Slides
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Roche Pharma Day 2026 London, 28 September 2026
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This presentation contains certain forward-looking statements. These forward-looking statements may be identified by words such as ‘believes’, ‘expects’, ‘anticipates’, ‘projects’, ‘intends’, ‘should’, ‘seeks’, ‘estimates’, ‘future’ or similar expressions or by discussion of, among other things, strategy, goals, plans or intentions. Various factors may cause actual results to differ materially in the future from those reflected in forward-looking statements contained in this presentation, among others: 1 pricing and product initiatives of competitors; 2 legislative and regulatory developments and economic conditions; 3 delay or inability in obtaining regulatory approvals or bringing products to market; 4 fluctuations in currency exchange rates and general financial market conditions; 5 uncertainties in the discovery, development or marketing of new products or new uses of existing products, including without limitation negative results of clinical trials or research projects, unexpected side-effects of pipeline or marketed products; 6 increased government pricing pressures; 7 interruptions in production; 8 loss of or inability to obtain adequate protection for intellectual property rights; 9 litigation; 10 loss of key executives or other employees; and 11 adverse publicity and news coverage. Any statements regarding earnings per share growth is not a profit forecast and should not be interpreted to mean that Roche’s earnings or earnings per share for this year or any subsequent period will necessarily match or exceed the historical published earnings or earnings per share of Roche. For marketed products discussed in this presentation, please see full prescribing information on our website www.roche.com All mentioned trademarks are legally protected. This presentation may include slides and information created by third parties. These materials, often previously presented by third-parties at medical conferences or information events, are typically included to support the diverse exchange of medical perspectives regarding clinical trial data and results. These third-party materials were generated and presented independently of Roche. Roche does not necessarily endorse, adopt, or concur with the content, opinions, or conclusions expressed in such slides or presentations. Furthermore, Roche assumes no obligation to correct, update, or provide its own view on such third-party content, and its inclusion in this deck should not be construed as an endorsement. 3
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Welcome Bruno Eschli Head of Investor Relations
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5 Agenda Introduction 09:30 BST Bruno Eschli, Head of Investor Relations Pharma Strategy and Commercial Growth Drivers Teresa Graham, CEO Roche Pharmaceuticals R&D Excellence Levi Garraway, CMO and Global Head of Product Development Revolutionizing drug R&D with Lab-in-a-Loop Aviv Regev, Head of Genentech Research and Early Development (gRED) Financial Excellence and Digitalization Alan Hippe, CFO Roche Group 11:15-11:40 Q&A – Strategy 11:40-12:30 Lunch Break Oncology/Hematology 12:30 BST Levi Garraway & Matt Hellman, SVP and Global Head of Oncology and Hematology Product Development Neurology Hideki Garren, SVP and Global Head of Neurology Product Development Immunology Larry Tsai, SVP and Global Head of Immunology Product Development Ophthalmology Christopher Brittain, SVP and Global Head of Ophthalmology Product Development Cardiovascular, Renal and Metabolism Manu Chakravarthy, SVP and Global Head of Cardiovascular, Renal and Metabolism Product Development 14:10-14:40 Q&A - Pipeline 14:40-15:00 Buffet reception StrategyPipeline
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Pharma Strategy and Commercial Growth Drivers Teresa Graham CEO Roche Pharmaceuticals
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Progress since Pharma Day 2025 Our strategy and capabilities Our commercialization excellence Future growth opportunities 7
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Significant progress made since Pharma Day 2025 Continued strong operational efficiency, supporting delivery of the next wave of innovation 8 1. At CER: Constant exchange rates (avg. full year 2025); 2. Positive Ph III interim data, study ongoing, in collaboration wi th Ionis; 3. Currently in Ph II/III study; 4. In collaboration with Nurix Therapeutics; 5. In collaboration with Zealand Pharma; COP: Core operating profit Significant pipeline progressPositive Ph III readoutsStrong financial performance1 +6% HY 26 sales growth +10% HY 26 COP growth +2.0%p HY 26 COP margin growth = Positive Ph III readout giredestrant Adj. ER+/HER2- eBC giredestrant Post CDKi ER+/HER2- mBC divarasib 2L+ KRAS G12C+ NSCLC Lunsumio 2L+ FL fenebrutinib RMS fenebrutinib PPMS Enspryng MOGAD Gazyva SLE Gazyva MN sefaxersen2 IgAN HER2 TKI3 HER2+ BC tambotatug pelitecan Lung cancer bexobrutideg4 CLL CD-20 Brainshuttle MS NLRP3 inhibitors AD, PD, CAD VEGF x IL6 DutaFab DME petrelintide5 Obesity ± T2D CT-996 Obesity ± T2D enicepatide + petrelintide Obesity ± T2D Neurology Immunology CVRMOphthalmologyOncology/Hematology +11% HY 26 operating free cash flow growth = Moving to Ph II = Moving to Ph III
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Substantial progress on Pharma R&D Excellence achieved R&D Excellence and strategic M&A driving pipeline value to all-time high 91. As of HY 2026; 2. From Lead Identification to end of Phase 3; aNPV: adjusted net present value; LI Go: Lead identification Go Achievements1 Improvement of the Ph3 success rate: 65% in 2025, >80% in 2026 YTD 2020 2021 2022 2023 2024 2025 HY 2026 +93% Pipeline evolution -27% Volume (project count) Pipeline value (aNPV) Introduction of the “Bar”: Portfolio value +93% since YE 2022 Introduction of the “Bar” Re-allocation of R&D resources with CHF ~1.6 bn savings reinvested since YE 2023 Shortened R&D cycle times by ~19 months until YE 20262 vs. YE 2023 Disciplined BD complementing in-house R&D Increased early stage research productivity with LI GOs growing to 104 at YE ‘25 vs. 51 YE ‘22
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Up to 20 NMEs with launch potential by 2030 Two recent additions: Tam-Peli in SCLC and NSCLC, and VEGF x IL6 DutaFab in DME 10 Peak sales shown unadjusted; 1. In collaboration with Ionis; 2. In collaboration with Nurix Therapeutics; 3. In collaboration with Zealand Pharma; 4. In collaboration with Alnylam; CVRM: Cardiovascular, renal and metabolism; NME: New molecular entity afimkibart IBD, RA, MASH sefaxersen1 IgAN zosurabalpin Bacterial infections trontinemab Alzheimer’s disease prasinezumab Parkinson's disease fenebrutinib RMS, PPMS giredestrant ER+ BC tambotatug pelitecan SCLC, NSCLC and others zemocimig Hemophilia A bexobrutideg2 CLL divarasib KRAS+ NSCLC cevostamab R/R MM HER2 TKI HER2+ BC VEGF x IL6 DutaFab DME vamikibart UME 0.5-1bn peak sales 1-2bn peak sales 2-3bn peak sales >3bn peak sales Oncology/Hematology Neurology Immunology Ophthalmology CVRM enicepatide Obesity +/- T2D CT-996 Obesity +/- T2D petrelintide3 Obesity +/- T2D pegozafermin MASH zilebesiran4 Hypertension
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22.5 22.6 24.0 23.6 11.2 11.4 12.5 12.5 Efficiency gains & cost control driving Pharma COP margin improvement 11 Note: Totals & subtotals may not add up due to rounding. Absolutes in CHF bn. Growth rates at CER; CER: Constant exchange ra tes of given year; COP: Core operating profit; OPEX: Operating expenditure; SG&A: Selling, general and administrative expenses HY Pharma sales & profit developmentHY Pharma OPEX development (% of OPEX) HY 2023 HY 2024 HY 2025 12.8 12.5 12.5 HY 2026 12.2 Cost of sales R&D SG&A (31.4%) (32.1%) (32.8%) (42.9%) (42.5%) (41.3%) (25.7%) (25.4%) (25.8%) +14% +13% +15% +9% Sales volume growth CHFbn 49.6% 50.4% 52.2% 53.0%COP margin +1.7%p CER+0.9%p CER HY 2023 HY 2024 HY 2025 HY 2026 Sales COP CHFbn +10% CER+5% CER +13% CER+7% CER (34.7%) (40.5%) (24.8%) +2.0%p CER +10% CER +6% CER 3.3 3.2 3.2 3.0 5.5 5.3 5.2 4.9 4.0 4.0 4.1 4.2 (31.4%) (32.1%) (32.8%) (42.9%) (42.5%) (41.3%) (25.7%) (25.4%) (25.8%) (34.7%) (40.5%) (24.8%)
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Sales 2025 2026E 2027E 2028E 2029E 2030E A strong base to deliver long-lasting future growth Year end 2025 pipeline successes provide a clear path for sustained and strong growth beyond 2030 12*Pending regulatory approval; **Positive Ph III interim data, study ongoing; Note: Graph is purely conceptual to outline port folio trends; AD: Alzheimer’s disease; CGM: Continuous glucose monitor; COP: Core operating profit; IBD: Inflammatory bowel disease; MASH: Metabolic dysfunction-associated steatohepatitis; PD: Parkinson’s disease; SBX: Sequencing by expansion; uHTN: Uncontrolled hypertension Diagnostics On-market Pharma portfolio Pharma pipeline Business development illustrative ▪ Diagnostics growth driven by on-market portfolio and key launches ▪ Unique blockbuster opportunities with SBX sequencing, mass spec and CGM ▪ Mid- to high-single digit sales growth ▪ COP growth ahead of sales growth ▪ BD to further accelerate pipeline growth ▪ Late-stage pipeline with major readouts in new diseases from 2027 to 2030 including IBD, AD, MASH, PD, obesity and uHTN ▪ On-market Pharma portfolio (including Gazyva in immunology, giredestrant and fenebrutinib) to deliver strong growth overcompensating for any generic erosion ▪ No patent cliff ahead ▪ Pharma COP margin at least stable Giredestrant launch* Fenebrutinib launch* Gazyva launch in LN Potential launches by YE 2027 divarasib in 2L NSCLC vamikibart in UME Enspryng in MOGAD & TED sefaxersen in IgAN** afimkibart in UC Primary endpoint met
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Progress since Pharma Day 2025 Our strategy and capabilities Our commercialization excellence Future growth opportunities 13
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Committed to innovate in our five TAs Providing clarity and intentional focus to leverage our scientific strengths and impact patients globally 14CVRM: Cardiovascular, renal and metabolism; DALY: Disability -adjusted life years; E2E: End -to-end; TA: Therapeutic areas Covering 60% of total global burden of disease Our five Therapeutic Areas Currently 11 disease areas where we invest E2E from discovery to commercial Oncology/ Hematology Immunology CVRM Ophthalmology Neurology -5% 22% 24% 33% 16% 22% Global burden of disease ‘23 and ‘35 (m DALYs) Growth p.p% 970 920 531 617 268 328 231 286184 22525 2023 33 2035 2,208 2,408 +9%
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Clear strategic focus across our five TAs Recent pipeline successes driving updated Oncology/Hematology strategy 15CVRM: Cardiovascular, renal and metabolism; E2E: End -to-end; RVD: Retinal vascular diseases; TA: Therapeutic areas Oncology/Hematology Achieve leadership through transformative anchors Neurology Immunology Ophthalmology CVRM Establish & expand position in key patient segments Secure position with next wave of innovations Extend #1 position in neurology post 2030 Broaden portfolio and lead in preventive neurology Transform patient journey E2E via integrated Pharma + Dia approach Maximize the value of our pipeline via multi- indication expansion Leverage pan-immuno pathways to create value & cross-TA synergies Pursue curative therapies for sustained remission Establish a strong position in Ophthalmology by becoming #1 in retina Broadly diversified and differentiated pipeline with transformational potential Expand portfolio beyond RVD into Dry eye disease and Glaucoma Secure a strong entry before 2030 with competitive products Differentiate our offering by unique Roche capabilities Become a top 3 player in obesity
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Core capabilities to succeed 16AI: Artificial intelligence; TA: Therapeutic area Modalities & technologies Devices Manufacturing Customer experience & access Data & AI Our People Focus on approaches with breakthrough potential in focus TAs & diseases Making devices an integral part of our assets, from R&D to commercialization Optimizing and future-proofing our manufacturing network Providing a holistic customer experience & enabling rapid, broad & sustainable access Leveraging data and generative AI to improve process efficiency Creating a culture that allows our people to thrive in our Pharma division
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Broad toolbox of modalities driving the next wave of innovation Leveraging internal capabilities and external partnerships 17*Pending deal closure; CAR-T: Chimeric antigen receptor T- cell Pipeline deals and platform collaborations Small molecules Antibodies Bispecifics/ trispecifics Antibody-drug conjugate Peptides Cyclic peptides Fusion proteins Gene therapy Protein degraders Stem cell therapy RNA-targeting therapeutics Allogeneic CAR-Ts Brainshuttle Neoantigen vaccines Radioligand therapy Port delivery platform Modalities & Technologies *
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Taking our global manufacturing network to the next level Accelerating facility readiness through virtual validation of manufacturing designs before implementation 18 1. Approval Time Using Reliance (240 days) was calculated as an average of the time taken to get 80% approvals from participating health authorities in the pilot. 2. Reliance: the act whereby a regulatory authority in one jurisdiction takes into account, and gives significant weight to, assessments performed by another regulatory authority or trusted institution, or to any other authoritative information, in reaching its own decision. The relying authority remains independent, responsible and accountable for the decisions taken, even when it relies on the decisions, assessments and information of others. (WHO Good Regulatory Practices: guidelines for national regulatory authorities for medical products, 2021) Integrated virtual model of the entire facility enables end-to-end testing of equipment, processes and system interactions before implementation Optimizing manufacturing performance to improve capital efficiency and accelerate facility readiness Next-gen. manufacturing platform to increase yields Regulatory innovation to accelerate medicines to patients1 5x yield increase 2x yield increase Fully integrated digital twin Regulatory Reliance² pilots: Achieved simultaneous FDA & EMA manufacturing expansion approvals for Lunsumio on the same day. Manufacturing 890 days 240 days Expected approval time Approval time using reliance
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Scaling digital twin capabilities enterprise-wide Unlocking value through repeatable deployment and expansion into device lifecycle innovation 19 “Partnering with Roche brings end-to-end digital twins to the forefront of pharmaceutical manufacturing. Roche’s deployment of NVIDIA Physical AI stack sets a new industry standard.” - Kimberly Powell, Vice President / General Manager, Healthcare Design Excellence Final Assembly Packaging & Distribution Reduce physical testing Right-first-time industrialization Improved design robustness A repeatable deployment approach brings new sites onboard faster and unlocks value across Roche Manufacturing Scaling digital twins enterprise-wide
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Building and scaling for the portfolio of tomorrow Novel device platforms & capacity investments enabling upcoming launches and improving patient experience 20 Devices Shanghai HillsboroHolly Springs Kaiseraugst Mannheim Global drug product manufacturing network Device technology platforms Device pilot plant in Basel Needle safety device Auto-injector On-body injector Port delivery system Oncology / Hematology Neurology Immunology Ophthalmology CVRM NSD AI OBI Multi-dose pen PDS Ocular PFS Prefilled syringe 6 device platforms will cover 90% of our anticipated future device needs
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Digital excellence to enhance our marketing performance Investing in AI-driven digital initiatives to drive speed, reduce costs, and increase effectiveness 1. Content Engine currently live in the US market with global roll -out ongoing. Our content engine1 is driving efficiency in content creation: -50% Avg. content creation time -83% Cost per asset +7% Content volume output leading to faster creation + approval cycles enabling highly personalized experiences Data & AI Return on promotional investment Incremental revenue driven by AI-enabled Marketing Automation & Revenue Simulation (MARS) tool Accelerated Go-To-Market Increasing the return on promotional investments over time 21 AI-enabled Traditional Earlier diminishing returns Greater impact at scale Sustained efficiency at higher scale Promotional investment
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Strengthening our R&D and GPS teams 22 Product Development Therapeutic Area Heads Global Pharma Strategy Therapeutic Area Heads Mark Dawson Head of Pharma Research and Early Development (pRED) Christopher Brittain Head of Ophthalmology PD Hideki Garren Head of Neurology PD Manu Chakravarthy Head of Cardiovascular, Renal & Metabolism PD Larry Tsai Head of Immunology PD Levi Garraway Head of Global Product Development (PD) and Chief Medical Officer Matt Hellman Head of Oncology/ Hematology PD Strengthening our Capabilities in Early Research & Development Saswata Talukdar VP Head of CVRM Discovery, pRED Kory Lavine VP Head of CVRM Research, gRED Louis Vermeulen SVP Head of Oncology, pRED Wendy Cheung Global Therapeutic Area Head Oncology / Hematology GPS Tanya Monga Global Therapeutic Area Head Immunology & Neurology GPS Morten Lammert Global Therapeutic Area Head Cardiovascular, Renal & Metabolism GPS Karsten Jung Head of Global Pharma Strategy (GPS) Nilesh Mehta Global Therapeutic Area Head Ophthalmology GPS Key new appointments since Pharma Day 2025 Our People
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Progress since Pharma Day 2025 Our strategy and capabilities Our commercialization excellence Future growth opportunities 23
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Commercialization archetypes: Entrench, expand, establish Leveraging our commercial execution and innovative pipeline to disrupt existing treatment paradigms 24KOL: Key opinion leader; NME: New molecular entity; SoC: Standard of care Maximize leadership positions in key disease areas Leveraging established disease areas by launching NMEs and expanding indications Entering into disease areas new to Roche by reshaping the current SoC Entrench Expand Establish ▪ Line extensions into adjacent indications ▪ Devices to boost convenience & adherence ▪ Commercial execution & customer experience ▪ Build on in-depth scientific and medical knowledge & KOL networks ▪ Leverage market expertise to address further unmet needs ▪ Drive commercial synergies while broadening market access ▪ Capabilities and infrastructure building ▪ Market understanding & value proposition articulation ▪ Disease awareness & unmet need scoping
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Portfolio mapping across the commercialization archetypes 25 Entrench Expand Establish Phesgo Tecentriq giredestrant divarasib fenebrutinib Enspryng Gazyva vamikibart trontinemab prasinezumab petrelintideafimkibart enicepatide pegozafermin zilebesiran CT-996 Hemlibra Columvi Lunsumio Polivy Ocrevus Vabysmo XolairEvrysdi sefaxersentambotatug pelitecan zemocimig bexobrutideg cevostamab HER2 TKI VEGF x IL6 DutaFab Neurology Immunology CVRMOphthalmologyOncology/Hematology Itovebi Susvimo Elevidys
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Entrench: Maximize potential by LEs, devices & commercial excellence 26 Neurology Immunology CVRMOphthalmologyOncology/Hematology Entrench Expand Establish Phesgo Tecentriq giredestrant divarasib fenebrutinib Gazyva trontinemab prasinezumab petrelintideafimkibart enicepatide pegozafermin zilebesiran CT-996 Hemlibra Columvi Lunsumio Polivy Ocrevus Vabysmo XolairEvrysdi sefaxersentambotatug pelitecan zemocimig bexobrutideg cevostamab HER2 TKIItovebi Susvimo Enspryng vamikibart VEGF x IL6 DutaFab Elevidys
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Breast cancer: Well-positioned to serve evolving needs in HER2+ Treatment landscape is becoming increasingly segmented as novel therapies enter the market 27 *Perjeta/Phesgo conversion rate calculated using volumes, currently taking 85 launch countries into account; e/ mBC: Early/metastatic breast cancer; HER2: Human epidermal growth factor receptor 2; PCR: Pathological complete response; SoC: Standard of care Oncology/Hematology ▪ eBC: Phesgo and Kadcyla expected to remain SoC in the majority of patients ▪ mBC: treatment strategy to evolve from 'one-size-fits-all' to tailored approaches anchored in disease biology and patient risk; Phesgo expected to remain a key treatment option ▪ HER2 franchise expected to peak in 2026, with a solid tail remaining by 2030 ▪ Innovative pipeline of combinations (e.g. Phesgo + giredestrant) and NMEs (e.g. HER2 TKI) HER2+ BC treatment paradigm to evolve further ▪ Phesgo global conversion rate climbing to 54%* ▪ Expecting to achieve >60% conversion rate at peak Phesgo conversion rate HER2+ eBC pts Residual Disease (45%) 65% 35% Adjuvant only Surgery PCR (55%) = Treatment paradigm expected to fragment based on latest clinical data giredestrant (heredERA) inavolisib (INAVO 122) DEMETHER Other (PATINA, HC-05) Kadcyla +Tecentriq (ASTEFANIA)* Neoadjuvant Adjuvant cont. First line
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NHL: Building on leadership with novel combinations Columvi and Lunsumio expanding into earlier lines 28BIC: Best in class; DLBCL: Diffuse large B-cell lymphoma; FL: Follicular lymphoma; NHL: Non -Hodgkin’s lymphoma; IPI: International prognostic index; SoC: Standard of care Oncology/Hematology ▪ Polivy established as SoC in 1L DLBCL; >120k pts treated globally ▪ Columvi: Leading bispecific in 2L+ DLBCL, supported by proven long-term OS benefit; Ph III SKYGLO combination with Polivy in 1L DLBCL with potential to bring well-tolerated outpatient regimen to larger patient population ▪ Lunsumio: Positive Ph III studies in 2L+ setting for both aggressive (DLBCL) and indolent (FL) lymphomas; outpatient community oriented doublet regimens with BIC tolerability and simplified dosing schedule Polivy in 1L DLBCL Columvi & Lunsumio in NHL Global patient count (1L DLBCL, thousands) DLBCL (patients, thousands) FL (patients, thousands) Columvi Lunsumio Primary endpoint met / filed / approved Ongoing Ph III
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Hemophilia A: Setting the SoC today, tomorrow and in the future Potential for Hemlibra autoinjector launch and Ph III zemocimig readout by YE 2027 29 *Commercial and WFH HA program; **Based RWD from McCary I, et al. Haemophilia 2020, Wall C, et al. ISTH 2020, Poon M -C, et al. ASH 2022 and Khairnar R, et al. ASH 2021; H2H: Head -to-head; Q2W/Q4W: Once every 2/4 weeks; RCT: Randomized-controlled trial; RWD: Real -world data; SC: Subcutaneous; SoC: Standard of care; VWD: Von Willebrand disease ▪ Growth driven by rising adoption and increased penetration in adult population ▪ Clinical confidence: ~80% of pts achieving zero treated bleeds** and without inducing FVIII inhibitors; RWD over >10 years in diverse patient populations, severities and clinical settings ▪ Autoinjectors in development to further improve convenience for Hemlibra and zemocimig Hemlibra in Hemophilia A Non-malignant heme pipeline ▪ Three Ph III trials of zemocimig in Hem A, incl. H2H vs. Hemlibra; data expected YE 2027 ▪ Zemocimig with potential to achieve hemostatic normalization Upcoming autoinjector Global patient count (thousands)* Ph I Ph II Ph III VWDHemlibra vs. FVIIIzemocimig vs. Hemlibrazemocimig Pediatric patientszemocimig SPK-8011QQ Time-saving administration Improved comfort & non-visible needle Ensures optimal therapeutic exposure Illustrative Oncology/Hematology
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Ocrevus: Expanding leadership to community and at-home settings #1 aCD20 in MS with >525k patients globally; Roche ranked #1 amongst MS patient organizations1 30 1. PatientView Corporate Reputation of Pharma - Multiple-Sclerosis Edition 2025; MS: Multiple sclerosis; OBI: On -body injector; SC: Subcutaneous; Ocrevus Zunovo with Halozyme’s rHuPH20/ Halozyme’s human hyaluronidase; Ocrevus OBI in partnership with Enable Injections Neurology ▪ Ocrevus proven efficacy & safety backed by 11+ years of data from clinical studies and 7+ years of experience from real-world studies ▪ Ocrevus Zunovo (SC) is the fastest growing aCD20 in the US, driven by uptake in community practices ▪ OBI is in development with the potential for convenient twice-yearly at-home self-administration; data expected in 2027 Ocrevus SC Upcoming Ocrevus OBI (on-body injector) Global patient count (thousands) Illustrative Novel high concentration formulation for lower injection volume vs. Ocrevus SC Twice-yearly at-home self- administration 9.6/10 preference rating amongst investigators Proven device: Partnership with Enable Injections
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Vabysmo: Expecting continued global market share gains Industry-leading Ophthalmology pipeline to further build on Vabysmo’s commercial success 31DME: Diabetic macular edema; DR: Diabetic retinopathy; GA: Geographic atrophy; nAMD: Neovascular age-related macular degeneration; RVO: Retinal vein occlusion Ophthalmology Vabysmo in RVD (nAMD, DME and RVO) Ophthalmology pipeline Global patient count (thousands) ▪ US branded market has stabilized; continued branded market share gains expected ▪ EU with strong volume growth overcompensating pricing effects ▪ ROW with strong growth driven by market share expansion; significant growth potential remaining Primary endpoint met Indication Ph II Ph IIIAsset Ph I New to Ph III vamikibart Enspryng Vabysmo VEGFxIL6 DutaFab Susvimo UME TED mCNV DME nAMD OpRegen GA CFB siRNA GA WNT DME trispecific Retinal disease undisclosed DR undisclosed GA
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Expand: Leverage existing footprint for NME launches 32 Neurology Immunology CVRMOphthalmologyOncology/Hematology Entrench Expand Establish Phesgo Tecentriq giredestrant divarasib fenebrutinib Gazyva trontinemab prasinezumab petrelintideafimkibart enicepatide pegozafermin zilebesiran CT-996 Hemlibra Columvi Lunsumio Polivy Ocrevus Vabysmo XolairEvrysdi sefaxersentambotatug pelitecan zemocimig bexobrutideg cevostamab HER2 TKIItovebi Susvimo Enspryng vamikibart VEGF x IL6 DutaFab Elevidys
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Giredestrant: Potential new SoC in adjuvant HR+ breast cancer Giredestrant to potentially overcome limitations of current treatment options 33 1. Estimates based on IQVIA and Flatiron data; 2. Risk definitions vary according to guidelines and tools used: stage at diag nosis based on internal estimates using SEER data; intermediate risk encompasses stage I, N0 included in the lidERA criteria, but excluded in NATALEE; AI: Aromatase inhibitor; (e)BC: (Early) breast cancer; CDKi: Cyclin dependent kinase inhibitor; ET: Endocrine therapy; HER2: Human epidermal growth factor receptor 2; HR: Hormone receptor; SoC: Standard of care Oncology/Hematology Treatment of HR+ HER2- eBC ET monotherapy + adjuvant chemo + CDK4/6i NATALEE (ET + ribociclib) monarchE (ET + abemaciclib) (giredestrant monotherapy) AI / tamoxifen Intermediate risk (~10%)2 High risk (~15%)2 Low risk (55-60%)2 Medium risk (15-20%)2 Potential key opportunities Intermediate risk (~10%)2 High risk (~15%)2 Low risk (55-60%)1 Medium risk (15-20%)2 Low risk Intermediate risk 20% Medium risk 50% High risk ET alone +CDK4/6i 2025 US adjuvant therapy utilization1 lidERA population vs. current treatments in adj. HR+ BC Pts. discontinuing/not tolerating CDKi Future combos with CDKi Pts. iniating ET monotherapy Pts. discontinuing/not tolerating ET Future use in low risk patients
