Kymera Therapeutics, Inc. · NASDAQ:KYMR

Kymera Therapeutics — Q4 2025 Earnings Presentation

71 slides from Kymera Therapeutics's earnings presentation, Feb 26, 2026

  1. Slide 1: Revolutionizing Immunology with Oral Medicines

    Revolutionizing Immunology with Oral Medicines February 2026

  2. Slide 2: Forward Looking Statements

    Forward Looking Statements This presentation contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995 and other federal securities laws. These statements include, but are not limited to, implied and express statements about our strategy, business

  3. Slide 3: Well Positioned to Redefine Immunology with Novel Oral Medicines

    Well Positioned to Redefine Immunology with Novel Oral Medicines Unrivaled science and expertise: Innovative, experienced team and capabilities to develop revolutionary oral therapies to transform the treatment of immunological diseases Patient-first mentality, with urgency: Rapidly advancing first-

  4. Slide 4: Kymera: Industry Leader in Developing Oral Degrader Medicines

    Kymera: Industry Leader in Developing Oral Degrader Medicines NOVEL INSIGHTS LEADING CAPABILITIES Translation: Deep expertise in target–drug interplay to optimize drug UNIQUE STRATEGIES Unique Chemistry Capabilities: disposition and degradation Finding ligands to historically across tissues and cell

  5. Slide 5: Immunology Remains a Large Underserved Market

    Immunology Remains a Large Underserved Market Millions of Patients Do Not Have Access to Advanced Systemic Therapies Untreated ~62M (39%) ~160M Advanced Therapies >$100B PATIENTS ~5M (3%) IN ANNUAL SALES DIAGNOSED WITH FOR ADVANCED IMMUNOLOGICAL THERAPIES2 DISEASES1 Non-Advanced Therapies ~90M (58%)

  6. Slide 6: Advanced Systemic Therapies Are Mostly Injectable Biologics

    Advanced Systemic Therapies Are Mostly Injectable Biologics Biologics Have Numerous Limitations, Making Orals Preferred by Most Patients • Inconvenient, burdensome, >90% and often painful for patients WOULD SWITCH TO AN ORAL • Immunogenicity risks OPTION1 • In-office injection training costs HCPs va

  7. Slide 7: Degraders Allow for Continuous, Biologics-like, Complete Pathway Blockade

    Degraders Allow for Continuous, Biologics-like, Complete Pathway Blockade Unlike Traditional Small Molecule Inhibitors (SMI) SMI Degrader STOICHIOMETRIC INHIBITION CATALYTIC DEGRADATION Pharmacodynamic effect (PD) correlated to drug exposure PD NOT directly correlated to PK (catalytic) allowing (PK)

  8. Slide 8: Unique Target Selection Strategy Drives Best-In-Industry Pipeline

    Unique Target Selection Strategy Drives Best-In-Class Pipeline Strong S TAT 6 Large clinical/ genetic/clinical commercial validation opportunities Undrugged or inadequately IRF5 Clear path to early clinical drugged IRAK4 differentiation targets FOCUS ON FIRST- AND BEST-IN-CLASS OPPORTUNITIES 8

  9. Slide 9: Oral Degraders with Biologics-like Efficacy Can Transform Immunology

    Oral Degraders with Biologics-like Efficacy Can Transform Immunology Existing Therapies Address 10% or Less of Diagnosed Patients1 STAT6 IRF5 IRAK4 TRANSCRIPTION FACTOR TRANSCRIPTION FACTOR SCAFFOLDING KINASE Key Indications: AD, Asthma, COPD, Key Indications: SLE, RA, UC, CD, Key Indications2: HS,

  10. Slide 10: Opportunity to Address a Wide Range of Immunology Indications

    Opportunity to Address a Wide Range of Immunology Indications Orals with Biologics-Like Activity to Transform Immunology Dermatology Respiratory GI Rheumatology Other (Neuro, Endocrinology, Heme) Immune Classes & AD HS CSU PN BP Vitiligo AA Asthma COPD CRSwNP IBD EoE RA SLE SSc Sjögren’s DM Myositis

