#1INVENTING NEW MEDICINES WITH TARGETED PROTEIN DEGRADATION KYMERA June 2023#2Forward-looking Statements This presentation contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995 (PSLRA) and other federal securities laws. These statements include information about our current and future prospects and our operations and financial results, which are based on currently available information. All statements other than statements of historical facts contained in this presentation, including express or implied statements regarding our strategy, future financial condition, future operations, projected costs, prospects, plans, objectives of management and expected market growth, are forward-looking statements. In some cases, you can identify forward-looking statements by terminology such as "aim," "anticipate," "assume," "believe," "contemplate," "continue," "could," "design," "due," "estimate," "expect," "goal," "intend," "may," "objective," "plan," "predict," "positioned," "potential," "seek," "should," "target," "will," "would" and other similar expressions that are predictions of or indicate future events and future trends, or the negative of these terms or other comparable terminology. These forward-looking statements include statements about our strategy, business plans and objectives for our programs; plans and timelines for the clinical development of our product candidates, including the therapeutic potential, clinical benefits and safety thereof; expectations regarding timing, success and data announcements of current ongoing clinical trials; the ability to initiate new clinical programs; the initiation, timing, progress and results of our current and future clinical trials and current and future preclinical studies and clinical trials of our product candidates and of our research and development programs; our plans to develop and commercialize our current product candidates and any future product candidates and the implementation of our business model and strategic plans for our business, current product candidates and any future product candidates. We may not actually achieve the plans, intentions or expectations disclosed in our forward-looking statements, and you should not place undue reliance on our forward-looking statements. You should not rely upon forward-looking statements as predictions of future events. Actual results or events could differ materially from the plans, intentions and expectations disclosed in the forward-looking statements we make. Any forward-looking statements are based on management's current expectations and beliefs and are subject to a number of risks, uncertainties and important factors that may cause actual events or results to differ materially from those expressed or implied by any forward-lo statements including, without limitation, risks associated with: the impact of COVID-19 on countries or regions in which we have operations or do business, as well as on the timing and anticipated results of our current and future preclinical studies and clinical trials, supply chain, strategy and future operations; the delay of any current and future preclinical studies or clinical trials or the development of our drug candidates; the risk that the results of current preclinical studies and clinical trials may not be predictive of future results in connection with current or future clinical trials, including those for KT-474, KT-333, KT-413 and KT-253; Our ability to successfully demonstrate the safety and efficacy of our drug candidates; the timing and outcome of our planned interactions with regulatory authorities; obtaining, maintaining and protecting our intellectual property; and our relationships with its existing and future collaboration partners. We undertake no obligation to update or revise any forward-looking statements, whether as a result of new information, the occurrence of certain events or otherwise, except as required by law. As a result of these risks and others, including those set forth in our most recent and future filings with the Securities and Exchange Commission, actual results could vary significantly from those anticipated in this presentation, and our financial condition and results of operations could be materially adversely affected. This presentation contains trademarks, trade names and service marks of other companies, which are the property of their respective owners. Certain information contained in this presentation and statements made orally during this presentation relate to or is based on studies, publications, surveys and other data obtained from third-party sources and the Company's own internal estimates and research. While the Company believes these third-party studies, publications, surveys and other data to be reliable as of the date of the presentation, it has not independently verified, and makes no representation as to the adequacy, fairness, accuracy or completeness of, any information obtained from third- party sources. In addition, no independent sources has evaluated the reasonableness or accuracy of the Company's internal estimates or research and no reliance should be made on any information or statements made in this presentation relating to or based on such internal estimates and research. KYMERA Ⓒ2023 KYMERA THERAPEUTICS, INC. PAGE 2#3KYMERA Recognized leader in Targeted Protein Degradation (TPD) Building a fully-integrated, global biotech company Initial I/I and Oncology focus, but a disease-agnostic platform Accelerating forward integration through key strategic partnerships KYMERA Ⓒ2023 KYMERA THERAPEUTICS, INC. ● ● ● ● ● ● Overview Key Accomplishments Advanced four programs to clinical stage Developed a deep pipeline positioned to deliver ≥1 IND/year First to advance degrader (KT-474/SAR444656) in healthy volunteers and patients with HS and AD Demonstrated degrader vs. small molecule inhibitors (SMI) biological and clinical differentiation, and potential best in class profile in I/I Demonstrated fidelity of translation of PK, PD and safety across three clinical programs in I/I and oncology patients Unique target selection strategy based on using TPD to unlock high value, undrugged targets Well-capitalized with $516m of cash, enabling expansion of clinical impact into areas with large clinical and commercial opportunities PAGE 3#4TARGET SELECTION Undrugged (UD) or inadequately drugged (ID) targets UD Transcription Factors (e.g. STAT3) ID Degrader Advantage Over SMI (e.g. IRAK4, MDM2) KYMERA Kymera's Differentiated Approach to TPD CLINICAL TRANSLATION Strong genetic validation within clinically validated pathway PLATFORM Significantly differentiated investments Tissue- selective E3 Ligases Enabling a whole new generation of clinical programs ©2023 KYMERA THERAPEUTICS, INC. New Molecular Glue Approach Novel strategy to address undrugged/ un-ligandable targets Fidelity of translation of PK, PD and safety now in 3 programs in