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Giredestrant: Enabling access for rapid patient uptake Generating clinical evidence to establish giredestrant as the new ET backbone across adjuvant settings 34 1. Since 1998 and until April 2026; 2. non -registrational study; 3. Pending final agreement, in collaboration with Natera and Al liance Foundation Trials; 4. Pfizer-managed, Ph III gated on positive Ph I; AI: Aromatase inhibitor; (e)BC: (Early) breast cancer; CDKi: Cyclin dependent kinase inhibitor; ET: Endocrine therapy; HCP: Healthcare professional; HER2: Human epidermal growth factor receptor; HR: Hormone receptor; MRD: Minimal residual disease; PDUFA: Prescription drug user fee act Oncology/Hematology Awareness Patient-centered, unbranded campaign to launch in the US >5 million pts treated globally across Roche’s BC portfolio1 >50% of target US HCPs engaged to date, with ongoing expansion Strong BC legacy and US launch readiness Development in adj. HR+ eBC ▪ Adjuvant HR+/HER2- eBC (lidERA): US filing acceptance under priority review, PDUFA set for Nov 30th ▪ Post CDKi HR+/HER2- mBC (evERA): US PDUFA set for Dec 18th ▪ Generating additional evidence across eBC populations (AI-intolerant, CDKi-intolerant, low-risk) and regimens (ctDNA-guided de-escalation) ▪ CDKi combination studies in eBC: Ph I with atirmociclib (CDK4i); single-arm lidERA substudies with abemaciclib and ribociclib Pts population Regimen Ph I Ph II Ph III Intermediate to high risk Giredestrant mono All risk, AI- intolerant Giredestrant mono2 All risk, upfront, switch from CDKi Giredestrant mono2 MRD-guided Giredestrant mono vs. ET + CDKi2,3 Intermediate to high risk Giredestrant + atirmociclib4 lidERA Ph IIIb (novERA) Ph IIIb (kalitERA) Primary endpoint met AFT-70 NAVIGATE IIS US Access Robust patient support programs to reduce access barriers and enable rapid clinically-driven adoption
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Fenebrutinib: First & only BTKi with positive Ph III in RMS/PPMS, filed in US Potential to be the first high efficacy oral therapy for RMS and PPMS, treating both relapses and progression 35 1. Hauser SL & Cree BAC, Am J Med, 2020: 133(12):1380-1390; 2. Singer BA et al., J Neurol, 2024: 271(6):3116 -3130; ARR: Annual relapse rate; BTK: Bruton’s tyrosine kinase; cCDP12: 12-week composite confirmed disability progression; FIC: First in class; H2H: Head -to-head; MS: Multiple sclerosis; (n) aSPMS: (Non-)active secondary progressive multiple sclerosis; PPMS: Primary progressive multiple sclerosis; RRMS: Relapsing-remitting multiple sclerosis; SPMS: Secondary progressive multiple sclerosis Neurology Fenebrutinib & Ocrevus in relapsing and progressive MS MS treatment landscape1,2 Low- to medium efficacy orals Low efficacy injectables Progressive biology (stop progression) Relapsing biology (stop relapses) OralsInjectables illustrative fenebrutinib ▪ Only BTKi with positive Ph III results in both RMS and PPMS, and only BTKi with positive H2H data vs. Ocrevus in PPMS; FIC potential in RMS and PPMS; planning real-world switch studies evaluating fenebrutinib post low or high efficacy therapies ▪ RMS: Significant reduction in relapses, down to one relapse every ~17 years, with the lowest ARR seen in Ph III MS trials; consistently positive trend in reducing disability progression vs. teriflunomide, incl. nominal significance in pooled cCDP12 ▪ PPMS: First and only medicine to reduce disability progression (cCDP12) with numerical benefit vs. Ocrevus MS biology Phenotypes RRMS aSPMS naSPMS PPMS Greater Relapsing Biology Greater Progressive Biology RMS PMS Fenebrutinib Ocrevus Positive Ph III results (fenebrutinib) / Approved in RMS & PPMS (Ocrevus) H2H vs. Ocrevus High efficacy treatments
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Enspryng: Differentiated risk-benefit profile in MOGAD and TED Potentially first approved treatment in MOGAD and first IL-6R inhibitor in active and inactive TED 36 AIE: Autoimmune encephalitis; MOGAD: Myelin oligodendrocyte glycoprotein antibody -associated disease; NMOSD: Neuromyelitis optica spectrum disorder; PDUFA: Prescription drug user fee act; TED: Thyroid eye disease Neurology Ophthalmology ▪ Enspryng engineered for maximal inhibition of IL-6 signaling, a key pathway across Neurology and Ophthalmology indications ▪ MOGAD: Highly significant reductions in annualized relapse rate, active MRI lesions, and rescue therapy use; US & EU filing achieved; US priority review granted with PDUFA Jan 10th ▪ TED: Totality of Ph III results show consistent, clinically meaningful improvements across key TED signs and symptoms; US priority review granted with PDUFA Oct 15th ▪ Ongoing Ph III in AIE with data expected 2027 MOGAD TED Potentially first approved treatment in MOGAD Highly favorable safety profile Significant, clinically meaningful reduced risk of new relapses Potentially first at- home SC treatment in TED Highly favorable safety profile Consistent, clinically meaningful improvements across key TED symptoms Indication Ph I Ph II Ph III Status NMOSD Launched in US/EU MOGAD Filed in US/EU TED Filed in US AIE 2027 readout SAkuraSTAR / SAkuraSky METEOROID SatraGO-1/2 CIELO Filed or approved Enspryng addressing unmet needs in MOGAD & TED Enspryng development program
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Establish: Enter disease areas new to Roche 37 Neurology Immunology CVRMOphthalmologyOncology/Hematology Entrench Expand Establish Phesgo Tecentriq giredestrant divarasib fenebrutinib Gazyva trontinemab prasinezumab petrelintideafimkibart enicepatide pegozafermin zilebesiran CT-996 Hemlibra Columvi Lunsumio Polivy Ocrevus Vabysmo XolairEvrysdi sefaxersentambotatug pelitecan zemocimig bexobrutideg cevostamab HER2 TKIItovebi Susvimo Enspryng vamikibart VEGF x IL6 DutaFab Elevidys
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Patient-driven Entry into new disease areas to address global burden of disease We deploy targeted investments and new approaches to ensure launch excellence in new disease areas 38 AD: Alzheimer’s disease; DME: Diabetic macular edema; IBD: Inflammatory bowel disease, MASH: Metabolic dysfunction -associated steatohepatitis; MS: Multiple sclerosis; nAMD: Neovascular age- related macular degeneration; PD: Parkinson’s disease; RA: Rheumatoid arthritis; RVO: Retinal vein occlusion; SMA: Spinal mus cular atrophy; T2D: Type-2 diabetes Ocrevus pegozafermin afimkibart trontinemabafimkibartVabysmoEvrysdiHemlibra Over the past 10 years, Roche has successfully entered new Disease Areas, primarily within targeted patient populations and specialty care settings In the next 10 years, Roche will enter broad-scale Disease Areas like obesity, T2D and Hypertension, necessitating different approaches and significant investment 20252015 2035 zilebesiran Bubble size is illustrative and represents prevalence of disease Care setting for majority of patients: enicepatide, CT-996 petrelintideprasinezumab
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Trontinemab with BID potential in Alzheimer’s disease 39 1. DRG (data available till 2036, extrapolated till 2050); AD: Alzheimer’s disease; APOE: Apolipoprotein E; ASO: Antisense ol igonucleotide; BID: Best-in-disease; CSF: Cerebrospinal fluid; PET: Positron emission tomography Neurology Alzheimer’s disease overview Roche in Alzheimer’s disease 2025 2026 2027 2028 Ph III (PrevenTRON) in preclinical AD initiated Ph III (TRONTIER 1 & 2) in early symptomatic AD fully enrolled Positive Ph Ib/IIa interim in AD Ph III readout in AD expected Ph III in early symptomatic AD initiated Global prevalence (Mn patients)1 ▪ Opportunity for trontinemab to differentiate on efficacy and safety as next gen Aβ antibody ▪ New Elecsys pTau217 blood test offers more accessible, reliable & faster diagnosis Key unmet needs 2029+ Diagnosis Invasive (PET/CSF), costly and not widely accessible Efficacy Faster and more complete amyloid clearance needed Safety ARIA-E and high monitoring needs Indication Asset Ph I Ph II Ph III Early symptomatic AD trontinemab Preclinical AD trontinemab AD nivegacetor AD NLRP3i AD APOE ASO TRONTIER 1 & 2 PrevenTRON GABRIELLA
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Prasinezumab with potential to become first DMT in Parkinson’s disease 40 1. Shalash A, et al., J Parkinsons Dis. 2026 Jun 23:1877718X261459875; 2. Bjornestad et al., Neurology 2016 Oct 11;87(15):1599-1606; 3. J Parkinsons Dis 2018, The Emerging Evidence of the Parkinson Pandemic Dorsey et al. 4. Global, regional, national epidemiology and trends of Parkinson’s disease from 1990 to 2021: findings from the Global Burden of Disease Study 2021 Luo et al.; DMT: Disease modifying treatment; PD: Parkinson’s disease Neurology Parkinson’s disease overview Roche in Parkinson’s disease Ph III prasinezumab readout in early stage PD expected Ph III prasinezumab in early stage PD initiated Ph II prasinezumab data suggests potential in early stage PD Global prevalence, (Mn patients)1 41% of initially independent patients lose functional independence with 5 years 46% stop working within 5 years of diagnosis Quality of life impact (% of patients)2-4 2025 2026 2027 2028 2029 Ph III (PARAISO) in early stage PD with strong recruitment ▪ Symptomatic treatments temporarily relieve motor symptoms, but benefits decline over time ▪ Multiple endpoints from Ph II (PASADENA & PADOVA) suggest potential to delay motor progression ▪ Ph III (PARAISO) in early stage PD ongoing; trial design optimized based on Ph II insights Indication Asset Ph I Ph II Ph III PD prasinezumab PD NLRP3i PARAISO 2030+
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Afimkibart spearheading our IBD entry, backed by next-gen MoAs 41 1. Evaluate Pharma; CD: Crohn’s Disease; IBD: Inflammatory bowel disease; MASH: Metabolic dysfunction -associated steatohepatitis; MoA: Mode of action; QoL: Quality of life; RA: Rheumatoid arthritis; SC: Subcutaneous; Tx: Treatment; UC: Ulcerative colitis Immunology IBD overview Global IBD market (CHF bn)1 Efficacy ceiling Initial response and remission limits of current Tx options Biologics sequencing Inconsistent guidelines, multiple cycles through Tx impacting QoL Key unmet needs Roche in IBD ▪ Afimkibart, the only TL1A offering the possibility of SC administration for induction & maintenance ▪ Exploring TL1A in multiple immunological diseases, incl. MASH and RA, in mono/combo Tx ▪ Developing next-gen IBD assets, e.g. bispecifics Indication Asset Ph I Ph II Ph III UC afimkibart CD afimkibart IBD p40 x TL1A IBD TL1A bispecific AMETRINE-1/2 SUNCREST SIBERITE-1/2 2025 2026 2027 2028+ Ph III in UC initiated Ph III in UC readout Ph II in RA readout Ph I in MASH readout Ph III readout in CD Launch in UC Ph II in RA initiated Ph I in MASH initiated Ph III in CD initiated Ph III initiations: AMETRINE SC-induction in UC AMETRINE-PEDS in pediatric UC SIBERITE-PEDS in pediatric CD
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CVRM pipeline advancing, primed to address growing disease burden 42 1. Sources: Hu SS et al. Chin Med J, 2025; Wang L et al. JAMA Intern Med, 2023; Zhou J et al. Clin Gastroenterol Hepatol, 202 5; Chen Y et al. J Clin Transl Hepatol, 2024; Estes C et al. J Hepatol, 2018; IDF Diabetes Atlas, 11th ed., 2025; Zhou B et al. Lancet, 2024; Phelps NH et a l. Lancet, 2024; Wang L et al. Lancet, 2021; Dandona L et al. Lancet Glob Health, 2018; Kalra A et al. Int J Environ Res Public Health, 2025; GBD 2023 CKD Collaborators Lancet, 2 025; Duseja A et al. J Hepatol, 2024; Kalra S et al. J Gastroenterol Hepatol, 2024; Misra A et al. Diabetes Ther, 2025; Anjana RM et al. Lancet Diabetes Endocrinol, 2023; Srivastava S et al. BMJ Open, 2025; Yusuf S et al. Lancet, 2004; *pending deal closure; ASC VD: Atherosclerotic cardiovascular disease; BID: Best In disease; BP: Blood pressure; CVRM: Cardiovascular, renal and metabolism; HFrEF: Heart Failure with reduced ejection fraction; MASH: Metabolic dysfunction-associated steatohepatitis; NIT: Non-invasive tests; T2D: Type-2 diabetes; uHTN: uncontrolled hypertension Cardiovascular, Renal & Metabolism 2025 2026 2027 2028+ Positive Ph II enicepatide in obesity + T2D Ph III Go for CT-996 Positive Ph II readouts: enicepatide in obesity zilebesiran in hypertension Study initiations: Ph III petrelintide in obesity Ph II enicepatide + petrelintide in obesity Ph III initiations: enicepatide in obesity pegozafermin in MASH zilebesiran in hypertension Ph III readouts: enicepatide in obesity and in T2D petrelintide in obesity pegozafermin in MASH zilebesiran in hypertension CVRM overview Roche in CVRM 2025 2035 Obesity Renal Diabetes CV Other metabolic Prevalence by disease type globally1 ( bn pts, not mutually exclusive) +6% +2% +2% +3%+1% CAGR Disease/Indication Asset Ph I Ph II Ph III Obesity, T2D, HFrEF, ASCVD enicepatide Obesity petrelintide Obesity CT-996 MASH pegozafermin uHTN zilebesiran Obesity UCN2 analog* Obesity/ diabetes MASH uHTN ▪ Positioned to capture market expansion & fragmentation ▪ Pts-centric care to meet evolving obesity/diabetes needs ▪ Leveraging advanced NITs for earlier diagnosis ▪ Potential BID innovative NME in a nascent market ▪ Potential to address poor oral adherence to boost control ▪ Leading the paradigm shift to continuous BP control
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Progress since Pharma Day 2025 Our strategy and capabilities Our commercialization excellence Future growth opportunities 43
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Updated 2025-30 consensus outlook* Long-term growth outlook improved; significant upside potential remains on the late-stage pipeline 44*All estimates are based on Post HY 2026 consensus collected by FTI Consulting on behalf of Roche (n=17) differences may occu r due to rounding; 1. Tecentriq, Alecensa, Elevidys, Susvimo, PiaSky, Activase/TnKase, Pulmozyme, CellCept, Xofluza, Rozlytrek: 2. included in >50% of sell -side models HER2 Herceptin 1.0bn Perjeta 3.0bn Phesgo 2.4bn Kadcyla 2.0bn MabThera 1.3bn Avastin 1.0bn Actemra 2.5bn Xolair 3.1bn 2025 Sales 2030E Sales Gap 6.2bn Xolair 1.6bn Avastin 0.5bn Actemra 1.1bn HER2 Herceptin 0.6bn Perjeta 1.0bn Phesgo 3.2bn Kadcyla 1.2bn MabThera 0.9bn Vabysmo 1.6bn Itovebi 1.0bn Columvi 0.9bn Polivy 0.9bn Gazyva 0.8bn Evrysdi 0.6bn Lunsumio 0.5bn Hemlibra 0.4bn Enspryng 0.3bn Ocrevus -0.1bn Other in-market1 0.1bn Pipeline Ph III2 9.2bn thereof giredestrant 3.5bn thereof fenebrutinib 1.1bn thereof enicepatide (CT-388) 0.8bn thereof afimkibart (TL1A) 0.7bn thereof divarasib 0.5bn thereof pegozafermin 0.4bn thereof petrelintide 0.4bn thereof trontinemab 0.4bn thereof vamikibart 0.3bn thereof sefaxersen 0.3bn thereof zemocimig (NXT007) 0.3bn thereof prasinezumab 0.3bn thereof zilebesiran 0.2bn Total 16.3bn Consensus sales growth (25-30)Biosimilar gap (25-30) Assets with low to no coverage in current sell side models: Cardiovascular & Metabolism: CT-996 in obesity +/- T2D; enicepatide + petrelintide in obesity +/- T2D; enicepatide in T2D Oncology/Hematology: cevostamab in r/r MM; bexobrutideg in r/r CLL; CDK4/2i in BC; HER2 TKI in HER2+ BC; tambotatug pelitecan in lung cancer; P-BCMA-ALLO1 in r/r MM Neurology: Enspryng in MOGAD & AIE; nivegacetor in AD; NLRP3i in AD/PD; CD-20 Brainshuttle in MS Immunology: Gazyva in immune-mediated kidney diseases; p40 x TL1A bispecific in IBD; Lunsumio and cevostamab in autoimmune diseases Ophthalmology: Enspryng in TED; VEGF x IL6 DutaFab in DME CHF Potential upside
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2027: Key newsflow outlook* 45*Outcome studies are event-driven: timelines may change Compound Indication Milestone Regulatory divarasib 2L KRAS G12C+ NSCLC US/EU approval Lunsumio + Polivy 2L+ DLBCL US approval Lunsumio 2L+ FL US/EU filing Hemlibra Autoinjector US/EU approval PiaSky aHUS US/EU approval fenebrutinib RMS US approval fenebrutinib PPMS US approval Enspryng MOGAD US/EU approval sefaxersen IgAN US filing Gazyva SLE EU approval Gazyva MN EU approval vamikibart UME US/EU approval Susvimo DME EU filing Clinical results Itovebi + Phesgo 1L PIK3CA-mut HER2+ mBC Ph III INAVO122 Columvi + Polivy + R-CHP 1L DLBCL Ph III SKYGLO zemocimig Hemophilia A Ph III ZEBRHA 1/2 Hemlibra VWD Ph III WILL-EMI Enspryng AIE Ph III CIELO Ocrevus OBI RMS/PPMS Ph III OCTAVIBE afimkibart UC Ph III AMETRINE-1/2 Susvimo AMD Q9M Ph III VELODROME nivegacetor AD Ph II GABriella afimkibart RA Ph II dRAvite p40 x TL1A UC Ph II SUNCREST
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R&D Excellence Levi Garraway CMO and Global Head of Product Development
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Recap | Our 2030 ambition 47 1. Reaching ‘Bar’ criteria: Future medicines that can have high impact for patients, high revenue potential, and optimized ri sk. Deliver 20 transformative medicines1 by 2030, addressing disease areas with the highest societal burden Reach top-quartile performance in R&D productivity across the biopharma industry to enable competitive end-to-end advantage
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Roche is on a path to materially elevate R&D productivity Prioritizing transformative assets by applying the Bar 48 AugmentationOperationalizationExecutionImplementationDiagnosis 2023 2024 2025 2026 2027+ Unlocks a path to value (e.g., robust revenue potential) Possesses worthy pharmacologic & developability characteristics Achieves meaningful therapeutic differentiation Answers a clear & addressable unmet need Engages a ‘foundational target’ Full adoption and early impact seen Sharper focus on critical aspects 100% adoption in Research and Development, enforced via Governance Boards Recent updates sharpen the focus on the ‘crux’ (single most important risk of program), path to value & therapeutic differentiation
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49 R&D Excellence: Our solutions Moving from implementation to “business as usual” Build a simplified system landscape and data foundation Evolve our R&D engine and invest in its excellence Transform our portfolio management & governance Adopt a unified portfolio framework Embrace ambitious R&D objectives Align our incentives with the new R&D strategy Access the best external innovation Implemented and moving into business as usual Implementation in progress
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50 R&D Excellence: Our solutions Moving from implementation to “business as usual” Build a simplified system landscape and data foundation Evolve our R&D engine and invest in its excellence Transform our portfolio management & governance Adopt a unified portfolio framework Embrace ambitious R&D objectives Align our incentives with the new R&D strategy Access the best external innovation Implemented and moving into business as usual Implementation in progress
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Pipeline prioritization since start of R&D Excellence Focus on high-impact projects and partnerships 1. Source: internal data, 28th September 2026; *pending deal closure; ADC: Antibody-drug conjugate; AGT: Angiotensinogen; BTK: Bruton’s tyrosine kinase; CAR -T: Chimeric antigen receptor T-cell; CDK4/2i: Cyclin dependent kinase-4/2 inhibitor; CSU: Chronic spontaneous urticaria; DLL3: Delta -like ligand 3; FGF21: Fibroblast growth f actor 21; GIP: Glucose-dependent insulinotropic polypeptide; GLP -1: Glucagon-like peptide-1; IBD: inflammatory bowel disease; LA: Long acting; mAb: Monoclonal antibody; MASH: Metabolic dysfunction -associated steatohepatitis; NME: New molecular entity; RA: Receptor agonist; SCLC: Small-cell lung cancer; siRNA: Small interfering RNA; TL1A: Tumor necrosis factor -like cytokine 1A; UCN2: Urocortin 2; Note: Chart Includes all assets from Ph I to Registration 4 8 3 3 5 3 4 5 5 5 3-5 - + -6 - -5 -3 - YTD Sep ’26 Q2 ’23 + -3 - + + -8 - 1 + - + -4 - + -9 - + -5 - + -2 - 1 + -5 + 81 65 - + -7 - -4 - + Portfolio evolution (NME additions / removals) Dual GLP-1/GIP RA in obesity ±diabetes Anti-AGT siRNA in hypertension Next gen. CDK4/2i in breast cancer DLL3 ADC in SCLC LA amylin analog in obesity ± diabetes FGF21 analog in MASH Anti-TL1A mAb in IBD Allogeneic CAR-T in Onc/Heme, Immuno and Neuro B7H3 ADC in solid tumors 51 Q3 Q4 Q1 Q2 Q3 Q4 Q1 Q2 Q3 Q4 Q1 Q2 Since HY ‘26 2023 2024 2025 2026 Adopt a unified portfolio framework Pipeline NMEs by TA 19 4 5 4 2 3 5 2 3 6 2 3 3 2Ph I 1 Ph II Ph III + Reg. 38 12 15 1 Oncology Neurology Immunology Ophthalmology CVRM Others BTK degrader in CLL UCN2 analog* in obesity
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52 Pipeline evolution since YE 2023 Growing share of potential best in disease assets and increasing peak sales for pipeline projects Adopt a unified portfolio framework 1. Source: Internal data; BID: Best-in-disease; YE: Year end Average peak sales per pipeline project, CHFbn1Share of late-stage projects with BID potential1 58% 65% YE 2023 HY 2026 +7%p 0.8 1.5 YE 2023 HY 2026 +79% Total portfolio value +72% since YE 2023
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53 Overall portfolio shift after introduction of the Bar Shifting portfolio to higher value and more balanced risk-reward 1. Based on all NMEs with PivGo decision since 2019, cut-off for pre the Bar at start of 2024; Values as of Ph III Go decision; aNPV: Risk-adjusted net present value (accounting for probability of launch); NME: New molecular entity; PivGo: Pivotal Go (pivotal study initiation decision point); PTS: Probability of technical success Risk-reward profile of assets with PivGo decisions post introduction of the Bar vs pre the Bar1, NMEs only Value (aNPV) PTS (Ph III) PivGo pre the Bar PivGo post the Bar (Pharma Day 2025) illustrative Adopt a unified portfolio framework
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54 Overall portfolio shift after introduction of the Bar Shifting portfolio to higher value and more balanced risk-reward 1. Based on all NMEs with PivGo decision since 2019, cut-off for pre the Bar at start of 2024; Values as of Ph III Go decision; aNPV: Risk-adjusted net present value (accounting for probability of launch); NME: New molecular entity; PivGo: Pivotal Go (pivotal study initiation decision point); PTS: Probability of technical success Risk-reward profile of assets with PivGo decisions post introduction of the Bar vs pre the Bar1, NMEs only Value (aNPV) PTS (Ph III) PivGo pre the Bar PivGo post the Bar (Pharma Day 2025) PivGo post the Bar (Pharma Day 2026) illustrative Adopt a unified portfolio framework
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55 R&D Excellence: Our solutions Moving from implementation to “business as usual” Build a simplified system landscape and data foundation Evolve our R&D engine and invest in its excellence Transform our portfolio management & governance Adopt a unified portfolio framework Embrace ambitious R&D objectives Align our incentives with the new R&D strategy Access the best external innovation Implemented and moving into business as usual Implementation in progress
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56 Pipeline acceleration through partnering and acquisitions Access the best external innovation External innovation to catalyze portfolio rejuvenationKey deals completed since start of R&D Excellence *pending deal closure; CLL: Chronic lymphocytic leukemia 2023 2024 2025 2026 ▪ Deals focusing on clinical stage assets (e.g. Ph III asset bexobrutideg in CLL) and platform technologies (e.g. access to DualityBio’s ADC platform for lead compound generation) ▪ Focusing on efficient integration processes and capabilities to remain the ‘Partner of choice’ for biotech ▪ Business development in combination with stringent R&D budget control to catalyze portfolio rejuvenation * Key deals completed to complement our pipeline across our five therapeutic areas
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57 R&D Excellence: Our solutions Moving from implementation to “business as usual” Build a simplified system landscape and data foundation Evolve our R&D engine and invest in its excellence Transform our portfolio management & governance Adopt a unified portfolio framework Embrace ambitious R&D objectives Align our incentives with the new R&D strategy Access the best external innovation Implemented and moving into business as usual Implementation in progress
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58 Our cumulative impact (2024 - YTD 2026) Embrace ambitious R&D objectives 1. Assets entering EIGLP (entry into GLP toxicology) studies; 2. From CHF 0.81 bn CHF to nearly CHF 1.45 bn; PTS: Probability of technical success Volume Success rateValue Effectiveness Cycle timeCosts Efficiency R&D Excellence Team-assessed Ph III PTS has increased since R&D Excellence roll-out CHF +0.64bn2 average peak year sales across late-stage portfolio Added 47 assets1 total from early R&D and high-value partnerships (+18 in 2026) Reinvested CHF ~1.6bn of savings from R&D back into the portfolio On track to achieve ~19 months acceleration by end of 2026 On track Longer follow-up needed
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59 Significant progress made since Pharma Day 2025 Embrace ambitious R&D objectives 1. From CHF 0.81 bn CHF to nearly CHF 1.45 bn Volume Success rateValue Effectiveness Cycle timeCosts Efficiency R&D Excellence Ph 3 success rate at >80% in 2026 YTD Average peak year sales across late- stage portfolio raised by CHF +0.19bn1 +18 assets added from early R&D and high-value partnerships Increased savings by CHF ~0.5bn Further accelerated cycle times by ~8 months On track Longer follow-up needed
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Significant acceleration achieved across late-stage pipeline Optimized R&D efficiency driving cycle time acceleration beyond fast-tracked assets 60 Source: Internal data; 1: Faster LPI not guaranteed to accelerate filing submission timelines for event -driven trials. 2: Other acceleration efforts include changes in study design/clinical development plan, Ph III ungating at interim and PoC biomarker analyses, and frontloading Ph III activities; LPI: Last patient in Embrace ambitious R&D objectives afimkibart prasinezumab trontinemab enicepatide 2 Faster LPI due to enrollment efficiency1 Faster to filing via other acceleration efforts2 5 8 216 92 8 7 27 11 zilebesiran 6 6 Fast-track asset Acceleration from initial projections (months)
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61 R&D Excellence: Our solutions Moving from implementation to “business as usual” Build a simplified system landscape and data foundation Evolve our R&D engine and invest in its excellence Transform our portfolio management & governance Adopt a unified portfolio framework Embrace ambitious R&D objectives Align our incentives with the new R&D strategy Access the best external innovation Implemented and moving into business as usual Implementation in progress
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Boston Innovation Center (opened Sep 18) ▪ Roche/Genentech collaboration with Harvard ▪ Focus: CVRM, Data & AI 62 Ongoing R&D investments Boston Innovation Center focusing on CVRM and AI in drug development opened AI: Artificial intelligence; CVRM: Cardiovascular, renal and metabolism Evolve our R&D engine and invest in its excellence >3500 Blackwell GPUs in hybrid-cloud AI factory, incl. 2 new data centers, one in the US and one in the EU SAIL (Shared AI license) foundation founding member, promoting collaborative exchange of AI algorithms & models 2026 AI milestones South San Francisco Boston Philadelphia London (Welwyn) Munich (Penzberg) Basel / Zurich Tokyo Shanghai (CiCor) Pharma R&D ChugaiRoche/Genentech
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63 R&D Excellence delivering the next wave of innovation aNPV: adjusted net present value; BD: Business development; KPI: Key performance indicator; NME: New molecular entity R&D Excellence drives… …our next wave of innovation ▪ Majority of solutions fully implemented, as tracked by R&D productivity KPIs ▪ Systematically applying the Bar to all in- house developed and partnered assets ▪ Continued augmentation of our R&D engine ▪ Up to 20 NMEs with launch potential by 2030, majority with a peak sales potential of CHF 3bn+ ▪ Balanced portfolio mix allowing for future development optionality of NMEs in the five focus TAs, including in disease areas new to Roche ▪ Disciplined resource reallocation leading to an all-time high in the total portfolio value (aNPV) On-track to reach our 2030 ambition
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64 Aviv Regev Genentech Research and Early Development (gRED) September 28th, 2026 Revolutionizing drug R&D with Lab-in-a-Loop
