#1Research & Development Day September 14, 2023 Illi Bristol Myers Squibb™ Not for Product Promotional Use#2Forward Looking Statements and Non-GAAP Financial Information This presentation contains statements about Bristol-Myers Squibb Company's (the "Company") future financial results, plans, business development strategy, anticipated clinical trials, results and regulatory approvals that constitute forward-looking statements for purposes of the safe harbor provisions under the Private Securities Litigation Reform Act of 1995. All statements that are not statements of historical facts are, or may be deemed to be, forward-looking statements. Actual results may differ materially from those expressed in, or implied by, these statements as a result of various factors, including, but not limited to, (i) new laws and regulations, (ii) our ability to obtain, protect, and maintain market exclusivity rights and enforce patents and other intellectual property rights, (iii) our ability to achieve expected clinical, regulatory and contractual milestones on expected timelines or at all, (iv) difficulties or delays in the development and commercialization of new products, (v) difficulties or delays in our clinical trials and the manufacturing, distribution and sale of our products, (vi) adverse outcomes in legal or regulatory proceedings, (vii) risks relating to acquisitions, divestitures, alliances, joint ventures and other portfolio actions and (viii) political and financial instability, including changes in general economic conditions. These and other important factors are discussed in the Company's most recent annual report on Form 10-K and reports on Forms 10-Q and 8-K. These documents are available on the U.S. Securities and Exchange Commission's website, on the Company's website or from Bristol-Myers Squibb Investor Relations. No forward-looking statements can be guaranteed. In addition, any forward-looking statements and clinical data included herein are presented only as of the date hereof. Except as otherwise required by applicable law, the Company undertakes no obligation to publicly update any of the provided information, whether as a result of new information, future events, changed circumstances or otherwise. Ill Bristol Myers Squibb™ Not for Product Promotional Use 2#3Agenda for today Chris Boerner, PhD, EVP - Chief Operating Officer Strategic Overview Robert Plenge, MD, PhD - EVP, Chief Research Officer, Head of Research Building on our strengths to deliver industry-leading R&D BREAK (10 min) Samit Hirawat, MD - EVP, Chief Medical Officer, Drug Development Accelerating Our Deep Development Pipeline (Immunology, Hematology, & Oncology) BREAK (10 min) Samit Hirawat, MD - EVP, Chief Medical Officer, Drug Development Accelerating Our Deep Development Pipeline (Cardiovascular & Neuroscience) Chris Boerner, PhD, EVP - Chief Operating Officer Closing BMS Leadership Q&A Conclusion, lunch reception Ill Bristol Myers Squibb™ Not for Product Promotional Use 3#4Strategic Overview Chris Boerner, PhD EVP, Chief Operating Officer CEO, effective Nov. 1, 2023 Ill Bristol Myers Squibb™ Not for Product Promotional Use 4#5Our business has significant opportunities beyond external expectations Strong Foundation • R&D has delivered: 9 new medicines, numerous milestones • Commercial execution is strong: Key Inline & New Products continue to grow Business momentum is robust: Strong base business & expanding New Product Portfolio 2023-2030 BMY External vs Internal Revenue Drivers Consensus Drivers Drivers of Internal Conviction ⚫ IRA • LOE Exposure In-line and recently launched products with significant commercial opportunities • 12 rapidly advancing new medicines in or near registrational development R&D productivity and efficiency enhancements Strong financial capacity for business development Bristol Myers Squibb™ Not for Product Promotional Use 5 LO#6Numerous levers to drive long-term growth $ $ Strong Base Business with unrecognized durability Increasingly de-risked New Product Portfolio Expanding registrational pipeline from 6 to 12 new assets over next 18 months Robust early pipeline with 30+ assets & opportunity to deliver ~10 INDs a year Increased R&D productivity Strategic optionality from Business Development Bristol Myers Squibb™ Not for Product Promotional Use 6#7Our goal is to deliver sustainable growth Four Key Enablers Evolve R&D for scientific leadership Strong commercial execution to realize value of our marketed portfolio Execute strategic capital allocation to further strengthen our growth profile Foster a high- performance culture and attract & retain industry-leading talent We are driven by our mission: Transforming patients' lives through science Ill Bristol Myers Squibb™ Not for Product Promotional Use 7#8Focus for today Four Key Enablers Evolve R&D for scientific leadership Strong commercial execution to realize value of our marketed portfolio Execute strategic capital allocation to further strengthen our growth profile Foster a high- performance culture and attract & retain industry-leading talent We are driven by our mission: Transforming patients' lives through science Ill Bristol Myers Squibb™ Not for Product Promotional Use 8#9Evolving BMS R&D: World-class organization with increased focus on productivity & scientific leadership Scientific Leadership Cardiovascular Hematology Oncology Immunology Neuroscience Top-tier productivity Increasing Probability of Success Increasing INDs Established leadership Reducing Cycle Times Re-establishing Capitalize on differentiated platforms Targeted Protein Cell Therapy Degradation Biotherapeutics Ill Bristol Myers Squibb™ Small Molecules Retain & attract the best talent in the industry Enabled by a high-performance culture Leveraging partnerships and Al/Digital Technologies Not for Product Promotional Use 9#10Build depth across our therapeutic areas Oncology Extend 10 leadership SC nivolumab, Opdualag, & next generation assets Cardiovascular Deepen leadership in cardiomyopathies & heart failure Diversification beyond 10 Ill Bristol Myers Squibb™ Expand expertise in thrombotic diseases Hematology Immunology Neuroscience Extend leadership across the Multiple Myeloma treatment paradigm Broaden portfolio across leukemias, lymphomas and non-malignant hematologic diseases Establish new standards of care in pulmonology Strengthen presence in dermatology, rheumatology, & gastrointestinal disorders Rapidly advance Cell Therapy into immunologic diseases Build a diverse pipeline across neurodegenerative & neuroinflammation diseases Advance promising clinical assets in Alzheimer's Disease & ALS Not for Product Promotional Use 10#11Differentiated Platforms: Significantly expand the opportunity in Targeted Protein Degradation & Cell Therapy Opportunity for Targeted Protein Degradation Positioned to deliver ~4 INDS annually ☑ Hematology Oncology And expand targets to new therapeutic areas: Immunology Neuroscience Abecma [idecabtagene vicleucel) First-in-Class anti-BCMA SUSPENSION FOR VINFUSION Waves of agents expected to launch over time: Building on Our Leadership in Cell Therapy Today Breyanzi (lisocabtagene maraleucel) SUSPENSION FOR IV INFUSION Best-in-Class anti-CD19 Future GPRC5D CAR T CD19 NEX T BCMA X GPRC5D dual binding CAR Innovative Technologies (e.g., allogeneic) Expansion into Immunology: Starting with CD19 NEX T1 Others Severe, refractory lupus AR LDD Other -3x MS golcadomide Multiple Sclerosis mezigdomide SLE iberdomide Other diseases with high unmet need LBCL Heme Malignancy B-cell Mediated Diseases 1.2023 estimates from Decision Resource Group & BMS Internal Analysis; represents U.S. total diagnosed prevalence Ill Bristol Myers Squibb™ Not for Product Promotional Use 11#12Three R&D productivity objectives to drive long term sustainable growth 1 Increase & Sustain INDS 2 Increase Probability of Success 3 Ill Bristol Myers Squibb™ ~10 INDs per year Increase success rate from first-in-human to approval to -20% Reduce Cycle Times Achieve median of -6.5 years from first- in-human to approval Not for Product Promotional Use 12#13Entering a data-rich period supporting potentially first-in-class/best- in-class assets with significant commercial potential cendakimab Ph III: EoE SOTYKTU (deucravacitinib) Ph III: PSA Induction II CAMZYOS™ (mavacamten) Ph III: nHCM SOTYKTU (deucravacitinib) Ph II: Alopecia Areata (AA) cendakimab Ph III: EGE AR LDD Ph II: 2L+ mCRPC Breyanzi Ph II: RR MZL Reblozyl (luspatercept-aamt) for injection 25mg 75mg Ph II: TD & NTD A-Thal Reblozyl (luspatercept-aamt) for injection 25mg 75mg Ph III: 1L TD MF anti-CCR8 Reblozyl (luspatercept-aamt) for injection 25mg 75mg Ph III: 1L NTD MDS Ph I: Solid Tumors Ph I: Solid Tumors CTLA4 NFPB Ph II: Solid Tumors 2024 - 2025 farletuzumab ecteribulin Ph II: NSCLC mezigdomide Ph III: 2L+ MM Vd combo LPA, Antagonist Ph III: IPF GPRC5D CAR T Ph II: RRMM DGK Inhibitor alnuctamab Ph III: 2-4L MM SOTYKTU (deucravacitinib) Ph III: PSA - Induction I MYK-224 Ph II: HFPEF BCL6 LDD Ph I: Lymphoma milvexian Phase III: SSP mezigdomide Ph III: 2L+ MM Kd combo BET inhib 158 Ph II: 1L MF farletuzumab ecteribulin Ph II: Ovarian ZEPOSIA. (ozanimod) Ph III: Moderate to severe CD - Induction II Opdualag Ph II: 1L Stage IV NSCLC CD19 NEX T Ph I: Severe refractory SLE Opdualag Ph II: 1L HCC Opdualag Ph I/II: 2L+ HCC (Post TKI) Opdualag Ph III: 2L/3L+ MSS MCRC Legend: Oncology Hematology Immunology 1. Japan or Asia study only 2. Confirmatory trial ll Bristol Myers Squibb" Note: excludes assets pending IND approval: HbF Inducer, BCMA x GPRC5D, CD19 NEXT in MS, & TYK2i-CNS Timeline represents data readouts or key data to inform clinical development (timeline not to scale) SOTYKTU (deucravacitinib) Ph III: Moderate to severe SLE Induction I SOTYKTU (deucravacitinib) Ph III: Moderate to severe SLE - Induction II TIGIT Bispecific Ph I: Solid Tumors iberdomide Ph III: 2L+ MM Breyanzi Ph III: RR FL (2L high risk)² Abecma decabrogene vicleucel) Ph III: 1L MM golcadomide Ph III: 1L LBCL once daily milvexian Ph III: ACS ONUREG (azacitidine) 2026 - 2030 Opdualag elF2B Activator Phase II: ALS Ph III: Adj. Melanoma Phase II/III: Low-or Int. Risk MDS ZEPOSIA (ozanimod) Ph III: Moderate to severe CD - Maintenance ZEPOSIA (ozanimod) Ph III: Moderate to severe CD Induction I Cardiovascular Neuroscience SOTYKTU (deucravacitinib) Ph III: SjS LPA1 Antagonist Ph III: PPF milvexian Ph III: AF anti-MTBR-Tau Ph II: Alzheimer's Disease iberdomide Ph III: NDMM Transplant Maintenance Not for Product Promotional Use 13#14What you will hear today яда We are focused on transforming our approach to R&D with an emphasis on: Strengthening scientific leadership in our TAs and platforms Significantly improving the efficiency and productivity of our R&D engine Building a culture of innovation that attracts and retains the best talent The evolved R&D engine will enhance the data-rich period in the second half of the decade A number of these assets have the potential to significantly exceed external expectations based on evolving science Successful execution of our R&D strategy is a core component to enable BMS achieve its strategic goal to achieve sustainable growth Bristol Myers Squibb™ Not for Product Promotional Use 14#15Building on our strengths to deliver industry-leading R&D Robert Plenge, MD, PhD EVP, Chief Research Officer, Head of Research Ill Bristol Myers Squibb™ Not for Product Promotional Use 15#16An integrated approach to research & development Oncology Hematology Thematic Research Centers (TRCs) Biology and translational teams Modalities and platforms Small molecules, biotherapeutics, cell therapy, targeted protein degradation, nucleic acid therapies Research functions Computational biology, clinical Research Immunology Drug Development Research & Development Cardiovascular Neuroscience Early and Late Clinical Development Global Development Operations Global Regulatory Sciences Global Biometrics & Data Sciences Worldwide Patient Safety Portfolio & Strategic Operations pharmacology, DMPK, toxicology, translational medicine Deliver new medicines with transformational potential with an increased probability of success in development Strategy & Capabilities Maximize innovation and productivity to deliver more medicines to patients faster Ill Bristol Myers Squibb™ Not for Product Promotional Use 16#17Three key Research principles to improve R&D productivity Causal human biology Application of human data (e.g., genetics, longitudinal profiling of patient samples) for rigorous target validation in drug discovery Matching modality to mechanism 88 Path to clinical proof-of-concept Invention of high-quality therapeutics that match a modality to a molecular mechanism of action Targeted patient selection (e.g., biomarkers) and clear translational endpoints for improved clinical success Our ambition is to increase the number of INDs with transformational potential and increased probability of success across all stages of clinical development Ill Bristol Myers Squibb™ Not for Product Promotional Use 17#18Investments in "causal human biology to proof-of-concept" research framework ensure we are industry-leading • Causal human biology • Human genetics (germline • and somatic) Translational insights from patients in the real world and BMS clinical trials Matching modality to mechanism Diverse modalities, including: - Small molecules Biotherapeutics Nucleic acid therapies Targeted Protein Degradation Cell Therapy Al-assisted molecule invention 88 Path to clinical proof-of-concept Technologies and diagnostics to enable mechanistic models for dose, schedule, and patient populations "T'EMPUS FINNGEN biobank Open Targets BROAD INSTITUTE Bristol Myers Squibb™ uk insitro SCHRÖDINGER. Exscientia BigHat BIOSCIENCES + 1-8 Not for Product Promotional Use 18#19Research framework is effective: TYK2 genetics and SOTYKTU in immunologic diseases Causal human biology Human genetics (P1104A): implicates TYK2 in multiple immunologic diseases Interferon signature (% reduction) % pSTAT3+ 100 80- 60- 40- 20- Matching modality to mechanism Allosteric inhibitor: A highly selective small-molecule drug ~70% TYK2 inhibition I TYK2 Regulatory domain Interferon signature (% reduction) Path to clinical proof-of-concept Initially psoriasis: now systemic lupus erythematosus (SLE) 110 40 20 20 Phenocopies P1104A homozygous genetic inhibition 0 -20 -40 -60 -80 BL 4 8 12 20 28 32 44 Week 0 G/G C/G CIC Active domain We now consistently apply this Research framework to all our programs to deliver transformational medicines with an increased probability of success in development Ill Bristol Myers Squibb™ Sci Transl Med 2016 Nov; 8(363): 363ra149 PLoS One 2015 April; 10(4): e0122271 Arthritis Rheumatol. 