immunology and oncology Percent Change from Baseline IRAK4 Percent Change from Baseline -20 -100 0 -20- -40- -80 -100- 0 4 0 8 12 16 20 24 28 32 36 40 2 24 96 192 15 Hours Days MAD PART C 0 2 24 192 15 Hours: Days ● TPD "FIRSTS" Accomplished several "firsts" in TPD: FIRST randomized, placebo- controlled trial in healthy volunteers with KT-474 (IRAK4) FIRST heterobifunctional degrader with clinical activity, outside of oncology, in patients with HS and AD with KT-474 (IRAK4) FIRST demonstration of biological and clinical differentiation of degrader vs SMI with KT-474 (IRAK4) FIRST heterobifunctional degrader against an undrugged transcription factor in clinic with KT-333 (STAT3) PAGE 4#5Validated Platform and Discovery Engine Demonstrated predictable translation of PK, PD and Safety in 3 oncology and immunology programs ● Successfully Applied TPD to Unmet Needs Outside of Oncology Reported clinical impact in complex inflammatory diseases such as HS and AD ● What Our Recent Accomplishments Mean for Kymera and TPD Demonstrated TPD Can Lead to Differentiated Clinical Activity Compared to Small Molecule Inhibitors Initial KT-474 data in HS and AD validates Kymera's unique target selection strategy ● Kymera is Building Franchises in Both Immunology and Oncology Focus is on areas of high unmet needs and large commercial opportunity, in targets with clear degrader rationale ● KYMERA ©2023 KYMERA THERAPEUTICS, INC. PAGE 5#6Scaffolding Proteins ● ● Building Franchises in Immunology and Oncology in Diseases with Large Unmet Needs and Commercial Opportunities ● Scaffolding proteins with clinically validated SMIs Protein degradation affords superior biological and clinical effect Transcription Factors Undrugged transcription factor with strong genetic validation Protein degradation only/best approach to deliver effective drug IRAK4 KT-474 UNDISCLOSED Scaffolding Kinase STAT3 IL4/13 PATHWAY Transcription Factor KYMERA ©2023 KYMERA THERAPEUTICS, INC. NOVEL MOLECULAR GLUE Immunology-Inflammation DERM. GI RHEU. RESPIR. IRAKIMID KT-413 MDM2 KT-253 UNDISCLOSED Scaffolding Kinase STAT3 KT-333 Oncology SOLID TUMORS LEUK. LYMPH. PAGE 6#7= Immunology-Inflammation Clinical Pipeline Programs with DC/IND's in 2023/24 Kymera's Pipeline of Novel Protein Degraders KYMERA Program IRAK4 IRAKIMID (IRAK4, Ikaros, Aiolos) STAT3 MDM2 = Oncology STAT3 Scaffolding Kinase Transcription factor IL4/13 Pathway Transcriptional Regulator Novel Glue Scaffolding Complex Indication(s) HS, AD, RA, others MYD88MT Tumors PTCL, LGL-L, CTCL, Solid Tumors Liquid & Solid Tumors Autoimmune & Fibrotic Diseases Psoriasis, IBD, Lupus, others AD, Asthma, COPD, EoE, PN Lupus, Auto-Ab Diseases, others Ovarian, Breast Ⓒ2023 KYMERA THERAPEUTICS, INC. Discovery IND Enabling Phase 1 00 KT-474 KT-413 KT-333 KT-253 Phase 2 Next Milestones Ph2 Start 2023 Clinical Activity 2023 Clinical Activity 2023 POM 2023 Rights KYMERA sanofi KYMERA KYMERA KYMERA KYMERA KYMERA KYMERA KYMERA KYMERA * *Option to participate equally in the development and commercialization of Sanofi-partnered programs in the US PAGE 7#8KYMERA KYMERA ● ● Kymera's 2023 Objectives Collaborate with Sanofi to initiate KT-474 Phase 2 Trials Publish results of KT-474 Phase 1 Trial including patient cohort Demonstrate KT-413 clinical anti-tumor activity in patients Demonstrate KT-333 clinical anti-tumor activity in patients Initiate KT-253 Phase 1 Trial in solid and heme tumors Establish KT-253 clinical proof-of-mechanism in patients Deliver at least 2 new DC/IND from the preclinical pipeline Expand novel molecular glue franchise ©2023 KYMERA THERAPEUTICS, INC. PAGE 8#9KYMERA IRAK4#10Degrading IRAK4: Best Approach to Block IL-1R/TLR driven Inflammation IRAK3 TLRs (TLR 2,4,5,7,8,9) signaling NFkB IL-1R/TLR Pathway IL-1 a/B, IL-18, IL-33, IL-36 Myddosome IKKS MyD88 IRAK4 IRAK 1 IRAK2 TRAF6 c-Jun KYMERA Ⓒ2023 KYMERA THERAPEUTICS, INC. IL-1R JNK/p38 secreted TNF-a, IFN-Y, IL-1B, IL-6, IL-8, IL-10, IL-12, IL-17, IL-23 Degrader Advantage Inhibitor Scaffolding Role JNK/p38 NFkB IRAK4 Degrader Kinase Role IRF5/7 Clinical Pathway Validation IL-1a/IL-1ß: Rheumatoid Arthritis, CAPS, Hidradenitis Suppurativa IL-1α: Atopic Dermatitis IL-1ß: Gout; CANTOS Outcomes Data in Atherosclerosis and Lung Cancer IL-18: Macrophage Activation Syndrome IL-36: Generalized Pustular Psoriasis, Atopic Dermatitis IRAK4 SMI: Rheumatoid Arthritis Human Genetics Adult humans with IRAK4 Null Mutation are healthy IRAK4 degrader has potential to achieve a broad, well-tolerated anti-inflammatory effect, providing multiple development opportunities in autoimmune inflammatory diseases PAGE 10#11● ● ● ● ● IRAK4 Degrader Best-in-class Potential in Immune-inflammation Potential for Broad Activity Across Th1-Th17 and Th2 Diseases KT-474 Lupus IBD Gout Psoriasis IL-1R/TLR ↓ IRAK4 Th1-Th17/Neutrophils Hidradenitis Suppurativa Rheumatoid Arthritis ● ● Th2/Eosinophils Atopic Dermatitis Asthma COPD CRSWNP $150B drug sales Combined global Source: EvaluatePharma; GlobalData; Dash. Allied Market Research. 2021; Koto. Modern Rheumatology. 2021; Ahn. JAMA Otolaryngol Head Neck Surg. 2016; UC: Ulcerative Colitis; CD: Crohn's Disease. KYMERA Ⓒ2023 KYMERA THERAPEUTICS, INC. Indication AD HS RA SLE IBD Gout Psoriasis Asthma COPD CRSWNP 2021 Prevalence US/EU5/JP ~82.5 M ~785 K ~4.6 M ~580 K ~3.2 M ~18.2 M ~15.8 M ~87.3 M ~61.7 M ~20.4 M 2021 Global Sales • Small Molecule Inhibitors o $5,760 M $1,106 M $27,634 M $1,333 M $21,710 M $1,319 M $23,268 M $15,664 M $9,960 M $2,622 M Limitations of Current Therapies Anti-Cytokine/Cytokine Receptor Antibodies Target only 1-2 cytokines Require injection Limited pathway blockade (IRAK4 SMI) Safety issues (JAK family) PAGE 11#12● ● ● KT-474 Phase 1 Trial Design and Summary Healthy Volunteers (HV), SAD and MAD 9 SAD cohorts 8 subjects per cohort (6:2 randomization) including 2 food-effect cohorts 72 adult healthy subjects dosed Single dose (25-1600 mg) 5 MAD cohorts 12 subjects per cohort (9:3 randomization) 60 adult healthy subjects dosed 14x daily doses (25-200 mg, MAD 1-4); 5x twice-weekly doses (200 mg, MAD5) Summary of Key Findings in Healthy Volunteers IRAK4 reduction to near lower limit of quantification with Mass Spectrometry Degradation associated with up to 85% inhibition of multiple disease-relevant cytokines and chemokines in ex vivo TLR stimulation assay at 100 mg dose Dose-dependent IRAK4 degradation in skin of >50% Generally well tolerated at doses up to 200 mg with no SAEs KYMERA ©2023 KYMERA THERAPEUTICS, INC. ● ● HS and AD Patients 1 cohort 21 HS and AD patients 75 mg (fed state) (~equivalent exposure to 100mg fasted MAD cohort dose level) Open-label 28x daily doses Summary of Key Findings in Patients Safety, PK and PD comparable to healthy volunteers Robust degradation of IRAK4 in blood and skin was associated with systemic anti-inflammatory effect in HS and AD patients Promising clinical activity observed in HS and AD exceeding