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65 Drug R&D is a challenging process with a low success rate Target discovery Drug discovery Preclinical Clinical studies Reg. review Manu- facture Approved medicine IND application NDA application Typically, only ~1-2 of 100 programs initiated in research will lead to a launch
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66 Why is drug R&D so difficult? BIG NUMBERS Enormous search spaces MULTI-SCALE Atoms, genes, proteins, cells, tissues, organs, patients MULTI-MODAL Multiple measurements / views of each entity VARIED No two research paths are quite the same
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67 VARIED AI has the potential to tackle each of these challenges BIG NUMBERS Enormous search spaces MULTI-SCALE Atoms, genes, proteins, cells, tissues, organs, patients MULTI-MODAL Multiple measurements / views of each entity No two research paths are quite the same
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68 LAB (OR CLINIC) IN THE LOOP Data Human biology, experiments & modalities AI/ML
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69 Lab-in-the-Loop in drug R&D Iterations with AI embedded E2E, across each component, from target discovery to the clinic Clinical candidate Lead optimization (LO) Lead identification (LI) Target discovery and assessment (TA) >> >> >> AI/ML, Artificial Intelligence and Machine Learning; FM, Foundation model; LI, Lead identification; LO, Lead optimization; R& D, Research and development; TA, Target assessment
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70 Our journey from build to delivery Build and iterate Deploy and deliver 2020 2021 2022 2023 2024 2025 2026 2027 2028 2029 2030 Transformative portfolio
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71 Our journey from build to delivery Strategy-driven investment across talent, AI capabilities, org design, data generation capacity & compute 1. Partnering/acquisition; 2. ~90% of eligible projects | Notes: BRAID: Biology Research AI Department; AI: artificial intell igence; LLM: large language model; LitL: Lab in the loop; LI: lead initiation; LO: lead optimization; SM: small molecules; IBD: Inflammatory bowel disease; gCS: gRED computational sciences; 2020 2021 2022 2023 2024 2025 2026 2020–2022 Build the foundation 2023–2024 Scale… 2025–2026 Transform… Strategy & capability Data generation Compute & software Organization & talent Example impact milestones Lab-in-the-Loop strategy Multiplicative Levers Prescient expansion (all molecules) Medra physical AI, MHS (Anthropic1) Autonomous Lab Accelerator gRED Computational Sciences (gCS) consolidated BRAID (biology AI) Computational Sciences Center of Excellence (serves both REDs) LLM trained on Roche data IBD pathobiology map + 15 LI targets LI target enters with AI agent support NVIDIA partnership Herophilus1 automation software A-alpha Bio collaboration AI factory (NVIDIA) LitL small molecule cycle LitL large molecule cycle LO small molecule scaffold with AI-supported design Antibody with AI support enters development portfolio (FPI) AI participating: 100% large molecules / 50% small molecules² PrescientDesign1 (antibodies AI) OpenAI pilot partnership1 Foundational Datasets for FMs initiative LitL2.0 initiative Cell & Tissue Genomics; Translational Genomics Recursion collaboration1 1st 1st 1st 1st 1st 1st 1st AWS Research Agent collaboration Caris collaboration
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72 Steady increase in research portfolio productivity 2022-2026 Increase from LI-Go to LO-Go to development candidates under nominally flat resources and halving LI CT Lead Identification Go Lead Optimization Go Internal Development Go Actual Forecasted Business deals Historical number +155% LI Go +75% LO Go +50% internal DevGo 2022-2025 growth CAGR 37% CAGR 20% CAGR 14% ~30% ~26% CAGR, Compound annual growth rate; LI, Lead identification; LO, Lead optimization
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73 Informative 10% Supportive 48% Fundamental/ Critical 41% ▪ Critical: Materially influenced ▪ Supportive: Meaningfully impacted decision confidence ▪ Informative: Informed thinking AI + computation contribute across the pipeline 40% of Q4 ’25 through Q2 ’26 pipeline decisions had a tracked AI / computational contribution Cumulative coverage: 40% (Q2 coverage reached 44%) Fundamental / Critical Supportive Informative 37% 36% 68% 43% 33% 25% Without computation contribution AI, Artificial intelligence; CS CoE, Computational sciences center of excellence; LI, Lead identification; LO, Lead optimization; Ph, Phase; TA, Target assessme nt Q4 ‘25 to Q2 ‘26 Role of contributions in decision making Impact on pipeline decisions by phase
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74 Lab-in-the-Loop in drug R&D Iterations with AI embedded E2E, across each component, from target discovery to the clinic Clinical candidate Lead optimization (LO) Lead identification (LI) Target discovery and assessment (TA) >> >> >> AI/ML, Artificial Intelligence and Machine Learning; FM, Foundation model; LI, Lead identification; LO, Lead optimization; R& D, Research and development; TA, Target assessment
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75 Increase in high quality volume of research portfolio entries Large-scale human and lab data, AI, and new processes increase high-quality volume and speed Conduct key experiments Anyone can propose a target for assessment (Target Champion) Target Champion assembles TAP data package TAP team advises Target Champion; recommendation within ~2 weeks LI entry proposal Cross-functional system to ensure speedy target assessment, expert guidance and prioritized resourcing Terminate project New enabling process: Target Assessment Portfolio (TAP) Teams Innovative scientific foundation: AI-enhanced pathobiology maps for target discovery Pipeline target hypotheses Output Genetics, disease atlases, perturbation screens, … Input Lab validation Pathobiology maps, AI Agent enablement AI disease model AI, Artificial intelligence; LI, Lead identification; TAP, Target assessment portfolio
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76 Pathobiology maps have scaled and accelerated our pipeline Example: IBD pathobiology maps PathoMap (FM) AI/ML Data Target Goal: Data & FMs to help break the efficacy ceiling Example: IBD Pathobiology Map v 2.0 ▪ Example map: cells x spatial context x human genetics ▪ Multi-modal data power IBD target discovery ▪ New biomarkers ▪ New combination therapies ▪ New drug targets ▪ Molecule discovery Clinical Histological Spatial Cellular Molecular Genetics Experiment Perturbation AI-informed cell modules and biology programs (IBD tissue) Portfolio programs Immune regulation Inflammatory signaling Fibrosis and remodeling targets cell / tissue programs AI, Artificial intelligence; IBD, Inflammatory bowel disease; FM, Foundation model; PathoMap, Patho-biology map
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77 AI-enhanced pathobiology maps across our TAs Cell surface targets across tumors COPD IBD Alzheimer’s MS Parkinson’s ALS AMD OphthalmologyNeurologyImmunologyOncology ✓ ✓ ✓ ✓ +155% increase in LI entries in 2 years First map deployed (IBD) 4 neurology maps deployed 1 YEAR 6 WEEKS ALS, Amyotrophic lateral sclerosis; AMD, Age-related macular degeneration; COPD, Chronic obstructive pulmonary disease; IBD, Inf lammatory bowel disease; LI, Lead identification; MS, Multiple sclerosis
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78 Foundational Datasets for Foundation Models initiative Large-scale data generation dedicated for training of AI models of relevant disease biology Target discovery and prediction → Find causal drivers Mechanistic insight → Understand how targets alter cell or tissue state Target-hopping → Find alternative therapeutic targets Target deconvolution → Identify what drives an observed compound’s effect Safety → Detect on- and of-target effects Foundation models (FM)Foundational datasets (FD) Cell & tissue FM Genomic FM Perturbation FM Patient tissues Healthy & disease Clinico-genomics Mechanisms & patient outcomes Perturbations Genetics and compounds Cells, organoids, tissues Sequence-to-phenotype Human genetics Massive scale lab assays Virtual cell / tissue a Experiment Data FD, Foundational datasets; FM, Foundation models
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79 Tackling biological search spaces with active learning Iterative AI-driven sampling efficiently explores the search space Active learning MSE Random selection of pairs MSE Active learning vs. baseline selectionExample: Iterative Perturb-Seq loop Active learning delivers better predicting model than strong baseline selection (random pairs over 600 impactful genes) Round #2 AI selected 600 pairs No AI ~700 selected pairs Round #3 AI selected 600 pairs Round #1 AI model Perturb platform Combinatorial CRISPRi Cells ~140 cells/ perturbation Data Predictions Combination effects Search space: ~180k pairs over 600 impactful genes Sampling: ~600 pairs / round Seeds where AI < Random: 20/20 (100%) AI: 0.083 ± 0.002 Random: 0.089 ± 0.003 Difference: -0.006 AI, Artificial intelligence; k, Thousands; MSE, Mean squared error +Baseline: 400 randomly selected pairs +Baseline: 400 randomly selected pairs
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80 TargetNexus Our AI agent for target assessment on track to be part of 80% of research portfolio decisions by Q4 Target discovery and assessment ▪ Causal mechanisms ▪ Disease biology ▪ Disease models ▪ Druggability ▪ Tractability ▪ Safety ▪ Modality ▪ Patient population ▪ Biomarkers ▪ Portfolio fit ▪ Competitive landscape Target Biology Drug Discovery Clinical & Portfolio Coverage across the pipeline
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81 Lab-in-the-Loop in drug R&D Iterations with AI embedded E2E, across each component, from target discovery to the clinic Target discovery and assessment (TA) Lead identification (LI)>> Clinical candidate Lead optimization (LO)>> >> AI/ML, Artificial Intelligence and Machine Learning; FM, Foundation model; LI, Lead identification; LO, Lead optimization; R& D, Research and development; TA, Target assessment Lead identification with functional screen (LI) >>
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82 Lab-in-the-Loop applied to cancer target & drug discovery Discovery of unique druggable MoA for a previously ‘undruggable’ pathway in oncology In collaboration with Start with biology Define Cell States Measure cellular response Identify and prioritize Reveal new biology Advance the best Undruggable pathway in cancer High-precision & high-bar hit validation Novel targets and novel mechanism of action On-pathway activity confirmed in vivo Challenge Anchor points Scale & screen AI prediction Discovery Optimization Perturb-Seq +Cell Painting PhenoMaps +TranscriptoMaps Novel mechanistic insights >250k compounds + whole-genome CRISPR screens Cell engineering of disease vs. healthy
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83 Virtual high-content small molecule phenotypic screens Scale discovery from constrained lab process to dramatically larger virtual scale Train foundation model Example public dataset 116K compounds Input compound structure Output measured phenotype Induce phenotype of interest in lab Anchor perturbation Anchor perturbation Measure phenotype Conduct phenocopy virtual screen Enamine virtual library 4B compounds screened Query the model virtually Discover anchor phenocopies ~220K compounds screened in a lab, 90B (10⁵-fold) space in ENAMINE to explore
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84 Prospective validation of a virtual cell phenotypic screen mTOR/PI3K pathway inhibitors Virtual screen and lab validation assays 3 rounds of experimental validation with increasing specificity No inhibitor FOXO3A in cytoplasm + PI3K inhibitor FOXO3A in nucleus Kinase inhibitionPathway activityMorphology ~500 compounds ordered (400 synthesized) Enamine REAL library PhenoCompass Predicted mTOR/PI3K pathway inhibitors ~4B compounds Hits with confirmed kinase inhibition; novel scaffolds Decreasing mTOR/PI3K pathway activity A B C D E F G H I J K L M N O Genes Morphology similarity Pathway activity Kinase inhibition
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85 Lab-in-the-Loop in drug R&D Iterations with AI embedded E2E, across each component, from target discovery to the clinic Clinical candidate Lead optimization (LO) Lead identification (LI) Target discovery and assessment (TA) >> >> >> AI/ML, Artificial Intelligence and Machine Learning; FM, Foundation model; LI, Lead identification; LO, Lead optimization; R& D, Research and development; TA, Target assessment
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86 Small and large molecule drug discovery AI can impact every stage of drug discovery Target assessment Lead optimizationLead identification Small molecules Druggability Hit generation Test Analyze Design Make Biologics Lead discovery Hit expansion Test Analyze Design Make
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87 AI-powered structural biology accelerates hit finding ICML 2026 GenBio Workshop Spotlight: Boltz-Jump: Accelerated Sampling of the Conformational Landscape of Biomolecular Structure Prediction Models. Daigavane et al. Identify druggable binding pockets Molecular hit finding Design of HDX-NMR experiments Generated ensembles of protein conformations HDX-NMR maps solvent- exposed regions VoxBind SAGE Pocket-conditioned voxel-denoising generative model Multi-property small molecule ligand design 1 2 3 Generic timeline First scaffold (New lab-based approach) First scaffold (AI-enabled virtual screen) X months X - 40% months X - 90% monthsX - 80% months Hit #1 (first synthesis) Hit #2
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88 Lab-in-the-Loop for small molecule optimization Weekly active learning improves both molecules and models Better molecules Better model Experimental synthesis and testing Synthetic & target aware idea generation Project data Potency & ADME prediction Selection for Active Learning Project ready designs Predicted P(active)True positive rate Measured pIC50 False positive rate
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89 AI+physics-guided scaffold hopping accelerates LO Optimizing metabolic stability while maintaining potency Virtual screen hit MedChem design Internal ML property filter Model molecular interactions Select lead compound Starting scaffold Expand Prioritize Optimize Binding optimization Compound enumeration (>90k) ↑ Stability New polar contact Predict relative potency Time <35 min to generate & filter ~100K structures WIP Learn Scale >1k compounds Potency ~40x improvement
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90 An AI Agent supports SM drug discovery Connecting context, SAR, design and computation to accelerate decisions Scientific foundation AI support Models & tools Skills Data Context Co-folding, docking, ADME and potency models, free energy perturbation, enumeration, etc. Structural biology, structure-activity analysis, model evaluations, plotting and visualizations, etc. Structure-activity project data, experimental structures, DesignHub, SM building blocks, etc. Project-specific context, documentations / history, medchem knowledge Reasoning Orchestration about project science and compound design tools, models and workflows LLM + Harness ADME, Absorption, distribution, metabolism, excretion; LLM, Large language model; SAR, Structure -activity relationship; SM, Small molecule
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91 Foundational building blocks for next-gen multi-specifics against relevant targetsData & AI driven target discovery Building next-gen multispecifics to improve outcomes Antibody building blocks and multi-program execution boost PTS, speed biologics, reduce costs Foundational building blocks (e.g. 100+) Assembly and optimization (e.g., 5 programs) Rapid generation of clinical candidate (e.g., 2 of 5 programs) Long-acting PathoMap Build & Opt AI/ML Clinical records Histological Spatial Cellular Molecular Human genetics Target Building blocks Clinical candidate Data AI/ML algorithms 1 2 3 1 3 1 32
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92 Integrated AI to optimize lead arms with low developability risk Rat, mice, rabbit, llama Potent function as monovalent arm High affinity and cross-reactivity Lead and backup arms for each target Example: Parallel efforts for each of 4 targets, for multiple bi- and tri-specifics Integrated experiments and computation help optimize lead arms to lower developability risk Immunogenicity (model 2) Pharmacokinetic Risk (model 1) X X Parent Sequence optimization High-throughput experimental affinity data set: ~1,200 single mutants Immunogenicity (model 2) Pharmacokinetic Risk (model 1) X X Parent Improved multi-specifics from building blocks
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94 Towards autonomous labs for drug R&D Our Autonomous Lab Accelerator to enhance the loop Human role: Operator Assistant Approver Auditor Observe Learn Predict Design Execute Analyze Results Report L0 Fully manual L1 Automated instruments L2 Connected workflows L3 AI-assisted workflows L4 Domain autonomy L5 Lab-wide autonomy Cheng et al. Preprints.org 2026 (in review) Including collaborations with
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95 Lab-in-the-Loop in drug R&D Iterations with AI embedded E2E, across each component, from target discovery to the clinic Clinical candidate Lead Optimization (LO) Lead Identification (LI) Target discovery and assessment (TA) >> >> >> AI/ML, Artificial Intelligence and Machine Learning; FM, Foundation model; LI, Lead identification; LO, Lead optimization; R& D, Research and development; TA, Target assessment
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96 Lab-in-the-Loop helps discover better molecules, faster Clinical-stage molecule with desired properties and reduced risk 2022 2023 2024 2025 2026 Target identification (novel target) Lead identification Go decision Lead optimization Go decision Clinical candidate First patient in Data Lead identification Lead optimization Phase 1 LI to clinical candidate in 18 months: 2x faster, reduced immunogenicity risk Data Variant sequence Screens In vitro function In vivo function Optimized lead Clinic
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97 CLINIC IN THE LOOP Lab-in-the-Loop to predict disease progression Disease, phenotype and progression Clinical trials AI/ML Covariate adjustment
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98 AI outperforms in predicting lesion growth “E2E” AI to predict lesion growth rate Trained and validated on >2,000 images from our past clinical trials in GA Baseline images (single/multi-modal) AI model Output PREDICTED GA GROWTH RATE Mahalo adjusted analysis using deep- learning FAF model Mahalo unadjusted analysis ▪ Covariate Adjustment with AI model (which wasn’t available at that time) changes Ph2 trial interpretation ▪ Precision of treatment effect estimate after adjustment is like running a trial >2x the size in this example Covariate adjustment with AI model False-positive effect ~20% (p=0.16) No effect ~4.5% (p=0.6) Sham High dose Low dose Sham High dose Low dose Anegondi N et al. Ophthalmology Retina. 2023 Mar;7(3):243-252. E2E, End-to-end; FAF, Fundus autofluorescence; GA, Geographic atrophy; Ph2, Phase 2 AI-based models allows covariate adjustment and better clinical decision making
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99 Clinic-in-the-Loop GWAS of novel AI-based outcomes identifies loci not detected in traditional risk studies OCT image AI layer segmentation Retinal zone mapping EZ loss 15.0 mm2 RPE loss 5.2 mm2 GWAS of novel outcomes Ellipsoid zone (EZ): photoreceptor health RPE supports the photoreceptors 15.0 5.2= High EZ/RPE = Poor patient prognosis Closing the loop E2E: added as new input for GA pathobiology map driving target discovery Illustrative cartoon Chromosome E2E, End-to-end; EZ, Ellipsoid zone; GWAS, Genome -wide association study; RPE, Retinal pigment epithelial cells; OCT, Optical c oherence tomography
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100 AI independence: owning the loop, learnings, improvements Data generation and AI independence needed to maximize competitive benefit of our learnings AI factory Multiple data generation streams at scale Proprietary Foundation models Expert domain agents and harness Ability to iterate (lab and AL/RL) Autonomous lab capabilities PartnershipsCapabilities Scientist
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101 Lab-in-the-Loop in drug R&D Iterations with AI embedded E2E, across each component, from target discovery to the clinic Clinical candidate Lead optimization (LO) Lead identification (LI) Target discovery and assessment (TA) >> >> >> AI/ML, Artificial Intelligence and Machine Learning; FM, Foundation model; LI, Lead identification; LO, Lead optimization; R& D, Research and development; TA, Target assessment
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Financial Excellence and Digitalization Alan Hippe CFO Roche Group
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Overview of key priorities Scalable automation and AI implementation driven by business process transformation 103 Scalable automation and AI implementation driven by business process transformation Efficiency in R&D through operational excellence and resource allocation Disciplined capital allocation to maximize long-term value creation
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104 AI strategic framework Leverage AI to increase effectiveness, transform business processes and realize value at scale …supported by four strategic pillarsStrategy developed for three levels of AI… EverydayAI Big Ideas Reshape Embed Everyday Al technologies in daily work to increase effectiveness Reshape processes to realize value at scale from existing AI technologies Invest in Big Ideas that use AI to disrupt the industry with emerging technologies People & change Value & impact Tech offering Policy
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105 ASPIRE driving business transformation Integrated and standardized system enabling advanced analytics and data-driven decisions In scope Partially in scope Value chain processes Enabling Processes Idea to product (Lifecycle) Marketing plan to cash (Commercial) Plan to deliver products (Manufacturing & Supply Chain) Plan to deliver services Subscribe / license to retire digital products Demand to pay (Procurement) Record to analyze (Finance) Plan to retire fixed assets Manage IT Manage quality & operational compliance Develop and manage business capabilities Conga iCollab Selection of solutions fully integrated in the ASPIRE portfolio Value Chain Processes Enabling Processes One common standard globallyMaster Data Transactions ASPIRE implementation (by year end 2026) 100% 80% 10% CorporatePharmaDiagnostics
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106 ASPIRE enabling productivity and efficiency Automation and agentic workflows to drive meaningful gains post-deployment Deploying ASPIRE (Status Sep 2026) ▪ Complex deployment of greenfield ASPIRE template and ecosystem: ▪ 118 company codes (44% deployed) ▪ ~950 process activities enabled1 ▪ 98% adherence to template ▪ Early value deployment and first benefits realized ▪ Full roll-out by 2029 Gains to be realized 2-5 years post-deployment Sustained productivity and efficiency enabled by ASPIRE Harmonization and standardization: ▪ Data ▪ Processes ▪ Systems Automation and AI enablement: ▪ Broad and simplified application ▪ Business insights at speed 1. Process classification framework according to APQC (American Productivity & Quality Center): Process activities are the ke y steps within the process chain that enable the 11 end -to-end processes, e.g. “Plan to deliver products (Manufacturing & Supply Chain)”
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Scalable automation and AI implementation driven by business process transformation Efficiency in R&D through operational excellence and resource allocation Disciplined capital allocation to maximize long-term value creation Overview of key priorities Disciplined capital allocation to maximize long-term value creation 107
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Sustainable financial development creating financial flexibility Balanced investments to support next wave of innovation while maintaining attractive shareholder returns 108Totals and subtotals may include differences due to rounding 69.7 -18.3 -32.2 -12.7 -4.6 -18.2 -16.2 Net Debt 2021 Operating FCF Dividend M&A All other effects Net Debt 2025 Roche net debt development 2021-2025 Core R&D 2022-2025: CHF –51.8bn (~12.9bn p.a.) Invest. in PP&E 2022-2025: CHF -14.5bn (~3.6 p.a.) Invest. in IA 2022-2025: CHF -5.5bn (~1.4 p.a.) CHFbn ~17.4 p.a. ~8.0 p.a. ~3.2 p.a. Non-operating FCF ~4.6 p.a. Taxes -14.6 (~3.6 p.a.) Treasury -3.7 (~0.9p.a.) ~1.1 p.a. -5.5bn 2022-2025: CHF 18.2bn (~4.6bn p.a.) for business development incl. intangible assets CHF -5.5bn (~1.4 p.a.)
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109 Group sales, Core OP and COP margin momentum past 5 years Accelerating growth after successfully navigating AHR cliff and COVID-19 pandemic Group sales and Core OP indexed at baseline, growing with CER/CHF rep growth rates of each year; CAGR calculated based on CER /CHF rep growth rates of each year; CER=Constant Exchange Rates; AHR: Avastin, Herceptin and Rituxan/MabThera; CAGR=Compound Annual Growth Rate; Source: Roche Finance Report 2021 -2025 Sales growth CHF rep vs CER 2021 2022 2023 2024 2025 -24% COP margin growth CHF rep vs CER CAGR 0% (CHF) 2021 2022 2023 2024 2025 -17% CAGR -1% (CHF) CAGR +7% (CER)CAGR +4% (CER) 2025: +7% (CER) 2024: +7% (CER) 2025: +2% (CHF)2024: +3% (CHF) 2025: +13% (CER) 2024: +14% (CER) 2025: +5% (CHF)2024: +8% (CHF) Core OP growth CHF rep vs CER 2021 2022 2023 2024 2025 -3.5%p COP margin development (CHF) COP margin development (CER) 2025: +1.9%p (CER) 2024: +2.1%p (CER) 2025: +1.1%p (CHF) 2024: +1.7%p (CHF) Group sales growth CAGR 2011-25: CER: +5%; CHF +3% Group Core OP growth CAGR 2011-25: CER: +6%; CHF +3% Group COP margin development 2011-25: CER: +6.4%p; CHF -0.1%p
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110 Roche investments worldwide (2016-2025) Strategic investments in R&D and manufacturing with complete value chain in key markets to ensure resilience 1. Percentage of Roche sales in 2025; totals and subtotals may include differences due to rounding; 2. Investments rest of wo rld 2016-2025: CHF 6bn; DP: Drug product investments in R&D and CAPEX (2016-2025)2CHF 158bn commitment into R&D and PP&E in the U.S. by 2029USD 50bn further investments planned at Basel site CHF 1.4bn Biologics Small Molecules Cell and Gene Therapy San Diego South San Francisco Hillsboro Philadelphia Holly Springs (under construction) Basel/ Kaiseraugst Mannheim Penzberg Singapore Shanghai (Biologics DP under construction) Tokyo Pharma manufacturing Oceanside Peptides USA thereof R&D thereof CAPEX % of Group sales1 % of Pharma sales1 CHF 64bn CHF 55bn CHF 10bn 48% 53% Asia (incl. Chugai) thereof R&D thereof CAPEX % of Group sales1 % of Pharma sales1 CHF 21bn CHF 13bn CHF 8bn 19% 15% Europe thereof R&D thereof CAPEX % of Group sales1 % of Pharma sales1 CHF 67bn CHF 50bn CHF 17bn 24% 19%
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111 Manufacturing: Network optimization and productivity improvement Freeing up resources to invest in new modalities, including peptides within existing budget CER: Constant Exchange Rates (avg. full year 2025 as basis calculating back with the CER growth rate of the respective year); COGS + PC: Manufacturing cost of goods sold and period costs Biologics network optimization since 2018 CVRM manufacturing strategy 2018 2019 2020 2021 2022 2023 2024 2025 6x faster volume growth Volume CAGR +12% COGS + PC CAGR +3% +19% +117% Volume and COGS+PC development1 rebased to 100 ▪ Clinical supply: Secured through several CDMOs ▪ Commercial supply: Optimized mix of in-house capacity and CDMOs, building resilient supply chains (regional & dual-sourced) ▪ Initial capacity secured through CDMO network ▪ Internal capacity (Holly Springs) operational by 2029, funded out of existing CAPEX budget Efficient site ramp-up via digital twins, reusable templates and standardized & harmonized data, processes, and systems.
