhertu DESTINY-Lung04 Imfinzi + Imjudo + CTx POSEIDON Tagrisso FLAURA volrustomig + CTx eVOLVE-Lung02 rilvegostomig ± Datroway TROPION-Lung10 Tagrisso + CTx FLAURA-2 Datroway + Tagrisso TROPION-Lung14 Imfinzi + ceralasertib LATIFY Datroway +/- Tagrisso TROPION-Lung15 Tagrisso + Orpathys SAFFRON/SAVANNAH Enhertu DESTINY-Lung02 Stg. II-III ~70K Tagrisso ADAURA2 3L+ ~70K Datroway TROPION-Lung05 rilvegostomig + CTx PDL1≥1 SQ ARTEMIDE-Lung02 rilvegostomig + CTx PDL1≥1 NSQ ARTEMIDE-Lung03 rilvegostomig PDL1≥50 ARTEMIDE-Lung04 AstraZeneca in non-small cell lung cancer Datroway TROPION-Lung17 NSQ TROP2-NMR+ established SoC launched indication DXd ADC IO TKI IO bispecificKey: Datroway + IO ± platinum TL08/TL07/AVANZAR A PP END I X | Oncology tumour maps

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54 All numbers are approximate. Illustrative settings and populations, not to scale. Breast Cancer map reflects Phase III/pivotal trials. Collaboration partners: Daiichi Sankyo (Enhertu, Datroway), Merck & Co., Inc. (Lynparza). Appendix: Glossary. RECURRENCE gBRCAm 5% of HR-positive 15% of TNBC HER2-positive 15-20% HR-positive 65-75% TNBC 10-15% Est. epi (G7, 2025) 540k 135k 100k 75k 60k 1st line 2nd line 3rd line 4th line + Early Neoadjuvant Adjuvant Metastatic CTx → Lynparza OlympiA Enhertu → THP DESTINY-Breast11 NST → residual disease → Datroway ± Imfinzi TROPION-Breast03 CTx → AI ± CDK4/6i 2-5 yrs → camizestrant CAMBRIA-1 Good outcomes with current SoC for low-risk patients CTx → camizestrant ± abemaciclib CAMBRIA-2 NST→ residual disease → Enhertu DESTINY-Breast05 PD-L1- 60% PD-L1+ 40%Datroway + Imfinzi TROPION-Breast04 Lynparza OlympiAD camizestrant + palbociclib SERENA-4 AI + CDK4/6i → camizestrant + CDK4/6i SERENA-6 ESR1m 35% Enhertu ± pertuzumab DESTINY-Breast09 Datroway TROPION-Breast02 Datroway + Imfinzi TROPION-Breast05 Truqap + Faslodex + CDK4/6i CAPItello292 saruparib + camizestrant EvoPAR-Breast01 tBRCAm, PALB2m 9% Enhertu DESTINY-Breast03 Enhertu DESTINY-Breast01/02 Datroway TROPION-Breast01 Enhertu DESTINY-Breast06 HER2-low (1+, 2+) 60% HER2-ultralow (0-1+) 25% Truqap + Faslodex CAPItello291 PIK3CA, AKT1, PTEN alt.40% HER2-low (1+, 2+) 35% DESTINY-Breast04 HER2-low (1+, 2+) 35% Enhertu DESTINY-Breast04 HER2-low (1+, 2+) 60% established SoC launched indication AstraZeneca in breast cancer DXd ADC PARPiIO ngSERD AKTiKey: A PP END I X | Oncology tumour maps PD-L1-inelig. 70% PD-L1-eligib. 30%