  11. Slide 11: Building a Best-In-Industry Oral Immunology Pipeline

    Building a Best-In-Industry Oral Immunology Pipeline Potential Patient Upcoming IND-Enabling Phase 1 Phase 2 Phase 3 Indications Opp.1 Milestones Immunology - Wholly-Owned Oral Small Molecule Degraders Ph2b AD Data: AD, Asthma, COPD, KT-621 – AD By mid-2027 STAT6 EoE, CRSwNP, CSU, >140M Ph2b Asthma

  12. Slide 12: First-in-Class Oral STAT6 Degrader Program

    First-in-Class Oral STAT6 Degrader Program Dupilumab-like activity in a pill 12

  13. Slide 13: KT-621 Summary

    KT-621 Summary Dupilumab-like Activity in a Pill KT-621 is the first • In preclinical in vitro and in • Phase 1b AD data showed deep STAT6 degradation in blood and skin, robust reductions in disease-relevant Type vivo studies, it is equal or highly selective, superior to dupilumab 2 biomarkers, mean

  14. Slide 14: STAT6 Transcription Factor: Highly Validated but Undrugged Target

    STAT6 Transcription Factor: Highly Validated but Undrugged Target STAT6 TRANSCRIPTION • STAT6 is the specific transcription factor in the FACTOR IL-4/IL-13 pathway Dupilumab IL-4 Dupilumab IL-4 IL-13 • IL-4/IL-13 is clinically validated by dupilumab across multiple Type 2 diseases: IL-4R⍺ γC IL-4R⍺

  15. Slide 15: Most Patients with Type 2 Diseases Remain Underserved

    Most Patients with Type 2 Diseases Remain Underserved Barriers Built Into the Current Treatment Paradigm ~2M Patients treated with • Do not address underlying drivers of Type advanced systemic therapy1 Local Therapies 2 disease, only manage symptoms (e.g., topicals, inhalers) > • Insufficient for mo

  16. Slide 16: Unlocking the Full Market Potential in Type 2 Disease

    Unlocking the Full Market Potential in Type 2 Disease Innovation Drives Growth >140M • New products and mechanisms have historically Diagnosed expanded the market by reaching more patients patients with Type 2 diseases1 Reducing Patient Burden Could Unlock Access Significant • An oral therapy that a

  17. Slide 17: KT-621 Has Significant Potential to Transform the Treatment of Type 2 Diseases

    KT-621 Has Significant Potential to Transform the Treatment of Type 2 Diseases CURRENT TREATMENT KT-621 PARADIGM LIMITATIONS SHIFT ⅹ Efficacy and incomplete disease ü Potential for biologics-like safety control and efficacy with robust durability ⅹ Side effects and safety issues ü Highly validated,

  18. Slide 18: Opportunity to Shift Treatment Paradigms for Type 2 Diseases

    Opportunity to Shift Treatment Paradigms for Type 2 Diseases Given the first-in-class profile of KT-621, there is significant opportunity to meet uncontrolled AD and Asthma patients earlier in their treatment journey Non-Rx. Management Topicals Injectables Atopic (Emollients, bathing, trigger (Stero

  19. Slide 19: KT-621 Development Plan Enables Efficient Path to Registration

    KT-621 Development Plan Enables Efficient Path to Registration Across All Type 2 Diseases Ph3 Ph2b AD Dose Ph3: AD (Initial), Dose Ranging EoE, CSU, PN, BP Ongoing Data expected by mid-2027 Ph1 HV Ph1b AD SAD-MAD Single Arm, Open Label ✓ Complete ✓ Complete Ph3 Ph2b Asthma Dose Ph3: Asthma (Initial)

  20. Slide 20: KT-621 Data Provide Validation and Derisk Future Clinical Trials

    KT-621 Data Provide Validation and Derisk Future Clinical Trials Relieves allergic rhinitis Preclinical In Humans symptoms (TNSS, RQLQ) POTENCY Blocks Type 2 inflammation in • <100 pM DC90 in all relevant human cell skin and impacts AD lesions types (EASI, vIGA-AD, and skin Deep STAT6 degradation tr