2023 Feb; 75(2): 242-252. Clin Transl Sci. 2023 Jan; 16(1): 151-164 Not for Product Promotional Use 19#20Research framework provides confidence in new programs: novel CNS penetrant TYK2 inhibitor for Multiple Sclerosis (MS) Transformational potential First-in-class, oral, CNS penetrant TYK2 inhibitor with direct anti-inflammatory effects in the CNS to treat neuroinflammatory neurodegenerative disorders. Causal human biology Mechanism is supported by human genetics (P1104A loss-of- function variant), human pathology, clinical fluid biomarkers. Microglia Astrocytes Lymphocytes Mean clinical score Matching modality to mechanism ▲ Wild Type ■Heterozygous ▼ Homozygous BMS TYK2i-CNS Phenocopies P1104A LoF in EAE No EAE control P1104A LOF TYK2 Variant Protects in EAE Model of MS 4.01 3.5 EAE vehicle control 3.0 EAE CNS-TYK2i #1 2.5 2.0 1.5 1.0 0.5 INS vs. PO tr. started on day -3 score of 0.0 0 2 4 6 8 10 12 14 16 Days after Immunisation @ 2 4 6 8 10 12 14 16 18 20 22 Days after Immunisation adapted from Dendrou, 2016 Mean Clinical Score (SEM) EAE CNS-TYK2i #2 phenocopies P1104A pSTAT3 pSTAT3, an indicator of TYK2 activation, is increased in key inflammatory cells of the brain in multiple sclerosis#. Path to clinical proof-of-concept Achieve CNS drug exposure to inhibit CNS TYK2 by at least 70% consistent with pre-clinical data in the EAE mouse model (above) and quantitative systems pharmacology modeling of SOTYKTU in psoriasis and SLE. Sci Transl Med 2016 Nov; 8(363): 363ra149 Ill Bristol Myers Squibb™ # Lu et al, J Neuropathol Exp Neurol 72:1135 (2013); Dendrou et al:Sci Transl Med 2016 Nov 2;8(363):363ra149. doi: 10.1126/scitranslmed.aag1974 Not for Product Promotional Use 20 20#21Research framework applied to Oncology builds on our scientific depth in immuno-oncology Strategy: Build a portfolio of foundational assets to address key tumor intrinsic and tumor extrinsic mechanisms, where combinations will be critical for durable responses with transformational potential. || || We have deep expertise in tumor extrinsic biology Immune Checkpoints Only company with three approved T cell checkpoint inhibitors (CPIs) Adaptive and Innate Immunity Insights from translational datasets to guide the next-generation of transformational medicines Bristol Myers Squibb™ Stroma Neoantigens Tumor Extrinsic Not for Product Promotional Use 21#22Research framework applied to Oncology builds on our scientific depth in immuno-oncology Strategy: Build a portfolio of foundational assets to address key tumor intrinsic and tumor extrinsic mechanisms, where combinations will be critical for durable responses with transformational potential. || || We have deep expertise in tumor extrinsic biology Immune Checkpoints Only company with three approved T cell checkpoint inhibitors (CPIs) Insights from translational datasets to guide the next-generation of transformational medicines Bristol Myers Squibb™ Tumor Extrinsic Adaptive and Innate Immunity Stroma Next-gen T cell CPIs Anti-CTLA4 next-gen, anti-TIGIT bi-specific, dual DGKα/ inhibitor Other immune cells Tregs anti-CCR8 Myeloid anti-ILT4 NK cells anti-NKG2A Aberrant Stromal Biology Neoantigens JNK inhibitor, TGFB inhibitor Not for Product Promotional Use 22#23Research framework applied to Oncology builds on our scientific depth in tumor intrinsic mechanisms Strategy: Tumor Intrinsic Build a portfolio of foundational assets to address key tumor intrinsic and tumor extrinsic mechanisms, where combinations will be critical for durable responses with transformational potential. Ill Bristol Myers Squibb™ Oncogenic Drivers Lineage Specific || || We have emerging expertise in tumor intrinsic biology Clinical and pre-clinical programs targeted to specific tumor types and patient subsets DNA Damage Synthetic Lethal Insights from translational datasets demonstrate the relationship between tumor intrinsic and tumor extrinsic to guide rational combinations Not for Product Promotional Use 23#24Research framework applied to Oncology builds on our scientific depth in tumor intrinsic mechanisms Strategy: Tumor Intrinsic Build a portfolio of foundational assets to address key tumor intrinsic and tumor extrinsic mechanisms, where combinations will be critical for durable responses with transformational potential. Oncogenic Mechanisms repotrectinib in ROS1+ lung cancer, RAS signaling (SHP2 inhibitor) Lineage-specific targets AR LDD in prostate cancer, anti-ganglioside fucosyl-GM1 in SCLC Cancer cell vulnerabilities Context specific dependencies (e.g., DNA damage), synthetic lethal interactions Oncogenic Drivers Lineage Specific DNA Damage Synthetic Lethal || || We have emerging expertise in tumor intrinsic biology Emerging clinical and pre-clinical programs targeted to specific tumor types and patient subsets Insights from translational datasets demonstrate the relationship between tumor intrinsic and tumor extrinsic to guide rational combinations Ill Bristol Myers Squibb™ Not for Product Promotional Use 24#25Research framework plus tumor intrinsic and extrinsic strategy will deliver productivity in Oncology Causal human biology Tumor Intrinsic Oncogenic Mechanisms repotrectinib in ROS1+ lung cancer, RAS signaling (SHP2 inhibitor) Lineage-specific targets AR LDD in prostate cancer, anti-ganglioside fucosyl-GM1 in SCLC Cancer cell vulnerabilities Context specific dependencies (e.g., DNA damage), synthetic lethal interactions Matching modality to mechanism Oncogenic Drivers Immune Checkpoints Lineage Specific Adaptive and Innate Immunity DNA Damage Stroma Synthetic Lethal 88 Path to clinical proof-of-concept Tumor Extrinsic Next-gen T cell CPIs Anti-CTLA4 next-gen, anti-TIGIT bi- specific, dual DGKα/ inhibitor Other immune cells Tregs Anti-CCR8 Myeloid Anti-ILT4 NK cells - Anti-NKG2A Neoantigens Aberrant Stromal Biology JNK inhibitor, TGFB inhibitor Ill Bristol Myers Squibb™ Not for Product Promotional Use 25#26Research framework in action: anti-CCR8 antibody depletes T regulatory cells (Tregs) with combination potential Transformational potential First-in-class, Treg-depleting monoclonal antibody (mAb) with broad combo potential across multiple tumor types. Causal human biology Clinical trial translational data demonstrate CCR8+ regulatory T cells (T regs) are a major barrier to effective immune response to anti-PD1 therapy in multiple cancer types. Matching modality to mechanism BMS-986340 is an anti-CCR8 IgG1 biologic with enhanced non-fucosylated (NF) Fc that binds CCR8 and potently depletes T regs while sparing effector CD8 T cells. Path to clinical proof-of-concept Depletion of CCR8+ Tregs in the tumor after 2 cycles Reduced ratio CCR8 Treg to CD8+ Teff in the tumor 1.5 Anti-PD1 mAb CCR8 Suppressed anti-tumor Tumor cells survive response Activated CCR8+ Treg Ill Bristol Myers Squibb™ Т Suppressed CD8 T cell * Treatment Screening CCR8:CD8 ratio 0.5- 1.0. 0.0 Screening C2D5 Not for Product Promotional Use 26#27Research framework in action: anti-CCR8 antibody depletes T regulatory cells (Tregs) with combination potential Transformational potential First-in-class, Treg-depleting monoclonal antibody (mAb) with broad combo potential across multiple tumor types. Causal human biology Clinical trial translational data demonstrate CCR8+ regulatory T cells (T regs) are a major barrier to effective immune response to anti-PD1 therapy in multiple cancer types. Hypothesis: Matching modality to mechanism BMS-986340 is an anti-CCR8 IgG1 biologic with enhanced non-fucosylated (NF) Fc that binds CCR8 and potently depletes T regs while sparing effector CD8 T cells. Path to clinical proof-of-concept Depletion of CCR8+ Tregs in the tumor after 2 cycles Reduced ratio CCR8 Treg to CD8+ Teff in the tumor 1.5 Anti-CCR8 mAb Deplete CCR8+ Treg Ill Bristol Myers Squibb™ Anti-PD1 mAb Reduce ratio, remove brake Activated CD8 T cell Activated anti-tumor response Tumor cell killing Treatment Screening CCR8:CD8 ratio 1.0. 0.5- 0.0 Screening C2D5 Not for Product Promotional Use 27#28Matching modality to mechanism: Leveraging expertise across multiple modalities Small molecule chemistry Biotherapeutics Allosteric inhibitors Nu Viral RNA Al-assisted screening ProbodyⓇ Therapeutic Immune cell engagers Active site inhibitors Nucleic acid therapies Lentivirus and AAV gene therapy Glycosylation -00120 arw Glycoprene Complex Proces of Host Cel Lipid Membrane Mairie Protein Targeted Protein Degradation Molecular glue Target protein Molecular glue molecule Hetero- bifunctional Target protein ADC degrader megrine Preverse Trip Pre 3 E3 ligase E3 ligase Established Ill Bristol Myers Squibb™ Emerging ⚫ Cysteine residue • Drug-Linker CELMOD LDD CELMOD ADC Discuss today Bi-specifics ADCs Cell Therapy Autologous Single CAR binder Next-generation Multiple other KO/KI TCR ΚΟ MHC-I Dual CAR binder KO MHC-II KO Dual CAR binder Allogeneic, iPSC-derived Not for Product Promotional Use 28#29Targeted Protein Degradation offers the promise of novel targets and clinical differentiation for existing targets Expanded universe of targets (e.g., scaffolding proteins, transcription factors) Drugged: Target with approved drugs (3%) "Dark 659 Genome": (3%) 1,607 No known disease 6,007 (30%) association (30%) Human protein - Coding genes -20,000 Ill Bristol Myers Squibb™ Druggable: No approved drugs, but bind small molecules with high potency (8%) (8%) 12,139 (61%) Disease- relevant: No known potent binders, but implicated in disease (61%) Small molecule enzyme inhibitor Not for Product Promotional Use 29#30Targeted Protein Degradation offers the promise of novel targets and clinical differentiation for existing targets Expanded universe of targets (e.g., scaffolding proteins, transcription factors) Drugged: Target with approved drugs (3%) "Dark Druggable: No approved drugs, but bind small molecules with high potency (8%) Small molecule enzyme inhibitor 659 Genome": (3%) 1,607 No known (8%) 6,007 disease (30%) association (30%) Human protein - Coding genes ~20,000 Disease- relevant: No known potent binders, but implicated in disease (61%) Scaffold 12,139 (61%) Opportunity for TPD Scaffold protein Transcription factor Ill Bristol Myers Squibb™ Not for Product Promotional Use 30#31Targeted Protein Degradation offers the promise of novel targets and clinical differentiation for existing targets Expanded universe of targets (e.g., scaffolding proteins, transcription factors) Drugged: Target with approved drugs (3%) "Dark Druggable: No approved drugs, but bind small molecules with high potency (8%) Small molecule enzyme inhibitor 659 Genome": (3%) 1,607 No known (8%) 6,007 disease (30%) association (30%) Human protein - Coding genes ~20,000 Disease- relevant: No known potent binders, but implicated in disease (61%) Scaffold 12,139 (61%) Opportunity for TPD Scaffold protein Ill Bristol Myers Squibb™ COAS Transcription factor Not for Product Promotional Use 31#32Targeted Protein Degradation offers the promise of novel targets and clinical differentiation for existing targets Expanded universe of targets (e.g., scaffolding proteins, transcription factors) Potentially superior efficacy (e.g., overcome resistance, higher selectivity) Drugged: Target with approved drugs (3%) "Dark 659 Genome": No known (3%) 1,607 (8%) 6,007 disease (30%) association (30%) Human protein - Coding genes -20,000 Ill Bristol Myers Squibb™ Druggable: No approved drugs, but bind small molecules with high potency (8%) Disease- relevant: No known potent binders, but implicated in 12,139 (61%) disease (61%) Scaffold Scaffold protein Small molecule enzyme inhibitor Transcription factor CELMOD Kinase Inhibitors Not for Product Promotional Use 32#33Our industry leading position in protein degradation is driven by portfolio breadth and depth of expertise Molecular glue Industry-leading capabilities Hetero- bifunctional Target protein ADC degrader Target protein Molecular glue molecule E3 ligase CELMOD evotec E3 ligase LDD Cysteine residue • Drug-Linker CELMOD ADC Berkeley UNIVERSITY SGC Ill Bristol Myers Squibb™ A-ALPHA BIO SyntheX Targeting the undruggable AMPHISTA THERAPEUTICS Not for Product Promotional Use 33#34Our industry leading position in protein degradation is driven by portfolio breadth and depth of expertise Industry-leading capabilities Molecular glue Target protein Molecular glue molecule E3 ligase CELMOD evotec Berkeley UNIVERSITY OF CALIFORNIA Hetero- bifunctional Target protein ADC degrader Cysteine residue E3 ligase • Drug-Linker LDD SGC A-ALPHA BIO Full Development Early Development CELMOD ADC IND-enabling studies SyntheX Targeting the undruggable AMPHISTA THERAPEUTICS Industry-leading pipeline iberdomide: Multiple Myeloma golcadomide: Lymphoma CK1a: Acute Myeloid Leukemia BCL6 LDD: Lymphoma HbF CELMOD: Sickle Cell Disease CELMOD Solid Tumors Discuss today mezigdomide: Multiple Myeloma AR LDD: Prostate Helios: Solid Tumors LDD: Prostate LDD: Autoimmune >15 pre-clinical programs across multiple therapeutic areas Potential to efficiently deliver -4 INDS annually and expand beyond Heme/Onc targets (Immunology, CV, Neuroscience) Ill Bristol Myers Squibb™ Not for Product Promotional Use 34#35The swift expansion of our CELMOD library has enabled key scientific insights and an increased number of IND candidates Diversify chemical library Novel substrates • -3 -2 -1 0 1 2 3 て 3 CELMOD library 2019 CELMOD library 2023 Ill Bristol Myers Squibb™ 0 Expanding CELMOD library identifies novel substrates and novel degrons Molecules profiled in proteomics Novel degrons Degron 1 Degron 2 Degron 3 Cereblon Not for Product Promotional Use 35#36The swift expansion of our CELMOD library has enabled key scientific insights and an increased number of IND candidates Diversify chemical library Novel substrates • -3 -2 -1 0 1 2 3 て 3 0 Expanding CELMOD library identifies novel substrates and novel degrons Molecules profiled in proteomics Novel degrons CELMOD library 2019 CELMOD library 2023 Ill Bristol Myers Squibb™ Causal human biology 10 CELMODs for Oncology in full discovery & IND enabling studies Not for Product Promotional Use 36#37Target protein Molecular glue molecule E3 ligase Targeting the previously undruggable: A novel CELMOD for Sickle Cell Disease Transformational potential Oral small molecule that increases fetal hemoglobin to functionally cure sickle cell anemia (e.g., eliminate pain crisis, prevent long term organ damage). Causal human biology Genetically validated targets that lead to persistence of fetal hemoglobin (HbF) are associated with improved clinical outcomes in patients with sickle cell anemia. Beta-globin locus 5 4 3 2 1 ε Gy Ay δ Β HbS Matching modality to mechanism Through our CELMOD proteomics initiative, we have identified CELMODs that degrade HbF genetic targets and increase HbF in pre-clinical models. HbF expression 8000- wwww 6000- Vehicle control CELMOD (high) CELMOD (low) 4000- 2000- TH Path to clinical proof-of-concept α B disease 10% HbF 20% 30% Hydroxyurea a LCR HSS Embryonic Fetal Adult 3'HS1 HbF Ill Bristol Myers Squibb™ healthy Reduced Reduced mortality recurring events Asymptomatic presentation Not for Product Promotional Use 37#38Ligand directed degraders (LDD) complement CELMODs in our approach to Targeted Protein Degradation Different from Same as CELMODS Ill Bristol Myers Squibb™ CELMODS E2 E3 ligase Ub NH₂ Target Protein Heterobifunctional molecule E2 E3 ligase LDD molecule recycling Ubiquitination NH₂ Ternary complex Ub NH2 Peptide fragments Proteasome Polyubiquitination Proteasomal degradation Early Development AR LDD: Prostate BCL6 LDD: Lymphoma IND-enabling studies LDD: Prostate LDD: Autoimmune Not for Product Promotional Use 38#39Target protein E3 ligase BMS-986458 is a novel ligand directed degrader (LDD) targeting BCL6 in lymphoma Transformational potential Oral small molecule medicine to treat B cell lymphomas driven by abnormalities in BCL6 signaling pathway. Causal human biology Gain-of-function somatic BCL6 mutations lead to B cell lymphomas and deletion of BCL6 prevents B cell maturation. Naive B cells Healthy, Germinal center Mature B cells Matching modality to mechanism that has exquisite We created a BCL6 LDD selectivity relative to the human proteome -log10 (nominal p-value) Only target degraded BCL6 GSNKAL BCL2CSPTIZE IKZFZFP91 WEE IVDP 4 CHEK1 IKZF3 -4 -2 0 2 4 Log² fold change (vs/ DMSO) Path to clinical proof-of-concept Correlate BCL6 degradation with clinical benefit BCL6 IHC high expression High BCL6 Malignant B cells (e.g., DLBCL) Ill Bristol Myers Squibb™ BCL6 LDD drug Conc. (μM) 100 -20 -10 Plasma conc. -0 10- 10 Tumor conc. -20 1 30 40 50 0.11 -60 0.01 BCL6 levels -70 80 98% 98% 95% 90 ☐ 0.001 -100 -2 Veh 2 4 6 8 10 12 14 16 Sample collection time (h) % BCL6 Degradation in -30% DLBCL Not for Product Promotional Use 39#40A new frontier: CELMOD ADCs to improve efficacy and safety in hematology/solid tumors Causal human biology Combine a clinically validated tumor targeted antibody with a clinically validated tumor cell-biased CELMOD to enhance efficacy and tolerability in hematology/solid tumors Path to clinical proof-of-concept Enhanced efficacy of ADC at lower levels of administered CELMOD Matching modality to mechanism Tumor cytotoxic CELMOD with catalytic activity Tumor targeted antibody to tumor antigen AF Tumor cell Ill Bristol Myers Squibb™ Tumor