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55 sonesitatug vedotin previously AZD0901. All numbers are approximate. Illustrative settings and populations, not to scale. Gastric cancer map reflects ongoing active Phase III/pivotal trials. Collaboration partners: Daiichi Sankyo (Enhertu), Compugen (rilvegostomig). Appendix: Glossary. RECURRENCE Other 20-25% HER2-positive 20% Est. epi (G7, 2025) 50k 90k 60k 30k 1st line 2nd line 3rd line Early Stage II/III Advanced/Metastatic Imfinzi + perioperative FLOT in resectable disease MATTERHORN Enhertu + rilvegostomig + FP ARTEMIDE-Gastric01 Enhertu + pembrolizumab + FP DESTINY-Gastric05 Enhertu DESTINY-Gastric02, 04 Enhertu DESTINY-Gastric01 sonesitatug vedotin CLARITY-Gastric01 established SoC launched indication AstraZeneca in gastric cancer DXd ADC IO AZN ADC IO bispecificKey: Claudin18.2- positive 45-50% sonesitatug vedotin Claudin18.2 ADC rilvegostomig PD-1/TIGIT bispecific Potential for new approaches with A PP END I X | Oncology tumour maps

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56 Significant progress with transformative technologies to drive 2030+ growth ADCs/RCs, next-gen IO and cell therapy/TCE progressed to Phase III 3 Phase III trials initiated with laroprovstat (oPCSK9) Multiple Phase II dose optimisation trials ongoing AZD5004 (oGLP -1) AZD6234 (SARA) Weight management and risk factors Establish and lead in new weight management paradigm 7 AZN ADCs in clinic, including sonesitatug vedotin (CLDN18.2) in Phase III for 2L+ GC/GEJA FPI-2265 (PSMA-targeted RC) in Phase II for pre-treated mCRPC ADCs and Radioconjugates Replace systemic chemotherapy and radiotherapy 14 Phase III trials with rilvegostomig and volrustomig initiated1 Encouraging early evidence for ADC combination presented at ASCO and ESMO 2025 Next-gen IO bispecifics Replace existing PD-1/ PD-L1 inhibitors AZD0120 (BCMA/CD19) CAR-T Phase III planned in multiple myeloma surovatamig (CD19/CD3) in Phase III for 1L FL EsoBiotec acquired Cell therapy and T-cell engagers Develop scalable cell therapies and T-cell engagers across therapy areas Preclinical and Phase I development ongoing across multiple platforms sAAVy and AAV capsid TALEN technology Gene therapy and gene editing Make cure possible for a range of rare diseases 1. Does not include eVOLVE-RCC02 which remains in Phase Ib. Updated as of 20 October 2025. Collaboration partners: Compugen (rilvegostomig). Appendix: Glossary.

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Please ensure you have added the correct confidentiality statement. Type the correct statement: ‘Company Restricted’ or ‘Strictly Confidential’ . No statement is needed for public information. ! AstraZeneca at WCLC and ESMO 2025 Highlights from key early programmes presented at the IASLC 2025 World Conference on Lung Cancer and European Society of Medical Oncology Congress 2025 September-October 2025

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Oncology at AstraZeneca 2 We have a bold ambition to provide cures for cancer in every form. We are following the science to understand cancer and all its complexities to discover, develop and deliver life-changing treatments and increase the potential to save the lives of people around the world. AstraZeneca attendance at the World Conference on Lung Cancer and European Society of Medical Oncology Congress 2025 4 35 >160 plenary presentations oral presentations abstracts “Our presence across WCLC and ESMO this year underscores AstraZeneca’s unwavering commitment to driving scientific innovation in Oncology. The depth and breadth of data we’re sharing highlights the strength of our science and the momentum behind our early pipeline as we work to transform outcomes for patients worldwide. ” – Susan Galbraith EVP , Oncology Haematology R&D For any questions or requests for follow-up information, please contact us at IRDirectors@astrazeneca.com

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AstraZeneca’s ambition in Oncology 3 Latest advances showcased at WCLC and ESMO 2025 Leading in next-wave IO bispecifics – rilvegostomig | ex vivo efficacy – ARTEMIDE-01 | rilvegostomig in checkpoint inhibitor-naïve metastatic NSCLC – TROPION-PanTumor03 | rilvegostomig + Datroway in locally advanced or metastatic urothelial cancer Expanding leadership position in growing ADC market – FONTANA | AZD5335 in platinum-resistant recurrent ovarian cancer – QCS platform | real world assessment of TROP2 NMR by QCS in NSCLC Progressing next generation PARP inhibition – PETRANHA | saruparib + ARPI in metastatic prostate cancer Our Oncology strategy is built with one goal in mind – to push the boundaries of science to change the practice of medicine and transform the lives of patients living with cancer. Our broad pipeline of next-generation medicines, together with our focus on excellence in execution, are aimed at expanding treatment options and improving outcomes for patients with solid tumours and haematological cancers. 1. 2. 3. 4. We focus on four strategic priorities: Pioneering research across seven scientific platforms: tumour drivers and resistance, immuno-oncology, DNA damage response, ADCs, radioconjugates, epigenetics and cell therapies Advancing innovative clinical strategies to treat early stages of disease and relapsed or refractory patients Building expertise and leadership in the most prevalent and highest mortality rate tumour types Delivering across our global footprint