benchmark placebo rates and comparing favorably to SOC biologics Results support advancing KT-474 into Phase 2 placebo-controlled trials; Sanofi has committed to start Ph2 clinical trials, initially in HS and AD PAGE 12#13● ● ● Healthy volunteer SAD and MAD cohorts demonstrated: Robust and sustained IRAK4 degradation in blood and skin with single and multiple daily doses Broad inhibition of ex vivo TLR-mediated cytokine induction Generally well tolerated ● ● ● Patient cohort demonstrated: PK, PD and safety comparable to healthy volunteers Modest, non-adverse QTcF prolongation spontaneously resolved back to baseline during dosing Robust IRAK4 degradation in blood and skin associated with systemic anti-inflammatory effect in HS and AD patients, validating pathway and target relevance in HS and AD ● Key KT-474 Phase 1 Accomplishments ● ● Promising clinical activity exceeding benchmark placebo rates and comparing favorably to SOC biologics in both HS and AD Sanofi has committed to start Ph2 clinical trials, initially in HS and AD KYMERA Ⓒ2023 KYMERA THERAPEUTICS, INC. PAGE 13#14Disease Severity Mild Moderate Severe Very Severe Extent of Disease AN Count Fistula Count Pain-NRS* Pruritus-NRS* EASI Score Baseline Disease Characteristics HS (n=13) (HS-PGA) Patients with any prior Therapy, n (%) Antibiotics/Antibacterials** Corticosteroids Adalimumab 10 1 2 Mean (min, max) 8 (5, 18) 4 (0, 15) 7 (3, 10) 5 (0, 10) 8 (62) 6 (46) 0 3 (23)² 1 (8)* AD (n=8) (VIGA-AD) 1 5 2 ! Mean (min, max) 8 (4, 10) 17.6 (4.4, 52.3) 7 (88) 1 (13) 7 (88) 0 0 Other Biologics includes 2 pts with very severe disease; *worst score over past week **includes clindamycin and chlorhexidine *1 patient with very severe disease received infliximab and bimekizumab (and adalimumab) AD=Atopic Dermatitis; AN=Abscess and Inflammatory Nodule Count; EASI-Eczema Area and Severity Index; HS-hidradenitis suppurativa; Min-minimum; Max-maximum; Pain-NRS-Skin Pain Numerical Rating Score; Pruritus-NRS-Peak Pruritus Numerical Rating Score; PGA-Physicians Global Assessment; IGA=Investigator Global Assessment KYMERA ©2023 KYMERA THERAPEUTICS, INC. PAGE 14#153 Enrolled patients Primary reason for Treatment Completion Completed Withdrawal by patient Withdrew treatment after 4 doses for personal reasons ** Withdrew treatment after 5 doses for personal reasons KYMERA Patient Disposition ©2023 KYMERA THERAPEUTICS, INC. HS 13 12 • 9 Moderate 1 Severe • 2 Very Severe ● 1* AD 8 7 • 1 Mild ● • 4 Moderate 2 Severe 1** Total 21 19 2 PAGE 15#16KT-474 Concentration (ng/mL) Mean (+ SE) 20 15 10 5 C ● KT-474 Plasma PK and IRAK4 Degradation in HS and AD Patients Dosed for 28 Days is Comparable to HV Part C KT-474 Plasma PK ● D1 D1-H6 n = 19 after Day 4; 2 patients discontinued treatment D4 D4-H6 D7-H6 D7 D11 D11-H6 D14 D14-H6 D21 D21-H6 D28 D28-H6 Mean Day 14 Cmax (MAD3: 100 mg QD) Mean Day 14 Ctrough (MAD3: 100 mg QD) KT-474 PK at the 75 mg QD dose (fed state) in patients is comparable to 100 mg QD (fasted state) in HV D31 KYMERA ©2023 KYMERA THERAPEUTICS, INC. 3 ng/mL threshold D35 D42 Mean Cmax and Ctrough levels at steady state in Part C are in line with MAD3 levels at Day 14 Mean half-life of 44 hours is within the range observed in MAD (34-59 hours) Percent Change from Baseline IRAK4 0 -20- -40- -60- -80 -100- PK/PD Correlation in Plasma/Monocytes (FLOW) 0 4 3 ng/mL threshold MAD PART C 8 12 16 20 24 28 32 36 40 KT-474 Ctrough/ng/mL KT-474 concentrations in plasma lead to same level of IRAK4 degradation in HV (n=48) and HS/AD (n=20) patients Concentrations above 3 ng/mL lead to same level of degradation (>80%) in HV and Patients protein] Mean (± SE) Absolute IRAK4 Levels by MS [fmol/µg IRAK4 Levels in PBMC in Patients at Day 28 (MS) 1.00- 0.75 0.50 0.25 0.00 Day 28 HS and AD Patients IRAK4 Levels at Day 28 (n=4) near LLOQ PAGE 16#17KT-474 Reduced IRAK4 in Skin Lesions of AD and HS Patients on Day 28 to at Least Same Level as Healthy Subjects KYMERA Mean (+SE) IRAK4 Levels in Skin (fmol/µg protein) N Mean (± SE) 0.3 0.2 0.1 0.0 MAD Healthy Subjects (Baseline) 46 0.123 (± 0.01) ©2023 KYMERA THERAPEUTICS, INC. ‒‒‒‒‒‒‒‒‒‒‒‒‒‒‒‒‒‒‒‒‒‒‒‒‒‒‒‒‒‒‒‒‒‒‒‒‒‒‒‒‒‒‒‒‒‒‒‒‒‒‒‒‒‒ AD Patients (Baseline) 7 0.216 (± 0.06) HS Patients (Baseline) 11 0.236 (± 0.05) AD Patients (Day 28) 6 0.103 (+ 0.05) ‒‒‒‒‒‒‒‒‒‒‒ ‒‒‒‒‒‒‒‒‒‒‒‒‒‒ HS Patients (Day 28) 9 0.112 (± 0.03) PAGE 17#18* Maximum % Change from Baseline -20 - -40- -60 - -80 -100 - HV (MAD3) Up to 98% Inhibition of 9 Disease-Relevant Cytokines Ex Vivo in both HS and AD Patients |'||||| IFNY IL10 IL12 IL17 IL1b IL23 IL6 IL8 TNFa -67% -45% -47% -20% -64% -54% AD -95% -98% -76% KYMERA LPS HS -36% -52% -84% -8% -44% -31% -50% -59% -57% -49% -60% -83% -63% -95% -70% -85% -74% Ⓒ2023 KYMERA THERAPEUTICS, INC. -41% MAD 3 Healthy Subjects 100 mg QD (n = 9) Part C AD Patients (n=7) Plots show median of the maximum change from baseline between Days 7-14 in MAD3, and Days 14-28 in Part C Part C HS Patients (n=9) Maximum % Change from Baseline |yp| -20- -40- -60- -80- -100- HV (MAD3) AD HS IFNY IL10 IL12 IL17 IL1b IL6 -87% -95% -76% -50% -71% -55% -67% -64% 0% -72% -54% -81% -74% -35% -69% -46% -57% -50% IL8 -33% -48% -43% R848 TNFa -62% -62% -54% PAGE 18#19In Vivo Inhibition of Disease-Relevant Plasma Cytokines and Acute Phase Reactants by KT-474 in HS/AD Patients IL-6 Analyte IL-6t CRPt IL-1B SAAT Mean Max* AD Mean Max* HS (n) (n) -56% (3) ΝΑ -36% (7) -51% (4) *Max % reduction through Day 42 +Analysis performed only on patients with values >ULN at baseline IL-6, IL-13 and CRP are high sensitivity assays KYMERA ©2023 KYMERA THERAPEUTICS, INC. -63% (8) -58% (5) -48% (8) -41% (10) Percent Change from Baseline 50 O -50 0 7 ed 14 TICH 28 Days + 35 AD (N=3) HS (N=8) 42 PAGE 19#20Disease-Relevant Genes Downregulated in Skin Lesions in ≥ 50% of Evaluable* AD (N=7) and HS (N=10) Patients at Day 28 (RNAseq) • Substantial downregulation of many disease relevant genes in both HS and AD patients Downregulation exceeded 90% for many genes Broad anti-inflammatory signature with downregulation of genes responsible for: KYMERA IL1 family cytokines Th1 Th17 Th2 Innate immunity AD HS CXCL1 ©2023 KYMERA THERAPEUTICS, INC. AD-3- AD-6- AD-7- AD-4- AD-5- AD-2- AD-1- IFNG HS-3- HS-8 HS-2- HS-5- HS-4- HS-12- HS-9- HS-1 HS-6 HS-7 -7.5 CSF3 HS-3- HS-8- HS-5 HS-1- HS-9 HS-2 HS-4- HS-6- HS-12- HS-7- 0 log2(fold change) -5.0 -7.5 -2.5 0.0 log2 (fold change) 2.5 IL2RB 0.0 AD-6- AD-3- AD-2- AD-7- AD-1- AD-4- AD-5- GZMB HS-5- HS-2- HS-3- HS-8- HS-12- HS-6- HS-7- HS-4- HS-9- HS-1- -3 HS-8- HS-1- HS-3- HS-4- HS-5- HS-7- HS-9- HS-12- HS-6- HS-2- -7.5 IL1B -5.0 -2.5 log2 (fold change) log2 (fold change) tlog2(fold change): -1 = 50% decrease, -2 = 75% decrease, -3 = 87.5% decrease log2(fold change) -5.0 -2.5 log2(fold change) 0.0 6 2.5 IL5 AD-4- AD-5- AD-1- AD-3- AD-7- AD-2- AD-6- IL8 HS-5 HS-4 HS-8 HS-1- HS-3- HS-12- HS-7 HS-9 HS-6 HS-2 -5.0 IL36A HS-5- HS-3 HS-4 HS-1 HS-8 HS-7 HS-9- HS-6 HS-2 HS-12- 0 -7.5 log2(fold change) -2.5 0.0 log2 (fold change) 2.5 5.0 0.0 NLRP3 AD-3- AD-5- AD-2- AD-4- AD-7- AD-1- AD-6- IL2RA HS-4- HS-5 HS-3- HS-8- HS-2- HS-1- HS-9- HS-12 HS-6 HS-7 -2 IL17A HS-5- HS-8- HS-3- HS-4- HS-1- HS-7- HS-2- HS-12- HS-9- HS-6- 0 2 log2(fold change) -5.0 -2.5 log2 (fold change) log2(fold change) *Evaluable patients for whom the samples were of sufficient quality for analysis. 