  21. Slide 21: KT-621: BROADEN2 Phase 2b Trial

    KT-621: BROADEN2 Phase 2b Trial Randomized, Double Blind, Placebo-controlled, Parallel-group, Multicenter Dose-ranging Design • Randomized, double-blind, placebo-controlled Key Trial Aim • ~200 patients • Daily dose for 16-weeks; Establish clinical activity and Adult & Adolescent 52-week open label

  22. Slide 22: KT-621: BREADTH Phase 2b Trial

    KT-621: BREADTH Phase 2b Trial Randomized, Double Blind, Placebo-controlled, Parallel-group, Multicenter Dose-ranging Design • Randomized, double-blind, placebo-controlled Key Trial Aim • ~264 patients • Daily dose for 12-weeks Establish clinical activity and safety in asthma to select Phase 3 Adult

  23. Slide 23: KT-621 Phase 1a Healthy Volunteer and Phase 1b BroADen AD Clinical Trial Data

    KT-621 Phase 1a Healthy Volunteer and Phase 1b BroADen AD Clinical Trial Data 23

  24. Slide 24: KT-621: Compelling Clinical Profile

    KT-621: Compelling Clinical Profile KT-621 Phase 1 Healthy Volunteer Data Suggests Potential for Dupilumab-like Activity in a Pill Robust STAT6 Degradation in Blood and Reductions in Multiple Disease-Relevant Skin Following Low Daily Oral Doses Type 2 Biomarkers 100 Serum TARC1 with Serum Eotaxin-32

  25. Slide 25: BroADen KT-621 Phase 1b AD Study Surpassed Objectives

    BroADen KT-621 Phase 1b AD Study Surpassed Objectives Effects on All Type 2 Biomarkers and Clinical Endpoints Were in Line with or in Some Cases Numerically Exceeded Published Data for Dupilumab at Week 4 BroADen Endpoints Phase 1b Results Highlights ü Strong fidelity of translation from Phase 1a he

  26. Slide 26: Design Phase 1b in Moderate to Severe Atopic Dermatitis Patients

    Design • Single arm, open label • 22 patients Phase 1b in Moderate to Severe • Oral, once daily dose for 28 days Atopic Dermatitis Patients • 14-day follow-up after dosing completed Baseline entry criteria: • Adult, moderate to severe AD patients Dosing • Two sequential dose cohorts EASI ≥16 • 100 m

  27. Slide 27: KT-621 Achieved Deep STAT6 Degradation in Blood and Skin

    KT-621 Achieved Deep STAT6 Degradation in Blood and Skin Degradation Maintained for 28 Days Across Both Dose Cohorts Median STAT6 Degradation in Blood Median STAT6 Degradation in Skin Method: Flow Cytometry Method: Targeted Mass Spec % STAT6 Change from Baseline % STAT6 Change from Baseline Median (

  28. Slide 28: Robust Impact on All Disease-Relevant Biomarkers of Type 2 Inflammation

    Robust Impact on All Disease-Relevant Biomarkers of Type 2 Inflammation in BroADen Phase 1b AD Trial TARC Eotaxin-3 IgE IL-31 FeNO (CCL17) (CCL26) Validated biomarker of Highly specific downstream IL-4 promotes B-cell class Key pruritogenic cytokine Marker of Type 2 airway Type 2 inflammation cytoki

  29. Slide 29: KT-621 Significantly Downregulated Core Type 2 Inflammation Gene Set

    KT-621 Significantly Downregulated Core Type 2 Inflammation Gene Set in Skin Lesions of AD Patients p < 0.01 KT-621 (n=18) Dupilumab2 (n=23) • Genes in signature1: • CCL26/Eotaxin-3 Signature Score • CCL17/TARC • CCL18/PARC • CCL13/MCP-4 • Changes in transcriptome comparable to published data for du

  30. Slide 30: KT-621 Achieved Rapid and Robust Reductions in EASI and SCORAD

    KT-621 Achieved Rapid and Robust Reductions in EASI and SCORAD Across All Patients Mean % Change from Baseline in EASI Mean % Change in Total SCORAD KT-621 100 mg QD (n=10)1 KT-621 100 mg QD (n=10)1 Mean (±SE) Percent Change from Mean (±SE) Percent Change from KT-621 200 mg QD (n=12) KT-621 200 mg Q