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Leading in next-wave IO bispecifics 1. Phase Ib/III trial (currently in Phase Ib) 5 Bispecific antibodies are engineered to bind to two different epitopes at the same time. This dual action principle can potentially improve target specificity by binding two antigens on the same cell. Drawing on our long history of protein engineering, we are designing bispecific antibodies that simultaneously target different immune checkpoints, as part of our efforts to harness the immune system against cancer. Fc attenuated triple-mutant IgG1 potentially maintaining and enhancing immune responses, and conferring improved safety Designed to fully inhibit PD-1 while preferentially inhibiting CTLA-4 on activated T cells rilvegostomig volrustomig Anti-PD-1 Fab KD 0.82nM Anti-CTLA-4 Fab KD 0.42nM Knob-into-hole IgG1-TM Fc Anti-PD-1 Fab KD 0.32nM Anti-TIGIT Fab KD 0.015nM Knob-into-hole IgG1-TM Fc Phase III trials across tumour types15 rilvegostomig TROPION-Lung12 | rilve ± Datroway | Stg. I NSCLC TROPION-Lung10 | rilve ± Datroway | 1L PD-L1>50% NSQ NSCLC ARTEMIDE-Lung02 | rilve + CTx | 1L PD-L1>1% SQ NSCLC ARTEMIDE-Lung03 | rilve + CTx | 1L PD-L1>1% NSQ NSCLC ARTEMIDE-Lung04 | rilve | 1L PD-L1 >50% NSCLC ARTEMIDE-Gastric01 | rilve + Enhertu/trast. + CTx | HER2+ PD-L1>1 1L GC/GEJC ARTEMIDE-HCC01 | rilve + bev ± Imjudo | 1L unresect./met. HCC DESTINY-BTC01 | Enhertu ± rilve | HER2+ adv. BTC DESTINY-Endometrial01 | Enhertu + rilve| pMMR HER2+ adv. EC eVOLVE-Lung02 | volru + CTx | 1L PD-L1 <50% NSCLC eVOLVE-Meso | volru + CTx | mesothelioma eVOLVE-Cervical | volru | high-risk LA cervical eVOLVE-HNSCC | volru | LA unresect. HNSCC ARTEMIDE-Biliary01 | rilve + CTx → rilve| resect. BTC eVOLVE-RCC021 | volru + casdatifan | 1L adv , ccRCC volrustomig

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New at WCLC – further insight into differentiated mechanism of action with rilvegostomig 6 Bispecific approach differentiated | Coordinated inhibition of PD-1/TIGIT induces greater ex vivo activity than its components n=46 NSCLC fresh patient tumours Fc-reduced functionality important for efficacy | Unmodified or enhanced Fc-functionality appears to be detrimental to rilvegostomig anti-tumour activity in NSCLC explants n=33 NSCLC fresh patient tumours Ratiu J et al. Abstract OA03.03 presented at the World Conference on Lung Cancer 2025. ADCC (Fc γRIIIa F158) reporter assay 0.0001 0.001 0.01 0.1 1 10 100 1000 0 100000 200000 300000 400000 Concentration ( nM) Luminescence (RLU) Rilvegostomig (Fc-reduced) Rilvegostomig (Fc-active) Rilvegostomig (Fc-enhanced) αTIGIT (Fc-enhanced) αTIGIT (Fc-active) αTIGIT (Fc-reduced) 20 30 40 50 60 -10 -9 -8 -7 -6 -5 -4 -3 hFcγRIIIa V158 hFcγRIIIa F158 hFcγRIIIb NSCLC ex vivo Immune activation (IFN γ production) Freq. tumors with drug activity (%) Log K D (M) Pears on r r = 0.90 r = 0.88 r = 0.90 αTIGIT mAbs in combination with pembrolizumab Fc-functionality correlates with ex vivo activity ADCC overlapping Rilvegostomig (Fc-enhanced) Rilvegostomig (Fc-reduced) αTIGIT (Fc-active) Rilvegostomig (Fc-active) Co lor Legend αTIGIT (Fc-reduced) FcγRIII affinity rilvegostomig