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Overview of key priorities Efficiency in R&D through operational excellence and resource allocation 112 Scalable automation and AI implementation driven by business process transformation Efficiency in R&D through operational excellence and resource allocation Disciplined capital allocation to maximize long-term value creation
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113 R&D Excellence: Optimization across portfolio and operations R&D savings achieved since 2024; existing initiatives expected to deliver additional savings 1. Source: Internal data including Spark, Flatiron, RMCS, PHC; E: Estimated savings by year -end 397 397 906 1,878 509 296 2024 2025 2026E 55 2030E 397 906 1,203 1,933 Net new Compounding Recurring savings (net new + compounding) in CHFm1One-off savings in CHFm1 Savings with long-lasting impact, reducing the cost base e.g. PD capacity optimization, clinical sourcing (vendor consolidation) 57 57 440383 316 2024 2025 2026E 57 440 755 One-off Prior years Non-recurring cost reductions e.g. portfolio prioritization (stopping programs early)
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114 R&D Excellence: 184 cost optimization initiatives identified Continued focus on excellence to deliver future portfolio in the most efficient way 184 cost optimization initiatives identified Key levers and opportunity areas across R&D ▪ Best-fit operating model; improve organizational structure and right-size capacity aligned to portfolio planning ▪ Efficient processes; reduce non-portfolio work and optimize processes through standardization and automation ▪ Best-cost footprint for repeatable standard task ▪ Vendor and demand management 9 2910 10 10 32 13 20 52 26 23 16 71 21 24 258 56 70 184 pRED gRED PD Total Best-fit operating model Efficient processes Best-cost footprint External vendor & demand management
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115 R&D Excellence: Resource reallocation to higher ROI projects CHF ~2bn will be reallocated to transformative programs and productivity initiatives by YE 2026 1. Source: Internal data including Spark, Flatiron, RMCS, PHC; AI: Artificial intelligence; BD: Business development; E: Esti mated savings by year-end; NME: New molecular entity; Note: Fast-track assets: afimkibart, enicepatide, trontinemab Reallocation of R&D budget in 2024-2026E (CHFm)1 Outcomes achieved through resource reallocation ▪ Enter CVRM as new therapeutic area via external innovation ▪ Maximize assets with transformational potential in existing therapeutic areas (e.g. giredestrant) ▪ Accelerate “fast track” and other key programs to ensure timely delivery (e.g. trontinemab, afimkibart, enicepatide, zilebesiran, prasinezumab) ▪ Increase investment in future capabilities and technology to enable sustained R&D efficiencies 454 892 612 R&D savings 2026E 2025 2024 1,958 486 364 1,108 Reallocation by investment type 1,958 Funding for BD NMEs Fast track & new PivGos Future capabilities (e.g. lab-in-the-loop, organoids)
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Oncology/Hematology Levi Garraway CMO and Global Head of Product Development
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117 Significant pipeline progress since Pharma Day 2025 Leveraging both internal capabilities and external innovation to rejuvenate Oncology/Hematology pipeline *Phase III to be initiated; **including deals pending closure; aHUS: Atypical hemolytic uremic syndrome; ADC: Antibody-drug conjugate; BD: Business development; BIC: Best in class; BTK: Bruton's tyrosine kinase; CLL: Chronic lymphocytic leukemia; (e/m)BC: (Early/metastatic) breast cancer; FIC: First in class; FL: Follicular lym phoma; HER2: Human Epidermal Growth Factor Receptor 2; HR: Hormone receptor; MIBC: Muscle-invasive bladder cancer; NSCLC: Non-small cell lung cancer; SCLC: Small cell lung cancer; TCE: T -cell engager Oncology/Hematology 2 NME Ph III decisions5 positive Ph III readouts 71% FIC/BIC assets External innovationKey late-stage successes Pipeline progress tambotatug pelitecan SCLC, NSCLC bexobrutideg R/R CLL giredestrant (lidERA) Adj. HR+/HER2- eBC divarasib (KRASCENDO 1) 2L+ KRAS G12C+ NSCLC Tecentriq (IMvigor011) MIBC Lunsumio (CELESTIMO) 2L+ FL PiaSky (COMMUTE-a/p) aHUS 6 platform deals / research collaborations** Novel candidates for challenging targets Small molecules Next-gen ADCs with novel cytotoxic payloads ADC platform Next-gen breast cancer targets Target discovery Degrader- Antibody Conjugates (DACs) DAC platform Novel antibody target combinations Bispecific antibodies Targeting cell cycle regulators in breast cancer Drug discovery 4 assets added through BD Ph III Tam-Peli (B7-H3 ADC) Lung CDH17 ADC CRC CD79a x CD19 x CD3 TCE Hem Ph III*Ph IPreclinical bexobrutideg (BTK degrader) Hem 28 NMEs in clinical development 18 Ongoing Ph III studies
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118 Oncology solid tumor pipeline Focus on breast and lung cancer as end-to-end investment areas **Phase III to be initiated; RG-No: Roche/Genentech; CHU: Chugai managed; 1. MediLink managed; 2. Innovent managed; 3. In collaboration with Hansoh Pharma; 4. In collaboration with BioNTech; AR: Androgen receptor; (e)BC: (Early) breast cancer; CDK: cyclin-dependent kinase; (Early)breast cancer; HCC: Hepatocellular carcino ma; HER2: Human epidermal growth factor receptor 2; HR+: Hormone receptor positive; (N)SCLC: (Non)small cell lung cancer; PDAC: pancreatic ductal adenocarcinoma; TKI: tyrosine kinase inhibit or RG6171 giredestrant RG6330 divarasib RG6505 Pan-RAS inhibitor RG6537 AR Degrader RG6620 KRAS G12D inhibitor RG6648 cMET ADC1 RG6810 DLL3 ADC2 RG6852 undisclosed RG6975 CDH17 ADC3 CHU codrituzumab CHU ROSE12 (anti-CTLA-4 switch Ab) CHU MINT91 CHU AUBE00 (Pan-KRAS inhibitor) CHU clesitamig (DLL3 trispecific Ab) CHU AQUA07 (allosteric ALK inhibitor) Phase I Phase II Phase III Registration Oncology/Hematology Breast cancer Lung cancer Prostate cancerColon cancer HCC Multiple indications Itovebi eBC HR+RG6114 RG6180 autogene cevumeran4 PDAC CDK4/2 inhibitor eBC HR+RG6794 ZN-1041 (HER2 TKI) eBC HR+RG6596 giredestrant multiple HR+ BC indicationsRG6171 RG6330 divarasib NSCLC Itovebi multiple BC indicationsRG6114 Alecensa LA stage III NSCLCRG7853 giredestrant HR+ BC adj and metastaticRG6171 Tecentriq stage III dMMR/MSI-H colon cancer RG7446 Tecentriq multiple indicationsRG7446 RG3502 Kadcyla HER2+ eBC high risk Small molecule Antibody Bispecific/trispecific Neoantigen vaccine Antibody-drug conjugate Cyclic peptides Protein degraders Itovebi CRPCRG6114 RG6919 tambotatug pelitecan1 SCLC** Itovebi HR+ BC PIK3CA wtRG6114 Pancreatic cancer
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119 Breast cancer: Portfolio of potentially BIC molecules to improve SoC Targeting key signaling nodes that drive etiology and progression of BC HER2 Itovebi: PI3K inhibitor with potentially greater safety margins allowing for combination with ET and CDK4/6i at standard doses with proven substantial benefit PI3K AKT mTOR 2 Giredestrant: Next generation SERD with the potential to become the ET backbone treatmentER1 RG6794 (GDC-4198): Highly potent CDK4/2 inhibitor with substantial activity against CDK2 to address a key mechanism of resistance to CDK4/6i CDK3 RG6596 (ZN-1041): Highly selective, brain-penetrant HER2 TKI, potentially combinable with established anti-HER2 backbonesHER24 Differentiated molecules with a potential to redefine BC treatment paradigm as monotherapy and in combinations Adapted from: Brufsky AM & Dickler MN. Oncologist 2018; BC: Breast cancer; BIC: Best -in-class; CDK: Cyclin-dependent kinase; ET: Endocrine therapy; HER2: Human epidermal growth factor receptor 2; HR+: Hormone receptor positive; PI3K: Phosphatidylinositol 3 -kinase; SERD: Selective estrogen receptor degrader; SoC: Standard o f care; TKI: Tyrosine kinase inhibitor Oncology/Hematology 4 2 1 3
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120 Giredestrant: Differentiated SERD with BIC potential *In preclinical studies; 1. Guan J & Zhou W, et al. Cell 2019; 2. Zhou W, et al. Cell Chemical Biology, 2026; 3. Liang J, et al. J Med Chem 2021; 4. Metcalfe C, et al. Cancer Res 2020; 5. Roche data on file; 6. van Kruchten M, et al. Cancer Discov 2015; 7. Not corrected for plasma protein binding; Human Cave (uM) = AUC0-24 ng*hr/mL/24 hr/MW; giredestrant: AUC0-24 (C2D1), 4320 ng*hr/mL [Cancer Res. Commun. 2023]; camizestrant: AUCτ (C1D15), 862.3 ng*hr/mL [Ann. Oncol. 2024]; palazestrant: Cave,ss (C2D1), 322 ng/mL [Breast Cancer Res. 2025]; vepdegestrant: AUC0-24 (C1D15), 15,459 ng•hr/mL (western patients) [Int. J. Clin. Oncol. 2025]; imlunestrant: AUCτ (C1D15), 2480 ng*hr/mL [J. Clin. Oncol. 2024]; Elacestrant: AUC0-24 (C1D6) 2440 ng*hr/mL [FDA approval label]; CDKi: Cyclin dependent kinase inhibitor; HR+: Hormone receptor positive; SERD: Selective estrogen receptor degrader; SoC: Standard of care Deep and sustained ER inhibition; superior potency over other SERDs*, allowing lowest therapeutic dose in class Selective ER degrader (SERD)1 ▪ Giredestrant suppresses ER signaling through ER immobilization and subsequent degradation ▪ Therapeutic potency is most associated with ER immobilization2 ▪ Full ER antagonist achieving deep and sustained ER inhibition ▪ Highest target coverage among SERDs Full ER antagonist2,6,7 Preclinical potency3-5 ▪ Highest preclinical potency vs other oral SERDs, allowing lowest therapeutic dose in the class ▪ Combinable with CDK inhibitors ▪ Well tolerated at all doses, with no dose-limiting toxicities 0 1,000 2,000 3,000 4,000 giredestrant 30mg camizestrant 75mg palazestrant 90mg imlunestrant 400mg elacestrant 400mg vepdegestrant 200mg CAMA-1 MCF-7 T-47D Human Cave/IC50 Target coverage at therapeutic dose Oncology/Hematology
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121 Giredestrant: Positive results in both adjuvant and metastatic HR+ BC 1. Bardia et al., SABCS 2025; 2. Mayer et al., ESMO 2025; CDKi: Cyclin dependent kinase inhibitor; CI: Confidence interval; DoR: Duration of response; ESR1m: ESR1 mutation; ET: Endocrine therapy; HER2: Human epidermal growth factor 2; HR: Hazard ratio; HR+: Hormone receptor positive; iDFS: invasive disease-free survival; INV-PFS: Investigator-assessed progression free survival; (m)BC: (Metastatic) breast cancer; ORR: Objective response rate; OS: Overall survival; SERD: Selective estrogen receptor degrader; SOC: Standard of care First and only oral SERD to show positive Ph III results in adjuvant HR+ BC Ph III (lidERA) iDFS results in adjuvant HR+ BC1 ▪ 30% reduction in recurrence or death vs SoC ET ▪ Clear positive OS trend (HR=0.79 at 32m) ▪ Lower discontinuation rates vs SoC ET in adjuvant BC; no photopsia ▪ PDUFA date November 30 under priority review ▪ PFS improvement in both ESR1m (HR=0.38) and ITT populations (HR=0.56) ▪ Clear OS trend favoring giredestrant across subgroups ▪ PDUFA date December 18 (US filing accepted in ESR1m patients) Ph III (evERA) INV-PFS results in post-CDK4/6i HR+ mBC2 Oncology/Hematology 0 6 12 18 24 30 36 42 100 80 70 97.7% 96.9% 94.6% 92.3% 92.4% 89.6% Time (months) 0 6 12 18 24 30 36 42 IDFS (%) 100 80 60 40 20 0 90 No. at risk gire SOC ET 2084 2086 2021 2016 1969 1958 1932 1898 1716 1683 1088 1048 345 325 26 25 Events, n (%) gire (n=2084) 140 (6.7) placebo (n=2086) 196 (9.4) Stratified HR, 0.70; p = 0.0014 Median, mo gire + eve (n=102) 9.99 SOC ET+ eve (n=105) 5.45 Stratified HR, 0.38; p < 0.0001 INV-PFS (%) 102 105 85 67 61 35 52 25 28 10 13 2 6 1 2 2 21 1 0 3 6 9 12 15 18 21 24 27 100 80 60 40 20 0 Time (months)No. at risk gire + eve SOC ET + eve ESR1m population 66.1% 40.5%38.1% 15.2%
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Giredestrant: Evidence generation in eBC to maximize opportunity Ph I/III with atirmociclib (CDK4i)* and Ph III in ctDNA-guided** to be initiated; abema combo data expected Q4 ‘26 *Pfizer-managed; Phase III gated on successful outcome of Ph I; **Pending final agreement, in collaboration with Natera and Alliance Foundation Trials 1. Risk definitions vary according to guidelines and tools used: stage at diagnosis based on internal estimates using SEER data; intermediate risk encompasses stage I, N0 included in the lidERA criteria, but excluded in NATALEE; †AI sensitive defined as patients who relapse >1yr after completion of adjuvant therapy; AI: Aromatase inhibitor; CDK: Cyclin-dependent kinase; CDP: Clinical development program; ESR1m: ESR1 mutation; ET: Endocrine therapy; FPI: First patient in; HER2: Human Epidermal growth factor receptor 2; HR+: Hormone receptor positive; IIS: Investigator initiated study (m)BC: (Metastatic) breast cancer; MRD: Minimal residual disease; PFS: Progression free survival; SoC: Standard of care 122 Oncology/Hematology metastatic BC Ph III lidERA giredestrant mono Tx Ph IIIb kalitERA giredestrant mono Tx Ph IIIb novERA giredestrant mono Tx SURGERY Intermediate risk (~10%)1 High risk (~15%)1 Low risk (55-60%)1 Medium risk (15-20%)1 Positive study Ongoing/to be initiated gire + CDK4/6i Non-registrational 2 giredestrant (lidERA) Adjuvant HR+/HER2- BC 8 giredestrant (pionERA) 1L HR+/HER2- mBC (ET-resistant, enriched for ESR1m) 7 giredestrant (persevERA) 1L HR+/HER2- mBC (ET-sensitive) giredestrant (evERA) 2L+ HR+/HER2- mBC9 gire + GDC-4198 (MoonROSE) 2L+ HR+/HER2- mBC gire + Phesgo (heredERA) 1L maintenance HR+/HER2+ mBC Ph Ib/II ongoing, FPI in Ph II achieved10 Readout 2028 Readout 2028 CDK4/6i single arm substudy Primary endpoint not met; numerical PFS improvement abemaciclib 100 pts (IA Q4 ’26); ribociclib 300 pts to be initiated 1 giredestrant (novERA) Adjuvant HR+/HER2- BC (AI-intolerant)4 giredestrant (coopERA) Neodjuvant HR+/HER2- BC1 Ph IIIb ongoing giredestrant (kalitERA) Adjuvant HR+/HER2- BC (all risk and switch from CDKi)3 Ph IIIb FPI imminent Adj Neoadj Interim OS data 2027 Ph I/III giredestrant + atirmociclib (CDK4i)* giredestrant (AFT- 70 NAVIGATE)** MRD-guided CDKi usage6 Ph III (IIS) to be initiated giredestrant + atirmociclib* giredestrant + atirmociclib intermediate to high risk 5 Ph I/III* to be initiated early BC Ph III AFT-70 NAVIGATE** gire mono, MRD-guided 2 3 4 5 6 Adjuvant studies added since lidERA readout ET ET ET±CDK4/6i ET±CDK4/6iSoC:
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2 giredestrant (lidERA) Adjuvant HR+/HER2- BC CDK4/6i single arm substudy abemaciclib 100 pts (IA Q4 ’26); ribociclib 300 pts to be initiated giredestrant (novERA) Adjuvant HR+/HER2- BC (AI-intolerant)4 giredestrant (coopERA) Neodjuvant HR+/HER2- BC1 Ph IIIb ongoing giredestrant (kalitERA) Adjuvant HR+/HER2- BC (all risk and switch from CDKi)3 Ph IIIb FPI imminent Interim OS data 2027 giredestrant (AFT- 70 NAVIGATE)** MRD-guided CDKi usage6 Ph III (IIS) to be initiated giredestrant + atirmociclib* giredestrant + atirmociclib intermediate to high risk 5 Ph I/III* to be initiated early BC Giredestrant: Additional opportunity in mBC Ph III studies in 1L mBC HR+/HER2- (pionERA) and HR+/HER2+ (heredERA) ongoing; FPI for Ph II CDK4/2i combo 1. Risk definitions vary according to guidelines and tools used: stage at diagnosis based on internal estimates using SEER data; intermediate risk encompasses stage I, N0 included in the lidERA criteria, but excluded in NATALEE; †AI sensitive defined as patients who relapse >1yr after completion of adjuvant therapy; AI: Aromatase inhibitor; CDK: Cyclin-dependent kinase; CDP: Clinical development program; ESR1m: ESR1 mutation; ET: Endocrine therapy; FPI: First patient in; HER2: Human Epidermal growth factor receptor 2; HR: Hormone receptor; (m)BC: (Metastatic) breast cancer; PFS: Progression free survival; SoC: Standard of care 123 8 giredestrant (pionERA) 1L HR+/HER2- mBC (ET-resistant, enriched for ESR1m) 7 giredestrant (persevERA) 1L HR+/HER2- mBC (ET-sensitive) giredestrant (evERA) Post-CDKi HR+/HER2- mBC9 gire + CDK4/2i (MoonROSE) 2L+ HR+/HER2- mBC gire + Phesgo (heredERA) 1L maintenance HR+/HER2+ mBC Ph Ib/II ongoing, FPI in Ph II achieved10 Readout 2028 Readout 2028 Primary endpoint not met; numerical PFS improvement Oncology/Hematology metastatic BC SURGERY Intermediate risk (~10%)1 High risk (~15%)1 Low risk (55-60%)1 Medium risk (15-20%)1 Positive study Ongoing/to be initiated gire + CDK4/6i Non-registrational 1 Adj Neoadj ET ET ET±CDK4/6i ET±CDK4/6iSoC: AI-resistant (40%)De novo/AI-sensitive† (60%) gire + mTORi gire + CDK4/2i gire + CDK4/6i 7 gire + CDK4/6i 8 gire + mTORi 9 9 10 1L 2L+ 7
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124 Itovebi: Defining new SoC in PIK3CAm HR+ BC Exploring combinations with giredestrant and CDK inhibitors (CDK4/6i, CDK4/2i, CDK4i) PI3Kα inh. with dual MoA Fold change (inavolisib vs alpelisib) Potency/selectivity1 ▪ Highly potent and selective PI3Kα inhibition and degradation ▪ Better in vivo efficacy ▪ Greater safety margins allow for combination with ET and CDK4/6i at standard doses 1. Jhaveri KL et al., SABCS 2023; 2. Turner N et al., ASCO 2025; AE: Adverse event; CDK: AI: Aromatase inhibitor; Cyclin -dependent kinase; CDP: Clinical development program; ET: Endocrine therapy; HER2: Human epidermal growth factor receptor 2; HR: Hazard ratio; HR+: Hormone receptor positive; (m)BC: (Metastatic) breast cancer ; mCRPC: Metastatic castration-resistant prostate cancer; MoA: Mechanism of action; ORR: Objective response rate; OS: Overall survival; PI3K: Phosphoinositide 3 -kinase; PIK3CAm: Phosphatidylinositol 3 -kinase, catalytic, alpha mutated; PFS: Progression-free survival; SoC: Standard of care Oncology/Hematology 58x 6x 26x 32x Pi3Kα potency β Pi3Kα selectivity vs δ γ Clinical development program inavolisib (INAVO121) Post-CDK4/6i HR+/HER2- mBC Readout 2026 inavolisib (INAVO123) 1L HR+/HER2- mBC (ET sensitive) Ongoing inavolisib (neoTOV) untreated, stage II—III HR+/HER2- BC Ph II ongoing inavo + Phesgo (INAVO122) 1L HER2+ mBC Readout 2027 inavolisib (INAVO120) 1L HR+/HER2- mBC (AI resistant) Approved ▪ Exploring combinations with giredestrant and CDK inhibitors (CDK4/6, CDK4, CDK4/2) in Ph Ib/II HR+/HER2- mBC ▪ Ph II (InavoPC) study in mCRPC ongoing ▪ Potential to expand into other tumors: Ph Ib/II signal seeking studies ongoing Ph III (INAVO120) OS results in 1L HR+/HER2- mBC2 ▪ Itovebi + palbociclib + fulvestrant reduced risk of death >30% compared with palbociclib + fulvestrant alone ▪ PFS benefit maintained during longer follow-up (17.2m vs 7.3m; HR=0.42) ▪ Low discontinuation rates due to AEs (6.8%) and hyperglycemia (1.2%), confirming manageable tolerability 0 25 50 75 100 0 3 6 9 12 15 18 21 24 27 30 33 36 4239 Months OS (%) 45 5148 96.8 87.0 74.3 65.8 56.590.1 76.7 67.2 56.3 46.3 Inavolisib Placebo Inavolisib (n=161) 34.0 Placebo (n=164) 27.0 Stratified hazard ratio, 0.67, p = 0.0190 Median, months inavolisib 1L HR+/HER2- PIK3CA wt mBC Ph II ongoing
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125 RG6794 (GDC-4198): CDK4/2i to overcome CDK2-driven resistance 1. Wander SA, et al. Cancer Discov. 2020;10:11174-1193. 2. Turner NC, et al. J Clin Oncol. 2019;37(14):1169 -1178. 3. Wander S, e t al. Poster presentation (PO3-18-06) at 2023 SABCS; 4. Wander S, et al. Poster presentation (PS1-11-07) at 2025 SABCS; BC: Breast cancer; BIC: Best -in-class; BID: Twice daily; CDK: Cyclin -dependent kinase; HR+ BC: Estrogen receptor positive breast cancer; ET: Endocrine therapy; HER2: Human epidermal growth factor receptor 2; HR+: Hormone receptor positive CDK4/6i resistance mechanism1,2 ▪ Highly potent CDK4 inhibitor with substantial activity against CDK2 ▪ More durable cell cycle arrest than approved CDK4/6is in preclinical studies ▪ CDK4/6i resistance remains a challenge; nearly all patients progress ▪ Data suggest that CDK2 activity is a potential mechanism of resistance IC50 (nM) CDK4 CDK2 GDC-4198 0.3 4.6 abemaciclib 0.8 270 palbociclib 2.3 >103 Encouraging activity in post-CDK4/6i setting; FPI in Ph II (MoonROSE) in combination with giredestrant Activity against CDK4 & CDK23 Preliminary activity in post-CDK4/6i setting4 ▪ Preliminary evidence of disease control with sustained responses in heavily pre-treated post-CDK4/6i setting ▪ Well-tolerated as a single agent and in combination with ET; safety profile consistent with approved CDK4/6i ▪ Achieved FPI in Ph II (MoonROSE) study of GDC-4198 + gire vs abema + gire in CDK4/6i-experienced HR+ mBC Oncology/Hematology
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126 RG6596 (ZN-1041): Highly selective, brain-penetrant HER2 TKI in Ph II/III Potential for combinations to improve HER2+ BC outcomes and prevent brain metastases 1. Ma F, et al. ASCO 2023 (Abstract 1040; poster presentation); 2. Andre et al, Ann Oncol 2024; 3. Lin NU, et al. ASCO 2026 (Abstract 1055; poster presentation); * AUCbr,u and AUCpl,u are measurements of the unbound drug concentrations over time in the brain and plasma, respectively; the ratio of these two values is the gold-standard assessment of brain penetration for drugs. A higher AUCbr,u/AUCpl,u ratio indicates a greater ability of the drug to enter and remain in the CNS from the systemic circulation; AUC: Area under the curve; BBB: Blood-brain barrier; BCRP: Breast cancer resistance protein; BC: Breast cancer; BM: Brain metastasis; CNS: Central nervous system; DCR: Disease control rate; HER2: Human epidermal growth factor receptor 2; ORR: Objective response rate; PH: Phesgo; P-gp: P-glycoprotein; T-DXd, trastuzumab deruxtecan; TKI: Tyrosine kinase inhibitor ZN-1041 properties1 ▪ Promising clinical activity in combination with standard anti-HER2 therapies (T-DXd and Phesgo) ▪ High disease control in combination with T-DXd (ORR >65%; DCR >90%) and notable continued responses in the PH maintenance setting (ORR >30.8; DCR 100%) ▪ Manageable safety profile, with predictable toxicity and low treatment discontinuations ▪ Initiated Phase II/III (BREnnA) study vs tucatinib in combination with Herceptin and capecitabine Global Phase 1c study results3 ▪ Despite recent advances in treating brain metastases, about half of patients still face CNS progression2 ▪ ZN-1041 is differentiated by high BBB permeability and CNS retention ▪ Better pre-clinical activity than tucatinib TKI AUCbr,u/ AUCpl,u* Efflux transporter (P-gp/BCRP) substrate? tucatinib 0.004 Yes lapatinib 0.010 Yes neratinib 0.013 Yes pyrotinib 0.024 Yes epertinib 0.080 Yes ZN-1041 0.470–0.770 No –100 –80 –60 –40 –20 0 20 40 + + + ++ + + + ++ –100 –80 –60 –40 –20 0 20 40 + + + ++ +++ + + + * + –100 –80 –60 –40 –20 0 20 40 + + Best change in sum of diameters of target tumor lesions from baseline (%) ZN-1041 + PH (n = 13)† ZN-1041 600 mg + T-DXd (n = 21) ZN-1041 800 mg + T-DXd (n = 20) CR PR SD PD + Patients with BM * Patient had ~45% reduction in tumor size, but also had a new lesion; therefore, the best overall response was progressive disease. † Patients with measurable disease at baseline Oncology/Hematology
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127 Multiple approaches to (K)RAS signaling inhibition, incl. combinations Leveraging Roche/Genentech/Chugai R&D engines to build a portfolio diversified across targets and mechanisms (e/m)NSCLC: (Early/metastatics) non small cell lung cancer; H2H: Head -to-head Oncology/Hematology ▪ Diverse portfolio with mutant-selective and pan-RAS/pan-KRAS inhibitors provide optionality for mono and combination therapy regimens in lung cancer and beyond ▪ Divarasib (KRAS G12Ci) and RG76620 (KRAS G12Di) potential for differentiation through greater potency and selectivity versus others Roche RAS-targeted pipeline Molecule Indication Precl. Ph I Ph II Ph III Status divarasib 2L+ mNSCLC H2H vs sotorasib/adagrasib divarasib + pembro 1L mNSCLC divarasib eNSCLC (adjuvant) KRAS G12Di solid tumors panRASi solid tumors pan-KRASi solid tumors multiple undisclosed solid tumors Primary endpoint met FPI exp. H2’26 KRASCENDO 1 KRASCENDO 2 KRASCENDO 3 KRAS GDP ⇆ GTP OFF ⇆ ON GDP GEF GTP SWII EFFON vs OFF inhibitors Stabilize inactive GDP state (OFF) or GTP active state (ON) Catalytic inhibitors Catalyzes GTP hydrolysis and conversion to OFF state Orthosteric Blocks GTP binding site directly Switch II pocket Specific allosteric site, reshapes GTP binding site Allosteric Blocks effector docking (e.g. RAF)CYPA Tricomplex Molecular glue traps; current generation leverage Cyclophilin A
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128 Divarasib: Potentially BIC oral KRAS G12C inhibitor Positive Ph III (KRASCENDO 1) divarasib in 2L KRAS G12C mNSCLC (H2H vs sotorasib and adagrasib) 1. Purkey H. et al., AACR 2022; 2. Skoulidis et al., ASCO 2026 * 3 patients did not receive treatment, 1 patient received divarasib 200 mg; (c)ORR: (Confirmed) objective response rate; CR: Complete response; H2H: Head-to-head; LFT: Liver functional test; (m)NSCLC: (Metastatic) non-small cell lung cancer; (m)PFS: (Median) progression free survival; OS: Overall survival Potency and selectivity1 IC50 (nM) / selectivity divarasib 0.18 / 16,000 sotorasib 3.4 / >1,800 adagrasib 1.0 / 340 ▪ 5-25 times more potent and 10- 50 times more selective in vitro than sotorasib and adagrasib Oncology/Hematology ▪ Positive Ph III (KRASCENDO 1) divarasib in 2L+ mNSCLC ▪ PFS superiority vs approved KRAS G12Ci; OS significance reached at interim analysis ▪ No new safety signals were observed ▪ Selected as Presidential Symposium at ESMO 2026 Ph III (KRASCENDO 1) in 2L mNSCLC ▪ PD-L1 pos.: reduction in tumor size in all patients with a post-baseline assessment, cORR 73%, mPFS 19.3m; PD-L1 neg.: unconfirmed ORR of 70% ▪ Divarasib plus pembro had a manageable safety profile ▪ Potential to be established as first ‘chemo-free’ regimen in 1L KRAS G12C NSCLC, regardless of PD-L1 status Ph II (KRASCENDO 170) in 1L NSCLC2 divarasib (400mg QD) sotorasib (960mg QD) or adagrasib (600mg BID) Primary endpoint: ▪ PFS per BICR Secondary endpoints: ▪ OS ▪ cORR ▪ PROs ▪ DoR ▪ Metastatic/ locally advanced KRAS G12C-mut NSCLC ▪ ≥1 but ≤3 lines of prior systemic therapy ▪ PD-L1 all- comers N=338 1:1 PD-L1 Positive Cohort, 400mg (N=59)*