  31. Slide 31: KT-621 Achieved Robust and Consistent Reductions in Itch Across Independent Clinical Measures

    KT-621 Achieved Robust and Consistent Reductions in Itch Across Independent Clinical Measures Mean % Change in Peak Pruritus NRS Mean % Change in SCORAD Itch 20 KT-621 100 mg QD (n=10) 20 KT-621 100 mg QD (n=10)1 KT-621 200 mg QD (n=12) KT-621 200 mg QD (n=12) 10 10 Mean (±SE) Percent Change from Me

  32. Slide 32: KT-621 Achieved Robust Improvement in Patient Reported Outcomes and Quality of Life Measures

    KT-621 Achieved Robust Improvement in Patient Reported Outcomes and Quality of Life Measures Mean % Change in SCORAD DLQI Responders POEM Responders - Sleeplessness1 (Improvement ≥ 4 points)3 (Improvement ≥ 4 Points) KT-621 100 mg QD (n=9)2 KT-621 100 mg QD (n=7) KT-621 100 mg QD (n=10) Baseline in

  33. Slide 33: KT-621 Achieved Robust Impact on FeNO and ACQ-5 in AD Patients with Comorbid Asthma

    KT-621 Achieved Robust Impact on FeNO and ACQ-5 in AD Patients with Comorbid Asthma ACQ-5 Responders Median % Change from Baseline in FeNO (n=4) Mean Point Change in ACQ-5 (n=4) (Improvement ≥ 0.5, n=4) 100 Baseline in ACQ-5 Score (Points) Median (Q1, Q3) Percent Change from 0.0 60 Mean (±SE) Change

  34. Slide 34: KT-621 Achieved Robust Impact on TNSS and RQLQ in AD Patients with Comorbid Allergic Rhinitis

    KT-621 Achieved Robust Impact on TNSS and RQLQ in AD Patients with Comorbid Allergic Rhinitis Mean Point Change TNSS Responders Mean Point Change RQLQ Responders in TNSS (n=7)1 (Improvement ≥ 0.55, n=7)1 in RQLQ (n=6)2 (Improvement ≥ 0.5, n=6)2 Baseline in RQLQ Score (Points) 100 100 Baseline in TNS

  35. Slide 35: KT-621 Demonstrated Robust Improvements Across All Key Clinical Efficacy Endpoints

    KT-621 Demonstrated Robust Improvements Across All Key Clinical Efficacy Endpoints Results in Line With or in Some Cases Numerically Exceeded Published Data for Dupilumab at Week 4 KT-621 100 mg QD KT-621 200 mg QD KT-621 Overall Dupilumab 300 mg Q2W Day 29 (n=10) Day 29 (n=12) Day 29 (n=22) D28 Ph3

  36. Slide 36: KT-621 BroADen Phase 1b Safety Summary

    KT-621 BroADen Phase 1b Safety Summary • Well-tolerated with favorable safety at both 100 mg and 200 mg with a profile similar to what was observed in the Phase 1a healthy volunteer trial • No SAEs or Severe AEs • No dose-dependent pattern in the TEAEs • No related TEAEs or TEAEs leading to disconti

  37. Slide 37: Kymera Completes the Clinical Translation of STAT6 Degradation

    Kymera Completes the Clinical Translation of STAT6 Degradation Potential for Study Data “Dupilumab-in-a-pill” Profile Human Genetics STAT6 is a key driver of Type 2 inflammation ✓ Preclinical KT-621 degraded STAT6 and blocked IL-4/13 Type 2-driven inflammation in vitro/in vivo as effectively as dupi

  38. Slide 38: First-in-Class Oral IRF5 Degrader Program

    First-in-Class Oral IRF5 Degrader Program Drugging a Genetically Validated Transcription Factor with an Oral Degrader 38

  39. Slide 39: KT-579 Overview

    KT-579 Overview Potential First-in-Class Opportunity with Oral Small Molecule Profile • IRF5 has the potential to • Human and mouse • IRF5 degradation in vivo • KT-579 fully KT-579 is be the first broad anti- genetics de-risk safety leads to robust cytokine degrades IRF5 a first-in-class, inflammato