0 log2(fold change) PAGE 20#21Mean % Change in EASI Score (+/-S.E. of Mean) -10 -20 -30 -40 -50 -60 O 0 AD: Significant Reduction in EASI Score and Pruritus Mean % Change in EASI Score Over Time (N=7) 7 14 -17.9 21 Day -37.1 28 35 -27.6 KYMERA ©2023 KYMERA THERAPEUTICS, INC. -36.4 42 Mean % Change (+/-S.E. of Mean) 10 -10 -20 -40 -50 -70 -80 0 Mean % Change of Worst Pruritus Over Time (N=7) -5.8 TH 7 -6.6 -32.1 14 -33.3 -43 | H H -35.6 -44.6 -51.2 21 Day Past Week Past 24 Hours 28 -38.9 -44.6 35 -51.9 -62.9 42 % of Pruritis Responders (80% CI) 100 90 80 70 60 50 40 30 20 10 O C Patients with ≥4 Unit Reduction from Baseline in Worst Pruritus (N=7) 7 29 14 43 29 21 Day Past Week Past 24 Hours 71 57 28 57 43 35 71 57 42 PAGE 21#22● 7 # of Patients by AD-IGA Score P 10 LO N 0 Investigator's Global Assessment (VIGA-AD) 2 1 4 4 ||| 2 Day 14 1 Baseline VIGA-AD Score Over Time (n=7) KYMERA ©2023 KYMERA THERAPEUTICS, INC. ■ Mild 1 2 Day 28 Moderate ■Severe IGA scores remained stable or improved in all patients 1 2 Day 35 1 3 3 Day 42 PAGE 22#23Percent Change from Baseline ● ● 51-year-old Hispanic/Latino male with severe AD (VIGA-AD) and EASI score of 28.2 at baseline Previously treated with topical betamethasone 2018-2020 Efficacy Endpoints IGA-AD Score EASI Score (% Change) Peak Pruritis NRS - past week (% Change) 150 125 100. 40 20 0 -20 -40- Plasma Cytokines 0 7 BL Severe 28.2 14 IL-1B IL-6 Percent Change from Baseline Day 28 Moderate 14 (-50) 1 (-75) 0- -25- -50- AD Case Study: Patient AD-3 Improvement in Disease Severity from Severe to Mild -75- -100- 21 28 35 42 49 Day KYMERA ©2023 KYMERA THERAPEUTICS, INC. Day 35 Moderate 16.45 (-42) 1 (-75) Day 42 Mild 9.2 (-67) 1 (-75) Skin Inflammation Biomarkers* (RNAseq) IL5 TNF NLRP3 CXCL1 CCL3 CXCL8 IL1B PTGS2 *Changes at D28 Day 1 - BL =1mm ADT =1mm Day 42 PAGE 23#24● ● KT-474 Showed Meaningful Signs of Clinical Activity in AD, Comparing Favorably to Placebo Benchmarks and SOC Encouraging initial EASI score reductions sustained after cessation of dosing Peak pruritus reductions, and responder rates, significantly greater than placebo and SOC benchmarks Investigator Global Assessment (IGA) scores improved in 2 of 7 patients and remained stable in the others AEASI APeak Pruritus NRS Peak Pruritus NRS Responder (week/24hrs) KT-474 Part C Day 28 -37% -52% 57%/71% Day 42 -36% -63% 57%/71% Placebo Benchmarks Week 4 -12 to -25%* -11%¹ 4 to 17%** Dupilumab Phase 3 Week 4 -52%¹ -34%¹ 23 to 40% 1,2 *Range from 7 different Phase 2 and Phase 3 trials; **Range from 10 different Phase 2 and Phase 3 trials; ¹Simpson EL, et al. NEJM 2016;375:2335-2348; 2Bieber T, et al. NEJM 2021;384:1101-1112; The Dupilumab clinical trial was conducted by other parties in a similar patient population with different enrollment criteria from Part 1C of our Phase 1 clinical trial evaluating KT-474. Results do not reflect a head-to-head trial and are shown for illustrative purposes only KYMERA Ⓒ2023 KYMERA THERAPEUTICS, INC. PAGE 24#25HS: Significant Reductions in AN Counts Leading to HiSCR Responses Mean % Change (+/- S.E. of mean) -10 -20 -30 40 -50 -60 Mean % Change in Total AN Counts Over time 0 7 KYMERA -27.4 -19.9 14 -49.6 21 Day -31.6 28 -45.4 All HS Patients (N=12)* Moderate to Severe (N=10) -40.6 35 -46.11 -50.7 42 ©2023 KYMERA THERAPEUTICS, INC. % of Patients with AN 0/1/2 (80% CI) 80 70 60 50 40 30 20 10 O 0 7 % of Patients with AN Count 0/1/2 20 14 17 21 Day 50 28 42 50 35 All HS Patients (N=12) Moderate to Severe (N=10) 42 40 33 42 % of HISCR Responders (80% CI) 80 70 60 50 40 30 20 10 O HISCR50 Responders 7 30 14 25 21 Day 30 *One patient is censored for Day 35 and Day 42 since the patient started on ustekinumab, steroids and abx on Day 34. 28 25 All HS Patients (N=12) Moderate to Severe (N=10) 50 42 35 50 42 42 PAGE 25#26Mean % Change (+/- S.E. of Mean) O -10 -20 -30 -40 -50 -60 -70 -80 O -26.9 KYMERA Mean % Change in Average Pain Over Past Week 7 -23.4 -38.7 14 -40.1 -56.1 HS: Significant Reductions in Pain/Pruritus % of Patients with ≥30% and ≥1 Unit Reduction in Worst Pain Over the Past Week -48.6 -64.6 21 Day -53.8 -65.7 28 All HS Patients (N=12)* Moderate to Severe (N=10) -59.7 F -60.1 35 -60.4 ©2023 KYMERA THERAPEUTICS, INC. 42 % of Pain Responders (80% CI) 100 90 80 70 50 40 30 20 10 O 0 20 7 17 50 14 42 70 58 21 Day 60 50 28 All HS Patients (N=12) Moderate to Severe (N=10) 60 60 50 35 50 42 Mean % Change (+/- S.E. of Mean) -10 -20 -30 -40 -50 -60 -70 -80 -90 -100 0 Mean % Change in Worst Pruritus Over Past Week -29.1 7 -17 -41.7 -26.1 -41.9 14 -24 *One patient is censored for Day 35 and Day 42 since the patient started on ustekinumab, steroids and abx on Day 34. -67.8 21 Day All HS Patients (N=12)* Moderate to Severe (N=10) -48.6 28 -62.3 -53.6 35 -61.6 -68.4 42 PAGE 26#27# of Patients by HS-PGA Score 12 10 00 2 O 2 1 9 HS-PGA Score Over Time (N=12*) Baseline 2 1 6 2 Physician's Global Assessment (HS-PGA) 1 Day 14 ■Clear ■Minimal ■Mild 2 1 5 3 1 1 1 4 3 KYMERA ©2023 KYMERA THERAPEUTICS, INC. 1 1 Day 28 Day 35 Moderate ■Severe ■Very Severe 1 1 4 1 Day 42 # of Patients by HS-PGA Score OHN W AUT a 5 *One patient is censored for Day 35 and Day 42 since the patient started on ustekinumab, steroids and abx on Day 34. 10 HS-PGA Score Over Time Moderate to Severe Patients (N=10) 1 9 Baseline Clear HS-PGA scores remained stable or improved in all patients Disease cleared in 1 patient with moderate disease at baseline 1 6 2 1 Day 14 Minimal 1 5 3 1 Day 28 1 4 3 1 1 Day 35 Mild Moderate ■Severe 1 4 1 Day 42 PAGE 27#28HS Case Study: Patient HS-3 Complete Clearing of Lesions and Symptoms in Patient with Moderate Disease at Baseline Day 1 - BL Day 42 45 year old Black Female with Moderate HS (HS- PGA); Baseline AN count = 7 Prior treatments: clindamycin (topical) and doxycycline Efficacy Endpoints HS-PGA Score AN Count (% Reduction) Skin Pain NRS - Worst, past week (% Change) Peak Pruritis NRS - past week (% Change) BL Moderate 7 7 6 Day 28 Day 35 Clear Clear 0 (-100) 0 (-100) 0 (-100) 0 (-100) 0 (-100) KYMERA ©2023 KYMERA THERAPEUTICS, INC. 0 (-100) Day 42 Clear 0 (-100) 0 (-100) 0 (-100) Percent change from baseline Area of swelling Beneath skin -25- -50- -75- -100- Resolution of Swelling Skin Inflammation Biomarkers* (RNAseq) '||| IIII CXCL8 IL1B PTGS2 IL36A IL17A IL5 CXCL1 GZMB IFNG *Changes at D28 PAGE 28#2939 year old Black Female with Moderate HS (HS-PGA); Baseline AN count 5 Prior treatments: benzocaine ointment Efficacy Endpoints HS-PGA Score AN Count (% Reduction) Skin Pain NRS - Worst, past week (% Change) Peak