volume (mm³) 2000- n = 5 1500 1000 500- IV dose 20 HH HH 中 ┤ 25 30 35 Days post-inoculation Vehicle control 10x CELMOD + Ab, unconjugated 1x CELMOD ADC 3x CELMOD ADC 10x CELMOD ADC ADC vs unconjugated components Not for Product Promotional Use 40#41Targeted Protein Degradation and Cell Therapy: Two differentiated platforms for optimizing therapies for patients Targeted Protein Degradation Molecular glue Target protein Molecular glue molecule Hetero- bifunctional Target protein ADC degrader Matching modality to mechanism Cell Therapy Autologous Next-generation Single CAR binder Multiple other KO/KI TCR KO Dual CAR binder E3 ligase E3 ligase Cysteine residue Invention of high- quality therapeutics that match a modality Dual CAR binder MHC-I KO MHC-II • Drug-Linker KO to a molecular mechanism of action CELMOD LDD Ill Bristol Myers Squibb™ CELMOD ADC These two platforms unlock novel targets and mechanisms to efficiently deliver INDS with the potential to improve the lives of patients Allogeneic, iPSC-derived Not for Product Promotional Use 41#42We are leveraging expertise to enable expansion beyond Hematology while increasing manufacturing efficiency Wave 1 Single CAR binder Wave 2 Dual CAR binder Wave 3 Multiple other KO/KI Dual CAR binder TCR KO Next-gen engineering Evolving delivery systems Optimizing manufacturing Ill Bristol Myers Squibb™ MHC-I KO MHC-II KO Monospecific CAR Dual Targeting CAR Engineered CAR/TCR Not for Product Promotional Use 42#43We are leveraging expertise to enable expansion beyond Hematology while increasing manufacturing efficiency Wave 1 Single CAR binder Wave 2 Dual CAR binder Wave 3 Multiple other KO/KI Dual CAR binder TCR KO Next-gen engineering Evolving delivery systems Optimizing manufacturing Ill Bristol Myers Squibb™ Monospecific CAR Surface GP200 Tran) MA (matrial Prote A p Dual Targeting CAR 3 VV NC nucleocap СА Lentivirus (LVV) MHC-I KO MHC-II KO Engineered CAR/TCR electroporation MINIMIN DNA MIN MINIMIM Adeno-associated virus (AAV) Lipid nanoparticles (LNP) Non-viral delivery (NVD) Not for Product Promotional Use 43#44We are leveraging expertise to enable expansion beyond Hematology while increasing manufacturing efficiency Wave 1 Single CAR binder Wave 2 Dual CAR binder Wave 3 Multiple other KO/KI Dual CAR binder TCR KO Next-gen engineering MHC-I KO MHC-II KO Evolving delivery systems Optimizing manufacturing Monospecific CAR Surface GP200 Tran) MA (matrial Prote A p Dual Targeting CAR 3 VV NC nucleocap CA Lentivirus (LVV) Autologous Breyanzi Abecma a/B T cells Adeno-associated virus (AAV) Ill Bristol Myers Squibb™ 2 seventybio Arsenal Bio editas OBSIDIAN MEDICINE Autologous NEX T platform Engineered CAR/TCR electroporation MINIMIN DNA MIN MINIMIM Lipid nanoparticles (LNP) Non-viral delivery (NVD) Allogeneic Healthy donor or iPSC a/B or y/o T cells, iNK/iT cells a/B T cells gentibio① CENTURY Not for Product Promotional Use 44 THERAPEUTICS Immatics#45Next-gen Cell Therapy pipeline: Oncology, Immunology, and Allogenic Hematology Early Discovery Late Discovery IND-Enabling Development Approved Breyanzi Abecma 2seventybio Partnered BMS-986393 GPRC5D CART (MM) ll Bristol Myers Squibb™ BCMAXGPRC5D CART (MM); Bristol Myers Squibb™ Allo Eng CART (NHL) Bristol Myers Squibb™ iPSC-derived iT/INK (AML) CENTURY Partnered THERAPEUTICS iPSC-derived iT/INK (MM) Discuss today. Immunology Oncology Eng Treg (IBD) CD19 NEXT (Multiple autoimmune disorders); Bristol Myers Squibb Next-gen CART (Multiple autoimmune disorders) Bristol Myers Squibb™ gentibio Partnered Allo Eng gd eTCR T (solid tumors) Logic-gated CAR T Program 1 (indication not disclosed) Logic-gated CART Program 2 (indication not disclosed) Allo Eng CART (RCC) ll Bristol Myers Squibb™ immatics Partnered O -ArsenalBio Partnered ll Bristol Myers Squibb Cell Therapy Platform: Autologous Allogeneic Not disclosed Cell Engineering Technologies: О editas CRISPR engineered program MEDICINE Ill Bristol Myers Squibb™ Multiple Eng CAR T Programs Multiple Eng eTCR T Programs Ill Bristol Myers Squibb Immatics OBSIDIAN Immune payloading programs not disclosed Not for Product Promotional Use 45#46Wave 2 Dual targeting BCMAXGPRC5D CART for relapsed/refractory multiple myeloma Transformational potential Primary and secondary non-response to standard of care therapies remains an unmet medical need in MM. Surface BCMA expression Causal human biology BCMA and GPRC5D are clinically validated targets independently expressed in multiple myeloma Antigen heterogeneity and clonal evolution are factors limiting efficacy of BCMA CAR T in multiple myeloma 40000 20000 10000 6000 4000 2000 1000 600 400 200 100 High BCMA Low GPRC5D 100 Low BCMA High GPRC5D 400 1000 4000 10000 40000 % BCMA positive tumor cells 1201 100- 80- Abecma trial 0 0 0 0 0 0 0 0 0 0 0 000000000000 Oooo 60- 0 هلم 40- 20- 0 000 ° ° ° . Matching modality to mechanism Optimized bispecific construct to overcome intra-and inter-patient antigen variability/heterogeneity and maintain functionality in cases of low BCMA Optimized manufacturing to develop at scale process improving product quality and manufacturing failures Myeloma burden (SBCMA) Path to clinical proof-of-concept Non-response Early relapse (3-6M) CART Infusion Getting into Depth of initial Maintaining response response response Loss of functional CAR T Late relapse Surface GPRC5D expression Ill Bristol Myers Squibb™ Baseline Biopsy Progression Biopsy Not for Product Promotional Use 46#47Wave 2 CD19 NEX T to reset the immune system in multiple Immunology indications Transformational potential Sequential immunotherapy offers the potential for a functional cure in autoimmunity: 1: Control inflammation; 2: Reset immune memory; 3: Promote homeostasis and repair Academic study Causal human biology 20 Before CAR-T After CAR-T 20 of CD19 CAR-T demonstrates B cell memory reset and functional cure in SLE. Ill Bristol Myers Squibb™ SLEDAI (disease activity) 15 15 10 T 5 Complete Remission • 0 ■Pt. 1 ■Pt. 2 ■Pt. 3 Pt. 4 Pt. 5 Pt. 6 ■Pt. 7 Adapted from Taubmann, J., et al EULAR (2023): 93-94 • Matching modality to mechanism Single CAR binder Chimeric antigen receptor (CAR): CD19 and intracellular domains same as Breyanzi Manufacturing: autologous, single train with shortened turn-around time, lower failure rates Path to clinical proof-of-concept Expand on findings from academic study in SLE Monitor biomarker predictors of cell therapy safety and efficacy Demonstrate evidence of resetting immune memory Not for Product Promotional Use 47#48Computational science, including Artificial Intelligence and Machine Learning, is applied at all stages of Research Leverage patient data and predictive analytics to define causal human biology Somatic mutations + SCNA Utilize computational power for predictive molecule invention to improve quality and accelerate timelines Predict: Molecular design and prioritization Make: Ligand synthesis Build mechanistic models to address specific problems to increase success and accelerate timelines in the clinic Patient State Drivers PSDA PSDB PSDC PSDD PSDE Regulon expression in patient states Ill Bristol Myers Squibb™ ΑΙ ML Learn: Model retraining Test: Dynamic profiling strategy BODY ON DRUG MECHANISM Concentration 1... I Time Fit-for-purpose Mechanistic Models DRUG ON BODY Not for Product Promotional Use 48#49Internal R&D strengths are amplified through extensive network of external partnerships SevenBridges biobank TEMPUS COTA PicnicHealth Memorial Sloan Kettering Cancer Center editas Genes & Health strandiji TWIST ENVISAGENICS -ArsenalBio Guardian RESEARCH NETWORK 1-O International Immuno-Oncology Network indivumed Concert Al GNS HEALTHCARE CENTURY THERAPEUTICS Fred Hutch Cancer Center Peter Mac Peter MacCallum Cancer Centre Victoria Australia Eisai →volastra ---- MEDIC Immatics 药明巨诺 B A-ALPHA BIO SGC CHARM THERAPEUTICS flatiron FINNGEN CROHN'S &COLITIS FOUNDATION NEW YORK GENOME CENTER HITGEN Scripps Research ADNI A AVIDITY BIOSCIENCES insitro AMPHISTA THERAPEUTICS prothena DARWIN HEALTH evotec 熊本大学 EMORY PRECISION THERAPEUTICS for CANCER MEDICINE Kumamoto University UNIVERSITY REPARE THERAPEUTICS SyntheX PathAl UNIVERSITY OF OXFC gentibio NORDIC BIOSCIENCE Roche santaris pharma a/s Fulcrum Therapeutics Logon OCTANT IMIDomics Agilent BD Adaptive BIOCARTIS illumina Thermo Fisher SCIENTIFIC HEMATOGENIX UNIVERSITY OF MIAMI Queen Mary University of London somalogic MAYO CLINIC МРААСТ THE ROYAL MARSDEN biopôle Open Targets Exscientia KeyBioscience SKYHAWK evotec THERAPEUTICE TUBULIS SCHRÖDINGER. Incentive Molecular Halozyme beLAB2122 LAB282 Templates JW Therapeutics Neuroscience Cardiovascular Protein Degradation Immunology Oncology & Hematology Computational Biology Small Molecule Drug Discovery Ill Bristol Myers Squibb™ Illi Bristol Myers Squibb™ > 100 active strategic collaborations BMS also has an extensive network of over 150 academic research alliances Translational Medicine DxTerity beLAB1407 JOHNS HOPKINS UNIVERSITY Cross- Therapeutic Mount Sinai Penn COLUMBIA UNIVERSITY Discovery Biotherapeutics X CYTOMX THERAPEUTICS zymeworks RECOMBINANT ANTIBODY NETWORK Adimab Not for Product Promotional Use 49#50We have the right strategy at the right time to develop transformational medicines & change patients' lives Causal human biology Path to improve R&D productivity Use of human data for rigorous target validation in drug discovery Build on our strength in five core therapeutic areas • Matching modality to mechanism Diverse portfolio of modalities supplemented with Al and ML Diverse modalities, including Targeted Protein Degradation and Cell Therapy 88 Path to clinical proof-of-concept Enable mechanistic models for dose, schedule, and patient selection All enabled by translational insights, computational science and BD partnerships Ill Bristol Myers Squibb™ . Increase number of INDs with transformational potential Increase success in clinical development Not for Product Promotional Use 50#51Program will reconvene following a short break Ill Bristol Myers Squibb™ (10 min) Not for Product Promotional Use 51#52Accelerating our deep development pipeline Samit Hirawat, MD EVP, Chief Medical Officer, Drug Development Ill Bristol Myers Squibb™ Not for Product Promotional Use 52#53An integrated approach to research & development Oncology Hematology Thematic Research Centers (TRCs) Biology and translational teams Modalities and platforms Small molecules, biotherapeutics, cell therapy, targeted protein degradation, nucleic acid therapies Research functions Computational biology, clinical pharmacology, DMPK, toxicology, translational medicine Research Immunology Drug Research & Development Development Cardiovascular Neuroscience Early and Late Clinical Development Global Development Operations Global Regulatory Sciences Global Biometrics & Data Sciences Worldwide Patient Safety Portfolio & Strategic Operations Strategy & Capabilities Deliver new medicines with transformational potential with an increased probability of success in Development Maximize innovation and productivity to deliver more medicines to patients faster Ill Bristol Myers Squibb™ Not for Product Promotional Use 53#54Phase 3 Phase 2 Phase 1 +AHR Antagonist*^ Solid Tumors +Anti-CCR8^ Solid Tumors + Anti-ILT4^ Solid Tumors +Anti-NKG2A^ Solid Tumors +AR LDD 1L, 2L mCRPC Oncology +Claudin 18.2 ADC Solid Tumors +DGK Inhibitor Solid Tumors +JNK Inhibitor Solid Tumors +Helios CELMOD Solid Tumors +MAGEA4/8 TCER* Solid Tumors +Anti-CTLA-4 NF ProbodyⓇ Solid Tumors Anti-Fucosyl GM1^ RR SCLC + Anti-IL-8^ Solid Tumors +BET Inhibitor (BMS-986378)^ Solid Tumors +farletuzumab ecteribulin Solid Tumors nivolumab+relatlimab Stage IV 1L NSCLC nivolumab+relatlimab 1L HCC nivolumab+relatlimab 2L+ HCC (Post-TKI) +SHP2 Inhibitor^ Solid Tumors +TGFB Inhibitor^ Solid Tumors +TIGIT Bispecific Solid Tumors +repotrectinib NTRK Pan-Tumor +alnuctamab RR MM +Anti-SIRPa BMS Pipeline Hematology +BET Inhibitor (BMS-986378)^ RR NHL Immunology +Anti-CD40 Autoimmune Disease afimetoran CLE +GPRC5D CAR T RR MM +CD19 NEX T Severe Refractory SLE +IL2-CD25 Autoimmune Disease +PKCe Inhibitor Autoimmune Disease Data as of September 14th, 2023 Cardiovascular +FXla Inhibitor Thrombotic Disorders Neuroscience +Anti-MTBR-Tau Alzheimer's Disease +elF2b Activator Neuroscience +FAAH/MGLL Dual Inhibitor Neuroscience +BTK Inhibitor Neuroscience Hematologic Malignancies CK1a Degrader Hematologic Malignancies +BCMA NKE RR MM +BCL6 LDD Lymphoma BET Inhibitor (BMS-986158) Hematologic Malignancies +golcadomide^ RR NHL +BET Inhibitor (BMS-986158) 1L MF ABECMA 1-4L+ MM BREYANZI 3L+ CLL golcadomide^ 1L DLBCL +CD33 NKE RR MM RR MZL BREYANZI +afimetoran SLE SOTYKTU Alopecia Areata BREYANZI RR MCL SOTYKTU DLE +TYK2 Inhibitor (BMS-986322) REBLOZYL A-Thalassemia ONUREG MDS BREYANZI RR FL Mod-to-Severe Psoriasis +MYK-224 OHCM +danicamtiv Dilated Cardiomyopathy CAMZYOS HFPEF +SC nivolumab + rHuPH20 (multi-indications) 2L RCC OPDIVO Adjuvant HCC OPDIVO Peri-adjuvant MIUC OPDIVO Stage IB-IIIA Adjuvant NSCLC* OPDIVO+YERVOY 1L HCC OPDIVO+YERVOY 1L MIUC OPDIVO+YERVOY St3 Unresectable NSCLC OPDUALAG Adjuvant Melanoma OPDUALAG 2L/3L+ MSS MCRC +iberdomide 2L+ MM iberdomide Post-ASCT Maintenance NDMM +mezigdomide 2L+ MM Vd INREBIC MF REBLOZYL 1L TD MF Associated Anemia REBLOZYL 1L NTD MDS Associated Anemia Ill Bristol Myers Squibb™ OPDIVO OPDIVO + YERVOY 1L+ MSI High CRC +SC nivolumab + relatlimab + rHuPH20 Peri-adjuvant NSCLC mezigdomide 2L+ MM Kd 1L Melanoma * Partner-run study; ^ Trials exploring various combinations; +NME leading indication; # BMS territory SOTYKTU SOTYKTU +cendakimab Eosinophilic Esophagitis SLE +LPA1 Antagonist IPF LPA1 Antagonist PPF SOTYKTU Psoriatic Arthritis Sjögren's Syndrome ZEPOSIA Crohn's Disease +obexelimab*# IgG4-Related Disease +milvexian Secondary Stroke Prevention* milvexian Acute Coronary Syndrome* milvexian Atrial Fibrillation* CAMZYOS nHCM Not for Product Promotional Use#55Immunology Ill Bristol Myers Squibb™ Not for Product Promotional Use 55#56Immunology LPA₁ Sotyktu Addressing high unmet medical need in Immunology Asset Approved Registrational+ CD19 NEX T Exploratory/PoC Studies* Moderate-to-severe Psoriasis Psoriatic Arthritis Alopecia Areata SOTYKTUO (deucravacitinib)ets Sjögren's Syndrome Systemic Lupus Moderate-to-severe Erythematosus Moderate-to-severe Crohn's ZEPOSIA. Ulcerative Colitis Disease (ozanimod) capsules 0.92 mg CD19 NEX T cendakimab LPA, Antagonist Ill Bristol Myers Squibb™ 1. Japan registrational trial; † ongoing or initiating 2023/2024 • Eosinophilic Esophagitis Eosinophilic Gastroenteritis¹ Idiopathic Pulmonary Fibrosis Progressive Pulmonary Fibrosis Severe, refractory Systemic Lupus Erythematosus Not for Product Promotional Use 56#57LPA₁ Sotyktu CD19 NEX T Immunology Significant unmet need in pulmonary fibrosis Disease • Fibrotic ILD: Associated with thickening of the lung lining, causing irreversible damage¹ • IPF: Fatal disease with 3-5 years median survival² PPF: Heterogenous group of ILDS with a progressive-fibrosing phenotype¹ • Unmet Need Ideal novel therapies which can be used alone or in combination with approved anti-fibrotics • Treatments needed to address underlying fibrosis and reduce decline in lung function ⚫ Tolerable treatment options to increase adherence and QoL improvement . Treatment Opportunity Deliver a potential new product with an improved efficacy and tolerability profile over current treatment options Approved therapies do not treat underlying fibrosis or halt disease progression 1. Raghu. Am J Respir Crit Care Med. 2022 May 1;205(9):e18-e47. 2. Raghu. Am J Respir Crit Care Med. 2011 Mar 15;183(6):788-824. Bristol Myers Squibb™ Not for Product Promotional Use 57#58Immunology LPA₁ Sotyktu CD19 NEX T LPA₁ signaling is central to the pathogenesis of fibrotic lung diseases 1. Epithelial cell apoptosis¹ LPA₁ signaling promotes apoptosis of alveolar epithelial cells Recurrent lung injury 2. Fibroblast recruitment2,3 LPA₁ signaling induces fibroblast chemotaxis to the site of injury LPA LPA₁ CYTOPLASM Profibrotic signaling 4. Fibroblast survival1 LPA₁ signaling increases fibroblast resistance to apoptosis 3. Fibroblast proliferation & activation 4,5 LPA₁ signaling stimulates fibroblast proliferation and collagen secretion 1. Funke M, et al. Am J Respir Cell Mol Biol. 2012;46(3):355-364. 