  40. Slide 40: IRF5: A New Treatment Paradigm for Complex Autoimmune Diseases

    IRF5: A New Treatment Paradigm for Complex Autoimmune Diseases Unmet Need: Designed for Disease Complexity • Heterogenous autoimmune diseases like lupus reflect broad immune Complex diseases are SLE, IBD, RA, others dysregulation, not isolated pathway disruption driven by multiple • Biologics have v

  41. Slide 41: Central Driver of Immune Dysregulation in Autoimmune Diseases

    Central Driver of Immune Dysregulation in Autoimmune Diseases Transient, Controlled Chronic, Dysregulated Activation Activation IRF5 Expression, Activation and Function Foreign Pathogens Immune Complexes • IRF5 is predominantly expressed and TLR4 BCR TLR4 activated in immune cell types: Dendritic Ce

  42. Slide 42: Opportunity to Address a Wide Range of Complex Autoimmune Indications Through Clinically Validated Pathways

    Opportunity to Address a Wide Range of Complex Autoimmune Indications Through Clinically Validated Pathways Potential to be a First-in-class Oral Advanced Therapy Individual Pathways Clinically Validated by Biologics Cytokines Deep degradation of Type I Autoantibodies (Myeloid/ IRF5 will modulate IF

  43. Slide 43: IRF5 Genetically Validated in Multiple Autoimmune Diseases

    IRF5 Genetically Validated in Multiple Autoimmune Diseases Human Genetics Mouse IRF5 KO Studies • Multiple GWAS studies identify IRF5 as an autoimmune • KO mice are viable and fertile; with normal B cell susceptibility gene1 development • IRF5 risk haplotypes and hyperactivated IRF5 levels in • IRF5

  44. Slide 44: IRF5: A Novel Mechanism in High Unmet Need Indications in I&I

    IRF5: A Novel Mechanism in High Unmet Need Indications in I&I >10M Systemic Advanced RHEUMATOLOGY RA PATIENTS1 4.7M Therapies: 7% Lupus2 1.2M Sjögren's 765K >$45B Market SSc 200K TOTAL POTENTIAL DM >100K PATIENT IMPACT1 GASTROENTEROLOGY IRF5 functional risk variants associate with increased suscepti

  45. Slide 45: KT-579: An Exquisitely Selective and Picomolar Oral IRF5 Degrader

    KT-579: An Exquisitely Selective and Picomolar Oral IRF5 Degrader Equipotent Degradation in Relevant KT-579: 10xDC90 in hPBMCs @ 24 hrs Equipotent Degradation in relevant hPBMC subsets @ hPBMC Subsets @ 24hrs 24hrs Cell Subsets KT-579 DC50 (nM) PBMC 0.8 Selectivity Binding and Cellular Assays KT-579

  46. Slide 46: KT-579 Potently Inhibits Production of Key Pro-Inflammatory Cytokines and Type I IFN

    KT-579 Potently Inhibits Production of Key Pro-Inflammatory Cytokines and Type I IFN in Human Primary Cellular Assays HuMonocytes + R848 HuMonocytes + ssRNA40 Cytokine KT-579 IL12p40 Production IFNb Production Biology Receptor Stim Cell Readout DC50 (nM) N-3 donors N-2 donors TLR8 ssRNA40 Monocytes

  47. Slide 47: KT-579 Effectively Blocks TLR Induced Pro-inflammatory Cytokines and Type I IFN

    KT-579 Effectively Blocks TLR Induced Pro-inflammatory Cytokines and Type I IFN Induction and Reduces Total IgG levels in SLE PBMC Samples Pro-inflammatory Cytokines + Type I IFN Total IgG TNFα IL-6 IFNb • KT-579 inhibits TLR7/8 pro-inflammatory cytokines and Type I IFN that are commonly elevated in

  48. Slide 48: KT-579 Superior Activity in the MRL/lpr Model of Lupus

    KT-579 Superior Activity in the MRL/Ipr1 Model of Lupus Sustained Reduction of Serum All KT-579 Treated Mice Plasmablasts2 Anti-dsDNA Survived Length of Study 2000 !"#A%&D()!*A"*+,-.L*0N"A#D2L34 *p=0.04 # Total 1.5 *p≤0.05 Treatment survival % of of CD45+ Cells + SEM 1500 Vehicle 10/15 1.0 1000 KT-5