Pruritis NRS - past week (% Change) - HS Case Study: Patient HS-10 Improvement in Disease Severity from Moderate to Mild BL Moderate 5 8 10 Day 28 Mild 2 (-60) 3 (-63) KYMERA ©2023 KYMERA THERAPEUTICS, INC. 2 (-80) Day 35 Mild 2 (-60) 3 (-63) 0 (-100) Day 42 Mild 1 (-80) 1 (-88) 0 (-100) Day 1 - BL Percent Change from Baseline Multiple Ulcerated 40 Plasma Cytokines/Acute Phase Reactants 20 O -20 -40 -60- -80 Nodules O 7 14 21 28 Day Day 42 Clearing of Ulcerated Nodules 35 IL-1B SAA 42 49 PAGE 29#30● ● ● KT-474 Showed Meaningful Signs of Clinical Activity in HS, Comparing Favorably to Placebo Benchmarks and SOC AN Count reductions most profound in moderate and severe patients Highly competitive HISCR response rates continued to improve after cessation of dosing Pain and pruritus response rates and reductions significantly higher than placebo and SOC benchmarks Physician Global Assessment (PGA) scores improved in 5 of 12 patients, including 1 moderate disease patient with full disease clearance, and stable in the others ΔΑΝ Count AN Count 0/1/2 HISCR50 HISCR75 Pain NRS30 Responder KT-474 Part C (All/Moderate to Severe) Day 28 Day 42 -46% / -51% -32% / -50% 42% / 50% 25% / 30% 8% / 10% 50% / 60% 33% / 40% 42% / 50% 25% / 30% 50% / 60% The Adalimumab clinical trial was conducted by other parties in a similar patient population with different enrollment criteria from Part 1C of our Phase 1 clinical trial evaluating KT-474. Results do not reflect a head-to-head trial and are shown for illustrative purposes only KYMERA Ⓒ2023 KYMERA THERAPEUTICS, INC. Placebo Benchmarks Week 4 -15%¹ 24 to 26%³ 19 to 30% 3,4 5%4 18 to 23% 3,5 Adalimumab Phase 2 and 3 Week 4 -31%¹ 28 to 47%2,3 29 to 51% 3,4 20%4 39 to 58%2,3,5 ¹Kimball AB, et al. Ann Intern Med 2012;157:846-55; 2Morita A, et al. J Dermatol 2021;48:3-13; 3Kimball AB, et al. NEJM 2016;375:422-434;4Glatt S et al. JAMA Dermatol 2021;157:1279-88; 5Scheinfeld, et al. Derm Online J 2016:22 PAGE 30#31Adverse Events Related to Study Drug (Occurring in > 1 Patient) Adverse Event (Preferred Term) Headache KYMERA Fatigue Diarrhea # of Patients ©2023 KYMERA THERAPEUTICS, INC. 6 4 2 Severity (# of Pts) Mild (5) Severe (1) Mild (4) Mild (2) Outcome (# of Pts) Recovered (6) Recovered (4) No SAEs, no drug-related infections, and no AEs observed leading to dose interruption or discontinuation Recovered (2) PAGE 31#32● ● ● QTc Prolongation Spontaneously Resolves to Baseline by Day 28 AQTCF in Part C is in the range observed in MAD3 (100 mg QD) up to Day 14 Declines to baseline with continued dosing and sustained plasma exposure through Day 28 Profile is maintained through day 42 upon cessation of dosing after Day 28 No QTc-related AEs observed AQTcF QTcF Mean MAD3 Part C MAD3 Part C n=9 for MAD3 and n=20 for Part C, except day 14 (n=19) KYMERA Ⓒ2023 KYMERA THERAPEUTICS, INC. Baseline 395 Change from Baseline QTcF (ms) Mean (± 90% CI) 403 20 15 10 5 O -5 Day 7 17 15 411 419 Day 14 13 12 408 416 Day 21 5.9 -- 410 MAD3 PART C Day 28 1.6 405 PAGE 32#33● ● Part C Summary KT-474 administered to HS and AD patients at 75 mg QD for 28 days shown to have safety, PK and PD comparable to healthy volunteers Modest, non-adverse QTcF prolongation observed to spontaneously resolve back to baseline during final 2 weeks of dosing in HS and AD patients Robust degradation of IRAK4 in blood and skin was associated with systemic anti- inflammatory effect in HS and AD patients Promising clinical activity observed in HS and AD exceeding benchmark placebo rates and comparing favorably to SOC biologics Data presented here validate IRAK4 degradation as a potential best in class mechanism in inflammatory diseases and its superior clinical potential over SMI Results support advancing KT-474 into Phase 2 placebo-controlled trials, Sanofi has committed to start Ph2 clinical trials initially in HS and AD KYMERA ©2023 KYMERA THERAPEUTICS, INC. PAGE 33#34KYMERA IRAKIMID#35IRAKIMiDs 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#36KT-413 Highly Active on Intermittent Dosing in Preclinical Models Complete Tumor Regressions Associated with Robust IRAK4 and Ikaros/Aiolos Degradation for ~72h +SEM Tumor Volume (mm³) Mean, ● KYMERA 2500 2000 1500- 1000 500 Drug (Day 33) IV vehicle CC-220, 3 mg/kg, PO, QD x 21 KT-413, 10 mg/kg, IV, D1,2,21,22 7 14 21 28 Days After Start of Treatment CC-220 KT-413 10 mg/kg T/C% (REG%) 9 (94) CR ©2023 KYMERA THERAPEUTICS, INC. 0 5 PR 0 2 35 SD 0 In the OCI-LY10 MYD88MT xenograft model, intermittent dosing of KT-413 induced strong antitumor activity, including complete regressions. Superior activity compared to IMID CC-220 alone PD 7 0 10000 KT-413 Concentration (ng/ml or ng/g) 1000 100 10- 1 0 •Tumor PK 48 HIH Plasma PK HH 96 Time (hr) 144 IRAK4 192 Ikaros HHHHH 240 150 100 50 O % of Vehicle Control Single 10 mg/kg dose showed extended tumor exposure and strong degradation of both IRAK4 and IMID substrates that was maintained for least 72hr in preclinical models Target PD 80-90% Ikaros KD and 50-70% IRAK4 KD in tumor for ≥72 hrs to achieve robust anti-tumor activity PAGE 36#37KT-413: Phase 1, Multicenter, Dose-Escalation and Expansion Trials to Evaluate KT-413 in Patients with R/R DLBCL 0.16 Key Objectives Primary 0.32 Secondary ● Ⓡ 0.51 ● Phase 1a (n up to 40) R/R B-cell NHL 0.82 Regimen: mg/kg IV Infusion q 3 weeks Predicted clinically efficacious doses DLX Phase 1a Safety/Tolerability and MTD and RP2D PK Parameters of KT-413 Preliminary Estimates of Activity Exploratory PD Effects of KT-413 MTD: Maximum Tolerated Dose. RP2D: Recommended Phase 2 Dose. ORR: Overall Response Rate KYMERA ©2023 KYMERA THERAPEUTICS, INC. ● ● ● MTD/RP2D Expansion * *Additional 3-6 pts for a total of 9 patients dosed at MTD Phase 1b (n=40) R/R DLBCL PD Effects of KT-413 Cohort 1: MYD88MT n=20 Cohort 2: MYD88WT n=20 Phase 1b Safety/Tolerability at RP2D in Patients with DLBCL Preliminary Clinical Activity (ORR, DOR, PFS, DCR, OS) PK Parameters of KT-413 PAGE 37#38Plasma KT-413 Concentration (ng/mL) 1000 100 10 O Plasma PK Showing Dose-Proportional Increase in Exposure 4 8 12 Cycle 1 Plasma PK 24 Time (h) KYMERA ©2023 KYMERA THERAPEUTICS, INC. 48 DL1: 0.16 mg/kg DL2: 0.32 mg/kg DL3: 0.51 mg/kg DL4: 0.82 mg/kg 72 PK Parameter Cmax (ng/mL) AUC inf (ug.h/mL) Vd (L/kg) CL (L/h/kg) t₁/2 (h) Cycle 1 PK Parameters DL2 DL1 DL3 0.16 mg/kg 0.32 mg/kg 0.51mg/kg (n = 1) (n = 1) (n = 1) 140 1380 10.1 0.116 60.3 546 3750 4.51 0.0853 36.7 598 7580 5.41 0.0673 55.8 Individual values shown for DL1-DL3; Mean (individual values) shown for DL4 since data from only 2 patients is available. DL4 0.82mg/kg (n = 2) 1500 (1140, 1850) 9340 (10800, 7860) 4.66 (3.92, 5.40) 0.0901 (0.0758, 00104) 35.9 PAGE 38#39DL3 and 4 Degradation Profile of IRAK4, Ikaros and Aiolos Consistent with Strong Antitumor Activity in Preclinical Models IRAK4 Ikaros Aiolos Percent Change from Baseline Percent Change from Baseline 150 100 50 0 -50 -100 0 -20- -40 -60 -80 -100 150 100 50 -50 Target Degradation in PBMC by FLOW DL1 DL2 DL3 0.16 mg/kg 0.32 mg/kg 0.51 mg/kg Cycle 1 -100 T 0 0 T 2 24 Hours T 2 24 Hours 02 24 Hours Note Cycle 1, 72 hours window = +24 hours 72 72 Cycle 2 M 72 T 8 Days 8 + 15 0 15 Days - T 2 Hours DL4 0.82 mg/kg T T T 24 8 15 Days T T 0 2 24 8 15 Hours Days 8 15 0 2 24 8 15 Days Hours Days KYMERA Ⓒ2023 KYMERA THERAPEUTICS, INC. Dose Level DL1 DL2 DL3 DL4 Dose Level DL1 D DL3 DL4 Dose Level DL1 DL2 DL3 DL4 Cycle 1 -4% -28% ΝΑ -70% Cycle 1 -82% -92% ΝΑ -89% Cycle 1 -95% -100% ΝΑ -95% Cycle 2 0 -40% -57% ΝΑ Cycle 2 -89% -95% -96% ΝΑ Cycle 2 - 89% -100% -100% ΝΑ ● • Five patients were treated across DL1-4.