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129 Tambotatug pelitecan: Potentially BIC B7-H3 ADC Accelerating global clinical development across key solid tumor indications 1. Ashman, et al. Chem Soc Rev 2022; 2. Cazzamalli, et al. Nat Cancer 2025; 3. Cai, et al. AACR 2023 (Abs 596), and adapted from MediLink materials available at MediLink website; 4. Roche internal study results; ADC: Antibody drug conjugate; DAR: Drug-antibody ratio; NSCLC: Non small cell lung cancer; SCLC: Small cell lung cancer Next gen. B7-H3 targeted ADC with dual-release mechanism1,2,3 ▪ Differentiated by a potent payload, high DAR=8 and highly hydrophilic and plasma-stable linker to minimize premature payload release and limit off- target toxicity, critical for future combination treatments ▪ Dual-release of payload: classical internalization amplified by tumor microenvironment activation Oncology/Hematology 88% 90% 97% 73% SCLC NSCLC Prostate cancer Breast cancer % tumor B7-H3 positivity4 expressing (>0) no expression (0) Global studies to initiate 1H’27 Global studies under consideration ▪ B7-H3 is broadly expressed across key tumors with limited expression in healthy tissue ▪ Accelerating clinical development with multiple global trials across indications, starting with SCLC Foundational, potentially multi-indication asset ADC B7-H3 Tumour microenvironment Tumour cell expressing antigen Tumour cell without antigenPayload uptake into neighbouring cells (“bystander effect”) Payload Extracellular payload release Intracellular payload release Cells in TME expressing antigen (e.g. CAF, TAMs) Target expression on non-tumor cells contributes to ADC accumulation in TME Payload release due to cleavage in tumor microenvironment 1 2 First global Ph III study to initiate Q4 ’26
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Positive Ph III (TAISHAN-302) results in 2L SCLC in Chinese patients Statistically significant improvement in PFS and OS; potentially differentiated safety profile with low ILD rates 1. Zhang et al. WCLC 2026; cORR: Complete overall response rate; ILD: Interstitial lung disease; NSCLC: Non -small cell lung cancer; PFS: Progression free survi val; OS: Overall survival; SCLC: Small cell lung cancer; TRAE: Treatment-emergent adverse events Ph III (TAISHAN-302) OS results1 ▪ Statistically significant and clinically meaningful OS improvement vs topotecan (54% reduction), PFS (71% reduction) and cORR (59.1%) ▪ Benefit maintained across all subgroups, incl. patients with baseline metastasis; intracranial PFS, OS and DCR superiority vs topotecan ▪ Significant proportion of patients with poor prognostic factors, e.g. metastatic burden, short chemo-free interval Oncology/Hematology Tam-Peli (N = 225) Topo (N = 226) Median OS, months 13.3 9.4 HR 0.46; P <0.0001 130 OS Tam-Peli (N = 224) Topotecan (N = 217) Median duration of exposure, weeks (range) 31.1 (3, 72.9) 10.1 (3, 70.4) TRAEs, n (%) All grades 221 (98.7) 216 (99.5) Grade ≥3 104 (46.4) 162 (74.7) Serious TRAEs 58 (25.9) 79 (36.4) Leading to dose interruption 78 (34.8) 80 (36.9) Leading to dose reduction 58 (25.9) 80 (36.9) Leading to discontinuation 13 (5.8) 6 (2.8) Leading to death 0 1 (0.5) Ph III (TAISHAN-302) safety1 ▪ Treatment-emergent ILD/pneumonitis events at 4.9% in the Tam- Peli arm vs 1.4% with topotecan; grade 3 events at 0.9% in each arm, and no grade 4 or 5 events ▪ Lower Grade ≥3 TRAE vs. topotecan (46.4% vs 74.7%) confirming favorable and manageable safety profile
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Hematology Matthew Hellmann SVP and Global Head of Oncology and Hematology Product Development
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132 Continuing to redefine the standard of care in hematology Oncology/Hematology Source: Zhang et al., Global burden of hematologic malignancies and evolution patterns over the past 30 years, Blood Cancer Journal 2023; DLBCL: Diffuse large B -cell lymphoma; FL: Follicular lymphoma; MCL: Mantle cell lymphoma; NHL: Non-hodgkin lymphoma; MM: Multiple myeloma; len: lenalidomide; Pd: pomalidomide and de xamethasone; MDS: myelodysplastic syndrome; MPNs: myeloproliferative neoplasms ; r/r: relapsed/refractory Pioneering new modalities and targets: ADCs, bispecifics, small molecule degraders MCL 4% MM 12% CLL 8% iNHL 8% Building on anchor assets with novel combinations in NHL Next-generation leadership in CLL Expanding into MM with differentiated modalities mAb Glycoeng. mAb ADC Bispecifics 2013 2019 2022/231997 2026+ Combinations & novel modalities 2016 SM Inhibitor bexobrutideg (BTK degrader) cevostamab (FcRH5 x CD3) P-BCMA-ALLO1 (Allogeneic CAR-T) CD79a x CD19 x CD3 (Trispecific) (CD20 mAb) (CD20 mAb) (BCL-2i) (CD79b ADC) (CD20x CD3) (CD20x CD3) DLBCL 22%
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Hematology R&D focus areas Building upon our leadership and experience with transformative medicines 133 Investing in key technologies to engage unique set of targets Degraders: Bexobrutideg (BTK degrader) has potential to overcome resistance mechanisms with BTK inhibition Building on top of anchor assets with novel combinations SKYGLO: Columvi + Polivy –R-CHP builds on top of POLARIX regimen as standard of care in 1L DLBCL Cevostamab: Novel target with lower risk of infection enables combinability in earlier lines Leverage best-in-disease assets, which offer the potential for cure / normalization of disease Zemocimig (NXT007): Potential to achieve hemostatic normalization Developing manageable regimens which can be used across treatment settings Hemlibra/zemocimig autoinjector: Continuing to improve administration with new delivery options Critical Capabilities Examples Improving patient experience Combinations Curative potential Oncology/Hematology Novel modalities
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134 Hematology pipeline Oncology/Hematology 1. In collaboration with Nurix Therapeutics; aHUS: Atypical hemolytic uremic syndrome; CLL: Chronic lymphocytic leukemia; DLBCL: Diffuse large B -cell lymphoma; FL: Follicular lymphoma; MCL: Mantle cell lymphoma; MDS: Myelodysplastic syndrome; MM: Multiple myeloma; R/r: Relapsed/refractory; VWD: Von Willebrand dise ase Ph I Ph II Ph III Registration PiaSky aHUSRG6107 Columvi monotherapy + combos heme tumors RG6026 Lunsumio 1L FL, 2L+ FLRG7828 SPK-8011QQ hemophilia ARG6797 RG6160 cevostamab r/r MM zemocimig (NXT007) hemophilia ARG6512 RG65381 P-BCMA-ALLO1 r/r MM Lunsumio monotherapy + combos heme tumors RG7828 Hemlibra Type 3 VWDRG6013 Columvi 1L DLBCL, 1L unfit DLBCL, r/r MCLRG6026 undisclosed r/r MMRG6733 undisclosed heme tumorsRG6735 Lunsumio + Polivy 2L+ DLBCLRG7828 bexobrutideg1 2L+ CLLRG74731 bexobrutideg combinations1 1L+ CLLRG74731 CLL MM Non-malignant heme NHL Small molecule Antibody Bispecifics Gene therapy Allogeneic CAR-T cells Protein degraders
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Data expected 2027 New Ph III study to be initiated in elderly, unfit, and frail pts Filed in US in Q2 (PDUFA: Feb 2027) Pivotal Ph I data expected 2027 (BTD) LPI achieved Met Primary Endpoint (PFS) 135 Extending the standard of care in NHL Oncology/Hematology 1. Zhang et al., Global burden of hematologic malignancies and evolution patterns over the past 30 years, Blood Cancer Journal 2023; * Sponsored by LYASRC; CLL: Chronic lymphocytic leukemia; DLBCL: Diffuse large B-cell lymphoma; FL: Follicular lymphoma; MCL: Mantle cell lymphoma; NHL: Non -hodgkin lymphoma; r/r: relapsed/refractory; BTD: breakthrough therapy designation Key Newsflow Indication Regimen Ph1 Ph2 Ph3 1L DLBCL Polivy + R-CHP 1L DLBCL Columvi + Polivy + R-CHP 1L DLBCL (unfit) Columvi + Polivy + R 2L+ DLBCL Lunsumio + Polivy 2L+ DLBCL Columvi + GemOx 3L+ DLBCL Columvi SKYGLO SUNMO STARGLO NP30179 EVERGLO POLARIX Indication Regimen Ph1 Ph2 Ph3 2L+ MCL Columvi 2L+ MCL Columvi GLOBRYTE Ph I Key NewsflowIndication Regimen Ph1 Ph2 Ph3 1L FL Lunsumio + len 2L+ FL Lunsumio + len 3L+ FL Lunsumio MorningLYTE* CELESTIMO GO29781 Approved or primary endpoint met Increasing the cure rate in DLBCL First-in-class potential in MCL Moving into earlier lines in FL Building on anchor assets with novel combinations
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50% 60% 70% 80% 90% R-CHOP POLARIX SKYGLO 1L DLBCL: SKYGLO has potential for BIC efficacy and safety Continuing to advance the standard of care in a curative setting 136 1. Topp M et al, ICML 2025; BIC: Best in class; CMR: Complete metabolic response; DLBCL: Diffuse large B cell lymphoma; FU: F ollow-up; HGBCL: High grade B-cell lymphoma; IRC: Independent review committee; NOS: Not otherwise specified; ORR: Overall response rate; PFS: Progression -free survival; Pola-R-CHP: Polivy + Rituxan + cyclophosphamide + hydroxydaunorubicin + prednisone; R -CHOP: Rituxan + cyclophosphamide + doxorubicin + vincristine + prednisone; SoC: Standard of care Ph Ib: 100% ORR with differentiated safety profile1 ▪ Polivy + R-CHP (POLARIX) is established SOC in 1L DLBCL, most prescribed 1L regimen among IPI 2-5 patients in the US ▪ Columvi+Polivy-R-CHP (SKYGLO) is the only regimen in Ph III to build on top of POLARIX in 1L DLBCL; readout expected 2027 ▪ Potential for best-in-class efficacy: Columvi + Polivy-R-CHP 100% ORR, 96% CMR, mPFS/mDOR not reached ▪ Potential for best-in-class safety: low CRS rates: 12.5% grade 1 CRS; no grade 2-5 CRS; regimen is suitable for outpatient administration Oncology/Hematology SKYGLO builds on POLARIX regimen in 1L DLBCL 1L DLBCL treatment evolution % Columvi + R-CHOP (n=56) Columvi + Polivy+ R-CHP (n=24) ORR 93% 100% CMR 86% 96% CRS Gr 1 Gr 2 10.7% 7.1% 3.6% 12.5% 12.5% 0 Efficacy Summary Safety Summary 70% 77% Illustrative + R-CHP + R-CHP 2-year PFS rate (%) R-CHOP Data exp 202720232006 POLARIX SKYGLO
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Lunsumio with chemo free combos in 2L+ DLBCL and 2L+ FL Expanding into earlier lines with positive Phase III SUNMO in 2L+ DLBCL and CELESTIMO in 2L+ FL 137 ▪ Lunsumio + Polivy tripled median PFS vs. R-GemOx ▪ Chemo-free, fixed duration regimen, suitable for outpatient use ▪ Lowest CRS incidence and severity among T-cell bispecifics; <5% of patients with Gr 2+ CRS 2L+ DLBCL: SUNMO shows strong efficacy and lowest CRS 1. Westin et al. ICML 2025; GemOx: Gemcitabine + oxaliplatin; PFS: Progression -free survival; R/R: relapsed/refractory Oncology/Hematology 0 20 40 60 80 100 3 6 9 12 15 Time (months) PFS (%) 18 21 24 27 300 Lunsumio-Pola: 11.5m R-GemOx: 3.8m HR (95% CI): 0.41 P-value: <0.0001 C1 C2 C3 C4 C1 C2 C3 C4 Ph III (CELESTIMO): 2L+ FL Lunsumio + len Lunsumio epcoritamab Rituxan ▪ Doublet regimen (Lunsumio + len) with simple dosing schedule, fixed duration ▪ Minimal steroid pre-medication required (3 days vs. 16 in C1) ▪ Suitable for outpatient administration, community 2L+ FL: CELESTIMO differentiated by convenience 14 fewer Infusions/ injections in first 4 cycles Ph III SUNMO: Lunsumio+Polivy in 2L+ DLBCL1 Ph III (EPCORE FL-1) epcoritamab + Rituxan + len Patients with ≥1 CRS AE (%) Lunsumio+Pola (n=135) Any grade 26% Grade 1 22% Grade 2 4% Grade 3 <1% Met primary endpoint Filed with FDA (PDUFA Feb 9)
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Bexobrutideg: Potential best-in-class BTK-targeted therapy Ph III in 2L+ CLL has been initiated; planned combinations in CLL (1L & R/R), MCL, and WM 138 Strong Ph I efficacy in late-line r/r CLL ▪ Complete target ablation and scaffold removal yield deeper pathway inhibition than BTK inhibitors ▪ Superior in vitro potency against both wildtype and mutant BTK ▪ Best-in-class potential, with improved selectivity vs. other BTK degraders, supporting differentiated tolerability profile ▪ Exceptional CNS penetrance BTK degradation addresses resistance to BTKi ▪ ORR: 83%, PFS of 22.1m in heavily pre-tx pts incl. difficult-to-treat subgroups (BTK mutations, high-risk mol. features, CNS disease) ▪ Potential for BIC safety with low rates of SAEs, ~5% D/C rate ▪ Ph III DAYBreak-CLL 306 in r/r CLL achieved FPI in Q3 ▪ Ph I/II combo with Venclexta +/- CD20 in CLL initiated Bexobrutideg in collaboration with Nurix Therapeutics; Source: Phase 1a, ASH 2025 update (Sep 2025 cutoff); *In CRISPR-engineered TMD8 cells; GI-50, growth inhibition 50%; r/r: relapsed /refractory; CLL: Chronic Lymphocytic Leukemia; MCL: Mantle Cell Lymphoma; WM: Waldenström’s Macroglobulinemia Superior mutation coverage vs. BTKi* Oncology/Hematology BTK mutation conferring BTKi resistance Mutant Improved selectivity vs. other BTK degraders
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Cevostamab: First-in-class FcRH5-targeted therapy in MM FcRH5 x CD3 bispecific, potential combination partner of choice with differentiated safety profile 139 Source: 1. Spencer et al., IMS 2026; *MRD-negative CR rates at the 10-5 level among MRD-evaluable CR+ patients; MRD by next generation sequencing ( ClonoSEQ); MRD-evaluable patients were those who achieved CR+ and had ≥1 valid MRD result (positive or negative) at any time; BCMA: B cell maturation antigen; FcRH5: Fc receptor-homolog 5; IVIG: Intravenous immunoglobulin; MM: Multiple myeloma; ORR: Overall response rate; Pd: Pomalidomide and dexamethasone; r/r: Relapsed/refractory; VGPR: Very good partial response; MRD: m inimal residual disease Strong efficacy and differentiated safety in r/r MM ▪ FcRH5 expressed in ~100% of MM cells, independent of BCMA or GPRC5D expression ▪ Unlike BCMAs, cevostamab not associated with persistent depletion of B-cells; lower risk of severe infection ▪ Unlike GPRC5Ds, cevostamab not associated with GI/skin toxicity FcRH5: high unmet need for new targets in MM ▪ Differentiated and favorable safety profile: At 70mg dose: • 17.2% gr 3 infection rate, no gr 4, one gr 5 • Restoration of humoral immunity without continuous IVIG ▪ Ph III (CEVOLUTION) cevostamab + Pd in r/r MM ongoing ▪ Initiating combinations in 1L 0 20 40 60 80 100 70 mg (n=29) Patients (%) VGPR+: 75.9% ORR: 86.2% PR VGPR CR sCR Oncology/Hematology MRD- CR rates* (CR+ evaluable pts) 93.8% 18m PFS 67.4% mPFS NR CR+: 62.1% Median follow-up: 20m Ph I: Cevostamab + Pd in r/r MM1 FcRH5 CD3
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Indication Regimen Ph1 Ph2 Ph3 Hemophilia A zemocimig vs. FVIII • Ph III data exp. late 2027 • ZEBRHA-2 is the only head- to-head trial vs. Hemlibrazemocimig vs. Hemlibra zemocimig (pediatric) SPK-8011QQ • FPI achieved in Ph II in Q3 VWD Hemlibra PNH PiaSky aHUS PiaSKy • Filing in aHUS expected 2026 Non-malignant hematology: Key newsflow ZEBRHA 1 Ph II ZEBRHA 2 ZEBRHA 3 WILL-EMI COMMODORE1/3 COMMUTE a/p Hemlibra autoinjector potential to launch by year end 2027 140 Roche is set to again transform care in Hemophilia A 1. Based on RWD from McCary I, et al. Haemophilia 2020, Wall C, et al. ISTH 2020, Poon M -C, et al. ASH 2022 and Khairnar R, et al. ASH 2021; aHUS: atypical hemolytic uremic syndrome; SC: subcutaneous; IV: intravenous Oncology/Hematology Approved or primary endpoint met Zemocimig is the only molecule going head-to-head vs. Hemlibra in Ph III Roche is leading evolution of the Hemophilia A standard of care FVIII prophylaxis ~80% bleed-free1 zemocimig (NXT007) Potential for Hemostatic normalization SPK- 8011QQ One-time treatment Daily to weekly IV Weekly to Q4W SC (autoinjector) Monthly SC (autoinjector) Potential for Hemostatic normalization Common breakthrough bleeds Dosing/admin Efficacy
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Ph I/II combined analysis1 141 Zemocimig (NXT007): BIC potential in Hemophilia A Next-gen FIXa/FX bispecific ▪ Zemocimig is a next-gen, bispecific, based on Hemlibra and optimized to provide increased FVIIIa- mimetic activity and a longer half life ▪ ~30-fold more potent than Hemlibra; low volume monthly injection with autoinjector ▪ Head-to-head trial vs. Hemlibra (powered for non- inferiority and superiority) Oncology/Hematology Potential to achieve true hemostatic normalization; Ph III data expected late 2027 ▪ >90% of pts with zero treated bleeds in the two highest dose cohorts.1 ▪ Thrombin generation at Ph II doses is well into the normal range of people without Hemophilia A** ▪ Favorable safety profile, with no observed thrombotic events ▪ Only one case of ADAs partially affecting PK out of 42 pts. NXT007 levels stabilized at ~2.5 μg/mL (considered equivalent to level of protection achieved with Hemlibra). Patient continued treatment with zero treated bleeds during study 0% 50% 100% Group Y (n=15) Group Z (n=14) Proportion of participants with zero treated bleeds during the NXT007 maintenance period1 93.3% (n=14/15) 92.9% (n=13/14) Group Y 0.70mg/kg (n=15) Group Z 1.08mg/kg (n=14) Hemostatic normalization achieved at Ph II doses2 1. Mancuso, et al., ISTH 2026; 2. Kiialainen et al., ASH 2025 *One notable outlier in Group Z had four treated spontaneous joint bleeds in the maintenance period. This participant had a leftknee replacement approximately 4 years prior to study entry and a left knee arterial embolization approximately 1 year prior to entry due to recurrent joint bleeds. The bleeds were considered secondary to direct trauma to an aberrant arterial vessel close to the replaced knee surface. **Normal range generated from plasma taken from 120 healthy volunteers; NXT007 TG peak height at steady state. ABR, annualized bleeding rate; CI, confidence interval. Zemocimig molecule design Cohort 2 (n=9) 0.70mg/kg Cohort 3 (n=6) 1.08mg/kg Upper limit of normal Lower limit of normalImproved PK profile Optimized binding affinity
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Neurology Hideki Garren SVP and Global Head of Product Development Neurology
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Neurology R&D focus areas End-to-end investment in MS and AD 143 Neurology AD: Alzheimer's Disease; CSF: Cerebrospinal fluid; E2E: End -to-end; MS: Multiple Sclerosis; NfL: Neurofilament light chain; PD: Parkinson’s Disease; PET: Positron emission tomography BrainshuttleTM in AD (trontinemab) readout in early 2028 BrainshuttleTM in MS (RG6035, aCD20) moving to Ph II TRAVELLER prescreening program in AD uses blood-based biomarkers to reduce diagnostic burden (CSF/PET) Elecsys® NfL blood test detects disease activity Initiating Ph III (PrevenTRON) of trontinemab in preclinical AD Invest end-to-end in Alzheimer’s disease and multiple sclerosis from discovery, R&D, to commercialization Invest into breakthrough innovation in Parkinson’s disease Critical Capabilities Examples Pharma + Dia partnership Therapeutic modalities Prevention approaches E2E investment
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Neurology pipeline Fenebrutinib filed in RMS and PPMS; Enspryng filing accepted in MOGAD with Priority Review 144 Neurology 1. Elevidys in partnership with Sarepta Therapeutics; 2. Ambulatory, 8 -<18 yrs; non-ambulatory, all ages; AIE: Autoimmune enceph alitis; DMD: Duchenne muscular dystrophy; GSM: Gamma- secretase modulator; MAGL: Monoacylglycerol lipase; MOGAD: Myelin oligodendrocyte glycoprotein antibody -associated disease; PPMS : Primary progressive multiple sclerosis; RMS: Relapsing multiple sclerosis; y.o.: year old Phase IIIPhase I Phase II Registration RG6627 APOE ASO Alzheimer’s RG6168 Enspryng AIE RD RG7935 prasinezumab Parkinson’s RG6168 Enspryng MOGAD RD RG6182 MAGLi Multiple Sclerosis RG6289 nivegacetor (GSM) Alzheimer's RG6434 NLRP3i Alzheimer’s, Parkinson’s RG6356 Elevidys1 DMD (0-<4 y.o.) RD RG6356 Elevidys1 DMD (>8 y.o.2) RD RG7845 fenebrutinib RMS, PPMS RG6102 trontinemab Early AD, preclinical AD RG6035 Brainshuttle CD20 Multiple Sclerosis RG6662 HTT miRNA GT (SPK-10001) Huntington’s RD Small molecule Antibody RNA-targeting therapeutics Bispecifics Gene therapy BrainshuttleTM Neuromuscular disorders Neurodegenerative diseases RD = Rare disease Neuroimmunologic disorders RD
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Fenebrutinib: Only BTKi with positive results across RMS/PPMS Fenebrutinib US filing completed in RMS and PPMS Neurology ▪ Fenebrutinib is the only non-covalent, reversible BTKi in MS ▪ Highly selective with unique structure and binding mode that targets dual drivers of disability in MS Designed to control relapsing and progressive biology 145 BTKi Progressive biologyRelapsing biology B cell Macrophage B cell Microglia fenebrutinib Non-covalent Reversible Sources: 1. Johnson A, et al. Presented at ACTRIMS 2025 (Poster P146); 2. Crawford J, et al. J Med Chem 2018;61:2227 –452; 3. Bar-Or A, et al. Presented at CMSC 2025 (Oral presentation PLA - A5); CSF: Cerebrospinal fluid; CNS: Central nervous system; PPMS: Primary progressive multiple sclerosis; RMS: Relapsing mult iple sclerosis ▪ Optimized PK profile maintains high systemic and CNS exposure ▪ Fenebrutinib achieves near maximal inhibition of B-cells and microglia in the CNS (associated with progressive biology)2,3 Inhibition of B-cells and microglia in CNS CSF: Concentration relative to microglia TNF-α IC90 1
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Fenebrutinib in RMS with lowest ARR seen in Phase III trials >50% improvement in ARR, >70% reduction in in new brain lesions, clinically meaningful improvements in cCDP Neurology Substantial impact on relapsing biology, MRI activity, and disease progression 146 ▪ >50% reduction in ARR vs. teriflunomide: translates to an average of one relapse every ~17 years (lowest ever demonstrated in a Ph III trial) ▪ >70% reduction in the number of new brain MRI lesions vs. teriflunomide (T1 Gd+ and NET2Ls) ▪ Ph II FENopta OLE showed sustained suppression of relapses and MRI lesions (Ph III longitudinal data to be presented at MSToronto) ▪ Clinically meaningful and nominally significant trend in both pooled cCDP12 and CDP12-EDSS+9HPT (composite endpoint used in ORATORIO-HAND study) FENhance 1 0.49 (0.33-0.73) P<0.001 FENhance 2 0.42 (0.28-0.61) P<0.00001 cCDP122 Adjusted ARR (95% CI)1 51.1% 58.5% 76.0% 82.5% Annualized number of NET2Ls FENhance 1 0.24 (0.19-0.31) P<0.0001 FENhance 2 0.17 (0.13-0.23) P<0.0001 Sources: Oh J, et al. AAN 2026, 1. Adjusted for the presence of T1 Gd+ lesions and EDSS score (<4.0 vs ≥ 4.0) at baseline. In FENhance 2, EDSS score was removed due to non -convergence of the model. 2. Defined as ≥ 1.0 or ≥ 0.5-point increase in EDSS, with baseline EDSS ≤5.5 or >5.5, respectively; or ≥20% increase from baseline in T25FWT; or ≥20% increase from baseline in 9HPT. Pooled results shown are not α controlled; Defined as ARR: Annualized relapse rate; cCDP12: 12 -week composite confirmed disability progression; EDSS: Expanded disability status scale; NET2L: new or enlarging T2 lesions; RMS: Relapsing multiple sclerosis; 9HPT: Nine -hole peg test
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Fenebrutinib ARR reduction positions it as a high efficacy DMT Fenebrutinib is the first and only oral to demonstrate >50% improvement in ARR in RMS Neurology 147Singer et al., J Neurol. 2024 Apr 14;271(6):3116–3130; ARR: Annualized relapse rate; DMT: Disease modifying therapy; RMS: Relapsing multiple sclerosis High efficacy: ~50-60% reduction of ARR Moderate efficacy: ~40-50% reduction of ARR Low efficacy: ~30-40% reduction of ARR Fenebrutinib
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Fenebrutinib: Only BTKi with positive results in PPMS and vs. CD20 Consistent numeric improvements on disease progression observed across all three MS studies Neurology 148 Fenebrutinib is the only molecule with head-to-head data vs. CD20 ▪ Curves started to separate by week 24, which lasted throughout the entire treatment duration of >120 weeks ▪ Fenebrutinib demonstrated nominally significant 22% reduction in disability progression on CDP12-EDSS+9HPT (composite endpoint used in ORATORIO-HAND study) FENtrepid cCPD12 Sources: Bar-Or A et al. ACTRIMS 2026; 1. Synthesis test statistic <−1.96 indicated noninferiority, with supplementary analysis based on pre-specified 95-95 fixed margin of 1.06 for the HR upper bound; cCDP12:12-week composite confirmed disability progression; EDSS: Expanded disability status scale; MS: Multiple sclerosis ; PPMS: Primary progressive multiple sclerosis; 9HPT: Nine-hole peg test
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Multiple sclerosis: Early development pipeline Diverse portfolio of modalities build on Roche’s leadership in MS Neurology 149 ▪ Leverages Roche’s proprietary BrainShuttleTM technology to address limitations of CD20 antibodies to penetrate CNS ▪ Advancing to Ph II in MS RG6035: BrainShuttle CD20 ▪ Unique and multimodal MoA to target compartmentalized inflammation in the CNS ▪ Ph II (Mintaka) trial in MS initiated; designed to evaluate MAGLi in combination with Ocrevus RG6182: MAGLi BBB Brain tissueBlood Transferrin receptor 1 Brain shuttle module CD20 binder BBB: Blood brain barrier; CNS: Central nervous system; DAG: Diacylglycerol; MAGLi: Monoacylglycerol lipase inhibitor; MoA: Mechanism of action; MS: Multiple sclerosis
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Enspryng: Potential to be the first approved treatment in MOGAD US filing in MOGAD accepted with Priority Review (PDUFA Jan 10) Sources: 1. Marignier R, et al. Lancet Nuerol. 2021;20:762-772; 2. Michael L, et al. AAN 2026. PL5; MOGAD: Myelin oligodendrocyte glycoprotein antibody -associated disease Neurology 150 ▪ MOGAD is a rare autoimmune condition that presents with inflammatory demyelinating attacks affecting the optic nerve, brain, and spinal cord ▪ No approved therapies; disease management frequently relies on acute treatment with high-dose corticosteroids1; relapse prevention is the main objective of maintenance therapy Disability in MOGAD driven by relapses ▪ Primary endpoint met: 68% reduction in risk of a new relapse vs. placebo; onset of response demonstrated as early as week 8 ▪ Highly significant reductions in annualized relapse rate, active MRI lesions, and rescue therapy use ▪ Enspryng was well tolerated with a safety profile comparable to placebo ▪ Enspryng autoinjector 120 mg granted FDA and EMA approval, 180mg under review Ph III METEOROID in MOGAD Vision loss Cognitive dysfunction Loss of ambulation IL-6 levels elevated in CSF and serum of patients with MOGAD, contributing to autoantibody production 87.3% 84.3% 66.5% 54.4% 0 20 40 60 80 100 0 24 48 72 96 120 Time to relapse (Weeks) Proportion relapse-free (%) Placebo (n=64) Enspryng (n=68) Censored HR (95% CI): 0.32 (0.15–0.70) p=0.0025 Time to relapse vs. placebo2