2. Tager AM, et al. Nat Med. 2008;14(1):45-54. 3. Swaney JS, et al. Br J Pharmacol. 2010;160(7):1699-1713. Ill Bristol Myers Squibb™ 4. Cheng PTW, et al. J Med Chem. 2021 Nov 11;64(21):15549-15581. 5. Decato BE, et al. Respir Res. 2022;23(1):61. Not for Product Promotional Use 58#59Immunology LPA₁ Sotyktu CD19 NEX T Robust Phase 2 IPF and PPF results support development of BMS-986278 across the spectrum of progressive lung fibrosis IPF1 PPF2 Rate of FVC decline ppFVC over 26 weeks³ 0 -0.5 60 mg n=93 30 mg n=91 Placebo n=92 -1 -1.5 -2 -2.5 -3 62% Relative reduction in FVC decline Rate of FVC decline ppFVC over 26 weeks³ 0 -0.5 60 mg 30 mg n=42 -1 -1.5 -2 -2.5 -3 -3.5 69% Relative reduction in FVC decline n=39 " Placebo n=41 -3.5 -4 -4 -4.5 -5 -5.5 Compelling reduction in the decline of lung function at 60 mg in both IPF and PPF cohorts, with a favorable and differentiated tolerability profile 1. Corte TJ, et al. Am J Respir Crit Care Med. 2023;207:A2785. 2. Corte TJ, et al. ERS 2023 [Presentation #RCT800]. 3. Mean +SEM, primary endpoint, linear model with Ill Bristol Myers Squibb™ supplementary estimand Not for Product Promotional Use 59#60Immunology LPA₁ Sotyktu ALOFT-IPF1 and ALOFT-PPF2: Two parallel Phase 3 registrational studies Key Inclusion: >40 yo (IPF); >21 yo (PPF) . FVC ≥40%, DLco >25% With or without concomitant background SoC Primary Endpoint: BMS-986278 (60 mg BID) Change in FVC (mL) at week 52 R 1:1:1 BMS-986278 (120 mg BID) Key Secondary Endpoint: Placebo Time to disease progression Patient-reported outcomes . Change in 6MWT 1. NCT06003426; 2. NCT06025578 Ill Bristol Myers Squibb™ Phase 3 studies initiating Data anticipated in 2026 (IPF) and 2028 (PPF) Primary Endpoint Week 52 CD19 NEX T Patients continue treatment and follow-up Not for Product Promotional Use 60#61Immunology Significant unmet medical need in lupus Complex Disease • Chronic auto-immune disorder of widespread inflammation leading to end- organ damage and death Impact on QoL due to multiple associated comorbidities (i.e., infections, CV disease) • LPA₁ Sotyktu CD19 NEX T Current Treatment Landscape Few approved branded therapies • Current options have limited efficacy • Many therapies require repeated injections Significant Need: Opportunity for patients to have a novel, oral, effective medicine Ill Bristol Myers Squibb™ Not for Product Promotional Use 61#62Immunology LPA₁ Sotyktu CD19 NEX T SLE Phase 2 results across endpoints provide rationale for Phase 3 100 SRI(4) response rates at week 481 A 22.7 (95% CI, 7.4-36.6) OR: 2.6 (95% CI, 1.4-4.8) Achievement of Lupus Low Disease Activity (LLDAS) at week 481 100 80 60 Response rate, % 50 60 40 40 20 20 P<0.001 57.1 47.3 47.2 34.4 0 n = 90 n = 91 n = 93 n = 89 Placebo deucravacitinib 3 mg BID 80 60 60 60 Δ 22.9 (95% CI, 9.6-35.3) OR: 4.0 (95% CI, 1.9-8.5) P<0.001 Response rate, % 40 20 20 36.3 25.8 23.7 13.3 n = 90 n = 91 n = 93 n = 89 0 deucravacitinib 6 mg BID deucravacitinib 12 mg QD Met the primary endpoint, and all secondary endpoints achieved or meaningfully improved at week 48 with a well tolerated safety profile consistent with earlier trials 1. Morand E, et al. Arthritis & Rheumatology. 2023 Feb;75(2):242-252.; Multiplicity-adjusted secondary end point; Primary endpoint was met: percentage of patients Ill Bristol Myers Squibb achieving SRI (4) at week 32 (P<0.001) Not for Product Promotional Use 62#63Response rate, % Immunology LPA₁ Sotyktu CD19 NEX T SLE Phase 2 data demonstrates compelling efficacy across domains Response rate, % Skin Domain: CLASI-501,2 Baseline CLASI activity score ≥ 10 with ≥ 50% decrease from baseline > Patient response treated with deucravacitinib in the PAISLEY Phase 2 study4 100 80 60 P<0.001 69.6 62.1 56.0 40 16.7 20 n = 24 n = 23 n = 25 0 n = 29 Week 48 Joint Domain: Joint Count-501,3 ≥ 6 active (tender + swollen) joints at baseline, with ≥ 50% decrease from baseline 100 80 68.3 40 20 642 56.5 60 52.3 45.3 Placebo 0 n = 64 n = 63 n = 65 n = 62 deucravacitinib 3 mg BID Week 48 deucravacitinib 6 mg BID deucravacitinib 12 mg QD Baseline Near complete resolution Day 1 Week 40 Day 1 Ill Bristol Myers Squibb™ 1. Morand E, et al. Arthritis & Rheumatology. 2023 Feb;75(2):242-252. 2. Multiplicity-adjusted secondary end point; A 52.9 (95% CI, 21.7-72.7), OR: 10.5 (95% CI, 2.5-43.0). 3. Exploratory non-multiplicity-controlled end point; 4. NCT03252587, Images used with investigator permission Not for Product Promotional Use 63 Week 20#64Immunology LPA₁ Sotyktu CD19 NEX T SLE Phase 3 registrational program (POETYK-SLE-11 and POETYK-SLE-2² parallel studies) Inclusion Criteria: • SLEDAI-2K > 6 with skin and/or joint involvement BILAG: 1A or 2Bs . Seropositivity R • Stable background therapy 1:1 • No severe organ- threatening disease Primary Endpoint: SRI(4) at Week 52 1. NCT05617677; 2. NCT05620407 Ill Bristol Myers Squibb™ Primary Endpoint Week 52 deucravacitinib 3 mg BID + SoC Placebo + SoC Optional long-term extension and follow-up Data anticipated in 2026 Not for Product Promotional Use 64#65Immunology LPA₁1 Sotyktu CD19 NEX T Development in Sjögren's Syndrome supported by Phase 2 results in SLE 88 M Unmet Need SjS is an autoimmune disease characterized by dry eye and mouth with potential involvement of other organs No approved therapies that slow the progression of SjS Most patients require supportive care to manage symptoms¹ • . Disease mechanism and genetic data support reason to believe Genetic studies implicate TYK2 pathways in SjS² Interferon activity is increased systemically and in tissue of patients with SjS³ SjS and SLE have shared pathogenesis with common biomarkers and lab findings Based on similarity to SLE and high unmet need, the Phase 3 trial in Sjögren's Syndrome is ongoing 1. https://sjogrens.org/understanding-sjogrens/treatment; 2. Khatri B, et al. Nature Communications. 2022;13(4287):1-17. 3. Ill Bristol Myers Squibb Brkic Z, et al. Ann Rheum Dis. 2013;72:728-735. Not for Product Promotional Use 65#66Immunology LPA₁ Sotyktu CD19 NEX T Sjögren's Syndrome Phase 3 study (POETYK-SjS-11) Inclusion Criteria: Meet 2016 ACR/EULAR criteria with disease duration ≤7.5 yrs Anti-SSA/RO+ •⚫ ESSDAI ≥5 Primary Endpoint: ESSDAI change from baseline at Week 52 Key Secondary Endpoint: ESSPRI deucravacitinib 3 mg BID R deucravacitinib 6 mg BID 1:1:1 Placebo Ill Bristol Myers Squibb™ 1. NCT05946941 Data anticipated in 2027 Primary Endpoint Week 52 Long-term extension and follow- up Not for Product Promotional Use 66#67Immunology LPA₁ Sotyktu CD19 NEX T First-in-class TYK2 inhibitor to treat PsO, with broad potential across PsA, SLE, SjS, and AA Today Psoriasis Sotyktu is approved for moderate-to-severe PSO and has reset the bar for oral treatments Near-Term Psoriatic Arthritis Leveraging strong relationship between PSO and PsA, sharing common pathogenic mechanisms1 Future Systemic Lupus Erythematosus, Sjögren's Syndrome, & Alopecia Areata Disruptive potential in SLE and new opportunity in SjS given similar disease pathogenesis Potential in AA based on inhibition of the IL-12/IFNY axis² Oral, tolerable, mechanistically differentiated TYK-2 targeting agent provides broad applicability across a range of immune-mediated diseases 1. Mease PJ, Armstrong AW. Drugs. 2014;74:423-441. 2. Edelkamp J, et al. ESDR 2022 [poster presentation]. Bristol Myers Squibb™ Not for Product Promotional Use 67#68Immunology LPA₁ Sotyktu CD19 NEX T Compelling CART data in lupus supports expanding new modality to address unmet need Potential transformational efficacy and favorable safety demonstrated with CD19 CAR T Disease Remission Post CART Treatment¹ SLEDAI Data Suggests Immune System Reset² Before CAR T After CAR T Before CAR T After CAR T 20 100% 20 100% 15 80% 15 All patients achieved complete remission 60% 10 10 5 5 40% Remission 20% 0 0 0 0 0 0 0 ■Pt. 1 Pt. 2 Pt. 3 Pt. 4 Pt. 5 Pt. 6 Pt. 7 80% 60% 40% 20% 0% 0% Pt. 1 Pt. 2 Pt. 3 Pt. 4 Pt. 5 Pt. 1 Pt. 2 Pt. 3 Pt. 4 Pt. 5 ■Pt. 1 Pt. 2 Pt. 3 Pt. 4 Pt. 5 Pt. 6 Pt. 7 7/7 pts achieved durable DORIS complete remission off all therapy; encouraging safety & tolerability with only grade 1 cytokine release syndrome and no neurotoxicity Patient immune system reset after CAR T treatment: Measurement of immunoglobulins shift from mature B-cells expressing IgA & IgG to naïve B-cells expressing IgM & IgD IgD ■IgM IgA IgG Ill Bristol Myers Squibb™ 1. Adapted from Taubmann, J., et al EULAR (2023): 93-94. 2. Adapted from Mackensen, A., Müller, F., Mougiakakos, D. et al. Nat Med 28, 2124-2132 (2022) Not for Product Promotional Use 68#69Immunology LPA₁ Sotyktu CD19 NEX T Potential transformative treatment option for patients with certain severe immunologic diseases BMS-986353 expresses the same CD19 specific CAR construct as best-in-class Breyanzi 1,2 Anti-CD19 Targeting Domain 1,2 Extracellular single-chain variable fragment to recognize CD19 CD28 Hinge/Transmembrane Domain³ 4-1BB Costimulatory Domain 1,2 Stimulates CD8+ central memory T-cell generation and favors CAR T-cell persistence4 CD3-Activation Domain 1,2 Breyanzi achieves rapid and complete B-cell depletion in patients with B-cell malignancies NEXT: Next generation technology manufacturing platform balances speed and robustness Faster turnaround time Optimized cell expansion time Increased productivity • Leverages a closed and automated manufacturing platform leads to increased yield and lowered cost Innovative technologies Proprietary harvest technology improves purity CD19 NEX T: Differentiated safety profile of Breyanzi with an enhanced manufacturing process 1. Makita S, et al. Drugs Context. 2019;8:212567. 2. Teoh J, et al. Blood. 2019;134:593. 3. Jayaraman J, et al. EBioMedicine. 2020;58:102931. 4. Weinkove R, et al. Clin Ill Bristol Myers Squibb Transl Immunol. 2019:8;e1049. Not for Product Promotional Use 69#70Immunology LPA₁ Sotyktu CD19 NEX T Severe, refractory SLE Phase 1 study Open label1: Assess the safety, preliminary efficacy, pharmokinetics Key eligibility criteria: 2019 ACR/EULAR classification criteria of SLE Presence of anti-dsDNA, anti-histone, anti-chromatin, or anti-Sm antibodies • ≥ 1 major organ system with a BILAG A score Inadequate response to glucocorticoids and to at least 2 treatments Part A Dose escalation Part B Dose expansion to optimize RP2D Data anticipated in 2024 Ill Bristol Myers Squibb™ 1. NCT05869955 Not for Product Promotional Use 70#71Immunology LPA₁ Sotyktu CD19 NEX T Rapidly expanding into other B-cell mediated diseases ጸ Numerous B-cell mediated diseases with select patient populations SLE Systemic Sclerosis Idiopathic inflammatory Multiple Myopathies Sclerosis Other indications Adding cohorts to Phase 1 severe, refractory SLE trial (e.g., myositis and others) Phase 1 trial in Multiple Sclerosis to be initiated Ill Bristol Myers Squibb™ Not for Product Promotional Use 71#72Immunology LPA₁ Sotyktu CD19 NEX T Rapidly building our portfolio in Immunology LPA₁ Antagonist: New potential standard of care in IPF & PPF with registrational Phase 3 programs initiating Sotyktu: Compelling Phase 2 data supports ongoing registrational Phase 3 programs in SLE & SjS CD19 NEX T: Phase 1 study in severe, refractory SLE initiated and expanding into other immunologic diseases Exciting additional registrational Phase 3 programs: Cendakimab in EoE & EGE Zeposia in CD Sotyktu in PSA Exploring 5 additional assets in early development across indications Addressing immunologic diseases with high unmet need impacting 8M+1 patients Ill Bristol Myers Squibb™ 1. 2023 estimates from Decision Resource Group & BMS Internal Analysis across indications in the U.S. & EU5 Not for Product Promotional Use 72#73Hematology Ill Bristol Myers Squibb™ Bristo Myers Sa Not for Product Promotional Use 73#74Hematology Reblozyl BET Inhibitor Breyanzi golcadomide Abecma alnuctamab GPRC5D Addressing high unmet medical need in Hematology Asset SUSPENSION FOR IV INFUSION Approved 5L+ R/R MM¹ • Registrationalt 3L+ triple-class exposed MM Sub-optimal response post-SCT iber/mezi Exploratory/PoC Studiest Abecma [idecabtagene vicleucel) Breyanzi (lisocabtagene maraleucel); Reblozyl (luspatercept-aamt) for injection 25mg. 75mg SUSPENSION 2L LBCL • 3L+ LBCL FOR IV INFUSION 1L MDS . 2L TD MDS-RS alnuctamab BET Inhibitor (BMS-986158) iberdomide golcadomide GPRC5D CAR T mezigdomide • • R/R CLL/SLL R/R MCL • ⚫ 2L+ FL; 3L+ FL • R/R MZL TD & NTD² Beta Thalassemia 1L NTD MDS TD MF 2-4L MM . Alpha Thalassemia³ NDMM post-SCT maintenance Novel combinations in MM Novel combinations in MF • 2-3L MM 1L LBCL Quadruple-class exposed MM 2-4L MM 2L+ MM 1L DLBCL R/R PTCL4 Novel combinations 1. Approved in 4L+ ex-US; 2. NTD approved ex-U.S.; 3. Asia-only study; 4. Japan-only study; † ongoing or initiating 2023/2024 Ill Bristol Myers Squibb™ Not for Product Promotional Use 74#75Hematology Reblozyl BET Inhibitor Breyanzi golcadomide Abecma alnuctamab GPRC5D Rapidly expanding use in the treatment of anemia FDA approved as first-line treatment of anemia in adults with lower-risk MDS OOX ㅁㅁ iber/mezi First and only therapy to demonstrate superiority over epoetin alpha in the head-to- head Phase 3 COMMANDS study Nearly doubled transfusion independence with concurrent hemoglobin increase vs epoetin alpha with a well-established safety profile Demonstrates more durable responses of transfusion independence vs epoetin alpha Expansion opportunities with ongoing studies in anemia associated with 1L TD MF, 1L NTD MDS, and alpha-thalassemia¹ Ill Bristol Myers Squibb™ 1. Asia-only study Not for Product Promotional Use 75#76iber/mezi Hematology Reblozyl BET Inhibitor Breyanzi golcadomide Abecma alnuctamab GPRC5D Phase 3 INDEPENDENCE 1L TD anemia in MF trial design1 Key Eligibility Criteria: MPN-associated MF • Stable dose JAK2 inhibitor • Transfusion dependent Stratification: Blinded Core Treatment Period (24 weeks) Extended Treatment (Week 25+) Luspatercept + JAK2i SQ every 3 weeks • BL RBC transfusion burden R DIPSS (intermediate vs. high) 2:1 Primary Endpoint: • RBC transfusion independence Placebo + JAK2i SQ every 3 weeks Day 169 Response Assessment: RBC-TI 12W/24W Continued Treatment Crossover from placebo to lusptercept allowed if no response at primary endpoint response assessment for ≥12 weeks Key Secondary Endpoint: RBC transfusion independence for ≥16 weeks Ill Bristol Myers Squibb™ 1. NCT04717414 Expected data readout 2025 Not for Product Promotional Use 76#77iber/mezi Hematology Reblozyl BET Inhibitor Breyanzi golcadomide Abecma alnuctamab GPRC5D BMS-986158: Potential-best in-class BET inhibitor with broad applicability BETi Mechanism of Action Unmet need in MF remains for new treatments which lead to strong & durable spleen volume reduction, symptom improvement, and extended survival BETI: Phase 1/2 study ongoing in MF2 Dose Escalation Phase Dose Expansion Phase Crosstalk JAK21 BETi 1L MF (rux-naïve) BMS-158 + ruxolitinib 15 mg BID JAK-STAT signaling BET (BRD2,BRD3, BRD4) H3K6me1 H3K27ac NF-kB activation Inflammatory NF-KB1 genes TGF-B Proinflammatory cytokines GLI1 Bone marrow fibrosis Inflammation signals Extramedullary hematopoiesis BET Inhibitors alone and in combination with JAK inhibitors have shown clinical benefit in patients with MF1 Ill Bristol Myers Squibb™ 1. Mascarenhas J, et al. Blood 2019; 134(suppl 1):670. 