* ● ● 1 each at DL1-3 and 2 at DL4 • PD results on first 4 patients Up to 70% KD of IRAK4 and 96- 100% KD of Ikaros and Aiolos in PBMC at DL1-4 • DL3-4 expected to be clinically active doses/profiles. Degradation consistent with target knockdown needed for antitumor responses in preclinical models of MYD88mut DLBCL (slide 36) * These included patients with transformed activated B-cell-like (ABC)-diffuse large B-cell lymphoma (DLBCL), follicular lymphoma, marginal zone lymphoma, and plasmablastic lymphoma, all of whom were MYD88 wild-type except for one who had a MYD88 gain-of-function mutation. PAGE 39#40● ● ● PK and PD profiles in DL1-4* consistent with preclinical data supporting once every three-week dosing regimen ● ● Desired Translation of PK, PD and Safety of KT-413 ● KT-413 achieved dose-dependent degradation of up to 70% IRAK4 and 96-100% Ikaros and Aiolos in PBMC after a single dose Consistent degradation in blood and tumor Profile that in preclinical species led to robust antitumor activity in MYD88 mutant tumors The most common adverse events were fatigue, cough and pyrexia.** No DLTs or drug-related neutropenia were observed in the study. Expect to be at potentially clinically active profiles at DL3-4 and beyond. *DL1-3 have been completed and DL4 remains open to accrual. **AEs related to KT-413 were all Grade 1 and 2; SAEs (Gr. 4 sepsis and Gr. 4 lung infection) reported in one patient in DL3 occurred outside of the DLT window at the end of Cycle 2 in the setting of disease progression. KYMERA ©2023 KYMERA THERAPEUTICS, INC. Potential to be First Precision Medicine in DLBCL to Target a Genetically- defined Population (MYD88MT) Profound antitumor activity in preclinical models both in single agent and combination Clinical strategy in place to enable accelerated approval: Monotherapy MYD88MT DLBCL for most direct path to registration Other MYD88MT lymphomas of interest include PCNSL, WM Combinations With SOC agents in MYD88MT DLBCL to enable earlier line therapy PAGE 40#41KYMERA STAT3#42● ● ● ● 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 ©2023 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 42#43KT-333 Highly Active on Intermittent Dosing Regimens Complete Tumor Regressions Associated with Robust STAT3 KD for ~48h in Preclinical Models KYMERA +SEM Tumor Volume (mm³) Mean, 3000 2000 1000 0+ 0 SU-DHL-1 Weekly Dosing Vehicle KT-333, 5 mg/kg, QW KT-333, 10 mg/kg, QW 10 5 15 Days (Post-randomization) HH 20 ©2023 KYMERA THERAPEUTICS, INC. 25 Dose- and degradation-dependent tumor growth inhibition observed with once-weekly dosing in ALK+ ALCL 10 mg/kg sufficient to drive full tumor regression in SU-DHL- 1 that was durable for multiple weeks after the last dose (on day 14) 100000 KT-333 Concentration (ng/ml or ng/g) 10000 1000 100 10- 0 Preclinical PK/PD •Tumor PK 48 Plasma PK Tumor PD 96 Time (hr) 144 192 240 Based on preclinical model (STAT3 dependent ALK+ ALCL), target PD >90% STAT3 KD for ~48 hours to achieve robust anti-tumor activity 150 100 50 -0 % of Vehicle Control PAGE 43#44KT-333: Phase 1, Multicenter, Dose-Escalation and Expansion Trial to Evaluate KT-333 in Adult Patients with PTCL, CTCL, LGL-L, and Solid Tumors 0.05 Key Objectives Primary 0.10 Secondary ● ● ● Phase 1a (n up to 40) R/R Lymphoma/Leukemia or Solid Tumors Regimen: mg/kg IV Infusion weekly 0.20 0.40 DLX Predicted clinically efficacious doses Phase 1a Safety/Tolerability and MTD and RP2D PK Parameters of KT-333 Preliminary Estimates of Activity Exploratory PD Effects of KT-333 MTD: Maximum Tolerated Dose. RP2D: Recommended Phase 2 Dose. ORR: Overall Response Rate KYMERA ©2023 KYMERA THERAPEUTICS, INC. ● ● MTD/RP2D Expansion* ● Phase 1b (n=40) Cohort 1: PTCL n=20 Phase 1b • Safety/Tolerability at RP2D in Patients with Lymphoma/Leukemia and Solid Tumors Cohort 2: CTCL n=20 PD Effects of KT-333 Cohort 3: LGL-L n=20 Cohort 4: Solid Tumors n=20 Preliminary Clinical Activity (ORR, DOR, PFS, DCR, OS) PK Parameters of KT-333 PAGE 44#45● As of May 1, 2023, thirteen patients received a mean of five doses across four dose levels. • Tumor types enrolled: CTCL (n=2), PTCL (n=1), and solid tumors (n=10, including colorectal [2], appendiceal, anal, pancreatic, cholangiocarcinoma, peritoneal, endometrial, ovarian and head & neck) Number of Patients with Adverse Event Occurring in ≥2 Patients (n, (%)) Preferred Term Fatigue Anemia Constipation Nausea Dehydration Dizziness Overall Safety Dose Level 1 0.05 mg/kg (n=4) All Related 2 (50) Dose Level 2 0.1 mg/kg (n=4) All Related Dose Level 3 0.2 mg/kg (n=3) All Related KYMERA Ⓒ2023 KYMERA THERAPEUTICS, INC. 1 (25) 2 (50) 2 (50) 1 (25) 1 (25) 1 (25) 1 (25) 1 (25) 1 (25) 1 (25) 1 (25) Skin infection 1 (25) (a) All Grade 1 and 2 events except the following: 1 patient with Gr. 3 abdominal pain and 1 patient with Gr. 3 fatigue that were not related to KT-333. (b) No Grade 4 or Grade 5 events. 1 (33.3) 1 (33.3) 1 (33.3) I Dose Level 4 0.4 mg/kg (n=2c) Related All I I I I Overall a, b (N=13) All 4 (30.8) 3 (23.1) 3 (23.1) 3 (23.1) 2 (15.4) 2 (15.4) 2 (15.4) Relatedd (c) At time of data cut off, DL4 had enrolled two patients and no AEs had been reported. (d) AEs related to KT-333 (n=1 each): Gr. 1: abdominal pain upper, LDH increase, and rash. Gr. 2: diarrhea; hypothyroidism; and squamous cell carcinoma (SCC) of the skin in CTCL patient with history of prior UVB treatment and recurrent skin SCCs considered possibly related. Safety Summary: At the time of the data cut off (May 1, 2023), KT-333 was well tolerated, with no dose limiting toxicity observed and no serious adverse events considered related to KT-333. PAGE 45#46Plasma KT-333 Concentration (ng/mL) Mean (± SE) 1200 1000- 800- 600- 400 200 0- 0 2 Consistent Plasma PK Across the Evaluated Dose Levels 4 Week 1 Plasma PK HOH 6 HH 8 Time (h) KYMERA ©2023 KYMERA THERAPEUTICS, INC. DL1: 0.05 mg/kg DL2: 0.1 mg/kg DL3: 0.2 mg/kg 24 PK Parameter Cmax (ng/mL) AUC last (ng.h/mL) Vd (L/kg) CL (L/h/kg) t₁/2 (h) DL1: 0.05, mg/kg (n=4) Day1 307 (30.5%) 1550 (65.7%) 0.277 (17.1%) 0.0447 (62.7%) Week 1 PK Parameters 6.25 (78.8%) Day 8 280 (22.9%) 1450 (35.2%) 0.270 (22.2%) 0.0380 (35.2%) 5.26 (28.2%) DL2: 0.1 mg/kg (n=2) Day 1 382 (405, 359) 1820 (2120, 1520) 0.315 (0.293, 0.337) 0.0565 (0.047, 0.0659) 3.93 (4.32, 