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Alzheimer’s disease: Opportunities to unlock patient benefit Despite approved therapies, significant unmet need remains 151 Neurology AD: Alzheimer’s disease; ARIA: Amyloid-related imaging abnormalities Ph I Ph II Ph III 2027nivegacetor (GSM) GABriella 1H 2028trontinemab TRONTIER 1 & 2 PrevenTRONtrontinemab RG6434 (NLRP3i) Ph II ▪ Ph III (TRONTIER 1 & 2) in early symptomatic AD achieved LPI; data expected 1H ’28 ▪ Ph III (PrevenTRON) in preclinical AD initiated Alzheimer’s disease development program Opportunities Diagnosis Blood tests enable early, convenient, at-scale detection, in symptomatic and presymptomatic individuals Efficacy Greater clinical benefit via: • Faster and more complete amyloid depletion via BrainshuttleTM • Targeting additional disease mechanisms, alone and in combination Safety Improved safety profile with low ARIA-E Dosing & Administration Induction/maintenance dosing regimen ensures rapid and robust removal of amyloid while reducing patient burden and further controlling AD pathology RG6627 (APOE ASO) Ph I
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Trontinemab has best-in-disease potential in Alzheimer’s disease BrainshuttleTM anti-Aβ engineered to increase brain penetration and distribution 152 Neurology Sources: 1. Kulic L et al. Presented at AAIC 2026; 2. Data on file: Poeschinger Lab, Roche Innovation Center Munich; 3. Villaseñor R, et al. Presented at AD/PD 2026, Copenhagen, Denmark. Whole-brain images show a 3D volume rendering of the whole brain acquired with a light-sheet microscope. Images highlight the distribution of classical IgG vs Brainshuttle IgG, targeting neurones in mouse brains. Brains were perfused and chemically fixed 5 days after a single IV dose of fluorescently labelled Brainshuttle IgG (3 mg/kg) or two consecutive IV doses of IgG (2× 6 mg/kg); 4. Grimm HP, et al. MAbs 2023;15:2261509; 5. Kulic L, et al. Presented at AD/PD 2025; Aβ: Amyloid β; BBB: Blood-brain barrier; ChP: Choroid plexus; CVO: Circumventricular organs; mAb: Monoclonal antibody ▪ Trontinemab is a novel bispecific 2+1 Brainshuttle Aβ-targeting mAb that crosses the BBB via TfR1-mediated transcytosis ▪ Brainshuttle technology enables 6- to 17- fold higher brain exposure with trontinemab observed compared with standard mAb1, and homogeneous distribution across brain regions2,3 ▪ Less engagement with vascular amyloid vs. standard mAb may lower ARIA incidence Active transport across the blood-brain-barrier enhances brain penetration BBB Brain tissueBlood Aggregated Aβ Transferrin receptor 1 Brain shuttle module Aβ binder Improved distribution vs. standard IgG mAb2,3 Active TfR1 transport at the capillary level Concentration of trontinemab in the brain vs a conventional mAb4,5
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Trontinemab demonstrates best-in-disease plaque removal Converging evidence suggests the rate and amount of clearance of amyloid is important1 153 Neurology †Amyloid positivity threshold defined as values ≤ 24; Sources: 1. Kulic L et al. Presented at AAIC 2026; CL: Centiloid unit; OLE: open label extension; PET: Positron emission tomo graphy ▪ 92% of participants were below the amyloid positivity threshold (≤24 CL) at 28 weeks, and 71% were below 11 CL† ▪ Substantial amyloid reduction in all patients (minimum -47CL change from baseline) ▪ An amyloid-negative threshold of approximately 24 CL appears to be critical for clinical response Rapid and robust amyloid plaque removal ▪ Patients previously treated with trontinemab assigned either to Q4W or Q12W dosing based on amyloid levels at OLE baseline ▪ Previously treated patients demonstrated continued amyloid reduction through 1 year of OLE Trontinemab OLE data PhIb/II OLE data Amyloid PET trontinemab 3.6 mg/kg
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Biomarkers of AD pathology and exploratory clinical outcomes 154 Neurology Sources: 1. Kulic L et al. Presented at CTAD 2025, Unblinded exploratory clinical efficacy data by dose levels (snapshot date: September 05, 2025). Completer analysis restricte d to participants with available assessment at both BL and Day 196. Exclusion of one participant with ischemic stroke and clinical aphasia in C ohort 4, Part 1, from the analysis; AD: Alzheimer’s disease; CDR -SB: Clinical dementia rating- sum of boxes; CSF: Cerebrospinal fluid; GFAP: Glial fibrillary acidic protein; MMSE: Mini -mental state examination; SE: Standard error ▪ Pronounced effects on key downstream biomarkers including CSF total Tau, CSF pTau181, plasma pTau 217, and plasma GFAP which is associated with AD pathology Effects on downstream biomarkers of AD pathology ▪ Numerically less decline on CDR-SB and MMSE with trontinemab compared with placebo at 28 weeks ▪ The BrainshuttleTMAD study design limits a robust quantitative evaluation of clinical scales: short duration, small sample size, heterogeneous population, 4:1 randomization active:placebo Trontinemab exploratory clinical efficacy outcomes1 Plasma GFAP 3.6 mg/kg double blind period Plasma pTau217 3.6 mg/kg double blind period CDR-SB change from baseline (±SE) MMSE change from baseline (±SE)
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Trontinemab has potential for best-in-class safety with <5% ARIA-E 155 Neurology Vascular engagement of standard anti-amyloid mAbs reduced with BrainshuttleTM ▪ In entering via CSF and perivascular spaces, anti-Aß mAbs binding to vascular amyloid pathology may exacerbate inflammation, leading to ARIA1,2 ▪ Murine surrogate of trontinemab shows enhanced plaque decoration with reduced vascular engagement compared with a standard mAb ARIA associated with vascular engagement ▪ Interim data demonstrated a consistent overall favorable safety profile with low incidence of ARIA-E (<5%) ▪ Anemia incidence mostly mild and transient, IRR were mild to moderate with severity and incident reduced with steroid premedication2 Ph Ib/II BrainshuttleTM safety data3 Part 1 + 2 (combined) (n=151)* Total number of participants, n (%) Cohort 3 1.8 mg/kg or Placebo (n=76) Cohort 4 3.6 mg/kg or Placebo (n=75) ARIA-E† Symptomatic ARIA-E 3 (3.9) 1 (1.3) 1 (1.3) 0 (0.0) ARIA-H Microhaemorrhage Superficial siderosis 5 (6.6) 2 (2.6) 3 (3.9) 3 (4.0) 2 (2.7) 1 (1.3) Concurrent ARIA-E + ARIA-H 0 (0.0) 0 (0.0) Other significant MRI findings Cerebral macrohaemorrhage§ 1 (1.3) 0 (0.0) Target engagement with BrainshuttleTM anti-amyloid mAb vs standard mAb Sources: 1. Mummery C, et al. Presented at AAIC 2025, Toronto, Canada; 2. Pizzo M, et al. Science 2025;389:eads3204; 3. Kulic L et al. Presented at CTAD 2025, Unblinded exploratory clinical efficacy data by dose levels (snapshot date: September 05, 2025). Completer analysis restricted to participants with available assessment a t both BL and Day 196. Exclusion of one participant with ischemic stroke and clinical aphasia in Cohort 4, Part 1, from the analysis; Aβ: Amyloid β; ARIA: Amyloid-related imaging abnormalities; CSF: Cerebral spinal fluid; IRR: Infusion -related reaction; mAb: Monoclonal antibody Vascular amyloid decoration 7 days post injection Standard mAb BrainShuttleTM anti-amyloid mAb Large vessels Amyloid plaques
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Nivegacetor: Gamma-secretase modulator (GSM) in Alzheimer’s GSM offers complementary approach to target amyloid beta; ideal for intervention at earliest stages 156Sources: 1. Cullen et al., Neurology 2022; 2. Von Kienlin et al. presented at CTAD 2018, Barcelona, Spain; A β: Amyloid beta; APP: Amyloid precursor protein; GSM: Gamma -secretase modulator Neurology ▪ GSMs selectively target processing of amyloid precursor protein (APP) and leave the other substrates (e.g. Notch) unchanged. ▪ Reduce amyloidogenic long peptides (Aβ40, Aβ42) and increase production of short, non-amyloidogenic peptides (Aβ38,Aβ37). Increased levels of shorter Aꞵ species reduce the risk of cognitive decline1,2 GSM alters APP processing, inhibits Aβ aggregation ▪ Ph I healthy volunteers: dose-dependent γ-secretase modulation with up to~70% Aβ42 reduction and strong increase in short Aβ forms. PK profile supports oral once daily dosing ▪ Ph IIa GABriella in early-AD recruitment completed; data expected 2027 Ph I nivegacetor in healthy volunteers1
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NLRP3i in neurodegenerative disorders RG6434 advancing to Ph II in Alzheimer’s disease and Parkinson’s disease 157 Neurology Sources: 1. Holbrook JA, et al. Fron Pharmacol 2021;12:643254; 2. Sutterwala FS, et al. Ann N Y Acad Sci 2014;1319:82 -95; 3. Jung ES, et al. Aging Cell 2022;21:e13623; 4. Pag ano G, et al. AD/PD 2026; 5. F. Hoffmann-La Roche Ltd. Data on file; Aβ, amyloid beta; AD: Alzheimer’s disease; CSF: Cerebral spinal fluid; PD: Parkinson’s Disease ▪ Amyloid fibrils activate NLRP3 in microglia; subsequent inflammatory signaling enhances tau phosphorylation1,2 ▪ Targeting NLRP3 offers potential to decouple Aβ accumulation from the subsequent neurodegenerative cascade3 ▪ Ph II study of RG6434 in Alzheimer’s to be initiated Alzheimer’s: NLRP3 links Aβ and Tau pathologies ▪ NLRP3 inflammasome activation associated with downstream dopaminergic neuronal death5 ▪ Ph Ib study of another NLRP3i (selnoflast) in early PD show proof of mechanism by downstream inflammasome biomarkers ▪ Potential to combine NLRP3i with orthogonal mechanisms in PD ▪ Ph II study of RG6434 in Parkinson’s to be initiated Parkinson’s: Ph I pharmacodynamics4 CSF IL-18 placebo (n=12) selnoflast (n=23)
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Prasinezumab: Trend towards delaying motor progression Signal of efficacy demonstrated beyond effective symptomatic therapy 158 Neurology Prasinezumab in collaboration with Prothena; Sources: 1. Nikolcheva et al. Presented at ADPD 2026; L -DOPA: levodopa; mAb: Monoclonal antibody; MDS-UPDRS: Movement disorder society-sponsored revision of the unified Parkinson’s disease rating scale; OFF: practically defined OFF state; PD: Parkinson’s diseas Anti-α-synuclein mAb Ph IIb PADOVA results ▪ Signal of efficacy in pre-specified L-DOPA subgroup (~74% of total study population) ▪ First biomarker evidence of prasinezumab impacting disease pathology: stabilization of neuromelanin and reduced iron accumulation in key brain regions ▪ Favorable safety profile ▪ Over 900 PD study participants, with more than 500 treated for 2.5 to 5 years Proposed effects: ▪ Reducing neuronal toxicity ▪ Preventing cell-to-cell transfer of pathogenic α- synuclein aggregates ▪ Slowing disease progression Prasinezumab selectively binds aggregated α-synuclein ▪ Prasinezumab has the potential to be the first disease modifying therapy in PD ▪ Ph III (PARAISO) enrolling in L-DOPA patients (n=900) Ph IIb PADOVA: Time to ≥5 points on MDS-UPDRS Part III OFF (L-DOPA subgroup)1
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Immunology Larry Tsai SVP and Global Head of Product Development Immunology
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160 Immunology IBD: Inflammatory bowel disease; CAR-T: Chimeric antigen receptor T cell Critical Capabilities Examples E2E investment Combinations Endotypes Cure Optimize pathways Build on known mechanisms and identify novel pathways/targets for transformational benefit Various approaches for enhanced B-cell depletion, TL1a pathway, and complement pathway Target multiple pathways to achieve improved efficacy and deeper remission p40xTL1A bispecific combines orthogonal targets to raise efficacy in IBD TSLPxIL33 bispecific targets key epithelial "alarmin" cytokines that trigger airway inflammation in COPD Identify patients’ subsets to improve efficacy and guide therapy Afimkibart IBD trials explore biomarkers to predict better response to treatment; COPD pipeline focused on patient identification on areas of high unmet need, e.g. muco-obstructive and non-Th2 disease Aim for curative treatment to achieve long-term remission Lunsumio and next-gen CD19/CD20 TCBs (in preclinical development) Invest end-to-end in select disease areas from discovery, R&D, to commercialization Inflammatory bowel disease (IBD) and chronic obstructive pulmonary disease (COPD) Immunology R&D focus areas
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Immunology pipeline 161 Phase I Phase II Phase III RG6299 sefaxersen IgAN RG7159 Gazyva SLE RG6631 afimkibart Ulcerative colitis RG6631 afimkibart Crohn’s disease RG7828 Lunsumio SLE/LN Immunology * Program to be initiated in Ph I; E2E: end to end: Ab; Antibody; COPD: Chronic obstructive pulmonary disease; IBD: Inflammat ory bowel disease; IgAN: IgA nephropathy; INS: Idiopathic nephrotic syndrome; LN: Lupus nephritis; SLE: Systemic lupus erythematosus Immune-mediated kidney & rheumatological diseases Respiratory & allergy Gastroenterology Others/undisclosed Registration RG6631 afimkibart Rheumatoid arthritis RG6730 p40 x TL1A Ulcerative colitis Broad development portfolio across E2E and breakthrough innovation disease areas RG7159 Gazyva LN Approved CHU anti-HLA-DQ2.5 x gluten peptides Celiac disease RG7159 Gazyva Membranous nephropathy RG7159 Gazyva Childhood onset INS Small molecule Antibody RNA-targeting therapeutics Bispecifics RG6767 undisclosed immunology RG6981 IL33:TSLP COPD/asthma RG6421 TMEM16A potentiator COPD CHU RAY121 (anti-C1s recycling Ab) Immunology RG6160 cevostamab SLE/LN RG6498 undisclosed IBD RG6527 undisclosed* COPD RG6644 undisclosed* COPD RG7159 Gazyva Childhood onset INS
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Immune-mediated diseases are a leading cause of CKD 162 Immunology Aiming to prevent progression to end-stage kidney disease and subsequent need for dialysis/transplantation 1. J. Jager, C. Kovesdy, R. Langham, et al. Kidney Int, 96 (2019), pp. 1048-1050; 2. Adapted United States Renal Data System. 2024 USRDS Annual Data Report: Epidemiology of kidney disease in the United States. NIH, 2024; 3. Arthritis Rheumatol. 2023 April ; 75(4): 567–573. doi:10.1002/art.42375; 4. Fervenza et al. 2019 N Engl J Med. 2019 Jul 4;381(1):36-46; 5. Pitcher D, Long-Term Outcomes in IgA Nephropathy. Clin J Am Soc Nephrol. 2023 Jun 1;18(6):727-738. doi: 10.2215/CJN.0000000000000135 ; 6. Roche Pharma Day 2025 Appendix-Epidemiology Overview7. US Dept of Health 2020; 8. A systematic EU approach to chronic kidney disease - European Parliament Question Feb 2022; aHUS: Atypical hemolytic uremic syndrome; CKD: chronic kidney disease; ESKD: End stage kidney disease; IgAN: IgA nephropathy; INS: Idiopathic nephrotic syndrome (Childhood onset INS also known as PNS: Pediatric nephrotic syndrome); LN: Lupus nephritis; MN: Membranous nephropathy; SLE: Systemic lupus erythematosus Development program in diseases driving kidney disfunction Molecule Indication Ph I Ph II Ph III Status Gazyva LN Approved SLE PDUFA Dec 4 MN PDUFA Nov 15 INS Approved PiaSky aHUS Filing 2026 sefaxersen IgAN Lunsumio SLE/LN Ph II RG6767 undisclosed Ph I initiated cevostamab SLE/LN Ph I initiated REGENCY ALLEGORY MAJESTY INShore COMMUTE SOLUNA CKD to be 5th leading cause of death globally by 20401 ▪ Immune-mediated kidney diseases are associated with high morbidity and mortality, ranking as the 3rd most common cause of ESKD ▪ Up to 25% of lupus, 50% of IgAN, and 30% of MN patients develop ESKD despite treatment with current available therapies3,4,5 Mortality significantly increases with increasing loss of renal function2 46 143 105 127 225 258 0 100 200 300 No CKD All CKD CKD Stage 1- 2 CKD Stage 3 CKD Stage 4- 5 Dialysis Deaths per 1000 patient years 1 EP met* *Based on interim analysis from ph III IMAgINATION study IMAgINATION Approved or primary endpoint met
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Gazyva: Deeper B-cell depletion key to improved clinical response B cells are central to immune mediated kidney disease pathogenesis Immunology 163 ▪ First glycoengineered type II aCD20 for LN, SLE, MN, INS to directly target B cells, an underlying cause of disease1 ▪ Type II anti-CD20 region with increased direct cell death, decreased CDC and reduced internalization ▪ Glycoengineered Fc region with higher FcƳR affinity and increased ADCC/ADCP1,2 Type II anti-CD20 mAbs binding capabilities result in superior direct cell death B cell depletion vs Rituxan3 1. Rahman A and Isenberg DA. N Engl J Med. 2008;358:929-938; 2. Gomez Mendez LM, et al. Clin J Am Soc Nephrol. 2018;13:1502-1509; 3. Adapted from Reddy V, et al. Rheumatology (Oxford).2017;56:1227-1237; 4. Rovin BH, et al. WCN 2025; ADCC: antibody-dependent cell-mediated cytotoxicity; FcγR: Fc gamma receptor; ADCP: antibody-dependent cellular phagocytosis; CDC: complement-dependent cytotoxicity; DCD: direct cell death; INS: Idiopathic nephrotic syndrome (Childhood onset INS also known as PNS: Pediatric nephrotic syndrome); LN: Lupus nephritis; MN: Membranous nephropathy; RA: Rheumatoid arthritis; SLE: Systemic lupus erythematosus ▪ Greater potency than Rituxan in depleting B-cells3 ▪ Tested in multiple immune mediated kidney diseases, including disease in which earlier generation anti-CD20s failed to demonstrate benefit4 Glycoengineered Fc region ● Higher FcƳR affinity ● Increased ADCC/ADCP Type II anti-CD20 region ● Increased direct cell death ● Decreased CDC ● Reduced internalization Gazyva (obinutuzumab): Type II anti-CD20 mAb B cell depletion by anti-CD20 mAbs Rituxan Gazyva RA SLE % B-cell depletion Only anti-CD20 approved for LN
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164 ▪ SLE affects 3.4M people worldwide, 50% develop LN which is associated with >6-fold increased mortality ▪ Primary endpoint of minimum four-point improvement in SLE Responder Index 4 (SRI-4) at 52 weeks was met with a statistically significant and clinically meaningful treatment difference of 23.1% ▪ Additionally, Gazyva demonstrated statistically significant and robust efficacy over placebo across all secondary endpoints, including a ~20% treatment difference on the DORIS remission score ▪ ACR update 2025 recommends earlier introduction of conventional and/or biologic immunosuppressive therapies Furie R et al. SLEuro 2026; ACR: American College of Rheumatology; SLE: systemic lupus erythematosus; SoC: standard of care; SRI-4: Systemic Lupus Erythematosus Responder Index 4; US: United States; W: week; *Plus standard therapy of antimalarial and/or immunosuppressant and/or prednisone (or equivalent) Gazyva: Type II aCD20 mAb transforming standard of care in SLE Filed in SLE in US/EU with PDUFA date Dec 4 Gazyva: First B-cell depleting agent to reduce SLE disease activity in a global Ph III study Immunology PH III ALLEGORY trial design SLE disease activity: Adjusted treatment difference 1 23.1% (95% CI, 12.5 to 33.6); P<0.001 DORIS remission score: Adjusted treatment difference 1 19.9% (95% CI, 10.6 to 29.2) Primary Endpoint: % of patients achieving SRI-4 at week 52 Additional Endpoints: % of patients achieving sustained response (week 40 to week52), % of patients achieving sustained corticosteroid control Gazyva intravenous D1 W104 Experimental arm Placebo arm W26 R W52 Primary Endpoint OLE Placebo intravenous Estimated Enrollment N=300 Study follow-up ≥12mo Gazyva* n=151 Placebo* n=152 Gazyva n=151 Placebo* n=152 DORIS at Week 52 (% of Responders) 0 10 20 30 40 50 60 70 80 90 100 33.8% 13.8%
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Gazyva: Best in disease potential for MN and childhood onset INS INS FDA approval achieved in Sep 2026; MN under FDA priority review with approval expected in Q4 165 First targeted therapy in MN to demonstrate efficacy in Ph III First approved targeted therapy in INS 1. Keri KC, et al. Postgrad Med J. 2019;95(1119):23-31; 2. Kanigicherla DAK, et al. Nephrol Dial Transplant. 2016;31(12):2108-2114; 3. Veltkamp F, et al. Pediatrics. 2021;148(1):e2020029249; 4. Ehren R, et al. BMJ Open. 2018;8(10):e024882; 5. Complete remission is defined as achievement of UPCR ≤0.3 g/g and eGFR <15% below baseline. eGFR is calculated using the Chronic Kidney Disease Epidemiology Collaboration equation. Patients experiencing intercurrent events of escape therapy, treatment failure or early study discontinuation were considered to be non-responders under the composite strategy; BTD: Breakthrough Therapy Designation; ESRD: End-stage renal disease; FRNS: Frequently relapsing nephrotic syndrome; INS: Idiopathic nephrotic syndrome (childhood onset INS also known as PNS:Pediatric nephrotic syndrome); LTFU: Long-term follow-up; MMF: Mycophenolate mofetil; MN: Membranous nephropathy; SDNS: Steroid-dependent nephrotic syndrome ▪ Up to 30% of patients with MN progress to kidney failure over 10 years despite current treatment approaches1,2 ▪ Primary endpoint of complete remission at week 104 met: Statistically significant and clinically meaningful treatment difference of 31.1% compared with tacrolimus ▪ Gazyva was superior to tacrolimus in achieving overall remission (complete or partial) at week 104 and complete remission at week 76 a) Obinutuzumab infusion of 1000 mg or 20 mg/kg if <45 kg on Week 0 (Day 1), Week 2 (Day 15), Week 24 (Day 168) and Week 26 (Day 182) b) MMF oral dose titrated by Week 4 to 1200 mg/m2/day is given orally twice daily until Week 52, after which administration must be discontinued or tapered over the subsequent 3 months a) Obinutuzumab dose: 1,000 mg infusion b) Tacrolimus dose: initially 0.05 mg/kg dry weight, titrated to maintain trough concentration of 5-7 ng/mL for up to 52 weeks, then tapered over 8 weeks. Participants who achieve complete proteinuric response (UPCR ≤0.3 g/g) may be considered for early taper starting at 9 months. Dose tapering must be complete by Week 60 c) LTFU, where patients will be observed and re-treated with obinutuzumab per clinical evaluation LTFU Open label treatment period Open label treatment period Gazyva n=44 MMF n=41 Week 52 Adjusted treatment difference 23.36% (95% CI, 6.85 to 38.9); P=0.0031 95.5% 73.2% Primary analysis Adjusted treatment difference 31% (95% CI, 18 to 44); P<0.001 Gazyva n=72 Tacrolimus n=152 Week 104 ▪ Childhood onset INS is the most common primary kidney disease in children3; 70% of patients cannot successfully taper steroids4 ▪ Primary endpoint met of complete remission at week 52 met : Statistically significant and clinically meaningful treatment difference of 23.4% compared with mycophenolate mofetil ▪ Gazyva could help children and young adults sustain remission, potentially with a reduced need for steroids LTFU Primary analysis Immunology
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Sefaxersen: First ASO with positive Ph III interim (IMAgINATION) in IgAN Clinically meaningful reduction in 24-hour proteinuria; BIC potential for selective complement suppression in IgAN 166 Sefaxersen (ASO Factor B) ▪ IgAN is driven by an autoimmune response to circulating abnormal IgA, leading to complement system activation and inflammation in the kidneys ▪ High levels of CFB are associated with IgAN1,2 ▪ Sefaxersen downregulates CFB production by inhibiting mRNA translation ▪ Primary endpoint met at interim with sefaxersen achieving statistically significant and clinically meaningful improvements in proteinuria reduction vs. placebo at 37wk as measured by UPCR ▪ UPCR signals early response; study is continuing for long-term functional eGFR confirming slower kidney-function decline (key secondary endpoint) at week 105 ▪ Data to be discussed with global health authorities and presented at upcoming conference Ph III (IMAgINATION) trial design ASO FB Alternative complement pathway Sefaxersen in partnership with IONIS Pharmaceuticals; Figure adapted from: Barbour et al. ASN Annual Meeting 2024; 1. Chiu et al. Front Immunol. 2021; 12: 638309; 2. Yeo et al. Pediatr Nephrol 2018: 33:763-777; ASO: Antisense oligonucleotide; CFB: Complement factor B; D: Day; GN: Glomerulonephritis; IgAN: IgA nephropathy; MoA: Mechanism of action; mRNA: Messenger RNA; OLE: Open label extension; Q4W: Every 4 weeks; SC: Subcutaneous; UPCR: Urine protein/creatinine ratio; UPE: Urinary protein excretion; W: Week Key eligibility criteria • Primary IgAN confirmed by kidney biopsy • UPCR ≥1 g/g or urine protein excretion ≥1 g/day (with UPCR ≥0.8g/g) from a 24-hour collection • eGFR ≥20ml/min/1.73m2 • Age min. 18 years D 1 D 15 W 105 Experimental arm Placebo arm R 1:1 D 29 sefaxersen subcutaneous Placebo subcutaneous W 37 Primary endpoint: Change in UPCR Q4W dosing until week 105Estimated Enrollment N=428 Open-label treatment Safety follow- up Immunology