2. NCT04817007 1L MF (rux-naïve) BMS-158 RP2D + ruxolitinib 10 mg BID 1L MF (add-on to rux) BMS-158 RP2D + ruxolitinib previously tolerated dose 2L MF (rux-exposed) BMS-158+ fedratinib 400 mg QD 2L MF (rux-exposed) BMS-158 RP2D + fedratinib 400 mg QD • • 2L MF (rux-exposed) BMS-158 RP2D monotherapy Primary Endpoint: Safety, tolerability, MTD and/or RP2D Key Secondary Endpoint: Preliminary efficacy based on SVR Proof-of-concept data anticipated in 2024 Not for Product Promotional Use 77#78Hematology Reblozyl BET Inhibitor Breyanzi golcadomide Abecma alnuctamab GPRC5D Breyanzi provides transformational benefits to patients Before Breyanzi infusion 10 iber/mezi One month after Breyanzi infusion Follicular Lymphoma Patient from TRANSCEND-FL1 1. Images used with investigator permission from TRANSCEND-FL Ill Bristol Myers Squibb™ h Not for Product Promotional Use 78#79Hematology Reblozyl BET Inhibitor Breyanzi golcadomide Abecma alnuctamab GPRC5D Best-in-class CAR T across the broadest array of B-cell malignancies 01 02 • • Best-in-class CAR T with the broadest label in 2L+ LBCL Differentiated efficacy & safety profile TRANSCEND-CLL: First & only pivotal trial in high-risk R/R CLL/SLL Demonstrated deep and durable responses LBCL Large B-Cell Lymphoma MCL Mantle Cell Lymphoma Aggressive Rapidly progressive but responsive to chemotherapy and often curable Bristol Myers Squibb™ CLL/SLL Chronic Lymphocytic Leukemia/ Small Lymphocytic Lymphoma . 03 iber/mezi Potential best-in-disease in R/R FL Unprecedented data in additional lymphoma types including R/R MCL FL Follicular Lymphoma MZL Marginal Zone Lymphoma Indolent Slowly progressive and responsive to therapy but not typically curable with standard approaches Not for Product Promotional Use 79#80Hematology Reblozyl BET Inhibitor Breyanzi golcadomide Abecma alnuctamab GPRC5D iber/mezi Expanding Targeted Protein Degradation into lymphoma Unmet Need in 1L LBCL: High-risk disease defined based on the IPI, where R-CHOP leads to cure in less patients Overall response rate, % High response rates seen with golcadomide + R-CHOP in 1L DLBCL1 100 ORR, 100% 80 67% 60 60 60 40 40 20 20 33% 0 All Dose Levels (n=15) CR, 100% . CR • 100 PR Dose Level 1 0.4 mg day 1-7 (n=7) Manageable Safety Profile1 No new safety signals were observed with golcadomide monotherapy Golcadomide was safely combined with rituximab, with no DLTs observed • Golcadomide has good combinability with R-CHOP, with manageable safety profile Plan to initiate 1L LBCL registrational trial in 2024 Data anticipated 2027+ 1. Munoz J, et al. ICML 2023 (poster #438). Ill Bristol Myers Squibb™ Not for Product Promotional Use 80#81Hematology Reblozyl BET Inhibitor Breyanzi golcadomide Abecma alnuctamab GPRC5D iber/mezi Moving into earlier lines of therapy in multiple myeloma Today Abecma (idecabtagene vicleucel) SUSPENSION FOR IV INFUSION 5L+ MM with differentiated real-world evidence Near-Term Moving into a triple-class exposed population KarMMa-3 is currently under review in U.S., EU, and Japan Future Phase 3, KarMMa-9 study initiating Expansion to NDMM with inadequate response to transplant Ill Bristol Myers Squibb™ Not for Product Promotional Use 81#82Hematology Reblozyl BET Inhibitor Breyanzi golcadomide Abecma alnuctamab GPRC5D Confidence in Abecma's competitive profile further reinforced by real world evidence R/R MM Efficacy Outcomes¹ Best ORR 84% 73% R/R MM Safety Outcomes¹ Best Response ≥ CR Any CRS/Grade ≥3 Any NT/Grade ≥3 42% 33% 84% 82% iber/mezi ide-cel RWE Predictable safety profile well understood Real world data confirms the efficacy profile in a real world population Strong manufacturing reliability confirmed: 94% success rate Data supports CAR T before other BCMA-targeted therapies in the real world² 18% 18% 5% 3% 3% 6% ide-cel KarMMa ide-cel RWE ide-cel KarMMa ide-cel RWE ide-cel KarMMa ide-cel RWE ide-cel KarMMa ide-cel KarMMa (Phase 2 cohort), n=128 ide-cel RWE, n=159 Ill Bristol Myers Squibb™ 1. Hansen DK, et al. J Clin Oncol. 2023;41:2087-97. 2. Ferreri CJ, et al. Blood Cancer J. 2023;13:117. Including antibody drug conjugate, bispecific antibody, or BCMA CART on clinical trial Not for Product Promotional Use 82#83Hematology Reblozyl BET Inhibitor Breyanzi golcadomide Abecma alnuctamab GPRC5D iber/mezi KarMMa-21: Strong data supports advancing Abecma into Phase 3 KarMMa-9 study Response, % 100% 80% Overall Response Rate ORR, 87.1% ISCR ■CR ■ VGPR PR 48.4% 60% CR, 74.2% 40% 25.8% 20% 0% 9.7% 3.2% n=31 PFS, % 100- 90- 80 70- 60- 50- 40- 30- 8 8 8 8 8 8 8 8 Progression-Free Survival Safety Grade ≥3 n=31 90.1% (SE: 5.43) 83.1% (SE: 6.89) H CRS 0 iiNT 3.2% Infections 12.9% 20- 10- All patients N=31 Number of events n=6 Median: 30.7 months (95% CI; NE, NE) 0. Manageable tolerability profile 0 -2 T T T T T T T T 4 6 8 10 12 14 16 18 20 22 24 26 28 30 8- - 32 with low rates of Gr≥3 Time, months NT and infections and At risk 31 31 29 29 29 29 27 27 27 26 26 26 22 15 9 3 0 no Gr≥3 CRS KarMMa-2 Cohort 2c studied Abecma in patients with clinical high-risk MM due to inadequate response (<VGPR) to frontline ASCT ll Bristol Myers Squibb™ 1. Dhodapkar M, et al. ASH 2022 [Presentation #3314]. Not for Product Promotional Use 83#84Hematology Reblozyl BET Inhibitor Breyanzi golcadomide Abecma alnuctamab GPRC5D iber/mezi Pivotal KarMMa-9 in patients with sub-optimal response post-ASCT Inclusion Criteria: Adult patients with PR or VGPR to ASCT Primary Endpoint: PFS Key Secondary Endpoint: • OS Stratification Factors: R-ISS III at initial diagnosis Anti-CD38 induction • VGPR vs PR Ill Bristol Myers Squibb™ NDMM after 4-6 Cycles Induction HDT/ASCT PR or VGPR lenalidomide maintenance 1 cycle R 1:1 Ide-cel manufacturing Apheresis Flu/Cy + ide-cel lenalidomide maintenance (start 1 month after ide-cel/counts recovery; continue until PD) lenalidomide maintenance until PD Pivotal KarMMa-9 study initiating Data anticipated in 2027 Follow-Up Not for Product Promotional Use 84#85Hematology Reblozyl BET Inhibitor Breyanzi golcadomide Abecma alnuctamab GPRC5D iber/mezi Alnuctamab demonstrates deep and durable responses in RRMM Response, % Overall Response Rate: Efficacy supports the optimal Phase 3 dose¹ 100 80 50 60 40 40 20 20 0 ORR = 41%2 14 ■SCR ■CR VGPR ORR = 65% PR 19 38 14 7 7 8 <30-mg target dose 30-mg target dose (n=29) (n=26) Deep and durable responses with clinically important MRD negativity1 Patients who achieved a response (n=29) Safety¹ 86% of responses ongoing and mDOR not reached Grade ≥3 n=73 CRS 0 ICANS 0 SCR CR MRD neg (10-6) MRD neg (10-5) Infections 10% VGPR PR PD Ongoing ▲ Death Hematologic: Neutropenia 42% Anemia 25% • Thrombocytopenia 14% T T T T T T T 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 Time (months) Responses deepened over time, with CRS limited to low-grade, short-lived events (median duration 2 days) Ill Bristol Myers Squibb™ 1. Wong SW, et al. EHA 2023 [Poster #P883]. 2. Values do not add to 41% due to rounding. Not for Product Promotional Use 85#86Hematology Reblozyl BET Inhibitor Breyanzi golcadomide Abecma alnuctamab GPRC5D iber/mezi Aggressive development plan to move into earlier lines and leverage proprietary combinations RRMM 1-3 prior lines alnuctamab monotherapy vs Investigator's Choice SOC Phase 3, placebo-controlled randomized study Anti-CD38 mAb & lenalidomide exposed and BCMA-targeting therapy naïve • RRMM ≥3 prior lines (dose escalation) alnuctamab + GPRC5D CAR T Phase 1b, dose escalation and dose optimization study Dose escalation: Triple class exposed; prior BCMA or GPRC5D therapies allowed • RRMM ≥3 prior lines (dose escalation) alnuctamab + mezigdomide Phase 1b, dose escalation and dose optimization study Dose escalation: Anti-CD38 mAb exposed or naïve Ill Bristol Myers Squibb™ Initiating Phase 3 trial in 2024 Not for Product Promotional Use 86#87Hematology Reblozyl BET Inhibitor Breyanzi golcadomide Abecma alnuctamab GPRC5D iber/mezi GPRC5D CAR T has differentiated MoA/construct, addressing unmet need in post-BCMA treated population GPRC5D-targeted CAR construct Anti-GPRC5D domain¹ Hinge and transmembrane domain¹ 4-1BB1,2 CD3-zeta1,2 Matching modality to mechanism TCE CAR T Repeated administration One-time infusion Critical need for new targets as the number of post-BCMA treated patients increases³ GPRC5D is a clinically validated receptor highly expressed on MM cells with limited expression in other tissues and shows great potential for treatment of advanced MM1 Overexpression of GPRC5D is associated with poor disease prognosis¹ Hypothesis: Deliver strong anti-tumor efficacy with a better on-target/off-tumor tolerability profile Though CART manufacturing and scalability is bespoke, therapy is a one-time infusion leading to significant efficacy and a manageable tolerability profile4 1. Smith EL, et al. Science Transl Med. 2019;11:eaau7746. 2. Song D-G, et al. Cancer Res. 2011;71:4617-4627. 3. Mailankody S, et al. N Engl J Med. 2022;387:1196-1206. Not for Product Promotional Use 87 Ill Bristol Myers Squibb 4. Bal S, et al. EHA 2023 [Presentation #S193].#88Hematology Reblozyl BET Inhibitor Breyanzi golcadomide Abecma alnuctamab GPRC5D iber/mezi GPRC5D CAR T in post-BCMA patients shows compelling efficacy and differentiated safety ORR = 96.3%¹ 100 SCR On-target/off-tumor TRAES, n (%) Any grade 90 ■ CR Skin 14 (20.9) All treated patients (n = 67) Grade > 3 0 (0) 80 ORR = 76%¹ 29.6 CRR VGPR Dysgeusia/taste disorder 12 (17.9) 0 (0) 40.7% PR 70 Nails 6 (9.0) 0 (0) Response, % 60 32.0 CRR 11.1 Dysphagia 1 (1.5) 0 (0) 36% 50 Neurotoxicity, n (%) 4.0 ICANS-type neurotoxicity 7 (10.4) 2 (3.0) 40 33.3 Dizziness 7 (10.4) 1 (1.5) 30 32.0 Headache 7 (10.4) 0 20 Ataxia 10 22.2 2 (3.0) 0 8.0 Neurotoxicity 2 (3.0) 0 0 Gait disturbance Prior BCMA (n=25) No prior BCMA (n=27) 1 (1.5) 0 Dysarthria 1 (1.5) Non-hematologic, n (%) Patients with prior BCMA-targeted therapy¹, n (%) CAR T-cell therapy (cilta-cel, ide-cel, orva-cel, ALLO 715, others not specified) Non-CAR T-cell therapy (ADC, belantamab mafodotin, TCE) n = 25 CRS 58 (86.6) 3 (4.5) 19 (76) 8 (32) GPRC5D CAR T on-target/off-tumor safety profile differentiated from bispecifics with lower rates of any grade events, and no Grade ≥ 3 events 1. Bal S, et al. EHA 2023 [Presentation #S193]. Ill Bristol Myers Squibb™ Not for Product Promotional Use 88#89Hematology Reblozyl BET Inhibitor Breyanzi golcadomide Abecma alnuctamab GPRC5D iber/mezi Registrational trial to be initiated 1H 2024 .. Quadruple class exposed IMID, PI, anti-CD38, anti-BCMA Demonstrate high ORR and DOR in a high-need population Explore novel combinations CELMODs or anti-BCMA TCE Expand development with combinations in earlier disease setting Expand in 2L+ vs SOC Key segment in RRMM Potential to explore head-to- head study vs standard therapies Registrational Trial Ill Bristol Myers Squibb™ Additional studies planned in 2024+ Not for Product Promotional Use 89#90Hematology Reblozyl BET Inhibitor Breyanzi golcadomide Abecma alnuctamab GPRC5D iber/mezi Two multiple myeloma CELMODs are in registrational trials iberdomide • Synergistic in vitro activity with anti-CD38 mAb¹ • Properties enable combinability, enhanced anti-MM activity, and favorable tolerability Potential to establish iberdomide in combination with anti- CD38 mAb in earlier lines • mezigdomide Highly potent, optimized for rapid and maximal degradation of target proteins • Induces tumor cell death and responses needed to regain control in advanced disease • ⚫ Potential to establish mezigdomide-Pl triplet combination in later lines, post-lenalidomide and anti-CD38 mAb Asset (indication) Phase 1 Phase 2 mezigdomide (RRMM 2-4L) SUCCESSOR-12 mezigdomide (RRMM 2L+) SUCCESSOR-23 iberdomide (RRMM 2-3L) EXCALIBER-RRMM4 iberdomide (post-SCT maintenance) EXCALIBER-MAINTENANCE5 Phase 3 Projected Data Readout 2026 2026 2026 2029 1. Hansen JD, et al. J Med Chem. 2020 Jul 9;63(13):6648-6676. 2. NCT05519085; 3. NCT05552976; 4. NCT04975997; 5. NCT05827016 Ill Bristol Myers Squibb™ Not for Product Promotional Use 90 90#91Hematology Reblozyl BET Inhibitor Breyanzi golcadomide Abecma I alnuctamab GPRC5D iber/mezi Extending leadership in multiple myeloma: Opportunity to help patients across their treatment journey 89 Patient Segments BMS Assets Ill Bristol Myers Squibb™ Newly Diagnosed Multiple Myeloma (1L) Early Relapse and Refractory Multiple Myeloma (2L-4L) Late Relapse and Refractory Myeloma (5L+) Quadruple class exposed Post-SCT consolidation Post-SCT maintenance anti-CD38 Sensitive/Naïve Post anti-CD38 Triple class exposed Abecma (idecabtagene vicleucel) iberdomide iberdomide SUSPENSION FOR IV INFUSION Abecma [idecabtagene vicleucel] SUSPENSION FOR VINFUSION mezigdomide alnuctumab mezigdomide alnuctumab GPRC5D CAR T GPRC5D CAR T Abecma [idecabtagene vicleucel] GPRC5D CAR T SUSPENSION FOR VINFUSION ☐☐ Planned Ongoing Approved Not for Product Promotional Use 91#92GPRC5D iber/mezi Hematology Reblozyl BET Inhibitor Breyanzi golcadomide Abecma alnuctamab Broadening leadership across malignant and benign Hematology - Reblozyl: • . Recent FDA approval in 1L MDS-associated anemia with a broad label 1L TD Myelofibrosis associated anemia Phase 3 ongoing Numerous assets to extend leadership in Multiple Myeloma: • . . Abecma is under regulatory review in the triple class exposed population; Phase 3 initiating in patients with sub- optimal response post-ASCT GPRC5D CAR T as a potential first-in-class CART with registrational program initiating next year iberdomide & mezigdomide registrational data expected in 2026 • alnuctamab initiating Phase 3 next year Strengthening breadth of leadership across leukemias, lymphomas, and benign hematology: Best-in-class Breyanzi expanding across the broadest array of B-cell malignancies • • Golcadomide moving into Phase 3 in 1L LBCL BET inhibitor (BMS-986158) as a potential new option for patients with Myelofibrosis Addressing hematologic diseases impacting 4M+1 patients Ill Bristol Myers Squibb™ 1. 2023 estimates from Decision Resource Group & BMS Internal Analysis across indications in the U.S. & EU5 Not for Product Promotional Use 92#93Oncology Ill Bristol Myers Squibb™ Not for Product Promotional Use 93#94Oncology Opdivo Opdualag TIGIT Bispecific DGK Inhibitor AR LDD Addressing high unmet medical need in Oncology Asset OPDIVO (nivolumab) Approved 26 approvals across 11 tumors Registrational+ 9 ongoing trials Exploratory/PoC Studies* Opdualag repotrectinib² subcutaneous nivolumab¹ AR LDD DGK Inhibitor farletuzumab ecteribulin TIGIT Bispecific 1L melanoma Adj. melanoma 2L/3L+ MSS CRC . 1L melanoma SC • 1L/2L+ HCC 1L NSCLC 1L ROS1+ NSCLC U.S. All Q2W & Q4W indications (bridging from 2L RCC) NTRK Pan Tumor 2L+ mCRPC Solid tumors NSCLC & ovarian NSCLC & gastric 1. U.S. Regulatory path opens up indications with Q2W and Q4W dose including melanoma, CRC, HCC, 2L NSCLC, UC, ESCC, & Gastric 2. U.S. PDUFA: November 27, 2023 Bristol Myers Squibb † ongoing or initiating 2023/2024 Not for Product Promotional Use 94#95Oncology Opdivo Opdualag TIGIT Bispecific DGK Inhibitor AR LDD Continuing to grow Opdivo / Dual 10 26 OPDIVO approvals 10 YERVOY approvals 11 Metastatic Setting Tumor/Trial Status Tumor/Trial Subcutaneous nivolumab CM-67T 2023 MSI-H CRC Readout CM-8HW Opdivo + Yervoy 1L MIUC CM-901 Opdivo + Yervoy vs SOC chemo Early-Stage Setting Tumor/Trial NSCLC (Peri-Adj) CM-77T Neo-adj Opdivo + chemo followed by Adj Opdivo vs chemo NSCLC (Adj) ANVIL Opdivo vs Observation 2024 Readout 1L HCC CM-9DW Opdivo + Yervoy vs sorafenib / lenvima Status Tumor/Trial 2024 Readout NSCLC Stage 3 (Unresectable) CM-73L 2024 Readout Opdivo mono, O+Y vs Imfinzi HCC (Adj) CM-9DX Opdivo vs Placebo Status 2025 Readout 2025 Readout Status 2025 Readout 2025 Readout MIBC (Peri-Adj) tumors CA017-078 Bristol Myers Squibb™ Opdivo+chemo vs chemo 2024 Readout Not for Product Promotional Use 95#96Oncology Opdivo Opdualag TIGIT Bispecific DGK Inhibitor AR LDD SC administration has clear benefits for patients, HCPs, and healthcare systems HCPs and Healthcare System Logistical: Complex scheduling demands due to higher patient volume1 Resource utilization: Overlapping duties for staff, inefficient patient to nurse ratios 1,2 Patients Time burden: Inconvenience 5, opportunity cost/income loss6 Emotional burden: Loss of normality long-term survivorship and 'chronic care'7 • Reduces chair time (~5 min)³ • Allows rapid drug delivery³ . Reduces staff needed for administration³,4 • Improves healthcare resource utilization³,4 • • Reduces time in clinic³ Improves scheduling and administration 8,9,10 Improves patient QOL 3,4,11 ¹Lopez-Vivanco G. Clin Transl Oncol. 