3.55) Day 8 497 (590, 403) 1620 (2090, 1140) 0.218 (0.200, 0.236) 0.0687 (0.048, 0.089) 2.36 (2.90, 1.82) Mean (%CV) shown for DL1; Mean (individual values) shown for DL2 and DL3. Subject 103-001 (DL2) excluded due to inconsistency in PK profile. DL3: 0.2 mg/kg (n=2) Day 1 1020 (1130, 902) 3150 (3050, 3250) 0.388 (0.374, 0.401) 0.0636 (0.0656, 0.0616) 4.23 (3.95, 4.51) Day 8 1070 (1200, 932) 4770 (4350, 5190) 0.243 (0.258, 0.229) 0.0422 (0.0459, 0.0385) 4.01 (3.89, 4.12) PAGE 46#47% Change from C1D1 Predose (Mean ± SEM) Strong Proof-of-mechanism for KT-333 with up to 88% Mean Maximum Nearing Desired Degradation Profile at DL3 0 IWA Cycle 1 weeks 1 & 2 T 4 5 6 7 8 9 10 11 12 -20 -40 -60 -80- KT-333 -100 Ⓡ ● Method: Targeted Mass Spectrometry ● T T 1 2 3 Days in Study Cycle 2 weeks 1 & 2 T T T T T T 29 30 31 32 33 KYMERA ©2023 KYMERA THERAPEUTICS, INC. +++ 35 36 37 38 DL1 DL2 DL3 Dose Level 0.05 mg/kg (n=4) 0.1 mg/kg (n=3) 0.2 mg/kg (n=2) Patient ID 105-001 105-002 102-001 105-003 105-004 103-001 180-004 180-001 180-002 Cycle 1 Maximum Degradation mean** (weekly max) -79.8% (-75.6 %, -84.1 %) -67.8 % (-73.5%, -62.0 %) -50.0 % (-47.4 %, -52.6 %) -67.8% (-66.1 %, -69.5 %) -65.5 % (-65.5 %, missing) -74.4 % (-68.1 %, -80.7%) -70.6 % (-66.9 %, -74.4 %) -75.5% (-73.9 %, -77.0%) -85.4 % (-80.3 %, -90.4 %) ** post doses 1 & 2; # = BLOQ Average -66.4% -70.2% -80.5 % Maximum Degradation mean (weekly max) N/A N/A N/A Cycle 2 Dose-dependent STAT3 degradation Mean maximum degradation of up to 85.4% in Cycle 1 and 88.4% in Cycle 2 Weekly maximum reductions of up to 90-91% Profile at or nearing STAT3 degradation that has been shown to lead to strong antitumor effects in preclinical models N/A -82.8 % -88.4 % (-91.0# %, -85.7#%) pending -83.6% (-88.6 %, -78.6%) -80.0 % (-72.7%, -87.2%) ** post doses 5 & 6; # = BLOQ ** Average N/A -85.6 % -81.8% PAGE 47#48KT-333 Achieved STAT3 Pathway Inhibition and Downregulation of Inflammatory Biomarkers in Blood Maximum % Decrease in Plasma SAA (Mean ± SEM) Maximum % Decrease in Plasma CRP (Mean ± SEM) -20- -40- -60- -80- -100 O -20 -40- -60- -80- -100- 00 D C to- OO O SAA O C1 Week 1 C1 Week 2 CRP O O to -●● O O C1 Week 1 C1 Week 2 DL1 DL2 DL3 DL1 DL2 DL3 KYMERA ©2023 KYMERA THERAPEUTICS, INC. % Change from C1D1 Predose (Mean ± SEM) ● ● ● ● 300 200 100 -50 -75 KT-333 DL1 T DL2 wal DL3 1 2 3 4 5 6 7 8 9 10 11 12 29 30 31 32 33 34 35 36 37 Days in Study SOCS3 % Change 100- -50- DL2 DL3 -75 -50 STAT3% Change -87.5 Dose-dependent reduction in SOCS3 mRNA during Cycles 1 and 2 Correlation between changes in STAT3 protein and SOC3 mRNA Additional gene expression changes measured in peripheral blood presently being analyzed Reductions in plasma SAA and CRP, STAT3 regulated acute phase proteins 1 0 PAGE 48#49Desired Translation of PK, PD and Safety of KT-333 ● PK and PD profiles in DL1-3* consistent with preclinical data Proof-of-mechanism for KT-333 demonstrated with up to 88% mean max degradation of STAT3 in peripheral blood mononuclear cells. This profile is nearing 90% target degradation that led to robust antitumor activity in STAT3-driven preclinical tumor models. • The most common adverse events were Grade 1 and 2 and included fatigue and gastrointestinal symptoms, with no DLTs observed or drug related SAEs. Expect to be at potentially clinically active exposures at DL4 and beyond. *DL1-3 have been completed and DL4 remains open to accrual. KYMERA Ⓒ2023 KYMERA THERAPEUTICS, INC. First-in-class Opportunity to Address STAT3-driven Pathology Across Diverse Indications First heterobifunctional degrader against an undrugged target in the clinic Clinical development strategy includes monotherapy direct registrational path in STAT3 dependent T cell malignancies Opportunity for expansion into solid tumors in combination with immune checkpoint inhibitors informed by planned analysis of PDL1 and TME markers in solid tumor sample from ongoing trial PAGE 49#50KYMERA MDM2#51● MDM2 is the E3 Ligase that Modulates p53, the Largest Tumor Suppressor Cancer genetics: p53 is NOT mutated in almost 50% of tumors • MDM2 overexpression and amplification can inactivate p53 Large opportunity in wide variety of cancers ● ● ● ● MDM2 Degraders In Oncology: KT-253 ● Benefits of MDM2 Degradation KT-253, unlike small molecule inhibitors, overcomes the feedback loop which up-regulates MDM2 production and in doing so more effectively stabilizes the tumor suppressor p53 Broad franchise opportunities available for this mechanism (over 50% of tumors are p53 WT), Kymera is focused on indications with specific sensitivity to degrader mechanism, through a biomarker strategy Opportunity to translate profile into clinical superiority of degrader over SMI, as has been shown with IRAK4 KYMERA ©2023 KYMERA THERAPEUTICS, INC. MDM2 CRISPR Sensitivity Score 0.6 Dependency of p53WT cells on MDM2 0.4 0.2 0 -0.2 -0.4 -0.6 -0.8 -1 -1.2 -1.4 -1.6 -1.8 -2 -2.2 p53MUT p53WT DNA Damage p53 Graph generated with data obtained from DepMap.org Cell Line Stressors Hypoxia Oncogenes MDM2 p53 p53 ub ub MDM2 Tumor Suppression Other p53 Targets CE p53 Degradation Feedback Loop Cell Cycle Arrest (p21, Ptprv) Apoptosis (Noxa, Bax, Puma) PAGE 51#52DNA Damage MDM2 Degradation, Not Inhibition, Efficiently Restores p53 • MDM2 SMI's show activity, but can induce feedback loop, limiting impact on pathway p53 KYMERA Stressors Hypoxia # Inhibitor 1 MDM2 T Degrader p53 Oncogenes p53 ub ub ub MDM2 Da Tumor Suppression p53 Targets Ⓒ2023 KYMERA THERAPEUTICS, INC. Other p53 Degradation Feedback Loop Cell Cycle Arrest (p21, Ptprv) Apoptosis (Noxa, Bax, Puma) MDM2 degraders remove the protein, can overcome the p53-dependent feedback loop that upregulates MDM2 • By inducing an acute apoptotic response in tumor cells, degraders can increase efficacy and therapeutic index vs a small molecule inhibitor MDM2 levels are kept at undetectable levels with MDM2 degrader KT-253, leading to p53 stabilization KT-253, IC90 Oh DMSO 2h 24h 4h 24h DMSO Oh DMSO 2h MDM2 levels are increased by the small molecule inhibitor (feedback loop), impairing p53 stabilization DS-3032, IC90 4h 24h MDM2 ACTB 24h DMSO MDM2 ACTB PAGE 52#53Kymera's MDM2 Degrader Investigational Drug, KT-253 is Superior to MDM2/p53 Small Molecule Inhibitors KT-253 is a potent MDM2 degrader % MDM2 Remaining Company 300 250- 200 150 100 80 60 40 20 0 0.00001 KT-253 p53 MSD, 2h -DS-3032 2500- 2000 GED 1500- 1000 500- Clinical stage RS4-11 IC50 KT-253 DS-3032 Baseline MDM2-HiBiT 0.0001 0.001 0.01 Compound Concentration, μM DC50=0.4nM (nM) (AML Cell Killing) MDM2-HiBiT, DC50 (nM) (Degradation) KT-253, unlike SMI's such as DS- 3032, strongly stabilizes p53... 