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New at ESMO – ARTEMIDE-01 follow-up confirms potential of rilvegostomig in checkpoint inhibitor-naïve NSCLC 7 ARTEMIDE-01 | Phase I/II open-label trial investigating rilvegostomig in patients with advanced or metastatic NSCLC Longer follow-up support extended duration of response PD-L1 TPS 1-49%, CPI-naïve (n=31) – ORR 29% – DoR 9.8 mo – Median PFS 6.1 mo – 12 mo PFS rate 27.2% PD-L1 TPS ≥50%, CPI-naïve (n=34) – ORR 61.8% – DoR NR – Median PFS 12.3 mo – 12 mo PFS rate 55.5% Well tolerated with low 3.1% discontinuation rate and only 6.2% patients reporting Grade ≥3 imAEs – Nearly all AEs were low grade, manageable and reversible – No Grade 4 or 5 TRAEs reported Data cutoff: 18 August 2025. Chul Cho B et al. Abstract 1853MO presented at the European Society of Medical Oncology 2025. rilvegostomig → → → → Time from first dose (months) 0 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 Change in target lesions from baseline (%) -100 -80 -60 -40 -20 0 20 40 60 80 100 Time from first dose (months) Change in target lesions from baseline (%) -100 -80 -60 -40 -20 0 20 40 60 80 100 0 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 2723 24 25 26 → →→ →→→ →→ → →→ → → → TRAEs ≥5% Grade ≥3 TRAEs Nausea GGT increased Decreased appetite Hypertriglyceridaemia Diarrhoea Fatigue ALT increased Constipation Rash Lipase increased Hypothyroidism Hypercholesterolaemia Myalgia AST increased Pruritus Patients (%) 100 100050 50 6.2% 6.2% 6.2% 7.7% 7.7% 7.7% 7.7% 7.7% 9.2% 9.2% 10.8% 10.8% 10.8% 10.8% 12.3% 3.1% 3.1% 3.1% 1.5% 1.5% 1.5%

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New at ESMO – rilvegostomig + Datroway data underscore potential of next-gen IO bispecific plus ADCs 8 TROPION-PanTumor03 cohort 6B | Phase II open-label trial cohort investigating Datroway + rilvegostomig in patients with locally advanced/metastatic urothelial cancer 1L cisplatin-ineligible (N=22) – cORR 68.2% – DCR at 12 weeks 95.5% – Median DoR NC – mPFS NC 2L cisplatin-ineligible (N=28) – cORR 38.9% – DCR at 12 weeks 83.3% – Median DoR NC – mPFS 12.5 mo Encouraging response rates and strong duration of response Manageable safety profile for combination in line with previous reports – No new safety signals Data support ongoing Phase III investigations into combinations and potential opportunity in bladder cancer – Discontinuation rate <20% in both cohorts Young Rha S et al. Abstract 3072MO presented at the European Society of Medical Oncology 2025. rilvegostomig Datroway Time (Months) Change in target lesion from baseline (%)−75 −50 −25 0 25 50 −100 0 1 2 3 4 5 6 7 8 9 101112131415161718192021 2322 24 Time (Months) −75 −50 −25 0 25 50 −100 0 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 Change in target lesion from baseline (%) Treatment ongoing Treatment discontinued