2017;19(12):1454-1461; 2Huang YL, et al. Journal of Oncology Practice. 2018; 14(2):e82-e91; 30'Shaughnessy J, et al. Eur J Cancer. 2021;152:223-232; BA. Cancer. 2008;112(11 Suppl):2556-2568. Harvey MJ, et al. Plos One. 2022;17(1):e0261336. Jonaitis L, et al. BMC Proc. 2021;15(suppl 17):25. 10 Schreiber S, et al. Adv Ther. 2022;39:2342-2364. 11Dent S, et al. Curr Oncol. 2019;26(1):e70-e80. ll Bristol Myers Squibb" "DuMond B, et al. J Oncol Pharm Prac. 2021;27(5):1214-1221. "De Cock E, et al. Cancer Med. 2016;5(3):389-397. 6Alzehr A, et al. Support Care Cancer. 2022;30(8):6385-6404. "Kim Y, Given Not for Product Promotional Use 96#97Oncology Opdivo Opdualag TIGIT Bispecific DGK Inhibitor AR LDD Subcutaneous nivolumab: Opportunity for a near-term launch potentially benefitting patients into the early 2030s Checkmate 67T1: Phase 3 study Patients with advanced or metastatic cc RCC who have received prior systemic therapy Primary Endpoint: • . Time-averaged serum concentration over 28 days (Cavgd28) Trough serum concentration at steady-state (Cmin) Key Secondary Endpoint: • ORR R 1:1 Arm A subcutaneous nivolumab + rHuPH20 Arm B intravenous nivolumab Data expected later this year & launch anticipated in 2024/2025 U.S. Regulatory path opens up indications with Q2W and Q4W dose² Indications encompass majority of Opdivo 2022 net sales in the U.S. Ill Bristol Myers Squibb™ 1. NCT04810078; 2. Supported with data from Checkmate-8KX Not for Product Promotional Use 97#98Oncology Opdivo Opdualag TIGIT Bispecific DGK Inhibitor AR LDD Next-generation IO medicine with significant potential to benefit patients into the next decade Today Near-Term Future Opdualag TM 2/3L+ MSS Colorectal Cancer & Adjuvant melanoma Strong launch supporting rapidly expanding dual 10 option for 1L melanoma patients Phase 3 trials ongoing Non-Small Cell Lung Cancer & Hepatocellular Carcinoma Phase 2 trials underway to inform path forward Ill Bristol Myers Squibb™ Not for Product Promotional Use 98#99Oncology Opdivo Opdualag TIGIT Bispecific DGK Inhibitor AR LDD Adjuvant Melanoma: High conviction indication with potential to benefit patients before disease spreads Clear evidence of neo-adjuvant activity with relatlimab and nivolumab complements proven benefit in metastatic setting PCR, n/N (%) Nivo + Rela² Nivo 1 3/12 (25) Nivo+Rela² 17/30 (57) Probability of Recurrence-Free Survival 0.0 0.2 0.4 0.6 0.8 1.0 PCR non PCR T T -5 p = 0.10 T T T 10 15 20 25 30 35 ФГ Months After Surgery PCR 17 17 15 13 10 5 1 0 non PCR 12 11 11 8 7 3 0 0 Combination relatlimab and nivolumab yields a high pCR rate and durable clinical benefit in resectable melanoma patients Favorable safety profile Opdualag: Potential therapy option for ~21K adjuvant patients vs ~13K 1L metastatic patients in the U.S.³ RELATIVITY-098 Phase 3 ongoing: Data expected in 2026 1. Amaria, et al. Nat Med 2018; 24: 1649-54; 2. Amaria, et al. Nat Med 2022; 611: 155-60; 3. Decision Resources Group, BMS Internal Analysis Ill Bristol Myers Squibb™ Not for Product Promotional Use 99#100Oncology Opdivo Opdualag TIGIT Bispecific DGK Inhibitor AR LDD MSS CRC: Combination benefit where PD-1 alone has not shown activity Patient with recurrent, metastatic MSS rectal adenocarcinoma after 3 lines of treatment in the metastatic setting DOD Baseline 3 months into treatment 9 months into treatment Partial Response (-38% decrease) in target lesions for 11+ months RELATIVITY-123 Phase 3 ongoing: Opdualag vs regorafenib or TAS-102 in later lines of metastatic colorectal cancer Data expected in 2025 Ill Bristol Myers Squibb™ Images courtesy of Dr. Eric Christenson and Dr. Dung Le, Johns Hopkins University Not for Product Promotional Use 100#101Oncology Opdivo Opdualag TIGIT Bispecific DGK Inhibitor AR LDD Ongoing Phase 2 studies to inform Phase 3 program 1L HCC1 nivolumab + relatlimab + bevacizumab VS nivolumab + bevacizumab Opdualag 2L + HCC (Post TKI)² 1L Stage IV NSCLC³ nivolumab + relatlimab VS nivolumab nivolumab + relatlimab + chemo VS nivolumab + chemo Key takeaways from Phase 2 studies inform and potentially de-risk the Phase 3 program Ill Bristol Myers Squibb™ 1. NCT05337137; 2. NCT04567615; 3. NCT04623775 Not for Product Promotional Use 101#102Oncology Opdivo Opdualag TIGIT Bispecific DGK Inhibitor AR LDD BMS-986442: Differentiated TIGIT & CD96 bispecific antibody in Oncology Antagonizes TIGIT & CD96 binding to CD155 MOA: Drives T & NK cell anti-tumor immunity Dual TIGIT & CD96 antagonist IL-2 [pg/mL] 400- 300- 200- 100- BMS-986442 Fc selected to enhance tumor- reactive T cell responses Program Overview: Licensed from Agenus Phase 1 single-agent trial complete Phase 1/2: Evaluating combinations (e.g., PD-1 ± chemotherapy) in dose escalation with data anticipated next year Positive data enables clinical development acceleration Initial tumors of interest: NSCLC & Gastric cancer CD96 & TIGIT are complementary targets in the same pathway & negatively regulate T & NK cell function in the tumor microenvironment 1,2,3 BMS-986442 potentially enhances the quality & magnitude of T cell responses (vs TIGIT & CD96 monospecific antibodies) through dual inhibition on APC or tumor cells4 IgG BMS-986442 anti-TIGIT anti-CD96 anti-TIGIT+ anti-CD96 APC: T-Cell Response (Bispecific vs monospecific(s)) T Ill Bristol Myers Squibb™ 1. Waight JD, et al., Cancer Cell. 2018. 2. Worboys JD, et al., Nat. Communi. 2023. 3. Banta KL, et al., Immunity 2023. 4. Dougall WC, et al., Immunol. Rev. 2017 Not for Product Promotional Use 102#103Oncology Opdivo Opdualag TIGIT Bispecific DGK Inhibitor AR LDD Dual DGKα/ inhibitor builds on our depth in Oncology to potentially deliver a transformational oral CPI Transformational potential First-in-class, oral therapy as a T cell checkpoint inhibitor (CPI) as monotherapy or in combination with approved CPIs Matching modality to mechanism A dual alpha/zeta inhibitor sensitizes CPI-resistant pre-clinical models through CD8 priming and clonal expansion, leading to tumor cell killing in combination with anti-PD1 and anti- CTLA4 therapies Path to clinical proof-of-concept Causal human biology Translational insights from IO-refractory patients demonstrates mechanisms of resistance related to low antigenicity, lack of co- stimulation, and T cell anergy. Clonal Expansion Amplifies CD8 priming & clonal expansion IL-2 IFNY TNFa Naive T cell Dendritic Cell Amplifies CD8 killing of tumor cells PFN GzmB T cell (effector) IFNY TNFa Cancer cell death IO Resistance Mechanisms Low TMB Low antigenicity Low MHCI Lack of co-stimulation T cell anergy Ill Bristol Myers Squibb™ DGKi Not for Product Promotional Use 103#104Oncology Opdivo Opdualag TIGIT Bispecific DGK Inhibitor AR LDD Effective & tolerable treatment options needed in metastatic castrate resistant prostate cancer (mCRPC) High unmet need remains in prostate cancer: . Expected U.S. mortality is -35K¹ men in 2023 5-year OS¹ decreases from >97% to -32.5% in the localized vs metastatic setting Current SOC - NHT2 • AR is a key driver of prostate cancer and AR-targeted therapies remain current SoC • • Traditional AR antagonists (e.g., enzalutamide) inhibit AR in a reversible manner This AR inhibition is overcome by upregulation of wildtype (WT) or mutation of AR in cancer cells, leading to resistance: - AR WT amplification (-50%)³ AR LDD AR LDD induces irreversible AR degradation in a catalytic manner leading to deeper, more potent AR inhibition • Potentially paradigm-shifting MoA overcomes resistance mechanisms to NHT including AR WT amplification and mutations Preclinical models demonstrated activity in both settings Potential to improve efficacy, safety, & tolerability in the post-NHT setting • - AR mutations (~15-20%)³ Post-NHT progression, limited options for patients (e.g., chemo) Ill Bristol Myers Squibb™ 1. SEER 2023; 2. NHT: e.g., enzalutamide and abiraterone; 3. Robinson, et al., 2015, Cell 161:1215; Abida et al., 2019, PNAS 116:11428. Not for Product Promotional Use 104#105TIGIT Bispecific DGK Inhibitor AR LDD Oncology Opdivo Opdualag AR LDD phase 1 design in 1L & 2L mCRPC Key eligibility criteria • • Open label¹: Assess the safety, tolerability and preliminary efficacy Histologically or cytologically confirmed adenocarcinoma of the prostate Progressed on ADT and ≥ 1 prior secondary hormonal therapy approved for CRPC ECOG performance status (PS) 0 or 1 Dose escalation/Dose expansion Primary endpoint Safety and tolerability Key secondary endpoints: Confirmed Prostate Specific Antigen (PSA) decline of ≥ 50% from baseline (PSA50) Objective soft tissue response (CR or PR), DOR, rPFS, PSA PFS Part A Dose escalation Part B Dose expansion to optimize RP2D Data anticipated in 2024 Ill Bristol Myers Squibb™ 1. NCT04428788 Not for Product Promotional Use 105#106Oncology Opdivo Opdualag TIGIT Bispecific DGK Inhibitor AR LDD AR LDD demonstrates on target AR degradation in tumor biopsy Patient Example Screening On Treatment AR protein is highly expressed in tumor cells 200 μm AR protein levels degraded with AR LDD after one cycle Ill Bristol Myers Squibb™ Source: Images from BMS internal database Not for Product Promotional Use 106#107Oncology Opdivo Opdualag TIGIT Bispecific DGK Inhibitor AR LDD Confirmation of mechanism of action of AR LDD from first-in-human study 69 yr old male with mCRPC since 20221 Prior Tx: ADT, enzalutamide, avelumab + talazoparib Pt entered study with AR amplification, BRCA2 mutation, rising PSA and progressive soft tissue disease Treated with AR LDD; responded rapidly with PSA90* *Observed PSA decreases in this patient only serve to illustrate MoA and are not intended to represent expected outcomes Ill Bristol Myers Squibb™ 1. Patient case from BMS internal database ng/ml 1051028 PSA 70- 60- 50- 40- 30 20- 10- 8 12 16 Weeks 20 -30% -50% 24 28 -90% Not for Product Promotional Use 107#108Oncology Opdivo Opdualag TIGIT Bispecific DGK Inhibitor AR LDD AR LDD: Opportunity to move into pivotal studies in next 18 months Phase 1 data across mutant/wildtype subgroups to be presented at a medical congress in 2024 + ФГ Next Steps Discuss pivotal study options with health authorities 艮 Consider expanding into hormone sensitive indications Δ Explore novel combinations to potentially enhance efficacy or synergy Ill Bristol Myers Squibb™ Not for Product Promotional Use 108#109Oncology Opdivo Opdualag TIGIT Bispecific DGK Inhibitor AR LDD ΙΟ Extending IO leadership while diversifying beyond 10 Extending leadership in 10 Subcutaneous nivolumab: Potential to benefit patients into early 2030s with data anticipated this year Opdualag: 3rd approved IO agent; Approved in 1L melanoma; Phase 3 studies in adjuvant melanoma and mCRC ongoing - Ongoing Phase 2 studies in HCC and lung to inform Phase 3 program Select next-gen 10 . BMS-986442: Differentiated TIGIT bispecific antibody targeting both TIGIT and CD96 DGK inhibitor: Potential transformational, oral dual inhibitor in solid tumors Diversifying beyond IO • AR LDD: Significant opportunity in mCRPC with data expected early next year; initiating pivotal trial in next 18 months repotrectinib: Potential best-in-class, next generation ROS1/NTRK inhibitor; PDUFA November 27, 2023 Addressing oncologic diseases impacting 1.2M+1 patients Ill Bristol Myers Squibb™ 1. 2023 estimates from Decision Resource Group & BMS Internal Analysis across indications in the U.S. & EU5 Not for Product Promotional Use 109#110Program will reconvene following a short break Ill Bristol Myers Squibb™ (10 min) Not for Product Promotional Use 110#111Cardiovascular Ill Bristol Myers Squibb™ Brick Not for Product Promotional Use 111#112Cardiovascular milvexian Camzyos MYK-224 Opportunity to develop medicines in important Cardiovascular indications Asset Approved CAMZYOS™ (mavacamten) capsules 15mg Obstructive Hypertrophic Cardiomyopathy milvexian MYK-224 danicamtiv Ill Bristol Myers Squibb™ † ongoing or initiating 2023/2024 Registrational+ Non-obstructive Hypertrophic Cardiomyopathy Secondary Stroke Prevention Acute Coronary Syndrome Atrial Fibrillation Exploratory/PoC Studies* • Obstructive Hypertrophic Cardiomyopathy • Heart Failure with preserved Ejection Fraction Dilated cardiomyopathy Not for Product Promotional Use 112#113Cardiovascular milvexian Camzyos MYK-224 Milvexian: Opportunity to expand anticoagulation beyond FXa to benefit millions of patients Opportunity to address multiple thrombotic conditions of high unmet need Target profile: Efficacy comparable or better to FXa with better bleeding profile ~7.5M patients² in U.S. with thrombotic diseases need treatment Anti-platelets • SSP Factor Xa ¡ milvexian · AF • ACS ✓ Robust phase 2 program has demonstrated a differentiated anticoagulant profile LIBREXIA program is the largest and most comprehensive phase 3 registrational program ongoing (SSP, ACS & AF) U.S. FDA granted Fast Track Designation to all 3 indications ongoing in Phase 3 studies Ill Bristol Myers Squibb™ 1. Current standard of care for indication(s); 2. Decision Resource Group, BMS Internal Analysis Not for Product Promotional Use 113#114Cardiovascular milvexian Camzyos Our framework reinforces confidence in milvexian as a next-generation anti-thrombotic Transformational potential Oral anti-coagulant with a potential for comparable/better efficacy with reduced bleed risk to a broader range of patients Causal human biology Congenital FXI-deficient patients: • Lower risk for venous thromboembolism & ischemic strokes Spontaneous bleeding is uncommon Risk of CV events lower by¹ 43% Risk of VTE lower by 48% 61% In patients with mild deficiency In patients with moderate-to- HR 0.52 severe deficiency In patients with mild deficiency HR 0.39 HR 0.571 Matching modality to mechanism MYK-224 Milvexian has high affinity and specificity for FXla, high oral bioavailability and demonstrates a wide therapeutic index in preclinical models of thrombosis Path to clinical proof-of-concept Human genetic data Epidemiologic observations No VTE events Pre-clinical models In patients with moderate-to- severe deficiency¹ Phase 2 studies Ill Bristol Myers Squibb™ 1. Preis M, et al. Blood. 2017; Mar;129(9):1210-1215. Not for Product Promotional Use 114#115Cardiovascular milvexian Camzyos MYK-224 TKR study demonstrates a differentiated monotherapy profile: Supports moving into AF Monotherapy 30% AXIOMATIC-TKR study¹ Major bleeding CRNM 0.25 0.236 ■ All VTE + all death 0.214 25% 0.209 20% 15% 0.113 0.09 0.076 AXIOMATIC-TKR 1 Phase 2 data Efficacy Robust efficacy with superiority vs enoxaparin Safety No major bleeds observed in milvexian arms 0.065 10% Dose Response 5% 0.014 0 0.014 0.007 0.007 0 0.013 0.007 in bleeding observed from existing anticoagulants Clear efficacy & no dose response distinct 0.003 0 0 0 0 0 0 0 0% 40 mg QD 25 mg BID 50 mg BID 100 mg BID 200 mg BID 25 mg QD 50 mg QD 200 mg QD Supports Phase 3 AF trial Enoxaparin milvexian Milvexian has potential to offer comparable/better efficacy with reduced bleed risk to a broader range of patients Ill Bristol Myers Squibb™ 1. Weitz J, et al. N Engl J Med. 2021; 385:2161-2172. Not for Product Promotional Use 115#116Cardiovascular milvexian Camzyos MYK-224 Data from the SSP Phase 2 study gives us confidence to move to Phase 3 in combination with anti-platelet treatments Combination Therapy AXIOMATIC-SSP study¹ Symptomatic ischemic stroke Fatal bleed & Symptomatic intracranial hemorrhage 12 7.7% Incidence rate (%, 95% CI) + a 00 10 ~ 30% RRR versus placebo 5.5% Ph3 SSP Dose 4.6% 3.8% 4.0% 3.5% 0.9% Efficacy Safety 2 0.3% 0.3% Dose 0% 0% 0% 0 Response Placebo 25 mg QD 25 mg BID 50 mg BID 100 mg BID 200 mg BID milvexian Ill Bristol Myers Squibb™ 1. Sharma et al, ESC 2022 Phase 2 data supports Phase 3 studies in SSP and ACS Clinically meaningful (-30%) reduction in ischemic stroke (primary endpoint for Phase 3 SSP) across several fold dose range . • • • • No fatal bleeding No signal for increase in intracranial bleeds No apparent dose response in bleeding Dose response in ischemic stroke with early plateau at 25mg BID Phase 3 dose 25mg BID Not for Product Promotional Use 116#117Cardiovascular milvexian Camzyos MYK-224 SSP data provides proof-of-concept in ACS Acute Coronary Syndrome Unmet Need Risk of recurrent CV events remains high despite dual antiplatelet therapy (5-10% annually) 1,2 Current treatments (antiplatelets & anticoagulants) decrease CV events, but increase risk of major bleeding 900K³ patients diagnosed in the U.S. Scientific rationale for milvexian in ACS Ischemic stroke and ACS share similar underlying pathophysiology and treatment ooo FXa on top of dual antiplatelet shows efficacy but with excess bleeding In AXIOMATIC-SSP, milvexian demonstrated efficacy in reducing recurrent ischemic stroke with no increase in severe bleeding vs. placebo. Phase 3 study in ACS underway Ill Bristol Myers Squibb™ 1. Steg G, et al. JAMA. 2007. 