  49. Slide 49: KT-579 Significantly Decreases IgG, Complement (C3) and Renal Disease Progression

    KT-579 Significantly Decreases IgG, Complement 3 (C3) and Renal Disease Progression Assessment of Terminal Kidney Collected from Surviving MRL/lpr Mice at Week 19 15 IgG 10 C3 6 Total Kidney Lesions % IgG+ Area of Renal Cortex Area + SEM % C3+ Area of Renal Cortex Area + SEM Total Kidney Lesion Scor

  50. Slide 50: IRF5 Degradation Demonstrated Generally Better Outcomes than Approved or Clinically Active Drugs

    IRF5 Degradation Demonstrated Generally Better Outcomes than Approved or Clinically Active Drugs in NZBW1 Spontaneous1 Mouse Lupus Model Early, Sustained and Complete Superior Activity Reducing Decreased Proteinuria Reduction in Anti-dsDNA Abs Anti-dsDNA at Week 37 **** **** ** *** # ** ** * le g/ r

  51. Slide 51: KT-579 Reduces Joint Swelling in a Mouse Model of RA

    KT-579 Reduces Joint Swelling in a Mouse Model of RA Treatment with KT-579 Leads to Significant Reduction in Joint Reduction in Circulating IL-12 Levels and Infiltrating Swelling Comparable to Tofacitinib in the AIA1 Mouse Model of RA Synovial IFNγ+ Th1 Cells IL-12p40 Serum Levels Day 2 IFNγ+ CD4+ T

  52. Slide 52: KT-579 Potently Degrades at Low Oral Doses in NHP with an Excellent Safety Profile

    KT-579 Potently Degrades at Low Oral Doses in NHP with an Excellent Safety Profile IRF5 Degradation in NHP Blood Post 7 Days of KT-579 QD Oral Dosing 0 IRF5 % Change from Baseline 24hrs After Last Dose • KT-579 potently degrades IRF5 across multiple preclinical species with low oral doses -50 • No a

  53. Slide 53: KT-579: First IRF5 Agent to Enter Clinical Evaluation

    KT-579: First IRF5 Agent to Enter Clinical Evaluation Phase 1 Trial: Double-blind, Placebo-controlled SAD and MAD in Healthy Volunteers • Safety & tolerability of Key Trial Aim Part A Primary escalating single and Single Ascending Dose multiple doses of KT-579 Key trial aim is to show that (SAD) KT-

  54. Slide 54: Partnered Oral Degrader Programs

    Partnered Oral Degrader Programs 54

  55. Slide 55: IRAK4 Overview

    IRAK4 Overview Combined Activity of Upstream Biologics (anti-IL-1/18/33/36) in a Pill • KT-485 has increased • Learnings from the • Phase 1 studies of KT- KT-485, a second selectivity and potency over clinical studies of KT-474 485 are expected to generation IRAK4 KT-474 including absence of will be

  56. Slide 56: CDK2 Overview

    CDK2 Overview Novel Molecular Glue (MG) Degrader • CDK2 is a master regulator of • Unlike inhibitors, CDK2 Potential best-in-class the cell cycle with strong genetic molecular glue degraders profile, with exquisite and clinical validation and broad selectively degrade CDK2 while selectivity for CDK2

  57. Slide 57: 2026: Catalysts for Growth

    2026: Catalysts for Growth • Complete enrollment in BROADEN2 Phase 2b AD KT-621 study in 2026; report data by mid-2027 First-in-Class Oral • Advance BREADTH Phase 2b asthma study; report STAT6 Degrader data in late-2027 KT-579 First-in-Class Oral • Report Phase 1 healthy volunteer data in the 2H 202

  58. Slide 58: Thank You

    Thank You NASDAQ: KYMR For additional information contact: www.kymeratx.com investors@kymeratx.com @KymeraTX media@kymeratx.com inquiries@kymeratx.com KYMERA THERAPEUTICS 500 North Beacon Street, 4th Floor Watertown, MA 02472

