Investor Presentaiton

Oncology 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

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