2. Sorbets E, et al. J Eur Heart J. 2020. 3. Decision Resources Group, BMS Internal Analysis Not for Product Promotional Use 117#118Cardiovascular milvexian Camzyos MYK-224 Confidence in profile supports three parallel Phase 3 trials in SSP, ACS, and AF Phase 2 Phase 3 Projected Data Readout Indication Phase 1 Secondary Stroke Prevention LIBREXIA-STROKE¹ (Dose: 25mg BID) Acute Coronary Syndrome LIBREXIA-ACS² (Dose: 25mg BID) Atrial Fibrillation LIBREXIA -AF3 2026 2026 2027 The LIBREXIA Phase 3 studies represent the largest, most comprehensive program for a Factor Xla inhibitor U.S. FDA granted Fast Track designation to all 3 indications Ill Bristol Myers Squibb™ 1. NCT05702034; 2. NCT05754957; 3. NCT05757869 Not for Product Promotional Use 118#119MYK-224 Cardiovascular milvexian Camzyos Expanding myosin inhibitor franchise in HCM and HFPEF Today CAMZYOS™ (mavacamten) capsules Strong launch momentum enabling more oHCM patients to benefit from Camzyos Medium-Term Expansion into nHCM & opportunity to expand diagnosis rates with Artificial Intelligence supported technology Long-Term Potential opportunity for myosin inhibitors in HFpEF Continued evolution of data suggests disease modifying ability of Camzyos Ill Bristol Myers Squibb™ Not for Product Promotional Use 119#120Cardiovascular milvexian Camzyos MYK-224 OHCM Patient Case (Electrocardiogram) Before Camzyos Treatment AVR aVL III AVE V2 A V4 ☺ ☺ + 6 Months of Camzyos Treatment aVL VE T V2 Normalizing trend in the ECG after 6 months of treatment with Camzyos Ill Bristol Myers Squibb™ Source: Courtesy of Dr. Matt Martinez Not for Product Promotional Use 120#121Cardiovascular milvexian Camzyos MYK-224 OHCM Patient Case (Echocardiogram) MHz/3.3 MHz B 4 dB br: 57 dB 1.4 0 cm 20- 15- Before Camzyos Treatment Ill Bristol Myers Squibb™ 10- Source: Courtesy of Dr. Matt Martinez V NE cm POST EXERCISE 5% 15 Med Pen G 3.2 6 Months of Camzyos Treatment x2 Not for Product Promotional Use 121#122Cardiovascular Camzyos: Phase 3 trial in nHCM underway milvexian Camzyos MYK-224 ODYSSEY H C M Patients with symptomatic nHCM (NYHA Class II or III) Key Inclusion: Diagnosis of HCM per ACC/AHA and ESC guidelines Peak LVOT < 30 mmHg at rest / < 50 mm Hg with provocation NYHA Class II or III Mavacamten Key Exclusion: R • Known infiltrative or storage disorder that mimics nHCM 1:1 H/o unexplained syncope within 6 months prior to screening Placebo • H/o SVT within 6 months prior to screening Assessment of Primary Endpoints at Week 48: • Exercise Capacity (PVO2) PRO (KCCQ) 1. NCT05582395 Ill Bristol Myers Squibb™ Data expected in 2025 Not for Product Promotional Use 122#123Cardiovascular milvexian Camzyos MYK-224 Significant unmet need remains in HFpEF HFrEF Normal HF affects -6.8 million individuals in the US1 HF is classified by clinical signs & symptoms Systolic Heart Failure Normal Heart • . as well as the heart's ability to eject blood 50% of HF patient have HFpEF which is a heterogenous disease contributed to by several comorbidities and/or specific causes, e.g., cardiomyopathy² Patients with HFPEF typically present with dyspnea and evidence of congestion. There may be evidence of diastolic dysfunction, ventricular stiffening and hypertrophy Less blood pumped out of ventricles HFPEF, heart failure with preserved ejection fraction; SGLT-2i, sodium-glucose cotransporter-2 inhibitors. Heidenreich PA et al. J Am Coll Cardiol. 2022 Bristol Myers Squibb 1. 2. Solomon SD et al. NEJM. 2022 HFPEF Diastolic Heart Failure Less blood fills the ventricles Not for Product Promotional Use 123#124Cardiovascular milvexian Camzyos Emerging data suggests a potential role for MYK-224 in HFPEF MYK-224 MYK-224 profile as a cardiac myosin inhibitor Pre-clinical animal models show similar exposure-response with mavacamten¹ MYK-224 OHCM Phase 2 MERCUTIO trial is ongoing to confirm exposure-response similarity in humans Role of cardiac myosin inhibitor in HFPEF Encouraging interim observations from mavacamten Phase 2a EMBARK suggests myosin inhibitor benefits in HFPEF Leveraging entirety of cardiac myosin inhibitor data and experience to support starting dose for MYK-224 in HFPEF Initiate MYK-224 PoC in HFpEF in 2023/2024 Ill Bristol Myers Squibb™ 1. Preclinical model only tested in 'prevention', not 'treatment' mode Not for Product Promotional Use 124#125Cardiovascular milvexian Camzyos MYK-224 Opportunity for sustained leadership in Cardiovascular 1 Successful history of developing leading CV medicines (e.g., Plavix & Eliquis) Extending our leadership in thrombotic diseases • Milvexian: Robust Phase 2 program supported differentiated clinical profile; Phase 3 studies in SSP, ACS and AF underway Potential opportunity for myosin inhibitors in cardiomyopathies and heart failure Camzyos: Expansion into nHCM with Ph3 trial underway MYK-224: Initiating PoC trial in HFPEF based on supportive data Addressing cardiovascular diseases impacting 17M+1 patients Ill Bristol Myers Squibb 1. Source: 2023 estimates from Decision Resource Group & BMS Internal Analysis across indications in the U.S. & EU5 Not for Product Promotional Use 125#126Neuroscience Ill Bristol Myers Squibb™ Not for Product Promotional Use 126#127Neuroscience Anti-MTBR-Tau elF2B Activator Building an exciting portfolio in neurodegenerative and neuroinflammatory conditions Neurodegeneration/Neuroinflammation ☐ In Development ALS Alzheimer's Disease Huntington's Disease Anti-MTBR- elF2B Activator Tau mAb Multiple Sclerosis Parkinson's Disease TYK2i-CNS1 22 active programs in discovery Ill Bristol Myers Squibb™ 1. TYK2i-CNS to transition into clinic soon FAAH-MGLL Powered by internal & external innovation Not for Product Promotional Use 127#128Neuroscience Anti-MTBR-Tau elF2B Activator BMS-986446 (PRX005): Potential best-in-class antibody to slow or halt the progression of Alzheimer's Disease The propagation of Tau pathology as Alzheimer's Disease (AD) progresses is thought to be mediated by Tau "seeds" containing the MTBR region of tau¹ Tau, not Ab, deposition correlates with age of AD onset, disease duration, and cognitive impairment¹ • A Tau fragment (MTBR-Tau 243) has recently been shown to correlate well with tau accumulation as measured by Tau- PET imaging and cognitive impairment³ BMS-986446 targets MTBR-Tau 243 and binds with high affinity to both the 3R and 4R isoforms of tau4,5 Abnormal A Normal- Normal Severe Biomarkers Mild cognitive impairment Dementia Disease progression - Amyloid-ẞ - Tau-mediated neural injury Clinical symptoms - Quality of life Cognitive impairment Social dependence - Motor abnormalities Figure adapted from Masters et al, Nat Rev Dis Prim 2015 Clinical symptoms Amino-terminal domain Nter 1- Proline-rich region Figure adapted from Colin et al, Acta Neuropathologica 2020 Microtubule-binding domain Cter R1 R2 R3 R4 441 carboxy-terminal tail BMS-986446: Preclinical models showed significant reduction of intraneuronal tau pathology and protection. against behavioral deficit in a tau transgenic mouse model in vivo and complete blockade of neuronal tau internalization in vitro5 Ill Bristol Myers Squibb™ 1. Horie, et al. Brain 2021. 2. Murray, et al. Brain. 2015. 3. Horie, et al. Nat Med. 2023. 4. Data on file: Prothena Press release 7/10/2023. 5. Dolan ADPD 2021 Not for Product Promotional Use 128#129Neuroscience Anti-MTBR-Tau elF2B Activator Phase 1 data supports rapidly moving BMS-986446 into Phase 2 Phase 1 Findings1 8 Safe and well-tolerated in Phase 1 across 3 dose cohorts; no deaths or SAEs observed in healthy participants Demonstrated dose-proportional anti-tau concentrations in plasma with CNS penetration in healthy participants Q No persistent anti-tau-induced anti-drug antibodies observed ㅁㅁㅁ Robust exposure in the CSF at 1-month predicts substantial target engagement in CNS R 1:1:1 PoC in Alzheimer's Disease to initiate in 1H 2024 Double-blind treatment period Placebo BMS-986446 Dose 1 BMS-986446 Dose 2 Optional long-term extension and follow-up Ill Bristol Myers Squibb 1. Martenyi, et al AAIC 2023 Poster 74181 Not for Product Promotional Use 129#130Neuroscience Anti-MTBR-Tau elF2B Activator elF2B Activator (BMS-986419): Potential across a range of neurodegenerative conditions Misfolded protein accumulation & evidence of ISR activation is present in multiple neurological conditions¹ Frontotemporal Dementia Amyotrophic Lateral Sclerosis Figure adapted from Hetz et al, Nat Rev Neur 2017 Alzheimer's Disease BMS-986419: Safe and well-tolerated in Phase 1 SAD/MAD study potential opportunity as monotherapy or combinations • Stressed cells that develop a chronically activated ISR accumulate misfolded proteins that impair cell functions and can lead to cell death The elF2 complex is an ISR "master regulator" that becomes dysfunctional in chronic disease BMS-986419 binds to a subunit in the eIF2 complex (elF2B) restoring normal ISR function, protein clearance and cellular homeostasis Phase 2 study in ALS initiating in 2024 ALS: Rapidly progressing & fatal neurodegenerative disease caused by death of motor neurons: • • Survival is typically only 2-5 years from symptom onset³ ~39k4 diagnosed prevalent patients in the U.S. Limited treatment options 1. Bristol Myers Squibb ISR: Integrated Stress Response Hetz et al, Nat Rev Neur. 2017. 2. Smith et al, Brain 2016. 3. Masron et al, Eur J Neur 2020. 4. Decision Resources Group, BMS Internal Analysis; Not for Product Promotional Use 130#131Re-establishing Neuroscience pipeline 川 Neuroscience Anti-MTBR-Tau elF2B Activator ☐ Δ Building a diverse pipeline across an array of neurodegenerative & neuroinflammation diseases Anti-MTBR-Tau moving into POC next year in Alzheimer's Disease elF2B is moving into a Phase 2 trial in ALS Ill Bristol Myers Squibb™ TYK2i-CNS to transition into clinic soon targeting Multiple Sclerosis Not for Product Promotional Use 131#132We are driving improved operational efficiency to accelerate speed to market Early Phase Phase III Development (I/II) Submission Activities Active future timeline Reduction from previous timeline Optimized study design World-class trial operations capabilities, ~40 countries footprint, robust site & patient engagement strategies Near-time data review and submissions Further enabled through Digital Innovation & Al Ill Bristol Myers Squibb™ Not for Product Promotional Use 132#133Implementing innovative Al/Digital tools to accelerate our R&D productivity What Significantly more powerful hypothesis generation Cytel Digital trial design optimization Enhancing clinical trial operations Rapid data interpretation and reporting TriNetX Ill Bristol Myers Squibb™ NVIDIA COTA :: nurocor ☑ OWKIN How Building predictive disease models using a vast proprietary data factory Powerful statistical simulation suite that aggregate millions of data points to enable decisions around effect-size, power, patient-selection, timelines & cost Real-time site selection based upon protocol required patient characteristics Effective automation and visualization technologies to enable timely data insights and clinical trial reporting COLUMBIA UNIVERSITY MEDICAL CENTER "T'EMPUS EDETEK flatiron Concert Al Not for Product Promotional Use 133#134Important updates today Expanding Currently Launched Products Sotyktu: Impressive Ph2 SLE data supports Ph3 programs in SLE & SjS Abecma: - KarMMa-3 under regulatory review in triple class exposed population KarMMa-9 registrational trial in post-transplant MM initiating this year Subcutaneous nivolumab: - Potential to benefit patients into early 2030's with data anticipated this year Camzyos: Data suggests myosin inhibitors remodel the heart New Wave of NME LPA₁ Antagonist: Demonstrated compelling Ph2 PPF data and Ph3 studies initiating CD19 NEX T: - Ph 1 study initiated in severe, refractory lupus with promise to reset the immune system & expanding into other immunologic diseases BET Inhibitor (BMS-986158): Proof-of-concept data expected early next year GPRC5D CAR T: - Differentiated profile addressing unmet need post-BCMA targeting treatment; initiating pivotal trial next year alnuctamab: - - Initiating Ph3 trial in 2024 in MM iberdomide/mezigdomide: - Ph3 data expected in 2026 golcadomide: Initiating Ph3 trial in 2024 in 1L LBCL AR LDD: Significant opportunity in mCRPC with data expected early next year - Initiating pivotal trial in the next 18 months milvexian: Compelling rationale for Ph3 programs • • Early Assets to Watch BCMA X GPRC5D: Entering into POC soon BCL6 LDD: Novel oral degrader in lymphomas TIGIT Bispecific: - Differentiated IO; targeting TIGIT & CD96 DGK inhibitor: Potential transformational oral, dual inhibitor Anti-CCR8: Treg depleting mAb therapy with broad combination potential Advancing Neuro PoC trials in 2024: Anti-MTBR-Tau in Alzheimer's Disease elF2B Activator in ALS TYK2i CNS (pre-clinical): Moving into clinic soon, targeting MS MYK-224: Progressing into HFPEF O Increasing registrational assets from 6 to 12 in next 18 months ll Bristol Myers Squibb™ Increase INDs to at -10 per year Productivity о Increase to -20% POS from FIH to approval Achieve median -6.5 years from FIH to approval Not for Product Promotional Use 134#135Conclusion Chris Boerner, PhD EVP, Chief Operating Officer CEO, effective Nov. 1, 2023 Ill Bristol Myers Squibb™ Not for Product Promotional Use 135#136Numerous levers to drive long-term growth $ Extended durability of our 10 business with subcutaneous nivolumab and Opdualag Increasingly de-risked the New Product Portfolio 稟 Registrational portfolio increasing from 6 to 12 new assets over the next 18 months Developing medicines in rapidly growing markets with significant commercial opportunities Leading positions with differentiated platforms in Cell Therapy and Targeted Protein Degradation Strategic optionality from Business Development Clearly establish BMS as an R&D leader by the end of the decade Ill Bristol Myers Squibb™ Not for Product Promotional Use 136#137Extended durability of our I-O business Today OPDIVO (nivolumab) INJECTION FOR INTRAVENOUS USE 10 mg/mL • Opportunity Subcutaneous nivolumab Potential to benefit patients into early years of next decade Roughly 65-75% of IV US revenue potentially on-label at launch • Today Opdualag TM (nivolumab and relatlimab-rmbw) Injection for intravenous use | 480 mg/160 mg Ill Bristol Myers Squibb™ Opportunity • • Benefits patients into the next decade in 1L melanoma Potential to benefit beyond melanoma (adj. melanoma, MSS CRC, lung, and HCC) Not for Product Promotional Use 137#138New product portfolio significantly de-risked with important catalysts ahead Milestones Achieved CAMZYOS™ ✓ Camzyos oHCM Future Catalysts • Camzyos nHCM $25B+ Non-Risk Adjusted* Opdualag Milestones Achieved Future Catalysts Breyanzi Opdualag 1L Mel FDC • Opdualag 1L NSCLC Milestones Achieved Breyanzi 3L+ LBCL ✓ Breyanzi 2L LBCL Future Catalysts $4B+ CAMZYOS™ Breyanzi 3L+ CLL . Breyanzi 3L+ iNHL • Opdualag Adj. Mel Opdualag 2L+ MSS CRC $4B+ Opdualag Milestones Achieved SOTYKTU Sotyktu PsO Future Catalysts • Sotyktu PsA • Sotyktu SLE Milestones Achieved Future Catalysts $4B+ SOTYKTUO ZEPOSIA. Zeposia MS ⚫ Zeposia CD ✓ Zeposia UC Milestones Achieved