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Expanding leadership position in growing ADC market 1. July 2025 Global Data (external data source) 10 Leveraging our internal ADC expertise, we are demonstrating the strength of our proprietary platform across several ADCs currently in clinical development. We are also working jointly with several external partners to bring ADCs to patients as quickly as possible and augment our clinical pipeline. ADCs now in clinic including 7 wholly owned ADCs and 5 using proprietary AZN platform9 Well positioned to lead with different payloads and opportunity for combinations across portfolio Antibody engineering with differentiated novel mAbs and chemistry bispecific mAb nnAA/ss conjugation Novel targets via surface proteomics Payloads match disease biology TOPO1 MTIs + alternative MoAs + Tumour + normal PDx models Tox species+ $45bn+ estimated global market size for ADCs in 2030 1 Preclinical Phase I Phase II Phase III Approved puxi-sam | B7H4 tila-sam | EGFR/cMET AZD5335 | FRα sone-vedo | CLDN18.2 AZD0305 | GPRC5D AZD9829 | CD123 Enhertu | HER2 Datroway | TROP2 AZD4360 | CLDN18.2 ● Alliance ADC ● AZN owned ADC ● AZN owned ADC using AZN proprietary platform

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New at ESMO – FONTANA demonstrates promise of AZD5335 in platinum-resistant recurrent ovarian cancer 11 FONTANA | First-in-human Phase I/IIa trial of AZD5335, a folate receptor alpha-targeted (FRα) antibody-drug conjugate, in patients with platinum-resistant recurrent ovarian cancer α TOP1i Warhead AstraZeneca proprietary linker technology AZD5335 | Specific, targeted TOP1i ADC that binds to FRα with high affinity – Average DAR of 8 – Cleavable peptide linker is bystander-capable and serum-stable1 1. Shapira-Frommer R et al. Abstract 754P presented at the European Society of Medical Oncology 2024. Interim response evaluable set, defined as all dosed patients with measurable disease at baseline who have ≥15 weeks follow-up or 2 post-baseline scans ≥4 weeks apart, according to RECIST v1.1 criteria. Data cutoff: 11 July 2025. *Confirmed ORR. Oaknin A et al. Abstract 1065MO presented at the European Society of Medical Oncology 2025. Robust efficacy and durable activity across dose range studied in FONTANA – 54% ORR across dose levels in heavily pre-treated population – Activity in both FRα-high- and low-expressing tumours Consistent safety profile with that previously reported1 – Manageable safety profile – No new safety signals AZD5335

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New at WCLC – data support ability of laboratories to effectively implement QCS into practice 12 In a real-world investigation of TROP2 NMR by QCS in NSCLC, TROP2 NMR assessment using the TROP2 (EPR20043) NSCLC NMR research use only algorithm was found to be: Reproducible across sites | Results were similar regardless of which lab conducted the analysis – When compared to the Roche CLIA lab, 9 external sites showed a PPA of 99.9%, NPA of 100.0%, and OPA of 99.9% – Across all 10 sites, the algorithm demonstrated a PPA of 99.9% and an NPA of 100.0%, resulting in an OPA of 99.9% Reproducible across readers | Results were consistent regardless of the scoring pathologist – Agreement between 30 participating pathologists remained consistently high, with a PPA of 99.9%, NPA of 100.0%, and OPA of 99.9% Whole Slide Imaging IHC with TROP2 Assay Automated Image Analysis (QCS) Calculates TROP2 NMR for every tumour cell C yto so l M em br ane N ucl eu s Membrane and cytoplasm optical density Measures OD in each tumour cell Differentiates tumour from non-tumour Membrane OD Membrane OD + Cytoplasm OD Lower NMR → higher cytoplasm proportion Patient Biomarker Status Determination ≥75% of tumour cells with TROP2 NMR ≤0.56 <75% of tumour cells with TROP2 NMR ≤0.561 QCS is a novel, fully-supervised computational pathology approach that quantifies and locates targets like TROP2 QCS technology is currently being validated in the Phase III Datroway programme, using the TROP2 (EPR20043) NSCLC NMR investigational use only algorithm 1 2 3 4 + - Lopez-Rios F et al. Abstract PL02.11 presented at the World Conference on Lung Cancer 2025. Datroway