3000- KT-253 Kymera IND enabling 0.3 0.4 0 ¹0000¹0 0.0001 0.001 0.01 DMSO Concentration, μM DS-3032 Sankyo/Rain Ph II / combo AML 67 RG7388 Roche Ph II / III ... which leads to superior tumor cell killing (pM range) RS4;11, 24h CTG 220 100 80- 60 40- 20 -20 10000'0 KT-253 DS-3032 0.0001 SAR405838 Sanofi 620 Paused 0.001 0.01 Concentration, μM HDM201 Novartis PhI/II 163 DMSO AMG-232 Amgen/Kartos Multiple Ph II; combo AML 280 KT-253 is >200-fold more potent in tumor cell killing assays than SMI's due to its mechanism of action Proteomics show selective degradation of KT-253 KYMERA Ⓒ2023 KYMERA THERAPEUTICS, INC. PAGE 53#54Single Dose of KT-253 Leads to Sustained Tumor Regression and is Superior to MDM2/p53 Small Molecule Inhibitors RS4;11 MV4;11 Tumor Volume (mm³) Mean ± SEM Probability of Survival 2500 2000 1500 1000 500 0 100 75- 50 0 25 0 7 7 14 Days Post Treatment 21 T 14 21 28 35 42 49 56 Days Post Treatment Vehicle → DS-3032 30 mg/kg PO, 3 on/11 off DS-3032 100 mg/kg PO, 3 on/11 off KT-253 0.3 mg/kg IV, QWx3 KT-253 1 mg/kg IV, SD → KT-253 3 mg/kg IV, SD 28 - Vehicle Control DS-3032 30 mg/kg PO, 3 on/11 off DS-3032 100 mg/kg PO, 3 on/11 off KT-253 0.3 mg/kg IV, QWx3 KT-253 1 mg/kg IV, SD KT-253 3 mg/kg IV, SD Tumor Volume (mm³) Mean ± SEM Probability of Survival 2500 2000- 1500 1000 500 0 100 75 50 25 0 0 0 7 7 14 Days Post Treatment ILL 21 28 14 21 28 35 42 49 56 63 70 Days Post Treatment Vehicle Control →DS-3032 30 mg/kg PO, 3 on/11 off DS-3032 100 mg/kg PO, 3 on/11 off KT-253 1 mg/kg IV QWx3 KT-253 3 mg/kg IV, SD Vehicle Control DS-3032 30 mg/kg PO, 3 on/11 off DS-3032 100 mg/kg PO, 3 on/11 off KT-253 1 mg/kg IV, QWx3 KT-253 3 mg/kg IV, SD RS4;11 ALL model, the median survival after a single dose of KT-253 at 3 mg/kg was 50 days vs 12 days for the clinically equivalent dosing regimen of DS-3032. MV4;11 AML model, a single dose of KT-253 at 3 mg/kg led to complete responses in 5 of 6 animals, and 4 of 6 remain tumor-free on study 80 days post dosing. KYMERA Ⓒ2023 KYMERA THERAPEUTICS, INC. PAGE 54#55Relative Quantification (% Vehicle, p53/ACTB) 2000 1500- 1000 500 KT-253 Potently Degrades MDM2 and Upregulates the p53 Pathway in Preclinical Leukemia Models %MDM2 Remaining (Normalized to Vehicle, ACTB) 250 KYMERA 200 150 100 50 0 MDM2 Protein Levels (1h post dosing) 19% 6% 8% I p53 Protein Levels 1 824 1 824 1 824 1 824 1 824 1 824 Time (Hours) .*.** 10000 8000 6000 4000 2000 0 ©2023 KYMERA THERAPEUTICS, INC. Vehicle KT-253 3 mg/kg SD KT-253 1 mg/kg SD KT-253 0.3 mg/kg QWx3 DS-3032 30 mg/kg QDx3 DS-3032 100 mg/kg QDx3 GDF15 Protein Levels p53 Activation 1 824 1 8 24 1 8 24 1 824 1 8 24 1 8 24 Time (Hours) 2000 1500 1000 500 0 Targeted proteomic analysis of RS4;11 tumors demonstrates robust degradation of MDM2 one hour post dosing. This is associated with activation of the p53 pathway as evidenced by a corresponding upregulation of proteomics biomarkers p53, GDF15, p21 (cell cycle arrest marker) and PHLDA3 (apoptotic marker) p21 Protein Levels 1 8 24 1 8 24 1 824. 1 8 24 1 824 1824 Time (Hours) 2000 1500- 1000 500 1 824 PHLDA3 Protein Levels 1 8 24 1824 1 824 Time (Hours) 1 8 24 1 8 24 PAGE 55#56KYMERA %hCD45+ in PB ● 100 ● 80 60 40 20 0 Strong Single Agent and Combinatorial Activity in Venetoclax Resistant AML Models Whole Blood DFAM-68555 Day 14 Vehicle KT-253 3.0mg/kg Q3W Venetoclax 100mg/kg QD O Study Day DFAM-6855 Characteristics: M5a (monoblastic); Mutations: FLT3, MLL3 KT-253 3 mg/kg Q3W dosing significantly reduces hCD45+ cells in Peripheral Blood 14 ©2023 KYMERA THERAPEUTICS, INC. Tumor Volume (mm³) Mean ± SEM 2000 1500 1000 500 ● 0 MOLM-13 AML XGs Vehicle IV KT-253 1 mg/kg IV Q3W Venetoclax 100 mg/kg PO QD KT-253 1 mg/kg plus Venetoclax 7 14 Days (Post-randomization) 21 1 28 Single dose of KT-253 in combination with daily dosing of Venetoclax achieves sustained tumor regression in MOLM- 13 xenograft model PAGE 56#57KT-253: Phase 1, Multicenter, Dose-Escalation and Expansion Trial to Evaluate KT-333 in Adult Patients with Liquid and Solid Tumors Hematological Malignancies ● AML identified as initial indication based on strong pre-clinical KT-253 activity Developed patient stratification strategy to target subsets of leukemias most sensitive to KT-253 as mono- and combination therapy Preclinical data also support potential development in other heme indications, such as ALL and P53WT lymphomas Solid Tumors Preclinical studies have identified several solid tumor types sensitive to KT-253 DLX KYMERA ©2023 KYMERA THERAPEUTICS, INC. DLx+1 Pharmacologically Active Dose in ST/L Solid Tumors/Lymphoma Phase 1a Phase 1b DLx+2 DLy Phase 1a DLY+1 DLn R/R high-grade Myeloid Malignancies/ALL DL₁ DLY +2 Key Objectives Primary Secondary Exploratory MTD/RP2D ● MTD/RP2D Phase 1a Safety, MED and/or RP2D PK Preliminary Efficacy PD . Phase 1b Solid Tumor TBD n=20 Lymphoma TBD n=20 R/RAML P53WT R/R AML n = 20 Phase 1b Safety at MED/ RP2D (AML) Preliminary Efficacy PK PD Initiate dose escalation in solid tumor/lymphoma (ST/L) Initiate dose escalation in AML once pharmacologically active dose identified in ST/L Initiate expansion in R/R AML Initiate expansions in select solid tumors and lymphomas based on data from 1a and ongoing preclinical efforts PAGE 57#58● First MDM2 Degrader, KT-253, in Clinic KT-253, unlike small molecule inhibitors, overcomes the feedback loop which up-regulates MDM2 production and in doing so more effectively stabilizes the tumor suppressor p53 KT-253 inhibits tumor cell growth with picomolar potency and is more than 200-fold more potent than clinically active MDM2 small molecule inhibitors Broad franchise opportunities available for this mechanism (>50% tumors are p53 WT), Kymera is focused on indications with specific sensitivity to degrader mechanism, through a biomarker strategy Opportunity to translate clinically, as for IRAK4, superiority of degrader over SMI First patient dosed May 2023 • POM data expected in 2023 KYMERA ©2023 KYMERA THERAPEUTICS, INC. First-in-class Opportunity to Address p53 WT Tumors Across a Variety of Tumor Types First degrader against a clinically proven but inadequately drugged target, MDM2 Profound single agent activity in preclinical liquid and solid tumor models Clinical development strategy includes accelerated registration path in p53 WT tumors with high sensitivity to degrader mechanism such as AML, lymphomas, and other solid tumors PAGE 58#59Kymera Well-Positioned for Continued Success • Kymera is executing on its mission to build a fully-integrated, global biotech company as a recognized leader in TPD • Our industry-leading R&D productivity has produced 4 clinical programs and a deep and innovative pipeline of valuable, high-impact programs We have demonstrated PK, PD and safety in Phase 1 trials that validate our platform, molecule design and target selection capabilities and strategies • We are well-capitalized with an experienced team that is highly focused • We are only at the beginning of our journey, as Kymera's knowledge, experience and drive positions us to maximize the untapped potential of TPD in areas with large clinical and commercial opportunities KYMERA ©2023 KYMERA THERAPEUTICS, INC. 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