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IgAN: Major cause of chronic kidney disease and kidney failure Up to 50–60% of IgAN patients remain uncontrolled even on advanced therapies 167 ▪ IgAN is the most common primary glomerulonephritis, globally affecting ~25 adults per million every year1,2 ▪ IgAN is one of the leading causes of chronic kidney disease and end-stage kidney disease in adults3 Clinical characteristics of IgAN 20-404 Current IgAN treatment paradigm7 IgAN diagnosis confirmed through kidney biopsy Patient risk stratification with proteinuria levels dosing Proteinuria < 0.5 g/day Proteinuria ≥ 0.5 g/day Complement inhibitors APRIL inhibitors, BAFF/APRIL inhibitors Patients at risk of progressive loss of kidney function 1. McGrogan A, et al. Nephrol Dial Transplant. 2011;26:414–30; 2. Rodrigues JC, et al. Clin J Am Soc Nephrol. 2017;12:677–86; 3. Zaidi O, et al. BMC Nephrol. 2024;25(1):136; 4. Caster DJ, et al. Kidney Int Rep. 2023;8(9):1792- 1800; 5. Pitcher D, et al. Clin J Am Soc Nephrol. 2023;18(6):727-738; 6. Jarrick S, et al. J Am Soc Nephrol. 2019;30(5):866-876; 7. Kidney International IgAN guidelines (2025); APRIL: A proliferation-inducing ligand; BAFF: B-cell activating factor; BIC: Best-in-class; DEARA: Dual endothelin and angiotensin receptor antagonist; ESKD: End-stage kidney disease; IgAN: IgA nephropathy; QoL: Quality of life; RASi: Renin-angiotensin system inhibitor; SC: Subcutaneous; SGLT2i: Sodium-glucose cotransporter-2 inhibitor Supportive care therapy : RASi OR DEARA +/- SLGT2i Targeted release budesonide Lifestyle modification11.4 yrs5 Mean kidney survival after biopsy 48 yrs6 Mean age at kidney failure or death Hematuria Severe hypertension Proteinuria End-stage kidney disease resulting in the need for dialysis or kidney transplantation ▪ Sefaxersen has BIC potential within complement inhibitors ▪ Focusing on high-risk 1L patients presenting persistent active inflammation / hematuria and 2L pts inadequately controlled by current frontline therapies ▪ Convenient SC monthly dosing provides potential for better patient adherence and improved QoL Age of onset (in years) Highest reported incidence in Asia Immunology
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Afimkibart: Broad anti-TL1A development program 168 ▪ TL1A/DR3 binding acts as a key amplifier of inflammatory pathways and tissue remodeling in immune-mediated diseases1,2,3 ▪ TL1A- and DR3-expressing cells are known drivers of different immune- mediated and fibrotic diseases1,2,3 ▪ Non-clinical and translational studies demonstrated its involvement in pathogenesis of fibrotic conditions TL1A is upstream of multiple immunological cytokine & cellular pathways, presenting pan-immunological potential ▪ Ph III UC studies completed enrolment Q3 2026 ▪ Pediatric UC and CD registrational studies ongoing ▪ Ph II RA data expected in 2027 ▪ Ph Ib FIBROLITE in MASH completed enrolment Q3 2025 Clinical development program TL1A is linked to multiple immunological diseases: IBD, MASH, RA trials ongoing RA MASH IBD = additional indications Indication Ph I Ph II Ph III Status Ulcerative colitis Data 2027 Crohn‘s disease Atopic dermatitis Rheumatoid arthritis Data 2027 MASH AMETRINE 1 & 2 SIBERITE 1 & 2 VELARITE dRAvite Immunology 1. Solitano V, et al. Med. 2024;5(5):386-400; 2. Hassan-Zahraee M, et al. Inflamm Bowel Dis. 2022;28(3):434-446; 3. Bamias G, et al. Gut. 2025;74(4):652-668; 4. Xu WD, et al. Front Immunol. 2022;13:891328; ; CD: Crohn’s disease; DR3: death receptor 3; FPI: First patient in; IBD: Inflammatory bowel disease; MASH: Metabolic dysfunction-associated steatohepatitis; RA: Rheumatoid arthritis; TL1A: Tumor necrosis factor-like cytokine 1A; TNFα: Tumor necrosis factor alpha; UC: Ulcerative colitis
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IBD: Chronic relapsing/remitting disease with high unmet need 169 Ulcerative Colitis1 Crohn’s Disease2 Continuous inflammation limited to the mucosal layer of the colon and rectum Inflammation in patches across the GI tract, commonly the terminal ileum & colon 2 common forms 1. CDC. https://www.cdc.gov/inflammatory-bowel-disease/about/ulcerative-colitis-basics.html; 2. CDC. https://www.cdc.gov/inflammatory-bowel-disease/about/crohns-disease-basics.html; 3. Ungaro R, et al. Lancet. 2017;389:1756-1770; 4. Feuerstein JD, et al. Mayo Clin Proc. 2014;89:1553-1563; 5. Storch I, et al. Inflamm Bowel Dis. 2003;9:104-115; 6. Adapted from Alsoud et al., 2021 [unable to verify full citation details, requires author input]; CD: Crohn's disease; CDC: Centers for Disease Control and Prevention; GI: Gastrointestinal; IBD: Inflammatory bowel disease; JAK: Janus kinase; N: Number; S1PR: Sphingosine-1-phosphate receptor; SoC: Standard of care; TNFα: Tumor necrosis factor alpha; UC: Ulcerative colitis; *Delta shown as average across drug class Despite options targeting different pathways, ~70-80% of patients fail to achieve remission within one year UC induction clinical remission rates of current therapies IBD pathophysiology ▪ All therapies exhibit an efficacy ceiling; initial response limited to 20-50% ▪ 20-30% of responders achieve remission within 1 year, durable remission is a long-term goal ▪ TL1a emerging as a novel MoA and treatment option ▪ Development combining multiple pathways, including TL1a, underway ▪ Dysregulated immune response to intestinal microbiota resulting in chronic inflammation and tissue injury3-5 ▪ High disease burden severely impacting quality of life % Induction of Clinical Remission6 (UC) Efficacy Ceiling leads to inconsistent biologic sequencing guidelines and cycling through multiple treatments resulting in poor quality of life 0 25 50 75 100 TNFα inhibitors (N=4) Integrin inhibitors (N=1) p19/p40 inhibitors (N=2) JAK inhibitors (N=6) S1PR modulators (N=3) Placebo group 10-15% 5-30% 10-20% 10-15% 5-30% *Delta shown as average across drug class Treatment group Immunology 15-30 Age of onset (in years) 63% of patients are 19-65 years old 50/50 Males and females Highest incidence in non-Hispanic White 65% moderate/severe, similar across countries and UC vs. CD
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Afimkibart in UC: AMETRINE-1&2 enrollment complete Potential for subcutaneous administration in induction and maintenance 170 ▪ Ph IIb (TUSCANY-2) in UC demonstrated strong efficacy and safety in a large group of pts (n=245) ▪ Sustained clinical remission and endoscopic improvement from induction to chronic phase Ph IIb (TUSCANY-2) in UC1 Ph III AMETRINE-1,2 and new AMETRINE–SC study design in UC ▪ Ph III (AMETRINE-1&2) completed enrolment Q3 2026 ; Ph III results expected 2027 ▪ Ph III UC SC study to assess the efficacy and safety of subcutaneous induction therapy to be initiated 2026 ▪ Exploring biomarker test which may predict better response to treatment 1. Danese S, et al. Lancet Gastroenterol Hepatol. 2025; ISSN 2468-1253; †Defined per FDA definition with an mMS 0–2 (endoscopic subscore = 0 or 1, and rectal bleeding subscore = 0); ‡Defined as endoscopic subscore = 0 or 1; aTL1A: Anti-tumor necrosis factor-like cytokine 1A; CD: Crohn's disease; CI: Confidence interval; FDA: Food and Drug Administration; FPI: First-patient-in; IV: Intravenous; MASH: Metabolic dysfunction-associated steatohepatitis; mMS: modified Mayo score; OLE: Open-label extension; Ph: Phase; pts: atients; Q: Quarter; R: Randomization; SC: Subcutaneous; UC: Ulcerative colitis; W: week AMETRINE-1: With treat-through design AMETRINE-2: Induction only afimkibart: SC Placebo: IV afimkibart: IV Efficacy assessment Efficacy assessment N=400 Placebo: SC W12 MaintenanceInduction W52 Efficacy assessment W12 Placebo: IV afimkibart: IV OLEN=350 Open label extension (OLE) AMETRINE-SC Placebo: SC afimkibart: SC Efficacy assessment W12 afimkibart: SC Induction Maintenance OLER Immunology
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Leveraging our multispecifics pipeline for success in IBD Establishing IBD portfolio with afimkibart, complemented by novel MoAs 171 p40xTL1A inhibits two key targets central to IBD pathology: IL-12/ IL-23 and TL1A *Global collaboration with Pfizer; 1. Solin KA, et al. J Crohns Colitis. 2021;15(11):1959-1973; 2. Schmitt H, et al. Gut. 2019;68(5):814-828; 3. Valatas V, et al. Front Immunol. 2019;10:583; 4. Strober W, Fuss IJ. Gastroenterology. 2011;140(6):1756-1767; 5. Li L, et al. Arch Dermatol Res. 2014;306(10):927-932; 6. Verstockt B, et al. Nat Rev Gastroenterol Hepatol. 2023;20(7):433-446; 7. Xu WD, et al. Front Immunol. 2022;13:891328; 8. Bamias G, et al. J Immunol. 2003;171(9):4868-4874; 9. ClinicalTrials.gov Identifier: NCT06536440; 10. ClinicalTrials.gov Identifier: NCT06979336; FPI: First patient in; IBD: Inflammatory bowel disease; IL: Interleukin; MOA: Mechanism of action; p40: Interleukin-12/23 subunit p40; Ph: Phase; TH: T helper; TL1A: Tumor necrosis factor- like ligand 1A; UC: Ulcerative colitis ▪ IL-12 and IL-23 are proinflammatory cytokines containing the p40 subunit, promote intestinal inflammation, and are strongly associated with IBD pathology3-7 ▪ The TL1A cytokine is an amplifier of immune responses that plays a key role in chronic inflammation and tissue damage ▪ Due to the diverse mechanisms driving IBD, simultaneously inhibiting multiple targets may overcome the therapeutic efficacy ceiling8-10 ▪ Ph IIb (SUNCREST) in UC ongoing, data expected in 2027 ▪ Other multispecific antibodies and oral therapies in development, targeting validated and novel driver pathways in IBD p40xTL1A bispecific*1,2 Molecule Pre- clinical Ph I Ph II Ph III Status p40xTL1A bispecific 2027 Bispecific Emerging combinatorial SUNCREST IBD pipeline Immunology
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Ophthalmology Christopher Brittain SVP and Global Head of Product Development Ophthalmology
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New MoAs to target a broader range of disease pathways and address additional indications Susvimo VELODROME trial exploring 9-month dosing expected in 2027 Expanded capabilities that apply biomarkers and data analytics, remote vision monitoring, and AI-supported clinical decision-making Invest end-to-end in retinal vascular disease (RVD), geographic atrophy (GA) and iAMD from discovery, R&D, to commercialization Ophthalmology R&D focus areas 173 Critical Capabilities Examples Extended durability & future technologies Novel MoAs & new indications, addressing multiple disease pathways Digital capabilities Ophthalmology MoA: Mechanism of action; iAMD: intermediate age-related macular degeneration E2E investment
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nAMD DME DR RVO Foundational Angiogenesis ▪ VEGF x Ang-2: Vabysmo ▪ WNT pathway: RG6697 ▪ WNT pathway: AntlerA platform Inflammation ▪ IL-6: Vamikibart ▪ VEGF x IL-6: RG6209 (DutaFab) ▪ Trispecific antibody: RG6913 Emerging Ischemia ▪ SEMA3A: SEMAthera Fibrosis Various preclinical targets Hallmarks of retinal disease and prioritized pathways/targets 174 Ophthalmology DME: Diabetic macular edema; DR: Diabetic retinopathy; nAMD: neovascular age-related macular degeneration; RVO: Retinal vein occlusion Investing in alternative pathways in pursuit of better outcomes beyond anti-VEGF alone Prioritized pathway/targetsHallmarks of Disease Relevance in disease Relevance: Low Moderate High
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Port Delivery Platform (PDP) Addressing key challenges in ophthalmology, such as the need for frequent IVT injections 175 Ophthalmology ▪ Unique platform; first and only approved surgically-implanted long-acting treatment for RVD Innovative platforms ▪ Unparalleled durability for almost all patients, with dosing confidence via continuous delivery ▪ Sustained, optimal drug levels in tissue over time with potential to lower safety risks ▪ Susvimo 9 mo dosing data (VELODROME) expected in 2027 Dosing confidence ▪ Optionality for future assets, customizing novel molecules ▪ Open for external innovation Potential for new assets IVT: Intravitreal; PDP: Port delivery platform: RVD: Retinal vascular disease
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Ophthalmology pipeline VEGFxIL6 DutaFab moving to Ph III; Susvimo approved in EU for nAMD 176 Phase II RG6501 OpRegen® cell therapy1 GA Ophthalmology 1. In collaboration with Lineage Cell Therapeutics (LCTX) 2. Licensed from SanegeneBio; CFB: Complement Factor B; CNV: Corneal neovascularization; DME: Diabetic macular edema; DR: diabetic retinopathy; DutaFab: Dual targeting fragment antigen-binding; GA: Geographic atrophy; nAMD: Neovascular age-related macular degeneration; NME: New molecular entity; TED: Thyroid eye disease; UME: Uveitic macular edema Phase I RG6209 VEGFxIL6 DutaFab DME RG6327 Undisclosed GA RG6441 Undisclosed DR Phase III RG6179 vamikibart UMERG7716 Vabysmo mCNV RG6321 Susvimo nAMD (36-week) GA DME/UME nAMD DR CNV TED Registration RG6168 Enspryng TED RG6697 Undisclosed DME RG6858 CFB siRNA2 GA Antibody RNA-targeting therapeutics Bispecifics Cell therapy Port Delivery Platform DutaFab RG6913 Undisclosed Retinal diseases
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Targeting IL-6 to achieve better visual outcomes Enspryng filed in TED, vamikibart filed in UME, VEGFxIL6 DutaFab advancing to Ph III in DME 177 Ophthalmology DME: Diabetic macular edema; DutaFab: Dual targeting fragment antigen-binding; IL-6: Interleukin-6; TED: Thyroid eye disease; UME: Uveitic macular edema; VEGF: Vascular endothelial growth factor ▪ Il-6 is a key pro-inflammatory cytokine in the pathogenesis of uveitis, retinal diseases, and thyroid eye disease Inflammation is a currently sub-optimally treated pathway in a number of ocular diseases ▪ Enspryng in TED US filing accepted with Priority Review (PDUFA Oct 15) ▪ Vamikibart in UME filed in the US and EU; Ph III (SANDCAT/MEERKAT) data presented at ASRS 2026 ▪ VEGF x IL6 DutaFab advancing to Ph III ▪ Trispecific antibody in development IL-6 targeted development IL-6 Inflammation Leukocyte adhesion & chemotaxis Angiogenesis BRB breakdown VEGF Molecule Indication Ph I Ph II Ph III Status Enspryng TED PDUFA Oct 15 Vamikibart UME Filed in US/EU VEGFxIL6 DutaFab DME Ph III to be initiated Trispecific SANDCAT/MEERKAT SatraGO-1 & 2
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Vamikibart: Potential first non-steroid IVT treatment in UME Filed in US and EU in Q3 178 Ophthalmology 1. Massa H et al. Clin Ophthalmol. 2019;13:1761-1777. 2. Lardenoye CWTA et al. Ophthalmology. 2006;113:1446-1449. 3. Kempen JH et al. Ophthalmology. 2011;118:1916 -1926. 4. Tomkins-Netzer O et al. Ophthalmology. 2015;122:2351-2359. 5. Pleyer U et al. Ophthalmol Ther. 2013;2:55-72. 6. Jobling AI and Augusteyn RC. Clin Exp Optom. 2002;85:61-75; 7. Glenn J Jaffe et al. Presented at ASRS; Jul 15-18; IOI: Intraocular inflammation; IOP: intraocular pressure; IVT: Intravitreal; UME: Uveitic macular edima; ▪ UME is the most frequent cause of vision loss in uveitis1, affecting around one-third of patients, primarily people of working age2 ▪ Despite immunomodulatory therapies, UME persists in 40% of eyes3,4 and corticosteroids, the mainstay of treatment, are associated with undesirable ocular and systemic side effects5,6 ▪ Intraocular, periocular, and systemic corticosteroids are the mainstay of treatment, but have recognized side effects and efficacy limitations High unmet need in UME ▪ Rapid improvements in vision and anatomical outcomes that were highly consistent across dose arms ▪ Well tolerated, with low incidence of treatment-related events of IOI, raised IOP, and cataract ▪ 52-week data to be presented at AAO Ph III (SANDCAT/MEERKAT) in UME7
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VEGFxIL6 DutaFab: Two Ph III in DME H2H vs. Vabysmo to be initiated 179 Ophthalmology *Primary endpoint: Change from baseline in BCVA in the BARDENAS treatment -naïve population; Sources: 1. Goldberg et al. ARVO 2026; BCVA: Best-corrected visual acuity; DME: Diabetic macular edema; DutaFab: Dual targeting fragment antigen-binding; IL-6: Interleukin-6; VEGF: Vascular endothelial growth factor Ph II with proof of concept for combining IL6 and VEGF pathways ▪ Intended to inhibit angiogenesis, vascular permeability and inflammation by binding and blocking VEGF and IL-6 ▪ Compatible with Port Delivery Platform ▪ In a treatment-naïve population, results show 44.7% of patients receiving anti-IL-6 + anti-VEGF gained ≥15 BCVA letters vs. 28.6% with anti-VEGF alone VEGFxIL6 DutaFab: Next generation bispecific Ph II data of anti-IL-6 + anti-VEGF shows superior efficacy to VEGF monotherapy in DME* +/- Ph II (BARDENAS): Change from baseline in BCVA for treatment-naïve patients1
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Enspryng in TED: Subcutaneous delivery with at-home autoinjector US filing accepted with Priority Review (PDUFA Oct 15) 180 Ophthalmology 1 Bartalena L, et al. Epidemiology, Natural History, Risk Factors, and Prevention of Graves’ Orbitopathy. Front Endocrinol. 2020;11:61599 3; AE: Adverse event; IL-6: Interleukin-6; IL-6R: Interlukin-6 receptor; NMOSD: Neuromyelitis optica spectrum disorder; QoL: Quality of life; SC: Subcutaneous; TED: Thyroid eye disease High unmet need in TED for disease modifying therapies that minimize long term complications ▪ Anti-IL-6 designed using novel antibody recycling technology, enabling extended subcutaneous delivery (autoinjector approved) ▪ Inflammation is central in the pathogenesis of TED (serum IL-6 elevated in patients with TED, and correlated with inflammatory disease activity ▪ Enspryng is approved for NMOSD treatment, with a well- established and highly favorable safety profile in >10,000 patients for up to 7 years ▪ Thyroid Eye Disease (TED) is a complex inflammatory autoimmune disease that causes facial disfigurement and visual disabilities impacting QoL, psychological wellbeing, and social interactions ▪ 80% of TED diagnoses are in women, with the median age of diagnosis being 43 (prevalence: 155/100,000)1 ▪ Current treatments are limited and associated with serious AEs such as muscle spasms, alopecia, hyperglycemia, menstrual disorders, hearing loss, and teratogenicity Enspryng is designed to enable maximal sustained IL-6 suppression and allow practical SC dosing
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Enspryng was efficacious and well tolerated in TED patients Ph III SatraGo-1 and SatraGO-2 results published in Ophthalmology 181 Ophthalmology 1. Sources: Subramanian P, et al. NASAOS 2026; Nominal P value, not adjusted for multiplicity; AE: Adverse event; CAS: Clinical activity score; TED: Thyroid eye disease Safety profile was highly favorable and distinct from other treatments ▪ Clinical benefits observed in both active and inactive TED population ▪ Showed clinically meaningful improvements across key efficacy endpoints, including proptosis, diplopia, and CAS in active TED ▪ There was a low incidence of serious adverse events and treatment discontinuation, and no serious infections ▪ No events of hearing loss, hyperglycemia and low rate (<3%) of neutropenia Ph III SatraGO-1 and SatraGO-21 Most common adverse events: active + inactive TED
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RG6858 (Complement Factor B siRNA) advancing to Ph II in GA Systemic therapy with extended durability for Geographic Atrophy Ophthalmology RG6858 in partnership with SanegeneBio; Sources: 1. GlobalData 2024 – Geographic Atrophy and Intermediate AMD Market & Epidemiology Reports; 2. Orozco et al; AMD; Age -related macular degeneration; 3. Data on file; 4. Jaffe et. Al AAO 2026; AP: A lternative pathway; ASO: Antisense oligonucleotide; CFB-ASO: Complement Factor B; GA: Geographic atrophy; KD: Knockdown; SAD: Single ascending dose 182 RG6858 demonstrates superior CFB inhibition3 ▪ On-market complement inhibitors in GA require frequent IVT injections1 ▪ CFB is produced primarily in the liver, with minimal expression in the eye; GalNAc conjugation in RG6858 enables targeted hepatocyte delivery for systemic CFB KD2 ▪ For Dose levels 3 and above, RG6858 achieved near 100% inhibition of CFB and AP activity at 3 mo follow-up ▪ Prior experience from the Ph II GOLDEN study, with CFB-ASO showed ~70% CFB knockdown and ~35% AP activity inhibition, resulting in small, but non-stat sig effect on GA lesion growth4 CFB siRNA with GalNAc liver targeting GalNAc (Liver targeting moiety) 22 nt Antisense Strand 20 nt Sense Strand Ph I Healthy Volunteer SAD Study: CFB Over Time 0.0 mg Dose 1 Dose 2 Dose 3 Dose 4 Dose 5
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Cardiovascular, Renal and Metabolism Manu Chakravarthy SVP and Global Head of Cardiovascular, Renal and Metabolism (CVRM) Product Development
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Unlocking the potential of our pipeline to address global CVRM disease burden 184 CVRM: Cardiovascular, renal, metabolism; NME: New molecular entity; MoA: Mechanism of action; TA: Therapeutic area Cardiovascular, Renal & Metabolism Critical Capabilities Holistic patient solutions Depth of research and technologies Combinations Next gen NMEs with broad MoAs Address the breadth of diseases across CVRM by tackling adiposity dependent and independent drivers Understand the interconnected science, utilize diverse modalities Establish a portfolio of combination therapies within CVRM and adjacent TAs Synergies with Roche Pharma + Diagnostics/Digital Health solutions to prevent and treat CVRM diseases
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Growing prevalence of CVRM diseases is driven by aging, obesity and multimorbidity 185 1. Numbers are rounded to the nearest 0.1 Bn; prevalence estimates based on scientific literature 2. Other metabolic includese.g., polyendocrine metabolic ovarian syndrome, gout 3. Liver includes mainly MASH, MASLD 4. Est. growth: SEA +15 pp, Western Pacific +13 pp, Eastern Mediterranean +12 pp, Africa +8 pp, Americas +9 pp, Europe +2 pp; 3. Clarivate DRG Epidemiology Dashboard 2025; Sources: Hu SS et al., Chin Med J, 2025; Wang L et al., JAMA Intern Med, 2023; Zhou J et al., Clin Gastroenterol Hepatol, 2025; Chen Y et al., J Clin Transl Hepatol, 2024; Estes C et al., J Hepatol, 2018; IDF Diabetes Atlas, 11th ed., 2025; Zhou B et al., Lancet, 2024; Phelps NH et al., Lancet, 2024; Wang L et al., Lancet, 2021; Dandona L et al., Lancet Glob Health, 2018; Kalra A et al., Int J Environ Res Public Health, 2025; GBD 2023 CKD Collaborators, Lancet, 2025; Duseja A et al., J Hepatol, 2024; Kalra S et al., J Gastroenterol Hepatol, 2024; Misra A et al., Diabetes Ther, 2025; Anjana RM et al., Lancet Diabetes Endocrinol, 2023; Srivastava S et al., BMJ Open, 2025; Yusuf S et al., Lancet, 2004; Satoh M et al., Hypertension Res, 2026; WHO Hypertension Key Facts, 2025 Cardiovascular, Renal & Metabolism Global prevalence in 2025 (Bn patients)1 Patient populations for these disease areas are overlapping due to comorbidities Total CVRM burden: 4+ billion Cardiovascular Diabetes3 Other metabolic2 Obesity3 ~0.8 Bn RenalLiver3 ~1.5 Bn 1.7 Bn ~0.2 Bn~0.6 Bn ~1.0 Bn 60-65% of the global adult population expected to have a CVRM disease by 2050 CVRM disease will remain significant in the future
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Adiposity is a key driver of multi-organ disease; however, adiposity-independent drivers also contribute 186 LEADER (NEJM 2016); SUSTAIN-6 (NEJM 2016); SELECT (NEJM 2023). NEJM: New England Journal of Medicine Cardiovascular, Renal & Metabolism Reducing body weight with incretin-based therapy improves obesity associated comorbidities CVRM diseases are interconnected with both adiposity and non- adiposity drivers impacting organ function and mortality Adiposity dependent CKDMASH T2D ASCVD HF Stroke Obesity Adiposity Independent pathways: Insulin resistance Fibro-inflammation Neurohormonal activation Mitochondrial, vascular dysfunction 20% MACE recurrence within 5 years 40% Residual elevated inflammation 6-8% Residual cardiorenal event Each disease treated in isolation Interconnected CVRM diseasesPathways/Pathophysiology
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A pipeline designed for multi-organ protection Addressing both adiposity dependent and independent drivers across the interconnected CVRM spectrum 187 1. Patients with obesity or overweight with at least one weight-related comorbidity including type 2 diabetes; 2. Petrelintide in partnership with Zealand Pharma; 3. Zilebesiran in partnership with Alnylam; 4. RG7985, HM17321 in collaboration with Hanmi Pharma, UCN2: Urocortin-2 (UCN2) analog, pending deal closure; ASCVD: Atherosclerotic cardiovascular disease; GC: Glycemic control; ; CAD: Coronary arterial disease; CVOT: Cardiovascular outcomes trial; HFrEF: Heart Failure with reduced Ejection Fraction; MASH: Metabolic dysfunction-associated steatohepatitis; OW/OB: Overweight/Obesity; T2D: Type-2 diabetes; uHTN: uncontrolled hypertension Cardiovascular, Renal & Metabolism Ph I Ph II Ph IIIMolecule Disease/Indication enicepatide (GLP-1/GIPRA) Obesity +/- T2D1 CT-996 (oral GLP-1RA) petrelintide2 (amylin) enicepatide + petrelintide2 Obesity +/- T2D Obesity +/- T2D Obesity T2D ASCVD afimkibart (anti-TL1A) MASH (F3-4) 103/104 Enith-1/2 201 ZUPREME-1/2 ZYNERGY (H2 26) 702/703 Eni-SPIRE GC (H1 27) Enith-MACE CVOT (H1 27) MetORA (H1 27) HFrEF Enith-rEF (H1 27) RG7985 (UCN2 analog)4 Obesity +/- T2D Update vs Pharma Day 2025 pegozafermin (FGF21) ENLIVEN NLRP3i ASCVD MASH (F2-3) zilebesiran3 (AGT siRNA) uHTN KARDIA-1, 2,3 ZENITH (CVOT) ZUPREME-3/4/5 (H2 26) MASH (F4) ENLIGHTEN-1 fibrosis ENLIGHTEN-2 cirrhosis
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▪ Native hormones and approved GLP-1R agonists signal through both cAMP and β-arrestin – “unbiased” agonism1 ▪ Enicepatide is G protein-biased limiting β-arrestin recruitment but retaining cAMP signaling potency2-4 ▪ Elimination of β-arrestin coupling minimizes receptor degradation potentially leading to prolonged pharmacological activity5 Minimal to no ß-arrestin recruitment results in prolonged glucose lowering and weight loss Enicepatide is a fully biased agonist Enicepatide is intentionally designed to be signal-biased Leveraging biased GLP-1/GIP agonism for potentially greater efficacy and tolerability 188 1. Jones B et al. Nature Communications. 2018;9:160 2. Rodriguez R et al. Presented at the American Diabetes Association 83rd Scientific Session, 23-26 June 2023; San Diego, CA. 3. Chakravarthy MV et al. Presented at the European Association for the Study of Diabetes, 59th Annual Meeting, 2-6 October 2023; Hamburg, Germany. 4. Luo J et al. Presented at the American Diabetes Association 84th Scientific Sessions; June 21-24, 2024; Orlando, FL.; 5. https://carmot.us/incretin-receptor-signaling-bias/; BG: blood glucose; BW: body weight; cAMP: cyclic adenosine monophosphate; GIPR: glucose-dependent insulinotropic polypeptide receptor; GLP-1R: Glucagon-like peptide 1 receptor Cardiovascular, Renal & Metabolism “on” state longer more signaling via cAMP more efficacy (BW and BG)1,3,4 Unbiased agonist Biased agonist 1