Abecma ✓ Abecma 5L+ Milestones Achieved Reblozyl 2L TD MDS Future Catalysts ✓ Abecma 3-5L ⚫ Reblozyl MF Reblozyl ✓ Reblozyl 1L MDS Ill Bristol Myers Squibb™ *Non-risk adjusted revenue potential, subject to positive registrational trials and health authority approval Note: Onureg & Inrebic <$1B NRA Financial projections may contain non promoted sales, BMS promotes only according to label $4B+ Reblozyl $3B+ Breyanzi $3B+ once-daily ZEPOSIA. $1B+ Abecma 2030 Not for Product Promotional Use 138#139We are increasing registrational portfolio from 6 to 12 potentially first-in-class/best-in-class assets over the next 18 months In registrational studies Registrational studies pending mezigdomide repotrectinib* CD19 NEX T BET Inhibitor (BMS-986158) iberdomide cendakimab GPRC5D CAR T alnuctamab milvexian LPA₁ Antagonist Ill Bristol Myers Squibb *Filed, U.S. PDUFA 11/27/2023 golcadomide AR LDD Not for Product Promotional Use 139#1402030 2023 Developing medicines in rapidly growing markets with significant commercial opportunities Oncology Hematology Immunology Cardiovascular* Neuroscience $85B+ $49B+ $60B+ $30B+ $23B+ $140B+ $90B+ $75B+ $21B+ $38B+ Ill Bristol Myers Squibb *CV markets impacted by generic entry in Atrial Fibrillation Source: EvaluatePharma estimates Not for Product Promotional Use 140#141Building a competitive advantage in Cell Therapy Manufacturing capacity is expanding Plan to deliver top-tier supply chain, manufacturing capacity & reliability: • Expanding drug product capacity • Strengthening vector supply • Increasing efficiency Ill Bristol Myers Squibb™ • Innovative pipeline is advancing Expanding to immunologic diseases Developing new targets Exploring innovative technologies e.g., dual binding CAR & allogeneic Well-positioned at the center of the innovation ecosystem Not for Product Promotional Use 141#142Targeted Protein Degradation platform is poised for a step-change in productivity Growing asset library • Extensive number of potential INDs identified Opportunities across therapeutic areas Industry-leading capabilities Significant experience applying preclinical, manufacturing, translational, Al/digital and clinical tools to optimize candidates Ill Bristol Myers Squibb™ Engine expected to deliver approximately 4 INDs annually Not for Product Promotional Use 142#143Enhancing BMS leadership by the end of the decade Strong track record 9 new products delivered since 2019 3 first-in-class medicines in 2022 20+ new indications & 45+ approvals across U.S., EU & Japan since 2020 High quality pipeline Registrational pipeline increasing to 12 new assets over the next 18 months Targeting high unmet need with growing commercial potential .. Improved productivity • Deliver -10 INDS per year Increase to -20% PoS from FIH to approval • Achieve median of -6.5 years from FIH to approval Continual generation of new first-in-class or best-in-class medicines Ill Bristol Myers Squibb™ Not for Product Promotional Use 143#144Q&A Bristol Myers Squibb TM 144#145Acronyms 6MWT Six Minute Walk Test HDT High Dose Therapy NTRK AA Alopecia Areata HFPEF Heart Failure with Preserved Ejection Fraction NYHA ACR American College of Rheumatology HFrEF Heart Failure with Reduced Ejection Fraction OHCM ACS Acute Coronary Syndrome IBD Inflammatory Bowel Disease ORR ADC Antibody-Drug Conjugate ICANS Immune Effector Cell-associated Neurotoxicity Syndrome OS ADT Androgen Deprivation Therapy iiNT Investigator-identified Neurotoxicity PFS AF Atrial Fibrillation ILD Interstitial Lung Disease PI Al Artificial Intelligence IMID Immunomodulary Drug PoC ALS Amyotrophic Lateral Sclerosis IND Investigational New Drug POS AML Acute Myeloid Leukemia 10 Immuno-Oncology PPF Neurotrophic Tyrosine Receptor Kinase New York Heart Association Obstructive Hypertrophic Cardiomyopathy Overall Response Rate Overall Survival Progression-free Survival Proteosome Inhibitor Proof of Concept Probability of Success Progressive Pulmonary Fibrosis APC Antigen-Presenting Cell IPF AR LDD Androgen Receptor Ligand-Directed Degrader IPI ASCT Autologous Stem Cell Transplant IRA Idiopathic Pulmonary Fibrosis Inflation Reduction Act PPFVC Percent of Predicted Forced Vital Capacity International Prognostic Index PR Partial Response PsA Psoriatic Arthritis BCMA B-cell Maturation Antigen ISR Integrated Stress Response PSA Prostate Specific Antigen BID Twice Daily JAK2i Janus Kinase 2 Inhibitor PsO Psoriasis BILAG BL British Isles lupus Assessment Group index Baseline LBCL Large B-cell Lymphoma PTCL Peripheral T-cell Lymphoma LDD Ligand-directed Degrader QD Once Daily CAR T Chimeric Antigen Receptor T-cell LOE Loss of Exclusivity QoL CD Crohn's Disease LPA1 Lysophosphatidic Acid Receptor 1 R CELMOD Cereblon E3 Ligase Modulator MAB Monoclonal Antibody RA Quality of Life Randomized Rheumatoid Arthritis CLASI Cutaneous Lupus Activity Index MCL Mantle Cell Lymphoma RBC Red Blood Cell CLL Chronic Lymphocytic Leukemia mCRPC Metastatic Castration-resistant Prostate Cancer RCC Renal Cell Carcinoma CPI Checkpoint Inhibitor MDOR Median Duration of Response ROS C-ros Oncogene CRPC Castration-Resistant Prostate Cancer MDS Myelodysplastic Syndrome RWE Real-World Evidence CRS Cytokine Release Syndrome MF Myelofibrosis SC Subcutaneous CV Cardiovascular MIUC Muscle-invasive Urothelial Carcinoma SCR DIPSS Dynamic International Prognostic Scoring System ML Machine Learning SjS Stringent Complete Response Sjogren's Syndrome DLT DMPK EGE Dose-Limiting Toxicity Eosinophilic Gastroenteritis MM Multiple Myeloma SLE Systemic Lupus Erythematosus Drug Metabolism Pharmacokinetics МоА Mechanism of Action SLEDAI-2K SLE Disease Activity Index 2000 mPC Metastatic Prostate Cancer SLL EoE Eosinophilic Esophagitis MPN Myeloproliferative Neoplasm SoC Standard of Care ESSDAI EULAR Sjögren's Syndrome Disease Activity Index MRD Minimal Residual Disease SRI(4) ESSPRI EULAR EULAR Sjögren's Syndrome Patient Reported Index European League Against Rheumatism MS Multiple Sclerosis SSP MSS MCRC Microsatellite Stable Metastatic Colorectal Cancer TA FL Follicular Lymphoma MZL Marginal Zone Lymphoma TCE Flu/Cy Fludarabine and Cyclophosphamide NDMM Newly Diagnosed Multiple Myeloma TD FVC Forced Vital Capacity NFPB Non-fucosylated Probody TIGIT FXa Factor 10a nHCM Non-obstructive Hypertrophic Cardiomyopathy TKI FXla Factor 11a NHL Non-hodgkin's Lymphoma TKR GI Gastrointestinal NHT GPRC5D HbF G Protein Coupled Receptor, Class C, Group 5, Member D Fetal Hemoglobin NSCLC NT HCC Hepatocellular Carcinoma NTD Novel Hormone Therapy Neurotoxicity Non-transfusion Dependent TRAE Small Lymphocytic Lymphoma Systemic Lupus Erythematosus Responder Index 4 Secondary Stroke Prevention Therapeutic Area T-cell Engager Transfusion Dependent T-cell Immunoglobulin and ITIM Domain Tyrosine Kinase Inhibitor Total Knee Replacement Treatment-related Adverse Event Non-small Cell Lung Cancer TYK2 Tyrosine Kinase 2 UC Ulcerative Colitis VGPR Very Good Partial Response Ill Bristol Myers Squibb™ Not for Product Promotional Use 145#146R&D efforts align with ESG values Addressing areas of high unmet need • 40+ disease areas studied, including several rare diseases Novel drugs with three first-in-class medicines launched in 2022 Diverse modalities with 10 drug platforms (e.g., cell therapy) Enhancing health equity and clinical trial diversity Numerous initiatives related to ensuring clinical trial diversity: 58% of US clinical trial sites located in highly diverse communities Racial diverse participants at 22% (goal 20%) in 2022 Responsibly driving innovation to maximize impact "Green by design" principles and a green chemistry approach, reducing total waste generated ⚫ "Green chemistry reviews" to identify opportunities for reducing safety and environmental impact Il Bristol Myers Squibb™ Representative examples, not exhaustive Not for Product Promotional Use 146#147Changes to the Development Pipeline Phase I Phase II New or Phase ◆BCL6 LDD in Lymphoma Transition Removed ✦NME 2 +CD47xCD20 +GSPT1 CELMOD (CC-90009) RIPK1 Inhibitor * Partner-run study; NME leading indication; # BMS territory Ill Bristol Myers Squibb™ + Anti-TIGIT +HSP47 Data as of September 14th, 2023 Phase III +LPA1 Antagonist in IPF LPA1 Antagonist in PPF ✦obexelimab*# in IgG4- Related Disease Registrational Submissions Oncology Hematology CV Immunology Neuroscience Approvals (n=2) • OPDIVO in Adj Melanoma (EU) REBLOZYL in 1L MDS associated anemia (US) Not for Product Promotional Use 147#148Addressing high unmet medical need in Oncology & Hematology Oncology Bladder $5B+ H&N $3B+ Hematology CLL $7B+ 2030 2023 $85B+ Lung $33B+ Renal $9B+ Liver $3B+ Melanoma $9B+ Ovarian $3B+ AML $1B+ MF $2B+ MDS $1B+ CHL $2B+ $49B+ MM $22B+ CRC $6B+ GI $1B+ NHL $14B+ Prostate $14B+ Renal $8B+ Bladder $10B+ H&N $5B+ Liver $4B+ CLL $11B+ Melanoma $14B+ AML $10B+ Ovarian $9B+ MM $31B+ $140B+ Lung $61B+ GI $4B+ Prostate $20B+ CRC $7B+ MF $3B+ CHL $3B+ MDS $6B+ $90B+ NHL $27B+ ll Bristol Myers Squibb™ Source: EvaluatePharma estimates; totals may not add due to rounding Not for Product Promotional Use 148#1492030 Addressing high unmet medical need in Immunology, Cardiovascular & Neuroscience Immunology Cardiovascular 2023 Psoriasis $26B+ UC $7B+ PSA $5B+ $60B+ Pulmonary Fibrosis $5B+ Lupus $2B+ Alopecia $0.6B+ EOE $40M+ SjS $19M+ Psoriasis $33B+ Stroke $1.8B+ ACS $0.5B+ HFPEF $8B+ $30B+ CD $16B+ AF $19B+ ACS $0.2B+ Stroke $3B+ UC $10B+ HFPEF $5B+ Pulmonary Fibrosis $2B+ HCM $5B+ $75B+ $21B+ CD $18B+ Alopecia $1B+ PSA $6B+ Lupus $5B+ SjS $0.4B+ EOE $0.4B+ ll Bristol Myers Squibb™ *CV markets impacted by generic entry in Atrial Fibrillation Source: EvaluatePharma estimates; totals may not add due to rounding AF $8B+ MS $23B+ Neuroscience MS $21B+ ALS $1B+ Alzheimer's $1B+ $23B+ $38B+ Alzheimer's $12B+ ALS $3B+ Not for Product Promotional Use 149#150Farletuzumab ecteribulin (FZEC) 1: Novel folate receptor alpha (FRA) ADC Overview . ⚫ FRa is a folate-binding protein that has limited expression on normal tissues and is overexpressed in malignant cells² MOA: Target delivery of differentiated payload, eribulin Tumour microenvironment FZEC binds to FRa on the surface of tumor cells, is internalized and cleaved to release the payload, eribulin - Eribulin inhibits microtubule growth resulting in cell death FZEC may potentially target tumors with heterogenous FRa expression through bystander effect of eribulin on nearby FRa-negative cells Development plan PoC trials ongoing in NSQ NSCLC, ovarian & endometrial cancers • In dose expansion to optimize the therapeutic index with data anticipated in 2024 FZEC FRa 2. Endocytosis 1. FZEC binds to FRO of FZEC 3. Lysosomal degradation, cleavage of linker and release of eribulin FRa-positive cancer cell 6. Released eribulin has bystander effects 4. Eribulin inhibits microtubule growth 5. Mitotic arrest leads to apopototic cell death and immunogenic cell death High addressable population based on range of FR expression Ill Bristol Myers Squibb™ 1. In partnership with Eisai; 2. Level of overexpression may vary depending on tumor type Not for Product Promotional Use 150#151Repotrectinib: Potential Best-in-Class ROS1 Inhibitor in NSCLC Highly Potent & Differentiated Small Molecule Repotrectinib ROS1+ TKI-Naïve NSCLC; ORR (95% CI) TKI-Pretreated Activity 79% (67.6, 87.7) ✓ ORRS of 28-42% (n=100) Market Potential Kinase CNS Activity (ROS1+ NSCLC) ROS1+ TKI-Naïve NSCLC Durability Solvent front mutation Gatekeeper mutation Ill Bristol Myers Squibb™ DOR ≥12-month DOR: 83.1% (73.1, 93.2) mDOR: 34.1 (25.6-NE) PFS • ≥12-month PFS: 76.6% (66.2, 87.0) •⚫ mPFS: 35.71 (27.40, NE) Generally Well Tolerated Safety Profile Source: Cho BC, et al. IASLC WCLC 2023 Clinically differentiated profile in NSCLC U.S. PDUFA November 27, 2023 ROS1 Prevalence: ~ 1.5% of NSCLC patients² Existing ROS1 market: ~$500-$600M³ Opportunity to roughly double the ROS1 market & achieve best- in-class share based on: Longer duration of response Higher response rate • Better safety profile tolerability Not for Product Promotional Use 151#152BMS-986288: A next generation CTLA-4 antibody Overview CTLA-4: established MOA, with Yervoy approved across solid tumors • Challenges (toxicity and patient selection) associated with targeting CTLA-4 have limited development BMS-986288 is a next-generation CTLA-4 designed to improve the benefit/risk: - NF (enhanced CD16 binding) biology increases immune priming via Fc engagement enhancing anti- tumor response Improves safety profile with ProbodyⓇ added to NF allowing for combinations and moving to earlier lines of therapy Development plan PoC trials in NSCLC & MSS CRC ongoing; data anticipated in 2024 MOA: A masked non-fucosylated anti-CTLA-4 antibody which improves immune priming and the safety profile APC T cell Enhanced binding BMS-986288 CTLA-4 CD16 CD80/86 MHC Tumor specific antigen CD80/86 Increased Interaction TCR. CD28. Broad range of development opportunities Ill Bristol Myers Squibb™ Not for Product Promotional Use 152#153PSA: Sotyktu Phase 2 responses provide confidence for Phase 3 Unmet need: Effective, tolerable, oral options with a novel mechanism to address both skin and joint involvement Phase 2 Primary Endpoint: ACR20 over time¹ POETYK-PSA-12 Phase 3 program ongoing data anticipated 2024/2025 Response rate, % 80 70 60 50 10 R320 40 • P < 0.001 62.7% Active disease; biologic DMARD-naïve ≥ 1 PSA-related hand and/or foot joint erosion on X-ray Week 16 Primary endpoint: ACR20 52.9% R Placebo deucravacitinib 6 mg QD 31.8% 1:1 LTE deucravacitinib 6 mg QD 0 1 2 4 8 12 16 Weeks Placebo deucravacitinib 6 mg QD deucravacitinib 12 mg QD All primary and key secondary endpoints were achieved in patients with active PsA Treatment was well-tolerate with a safety profile consistent with prior studies 1. Mease PJ et al. Ann Rheum Dis. 2022;81:815-822. 2. NCT04908202; 3. NCT04908189 Ill Bristol Myers Squibb™ POETYK-PSA-23 . Active disease; biologic DMARD-naive OR TNF inhibitor experienced Week 16 Primary endpoint: ACR20 deucravacitinib 6 mg QD R 3:3:1 Placebo deucravacitinib 6 mg QD apremilast 30 mg BID LTE Not for Product Promotional Use 153#154Established IBD presence with Zeposia in UC, with potential expansion to Crohn's Disease Zeposia in IBD Ulcerative Colitis Approved in the U.S. & EU Zeposia provides UC patients with efficacy comparable to biologics, and a favorable safety profile in an oral medicine Primary endpoints: • Induction studies: Week 12 clinical remission • Maintenance study: Co primary @ Week 52 Crohn's Disease Phase 3 YELLOWSTONE program ongoing Maintenance study data anticipated 2026 Study 32011 N = 400 Zeposia N = 200 Placebo N = 400 Zeposia clinical remission Study 32022 N = 200 Placebo and endoscopic response 12 wk induction study Ill Bristol Myers Squibb™ 1. NCT03440372; 2. NCT03440385; 3. NCT03464097 Zeposia responders or remitters are re-randomized 1:1 to Zeposia or Placebo Zeposia Placebo 52 wk maintenance study³ Not for Product Promotional Use 154#155Cendakimab: High-Affinity IL-13 Neutralizing Antibody for EoE Eosinophilic Esophagitis + Cendakimab EoE: Currently Enrolling Phase 3 study² • ⚫ Binds to IL-13 ligand IL-4 IL-13 IL-13 • ⚫ Blocks IL-13 binding to IL-13 IL-13Ra2 both IL-13Ra1 & IL-13Ra2 subunits Induction Phase Placebo 24 weeks Maintenance Phase Week 24 Co-Primary Endpoints 24 weeks Week 48 Secondary Endpoints • Tissue Inflammation Fibrosis and Remodeling EoE is a life altering disease affecting -700k¹ prevalent patients (combined U.S./EU5) Potentially differentiated MoA addressing a significant unmet need for a highly efficacious treatment that improves both inflammation & fibrosis/remodeling Cendakimab 360 mg SC QW Cendakimab 360 mg SC QW Co-primary (week 24): • Change in dysphagia days • Histologic response: eos ≤6/hpf Cendakimab 360 mg SC Q2W Key secondary (weeks 24 & 48): Histologic response: eos <15/hpf EREFS EOE-HSS • mDSD composite score Data anticipated in 2024 Ill Bristol Myers Squibb™ 1. Source: Decision Resources Group; BMS Internal Analysis; 2. NCT04753697 Not for Product Promotional Use 155