Kymera Results Presentation Deck

● ● ● ● STAT3 Degraders In Oncology: KT-333 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 STAT3 Has Unique Tumor Cell Intrinsic and Extrinsic Mechanisms 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-dep. malignancies (e.g., T cell maligs., DLBCL, AML) and drug resistant tumors (e.g., TKI res. oncogene- driven solids) KYMERA Ⓒ2022 KYMERA THERAPEUTICS, INC. Prevalence Incidence ~13k ~6.5k ~30k ~2.6k ~4.5k <1k Solid Tumors, PD-1 Combo (e.g. Stage IV MSI-H CRC) ~30k ~5k Source: Bionest, SEER. GlobalData; ROW includes EU, UK, Japan and China. Extrinsic: STAT3 promotes the differentiation and activity of immunosuppressive and endothelial cells, resulting in an immunosuppressive tumor microenvironment Peripheral T-cell lymphoma (PTCL) Large granular lymphocyte leukemia (LGL-L) Opportunities in multiple heme and solid tumor indications that are not responsive to immune checkpoint inhibitors Cutaneous T-cell lymphoma (CTCL) Cytokine Receptor JAK JAK U.S. Growth Factor Receptor P P STAT3 SRC STAT3 STAT3 STAT3 STAT3 # P R.O.W. Prevalence Incidence ~27k ~15k ~67k ~6k ~24k ~3k ~78k ~20k Adrenergic Receptor PAGE 8

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