Kymera Investor Day Presentation Deck

STAT3 Has Unique Tumor Cell Intrinsic and Extrinsic Mechanisms Survival, proliferation, EMT, stemness ● STAT3 as a Target Growth Factor Receptor Cytokine Receptor JAK JAK P P SRC STAT3 STAT3 STAT3 P P STAT3 STAT3 NAMO Adrenergic Receptor W High degree of validation of JAK-STAT pathway in oncology and immuno- oncology supported by >25k publications Traditionally undrugged target First-in-class opportunity to address STAT3 driven pathology across large and diverse indications KYMERA ©2021 KYMERA THERAPEUTICS, INC. Cancer Cells P P STAT3 STAT3 Cytokines (e.g., IL-6, IL-10, VEGF) Myeloid Cells (Macrophages, MDSCs) Tregs Immature DCs PD-L1 P STAT3 Endothelial Cells Vascularization Immune- suppression KYMERA R&D DAY - December 16th, 2021 ● Tumor Cell Intrinsic Hyperactivation of STAT3 via either receptor signaling, or hotspot mutations promotes gene expression programs involved with survival, proliferation, stemness and metastasis of tumor cells Opportunities in STAT3-dependent malignancies (e.g., T cell malignancies, DLBCL, AML) and drug resistant tumors (e.g., TKI resistant oncogene-driven solid tumors) Tumor Cell Extrinsic STAT3 promotes the differentiation and activity of immunosuppressive and endothelial cells, resulting in an immunosuppressive tumor microenvironment. Opportunities in multiple heme and solid tumor indications that are not responsive to immune checkpoint inhibitors. PAGE 59

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