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Building the next generation of PARP inhibition 14 Targeted DDR inhibitors such as PARPi can be used to maximise DNA damage and selectively kill cancer cells, providing a targeted approach to cancer treatment with the potential to improve patient outcomes across multiple tumour types. saruparib New at ESMO – promising profile in PETRANHA for saruparib + androgen receptor pathway inhibitor in metastatic prostate cancer Leading PARPi globally Approved in ovarian, breast, prostate and pancreatic cancers PARP1 selective In Phase III for prostate and breast cancers Strong heritage and exciting potential in PARP inhibition PETRANHA part A | Phase I/IIa multi-arm study of saruparib + ARPIs in patients with metastatic prostate cancer – Responses occurred irrespective of HRRm status with promising rates of PSA-90 and undetectable PSA levels – Comparable or lower incidence of Grade ≥3 AEs than similar combinations containing non-selective PARPi Phase III programme for saruparib spans multiple settings in breast and prostate cancer EvoPar-Prostate01 |EvoPar-Prostate02 | EvoPar-Breast01 Data presented from the Interim Response Evaluable Analysis Set (i.e., all dosed patients who received ≥1 dose of any study intervention with measurable disease at baseline) at data cutoff: 28 October 2024. Azad A at al. Abstract 2384MO presented at the European Society of Medical Oncology 2025. saruparib

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Please ensure you have added the correct confidentiality statement. Type the correct statement: ‘Company Restricted’ or ‘Strictly Confidential’ . No statement is needed for public information. ! Investor Enquiries Registered office and corporate headquarters AstraZeneca PLC 1 Francis Crick Avenue Cambridge Biomedical Campus Cambridge CB2 0AA UK Corporate access CorporateAccess@astrazeneca.com Contact us IRDirectors@astrazeneca.com +44 20 3749 5000 Shareholder Helpline +44 800 389 1580

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Glossary 16 (c)ORR (confirmed) objective response rate (un)resect. (un)resectable 1L, 2L, 3L first-, second-, third-line ADC antibody conjugate ADCC antibody-dependent cellular cytotoxicity adv. advanced AE adverse event ALT alanine transaminase ARPI androgen receptor pathway inhibitor AST aspartate aminotransferase B7H4 B7 homolog 4 bev bevacizumab BTC biliary tract cancer ccRCC clear cell renal cell carcinoma CD123 interleukin-3 receptor alpha chain CLDN18.2 Claudin-18.2 CLIA Clinical Laboratory Improvement Amendments cMET mesenchymal -epithelial transition factor receptor CPI checkpoint inhibitor CTLA-4 cytotoxic T -lymphocyte -associated protein 4 CTx chemotherapy DAR drug to antibody ratio DCR disease control rate DDR DNA damage response DoR duration of response EC endometrial cancer EGFR epidermal growth factor receptor NSQ non-squamous OPA overall percentage agreement PARP poly (ADP-ribose) polymerase PD-(L)1 programmed death -(ligand) 1 PDx patient-derived xenograft PFS progression free survival pMMR proficient mismatch repair PPA positive percentage agreement PSA prostate-specific antigen puxi-sam puxitatug samrotecan QCS quantitative continuous scoring R&D Research & Development rilve rilvegostomig RUO research use only sone-vedo sonesitatug vedotin SQ squamous TIGIT T-cell immunoreceptor with immunoglobulin and ITIM domains tila-sam tilatamig samrotecan TOPO1 topoisomerase I TPS tumour proportion score TRAE treatment-related adverse event trast. trastuzumab TROP2 trophoblast cell surface antigen 2 volru volrustomig WCLC World Conference on Lung Cancer ESMO European Society of Medical Oncology Fab fragment antigen -binding region Fc crystallisable region FRα folate receptor alpha GC gastric cancer GEJC gastroesophageal junction adenocarcinoma GGT gamma-glutamyl transferase GPRC5D G protein-coupled receptor, class C group 5 member D HCC hepatocellular carcinoma HER2 human epidermal growth factor receptor 2 HNSCC head and neck squamous cell carcinoma HRRm homologous recombination repair mutation IgG1-TM Fc modified immunoglobulin G1 antibody imAE immune mediated adverse event IO immuno-oncology IUO investigational use only LA locally advanced mAbs monoclonal antibodies met. metastatic mo month MoA mechanism of action MTI microtubule inhibitor NC non-calculable nM nanomolar NMR normalised membrane ratio NPA negative percentage agreement NSCLC non-small cell lung cancer

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