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Enicepatide Ph II (103) in OW/OB: Robust weight loss with no plateau More than a quarter of treated participants achieved ≥ 30% weight loss by 48 weeks 189 1. Lingvay I et al., ADA 2026, Poster-2813-LBA; *p ≤ 0.001 vs placebo; **The denominator to calculate the proportion is based on the number of participants who have reached week 48. †Prespecified endpoint; BIC: Best in class; BP: blood pressure; BW: body weight; CI: Confidence interval; CRP: C-reactive protein; CVOT: Cardiovascular outcomes trial; T2D: Type 2 diabetes; WL: weight loss Cardiovascular, Renal & Metabolism Ph II (103) results in overweight/obesity1 ▪ Dose-dependent WL with up to 22.7% change in BW without a plateau at 48 weeks → potential to achieve additional WL with longer treatment ▪ At 48 weeks, 48% of participants achieved ≥ 20% WL, 38% ≥ 25% WL, and 26% ≥ 30% WL at the highest dose ▪ Tolerability profile generally consistent with other incretin-based therapies at similar development stage ▪ @EASD 2026: changes in BP, lipids, CRP and body composition Placebo 4mg 8mg 12mg 16mg 24mg • Ph II (103) study results in OW/OB pts at 48-weeks (ORAL) Enicepatide reduced vascular, haemodynamic and body fluid parameters in OW/OB people, Ph II (103) study (short oral) Enicepatide reduced cv prognostic markers of central and visceral adiposity in OW/OB adults with ≥ 1 comorbidity, Ph II (103) study (short oral) Enicepatide reduced cardiovascular risk factors in OW/OB people, Ph II (103) study (short oral) Weight loss (efficacy estimand) Weight reduction thresholds (at 48 weeks) EASD 2026 data presentations
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• Enicepatide Ph II (104) in OW/OB + T2D: Potential for BID glycemic control 190 Cardiovascular, Renal & Metabolism Ph II (104) Enicepatide in T2D pts with overweight/obesity • HbA1c reduction (efficacy estimand) Placebo Enicepatide 24mg 1. Semaglutide: -1.3% (SUSTAIN 2, semaglutide 0.5 mg) to -2.2% (SUSTAIN FORTE, semaglutide 2 mg); 2. tirzepatide: -1.93% (SURPASS 3, tirzepatide 5 mg) to -2.37% (SURPASS 3, tirzepatide 15 mg); 3. cagrisema: -1.9% (REIMAGINE 2, cagrisema 2.4/2.4 mg) to -2.1% (REDEFINE 2, cagrisema 2.4/2.4 mg); 4. retatrutide: -1.7% (TRANSCEND T2D-1, retatrutide 4 mg) to -2% (TRANSCEND T2D-1, retatrutide 9 mg): only published trial in T2DM population; 5. semaglutide: -2.8% (SUSTAIN 1 trial); 6. tirzepatide: - 3.24% (SURPASS 3); 7. cagrisema: -2.58% (REIMAGINE-2); AEs: adverse events; BID: best-in-disease; BL: baseline; BMI: body mass index; BW: body weight; Co-1 EP: co-primary endpoint; CV: cardiovascular; FU: follow-up; HbA1c: glycated hemoglobin; OW/OB: overweight/obesity; pbo: placebo; Ph: phase; reta: retatrutide; SE: standard error; sema: semaglutide; SGLT2i: sodium-glucose cotransporter-2 inhibitor; T2D/T2DM: type 2 diabetes / type 2 diabetes mellitus; WL: weight loss Molecule HbA1c reduction* semaglutide tirzepatide cagrisema retatrutide -1.3 to -2.2%1 -1.93 to -2.37%2 -1.91 to -2.1%3 -1.7 to -2.0%4 > 60% of treated pts achieved normoglycemia, those with baseline HbA1c >8.5 dropped HbA1c >4% by 48 wks Adjusted Mean change from baseline (+/-SE) -2.65% -0.43% All comers BL A1c > 8.5% -3.24%6 -2.8%5 ▪ Clinically meaningful and statistically significant HbA1c reduction from baseline to W48 of 2.65% (baseline HbA1c 8.1%) ▪ HbA1c reduction of 4.13% in patients with poor baseline glycemic control (baseline A1c >8.5%) ▪ Proportion of patients at W48 achieving target HbA1c ≤6.5% = 90% and <5.7% = 62% ▪ WL at W48: -15.5% with no plateau ▪ Discontinuation due to AEs: 2.0% in enicepatide arms vs 0% in placebo; no level 2 hypoglycemia; safety & tolerability in line with incretin class *Values are non-pbo adjusted HbA1c reductions using the efficacy estimand; studies with similar baseline HbA1c to study104. Standard cross-trial comparison caveats apply, incl. variations in background medications, body weight, treatment duration, etc. -2.58%7 HbA1c reduction by current therapies Enicepatide -2.65% -4.13% Baseline Week 8 Week 16 Week 28 Week 36 Week 48
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Enicepatide: Broadening Ph III clinical development program Ph III in Glycemic control, HFrEF and CVOT will be initiated in H1 2027 191 ASCVD: Atherosclerotic cardiovascular disease; CWM: Chronic weight management; CV: Cardiovascular; CVOT: Cardiovascular outco mes trial; GC: Glycemic control; GIP: Glucose-dependent insulinotropic polypeptide; GLP-1: Glucagon-like peptide-1; HF: Heart failure; HFrEF: Heart failure with reduced ejection fracti on; MACE: Major adverse cardiovascular events; RA: Receptor agonist; QW: Once weekly; OW/OB: Overweight/Obesity; T2D: Type 2 diabetes Cardiovascular, Renal & Metabolism ▪ Ph III CWM studies (Enith-1/2) in people with overweight/obesity is ongoing with recruitment on track ▪ Ph III GC study in people with T2D, including a head-to-head study against tirzepatide – H1 2027 ▪ Ph III CVOT-MACE and CVOT-HFrEF in people with ASCVD/heart failure – H1 2027 Clinical development program Ph I Ph II Ph IIIMolecule Disease/Indication Ph I Ph II Ph III Status Enicepatide GLP-1/GIP RA (QW) OW/OB OW/OB OW/OB + T2D OW/OB Ongoing OW/OB + T2D Ongoing T2D To be initiated H1 27 ASCVD ± T2D To be initiated H1 27 HFrEF ± T2D To be initiated H1 27 CT-388-101 CT-388-103 CT-388-104 Enith-1 (CWM) Enith-2 (CWM) Eni-SPIRE (GC) Enith-MACE (CVOT, including T1D subgroup) Enith-rEF (CV death/HF event reduction) Primary endpoint met
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CT-996: Oral small molecule with positive Ph II, moving into Ph III Additional Ph I data in T2D to be presented Oct 1 at EASD, demonstrating strong reduction of HbA1c 192 1. NCT07081958; BL: Baseline; CI: Confidence interval; EASD: European Association for the Study of Diabetes; EoP2: end of Pha se 2; GI: Gastrointestinal; HbA1c: Glycated hemoglobin; OW/OB: Overweight/Obesity; QD: Once daily; T2D: Type 2 diabetes; TEAE: Treatment -emergent adverse event; WL: weight loss Cardiovascular, Renal & Metabolism CT-996: Ph II in overweight/obesity ▪ Wide dose ranging and various titration regimens explored ▪ Overall data support advancing the program to Phase 3 CT-996 Ph II obesity trial without T2D participants1 Screening Week 3820 CT-996 dose regimen 7 5-week safety follow- up CT-996 dose regimen 6 Placebo Eligibility criteria: • Adults ≥ 18 yrs • OW/OB + one comorbidity (excluding T2D) CT-996 dose regimen 1 1:1:1:1:1: randomization CT-996 dose regimen 2 CT-996 dose regimen 3 CT-996 dose regimen 4 CT-996 dose regimen 5 Primary analysis at week 30 30 Ph I 4wk data in OW/OB +T2D CT-996 Ph I (201, arm 3) OW/OB + T2D, 4 wks Mean change from BL in HbA1c (95% CI), % -0.3 (-0.84,0.20) -1.0 (-1.32,-0.66) -1.3 (-1.55,-0.99) Days HbA1c reduction up to 1.3% CT-996 120mg, n=11 Placebo, n=5 CT-996 90mg, n=11 HbA1c ▪ HbA1c reduction of up to 1.3% within 4 weeks ▪ Strong FPG lowering with no glycemic excursions during MMTT ▪ WL up to 4.9% and no plateau ▪ PK supports once-daily dosing without food/water restrictions ▪ Data to be presented at EASD 2026 on Oct 1 Body weight (%) Days Mean change from BL in Body Weight (95% CI), % -1.8 (-3.43,-0.22) -4.2 (-4.67,-3.73) -4.9 (-5.73,-4.1) Body weight reduction up to 4.9%
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CT-996: Ph III initiation for chronic weight management Oral small molecule combining convenience with efficacy to optimize real-world adherence 193 GLP-1: Glucagon-like peptide-1; RA: Receptor agonist; QD: Once daily; OW/OB: Overweight/Obesity; T2D: Type 2 diabetes; CWM: Chro nic weight management Cardiovascular, Renal & Metabolism Clinical development program Ph I Ph II Ph III Molecule Disease/Indication Ph I Ph II Ph III Status CT-996 GLP-1 RA (QD) OW/OB Obesity OW/OB + T2D OW/OB OW/OB + T2D Ongoing OW/OB + T2D To be initiated H1 27 CT-996-201, Arm 1 CT-996-201, Arm 2 CT-996-201, Arm 3 CT-996 (-702 study) CT-996 (-703 study) Primary endpoint met MetORA CMW Program
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Petrelintide: Potential to redefine weight management experience with double-digit weight loss and improved tolerability 194 1. Developed in collaboration with Zealand Pharma; 2. Data on file; 3. Brændholt Olsen et al. Poster 92-LB. Presented at ADA 83rd Scientific Sessions, June 23–26, 2023, San Diego, CA; 4. Eriksson et al. Presentation at ObesityWeek, November 1–4, 2022, San Diego, CA; 5. Hayes et al. Annu Rev Nutr 2014;34:237–260; 6. Weight-related comorbidities include prediabetes, hypertension, dyslipidemia, obstructive sleep apnea, or cardiovascular disease; BID: Twice daily; FDC: Fixed-dose combination; FPI: First patient in; GIP: Glucose-dependent insulinotropic polypeptide; GLP-1: Glucagon-like peptide-1; MoA: Mechanism of action; OW/OB: Overweight/Obesity; Q1W/QW: Once weekly Cardiovascular, Renal & Metabolism ▪ Potent balanced agonist effect on amylin and calcitonin receptors2,4 ▪ Restores leptin sensitivity to increase satiety (vs. suppressing appetite)5 along with improved insulin sensitivity Petrelintide: Long-acting amylin analog suitable for Q1W dosing1-3 36 amino-acid acylated peptide Enicepatide + petrelintide: Complementary MoA with potential for BID weight loss and glycemic control ▪ Amylin and GLP-1/GIP signaling may support satiety through distinct pathways, potentially offering BID weight loss while maintaining a favourable tolerability profile ▪ Ph II (ZYNERGY) will evaluate the efficacy and safety of petrelintide + enicepatide combination in pts with OW/OB6; FPI expected Q4 2026 ↓ appetite ↓ nausea ↑ insulin ↓ glucagon ↓ gastric acid secretion ↑ lipid deposition ↑ lipogenesis ↓ bone resorption ↓ appetite ↑ nausea ↓ food intake ↑ insulin ↓ glucagon ↓ gastric emptying ↑ lipolysis ↑ cardioprotection ↑ heart rate GIP (Duodenum) GLP-1 (Illeum) amylin (Pancreas) ↑ satiety ↓ food intake ↓ glucagon ↓ gastric emptying ↑ energy expenditure ↓ osteoclast activity ↑ osteoblast activity
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Petrelintide: Ph III monotherapy program in OW/OB +/- T2D initiated Ph II data in OB/OW achieved double digit WL with improved tolerability 195 Petrelintide developed in collaboration with Zealand Pharma; ADA: American Diabetes Association; AE: Adverse event; BMI: Body mass index; CI: Confidence interval; EASD: European Association for the Study of Diabetes; FPI: First patient in; H2: Second half; OW/OB: Overweight/Obesity; QW: Once weekly; SAE: Serious adverse e vent; T2D: Type 2 diabetes Cardiovascular, Renal & Metabolism Clinical development programPh II ZUPREME-1 results ▪ Statistically significant and clinically meaningful weight loss from baseline after 28 weeks in all five treatment arms vs. placebo ▪ Weight loss of up to 10.7% sustained through week 42 vs 1.7% on placebo ▪ AE rates comparable to placebo 0 – 2 – 6 – 10 – 12 0 4 8 1 2 1 6 2 0 2 4 2 8 3 2 3 6 4 0 4 2 Weeks since first dose – 8 – 4 Mean change (%) [95% CI] Placebo -1.7% 8.7% 9.2% 10.2% 10.5% 10.7% 70.8 3.5 60.9 32.9 3.5 69.1 3.7 59.3 34.6 6.2 0 20 40 60 80 100 Pooled petrelintide (N=404) Pooled placebo (N=81) Baseline characteristics: 53% female, mean BMI 37 Molecule Disease/Indication Ph I Ph II Ph III Status Petrelintide amylin analog (QW) OW/OB OW/OB OW/OB + T2D Data 2026 OW/OB FPI Q4 2026 (for Z-3)OW/OB + T2D OW/OB ZUPREME-1 ZUPREME-2 ZUPREME-3 ZUPREME-4 ZUPREME-5 Primary endpoint met ▪ Ph II (ZUPREME-1) in obesity met primary endpoint in H1 2026; data presented at ADA, additional data at EASD 2026 ▪ Ph II (ZUPREME-2) in obesity with T2D data expected H2 2026 ▪ Ph III studies in OW/OB (ZUPREME-3) FPI expected Q4 2026 ▪ Evaluating initiation of additional Ph III trials
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Zilebesiran: Novel MoA with potential to transform HTN management Continuous control of blood pressure with 2x yearly dosing aiming to reduce cardiovascular risk 196 1. Figure adapted from Kario K. Prog Cardiovasc Dis. 2016;59(3):262 –281; 2. Pagidipati et al. ESC 2026; Zilebesiran in partnersh ip with Alnylam Pharmaceuticals; ACE: Angiotensin -converting enzyme; AGT: Angiotensinogen; Ang I/II: Angiotensin I/II; ARB: Angiotensin receptor blocker; BP: Blood pressure; CV: Cardiovascular; CVD: Cardiovascular disease; CVOT: Cardiovascular outcomes trial; HF: Heart failure; HTN: Hypertension; K-3: Kardia-3; MI: Myocardial infarction; RAAS: Renin -angiotensin-aldosterone system; SBP: Systolic blood pressure Cardiovascular, Renal & Metabolism Zilebesiran targets most upstream precursor to RAAS pathway1 Reduced Blood Pressure AGT Ang I Ang II Zilebesiran ACE inhibitors ARBs Aldosterone ACE Diuretics Renin Ph II Kardia-3 posthoc analysis in pts on baseline diuretic with office SBP ≥140mm Hg at month 62 Placebo, N=39 Zilebesiran (300 + 600 mg pooled), N=71 Nighttime (−14.6, −2.5)−8.6 Daytime −7.9 (−13.8, −2.0) Change from baseline (pbo-adj) in Daytime, Nighttime, and 24-hour SBP at mo 6 • 11,000 patients with CVD/risk, SBP >140 mmHg on stable treatment including a diuretic) • Primary Outcome: Composite endpoint of CV death, nonfatal MI, nonfatal stroke, or HF event • Recruitment on track Phase III CVOT (ZENITH) ▪ K-3 post hoc analysis: −8.1 mm Hg (−13.9, −2.4) reduction in 24h SBP at month 6 in pts receiving diuretic with office systolic BP ≥140 mmHg → informed design for ZENITH ▪ Significant reduction in nighttime SBP → single strongest predictor of CV mortality (JACC Advances 2024) ▪ Despite existing oral therapies, less than 50% of patients achieve BP control due to poor adherence ▪ Zilebesiran offers potential for tightest and continuous control of BP thereby improving CV outcomes
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Pegozafermin: Potential best-in-disease therapy in MASH Further strengthens CVRM portfolio and offers optionality for future combination development 197 1. Loomba et al. EASL 2023; *Fourteen ENLIVEN F2/F3 subjects were reclassified as F4 by 3 -panel read; CVRM: Cardiovascular, rena l and metabolism; GLP-1: Glucagon-like peptide-1; MASH: Metabolic dysfunction-associated steatohepatitis; Q2W: Every two weeks; QW: Once weekly Cardiovascular, Renal & Metabolism Ph II (ENLIVEN) week 24 results in pts with MASH and fibrosis (F2-F4)1 ▪ Within 24 weeks, improvements in both MASH resolution and fibrosis observed, including fibrosis improvement in those with compensated cirrhosis (F4c) at baseline* ▪ Sustained benefits on fibrosis markers were observed vs. placebo in patients on background GLP-1 therapy at week 48 (ENLIVEN 48-week extension data) ▪ Pegozafermin was well tolerated across patients Fibrosis improvement ≥ 1stage without worsening of MASH MASH resolution without worsening of fibrosis Pts with F4 at baseline: Fibrosis improvement ≥1 stage without worsening of MASH Clinical development program ▪ Ph III ENLIGHTEN-Fibrosis (F2-F3): Topline histology data exp. in H1 2028 ▪ Ph III ENLIGHTEN-Cirrhosis (F4): Topline histology data exp. in 2028+ ▪ MASH diagnosis: Elecsys PRO-C3 test combined with the ADAPT algorithm Indication Ph I Ph II Ph III Status MASH F2-F3 Ongoing MASH F4 Ongoing ENLIGHTEN-Fibrosis ENLIGHTEN-Cirrhosis
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RG79851: UCN2 analog in obesity with FIC potential Pleiotropic effects for weight loss, improved insulin sensitivity, muscle preservation, and cardiac protection 198 1. RG7985 (HM17321) in collaboration with Hanmi Pharma, pending deal closure; BW: Body weight; BWL: Body weight loss; CRF: Corticotropin-releasing factor; CRFR2: Corticotropin-releasing factor receptor 2; CRFR1: Corticotropin-releasing factor receptor 1; DIO: Diet-induced obese; EASD: European Association for the Study of Diabetes; EoT: End of treatment; FIC: First-in-class; FM: Fat mass; HPA: Hypothalamic-pituitary-adrenal; LM: Lean mass; QW: Once weekly; Sema: Semaglutide; UCN: Urocortin; Cardiovascular, Renal & Metabolism CRFR2-selective biased urocortin 2 (UCN2) analog ▪ Long-acting UCN2 selectively targeting the corticotropin-releasing hormone receptor 2 (CRFR2) in brain, skeletal muscle and heart ▪ The UCN2 pathway has profound pleiotropic potential, enabling a single molecule to simultaneously drive fat breakdown, improve ins sensitivity, preserve muscle, and support cardiovascular function • Hypertrophy • Insulin sensitivity • Energy expenditure • Lipolysis • Appetite • Cardiac protection (under investigation) • High selectivity to on-target • Long-acting suitable for QW Preclinical data in DIO mice Figure adapted from Kim J et al, Hanmi Pharmaceutical, EASD Sep15-19, 2025 Effects of HM17321 (RG7985) in combination with incretin-based drugs on body weight and body composition Body weight (BW) change at EoT DIO, vehicle DIO, HM17321 100nmol/kg DIO, semaglutide 10nmol/kg DIO, HM17321 + semaglutide BW change (% vs D0) HM17321 showed similar WL to semaglutide alone with additive WL effects in combination Fat (FM) and lean mass (LM) change at EoT FM change (% vs D0) LM change (% vs D0) HM17321 + Sema resulted in greater fat mass loss while maintaining/enhancing lean mass Such a profile suggests enhanced muscle insulin sensitization, and could contribute to durable WL maintenance
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Treating and preventing CVRM diseases holistically for those living with or without obesity 199 Cardiovascular, Renal & Metabolism Prevent organ damage Reduce Global Health burden Treat organ dysfunction CKDMASH T2D ASCVD HF Stroke Obesity Adiposity Dependent + Independent Drivers Our focus: Address both adiposity-dependent and –independent drivers using both external + internal R&D to develop transformative medicines to reduce the burden of CVRM diseases
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Doing now what patients need next 200 Translating operational rigor and R&D excellence into sustainable, long-term growth R&D excellence Operational excellence Commercial excellence All major solutions embedded as business-as-usual The Bar applied across all-inhouse and partnered assets Total pipeline value (aNPV) at an all-time high Augmented manufacturing productivity & network optimization Disciplined capital allocation to maximize long-term value creation AI integration across the full value chain Maximizing key on-market assets, incl. via line extensions and devices Targeted execution across entrench, expand and establish archetypes Scaling capabilities for upcoming NME launches across TAs Launching the next wave of innovations Near-term catalysts Giredestrant & fenebrutinib leading the first wave, plus up top 4 additional NME launches by YE 2027 20 NMEs by 2030 Total wave of up to 20 NME launches projected by 2030 6 new Phase III transitions Refueling the pipeline with 6 NMEs advancing to Ph III since Pharma Day 2025 aNPV: adjusted net present value; NME: New molecular entity; TA: Therapeutic areas
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Appendix
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Status as of September 28, 2026 Changes to the development pipeline Pharma Day update 202 New to phase II New to phase III New to registration Removed from phase I Removed from phase II Removed from phase III Approvals New to phase I 1 NME: RG6237 emugrobart (GYM 329) – obesity 1 AI: RG6631 afimkibart (anti-TL1A) - atopic dermatitis 1 NME: RG6794 CDK4/2i - HR+ HER2- BC Phase II initiation* (2 NMEs) : RG6434 NRLP3i – AD, PD (exp Q4 26) RG6035 BrainshuttleTM CD20 - multiple sclerosis (exp H1 27) Phase III initiation* (5 NMEs) : RG68492 petrelintide - obesity +/- T2D (H2 26) RG6209 VEGF x IL6 DutaFab - DME (exp H1 27) RG6652 CT-996 - obesity +/- T2D (exp H1 27) RG6640 enicepatide (CT-388) - obesity +/- T2D, ASCVD, HFrEF (exp H1 27) RG6919 tambotatug pelitecan – 2L+ SCLC (Q4 26) 1 NME: RG6795 CDK4i - HR+ HER2- BC 3 NMEs: RG79851 UCN-2 analog - obesity +/- T2D CHU allosteric ALK inhibitor (AQUA07) – NSCLC RG6767 NME - immunology Phase I initiation* (3 NMEs + 1 AI) : RG6375 CEA12Pb PRIT - mCRC (exp Q3 26) RG6527 NME - COPD (exp Q3 26) RG6644 NME - COPD (exp Q4 26) RG6160 cevostamab - SLE +/- LN (exp Q3 26) 1 AI (US): RG6168 Enspryng - MOGAD 2 NMEs (US): RG7845 fenebrutinib - RMS, PPMS RG6179 vamikibart - UME *FPI pending, not yet accounted for in the pipeline/count ;1. in collaboration with Hanmi Pharma, pending deal closure; 2. Zealand Pharma managed 1 NME (EU): RG6321 Susvimo – wAMD 1 AI (US): RG7159 Gazyva – childhood onset idiopathic nephrotic syndrome
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Status as of September 28, 2026 Roche Group development pipeline RG6026 Columvi monotherapy + combos heme tumors RG6171 giredestrant monotherapy + combos solid tumors RG6330 divarasib monotherapy + combos solid tumors RG6411 enzelkitug (anti-CCR8) solid tumors RG6505 PanRAS inhibitor solid tumors RG6537 AR degrader mCRPC RG6538 P-BCMA-ALLO1 r/r multiple myeloma RG6540 P-CD19 x CD20 - ALLO1 heme tumors RG6620 KRAS G12D inhibitor solid tumors RG66481 cMET ADC solid tumors RG6733 - MM RG6735 - heme tumors RG68102 DLL3 ADC SCLC RG6852 - mCRPC RG69191 tambotatug pelitecan (B7-H3 ADC) solid tumors RG69753 CDH17 ADC CRC RG7828 Lunsumio monotherapy + combos heme tumors CHU clesitamig (DLL3 trispecific) solid tumors CHU codrituzumab HCC CHU MINT91 solid tumors CHU anti-CTLA-4 switch antibody solid tumors CHU pan-KRAS inhibitor (AUBE00) solid tumors CHU allosteric ALK inhibitor (AQUA07) NSCLC Phase I (38 NMEs + 5 AIs) Phase II (12 NMEs + 5 AIs) RG-No - Roche/Genentech; CHU - Chugai managed;1. MediLink managed; 2. Innovent managed; 3. In collaboration with Hansoh Pharma; 4. Qyuns Therapeutics managed; 5. In collaboration with IONIS; 6. In collaboration with Pfizer; 7. Zealand Pharma managed; 8. US rights with Sarepta; 9. In collaboration with Hanmi Pharma, pending deal closure RG6421 TMEM16A potentiator Muco-obstructive respiratory disease RG6498 - IBD RG6767 - immunology RG69814 Il33:TSLP COPD/Asthma CHU anti-C1s recycling antibody immunology RG6622 - coronary artery disease RG6631 afimkibart (anti-TL1A) MASH RG79859 UCN-2 analog obesity +/- T2D RG6035 Brainshuttle CD20 multiple sclerosis RG6434 NLRP3i neurodegenerative disorders RG66275 APOE ASO Alzheimer's disease RG6662 HTT miRNA GT Huntington’s Disease RG6209 VEGF x IL6 DutaFab DME RG6327 - geographic atrophy RG6441 - DR RG6697 - DME RG6858 - retinal diseases RG6913 - DME RG6006 zosurabalpin bacterial infections CHU REVN24 acute diseases RG6114 Itovebi + enzalutamide CRPC RG6114 Itovebi + ribociclib + fulvestrant 1L HR+ Chr8P-loss PIK3CA-wt mBC RG6180 autogene cevumeran solid tumors RG6596 HER2 TKI (ZN-1041) HER2+ mBC RG6794 CDK4/2i HR+ HER2- BC RG6797 dirloctocogene samoparvovec (SPK-8011QQ) hemophilia A RG6631 afimkibart (anti-TL1A) rheumatoid arthritis RG67306 p40xTL1A bispecific antibody UC RG7828 Lunsumio SLE CHU anti-HLA-DQ2.5 x gluten peptides antibody celiac disease RG6418 selnoflast (NLRP3i) coronary artery disease RG6652 GLP-1 RA (CT-996) obesity/ T2D glycemic control RG68497 petrelintide obesity +/- T2D RG6182 MAGL inhibitor multiple sclerosis RG6289 nivegacetor (γ-secretase modulator) Alzheimer’s RG63568 Elevidys DMD, <4 years RG6501 OpRegen geographic atrophy New Molecular Entity (NME) Cardiovascular, Renal & Metabolism Additional Indication (AI) Neurology Oncology / Hematology Ophthalmology Immunology Other 203
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Status as of September 28, 2026 Roche Group development pipeline 204 New Molecular Entity (NME) Cardiovascular, Renal & Metabolism Additional Indication (AI) Neurology Oncology / Hematology Ophthalmology Immunology Other Phase III (12 NMEs + 19 AIs) Registration US & EU (3 NMEs + 9 AI) RG3502 Kadcyla + T HER-2+ eBC high-risk RG6013 Hemlibra Type 3 VWD RG6026 Columvi + Polivy + R-CHP 1L DLBCL Columvi r/r MCL RG6107 PiaSky aHUS RG6114 Itovebi + fulvestrant post CDKi HR+ PIK3CA-mut. BC Itovebi + Phesgo 1L HER2+ PIK3CA-mut. mBC Itovebi + CDK4/6i + letrozole 1L ES PIK3CA-mut. HR+ HER2- advanced BC RG6160 Cevostamab r/r MM RG6171 giredestrant + Phesgo 1L ER+/HER2+ BC giredestrant + CDK4/6i 1L ET resistant ER+/HER2- BC RG6330 divarasib 2L NSCLC divarasib + pembrolizumab 1L NSCLC RG6512 zemocimig (NXT007) hemophilia A RG7473 bexobrutideg r/r CLL RG7828 Lunsumio + lenalidomide 2L+ FL RG7853 Alecensa LA stage III NSCLC RG6149 astegolimab COPD RG62992 sefaxersen (ASO factor B) IgA nephropathy RG6631 afimkibart (anti-TL1A) ulcerative colitis afimkibart (anti-TL1A) Crohn’s disease RG66151 zilebesiran Hypertension RG6640 enicepatide (CT-388) obesity +/- T2D RG6881 pegozafermin MASH with fibrosis stage F2 or F3 pegozafermin MASH with fibrosis stage F4 RG6102 trontinemab early Alzheimer’s RG6168 Enspryng autoimmune encephalitis RG63563 Elevidys DMD, 8 years and older RG7935 prasinezumab Parkinson´s RG6321 Susvimo wAMD, 36-week RG7716 Vabysmo CNV RG6171 giredestrant + everolimus† post-CDK4/6 ER+/HER2- BC giredestrant† ER+ BC adj RG7446 Tecentriq stage III dMMR/MSI-H colon cancer RG7828 Lunsumio + Polivy† 2L+ DLBCL RG7159 Gazyva systemic lupus erythematosus Gazyva†† childhood onset idiopathic nephrotic syndrome* Gazyva membranous nephropathy RG6168 Enspryng† TED RG6179 vamikibart UME RG6168 Enspryng MOGAD RG7845 fenebrutinib† RMS fenebrutinib† PPMS †Filed in US ††Filed in EU, approved in US 1. Alnylam Pharmaceuticals managed; 2. In collaboration with IONIS; 3. US rights with Sarepta; T:Tecentriq, *also known as pediatric nephrotic syndrome (PNS)
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