Kymera Investor Presentation Deck

● ● • KT-333 is a potent highly selective heterobifunctional small molecule degrader of STAT3 ● ● KT-333: STAT3 Degrader in Oncology 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 Opportunities in STAT3-dep. malignancies (e.g., T cell maligs., DLBCL, AML) and drug resistant tumors (e.g., TKI res. oncogene-driven solids) KYMERA 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 ● ©2023 KYMERA THERAPEUTICS, INC. ● Prevalence Incidence ~75k ~4-8k ~30k ~3k ~4.5k <1k Solid Tumors, PD-1 Combo (e.g. Stage IV MSI-H CRC) ~30k ~5k Source: Bionest, NCI, SEER. GlobalData, LLS; ROW includes EU, UK, Japan and China. Peripheral T-cell lymphoma (PTCL) Cutaneous T-cell lymphoma (CTCL) Potential Clinical Activity Based on Preclinical Data: Single agent activity in heme (i.e. CTCL, PTCL, LGL-L); potential activity in solid tumors in combination Large granular lymphocyte leukemia (LGL-L) 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 Cytokine Growth Factor Receptor Receptor JAK JAK U.S. P P STAT3 SRC STAT3 STAT3 STAT3 STAT3 P R.O.W. Prevalence Incidence ~27k ~15k ~67k ~6k ~24k ~3k ~78k ~20k Adrenergic Receptor W RT PAGE 22

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