Kymera Investor Presentation Deck

IRAKIMiDs are Potent Degraders of IRAK4 and IMID Substrates Targeting Redundant Pro-survival Pathways in MYD88MT DLBCL Single-agent therapies targeting activated NFkB signaling in DLBCL show limited activity • Redundant NFKB pathway activation and downregulation of Type 1 IFN common in MYD88MT lymphoma • Simultaneous degradation of IRAK4 and IMiD substrates Ikaros and Aiolos shows synergistic activity in MYD88MT models MYD88 MT DLBCL Prevalence ~8k U.S. ~9k ~2k Incidence 2.8 / 100k MYD88 MT Waldenström's Macroglobulinemia MYD88 MT PCNS Lymphoma Source: Bionest and Global Data. ROW includes E.U., U.K. and Japan. 0.3/ 100k 0.6/ 100k KYMERA ©2023 KYMERA THERAPEUTICS, INC. R.O.W. Prevalence Incidence 1.2/ 100k ~10k ~26k ~10k 0.7/ 100k 0.6/ 100k TLRs JNK * AP1 Pathway P IL-1R MYD88MYD88 IRAK4 IRAK4 IRAK1 IRAK1 * TRAF6 TRAF6 P IKKy IKKBIKKa NFkB Pathway PROLIFERATION & SURVIVAL B Cell Receptor BTK CARD11 MALT1 BCL10 * A20 * IRF4 Autoantigens * CD79A/B Ikaros Aiolos IRF7 IFN IFNAR1/2 IFN Pathway IFITS Pathway-activating alterations in DLBCL Adapted from Yang et al. (2012) Cancer Cell 21, 6, pp723-737 PAGE 35

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