  59. Slide 59: Appendix: First-in-Class Oral STAT6 Degrader Program

    Appendix: First-in-Class Oral STAT6 Degrader Program 59

  60. Slide 60: KT-621: Compelling Preclinical Profile

    KT-621: Compelling Preclinical Profile Preclinical Package Suggests Potential for Dupilumab-like Activity in a Pill Full Inhibition of IL-4/IL-13 Excellent Preclinical Exquisite Robust Degradation Pathways, More Potent Activity Comparable or Selectivity in Relevant Cell Types than Dupilumab Superior

  61. Slide 61: KT-621 Phase 1a Healthy Volunteer Trial: Safety Summary

    SAD & MAD KT-621 Phase 1a Healthy Volunteer Trial: Safety Summary Well Tolerated Across All Doses Evaluated and Safety Profile Undifferentiated from Placebo • No Serious Adverse Events TRAEs by Preferred Term: SAD Cohorts • No Severe Adverse Events SAD SAD AE Term (severity) Placebo KT-621 • No dose

  62. Slide 62: KT-621 BroADen Phase 1b Demographics

    KT-621 BroADen Phase 1b Demographics Generally Well-Balanced Across Treatment Cohorts 100 mg 200 mg Overall (n=10) (n=12) (n=22) Gender, n (%) Female 6 (60) 7 (58.3) 13 (59.1) Male 4 (40) 5 (41.7) 9 (40.9) Age, years, mean (SD) 30.1 (8.5) 33.0 (11.4) 31.7 (10.1) BMI, kg/m2, mean (SD) 32.8 (11.5) 30.

  63. Slide 63: KT-621 BroADen Phase 1b Baseline Disease Characteristics

    KT-621 BroADen Phase 1b Baseline Disease Characteristics Generally Well-Balanced Across Treatment Cohorts 100 mg 200 mg Overall (n=10) (n=12) (n=22) vIGA-AD, n (%) Moderate (3) 6 (60) 6 (50) 12 (54.5) Severe (4) 4 (40) 6 (50) 10 (45.5) EASI Score, mean (SD) 23.5 (7.5) 26.1 (9) 24.9 (8.3) Other Disea

  64. Slide 64: Example of Clinical and Biomarker Response to KT-621 in BroADen

    Example of Clinical and Biomarker Response to KT-621 in BroADen Patient with Severe AD and Prior Dupilumab Treatment Pre and Day 29 Photos for EASI-75 Responder STAT6 Staining IHC Baseline Day 29 Baseline Day 29 % Change in EASI and Itch1 EASI SCORAD ITCH and PPNRS Percent Change from Baseline in Pe

  65. Slide 65: Atopic Dermatitis: Intensely Pruritic, Chronic and Underserved Disease

    Atopic Dermatitis: Intensely Pruritic, Chronic and Underserved Disease Opportunity Exists to Transform the Treatment Paradigm • Chronic inflammatory disease that causes inflamed and irritated skin, making it itchy and painful • Majority of patients have disease onset as children and carry the diseas

  66. Slide 66: Asthma: Chronic, Inflammatory Lung Disease

    Asthma: Chronic, Inflammatory Lung Disease Opportunity Exists to Transform the Treatment Paradigm • The airways in lungs to become swollen and inflamed, causing coughing, shortness of breath, chest tightness or pain, and making it harder to breathe • Symptoms may resemble other lung conditions, call

  67. Slide 67: Appendix: Partnered Programs

    Appendix: Partnered Programs 67

  68. Slide 68: IRAK4 Biology and Target Rationale

    IRAK4 Biology and Target Rationale IRAK4 SCAFFOLDING KINASE Target Rationale IL-1R/TLR Pathway • IRAK4 is an obligate node in IL-1R/TLR signaling, and its degradation is TLR Cytokines IL-1, IL-18, the only approach to fully block the pathway Agonists IL-33, IL-36 TLRs IL-1R Human Genetics • Adult hu

  69. Slide 69: CDK2 Molecular Glue Degrader Advantage

    CDK2 Molecular Glue Degrader Advantage CDK2 MASTER CELL CYCLE REGULATOR Target Biology and Rationale • Regulates the G1-S transition, with its partner CCNE CDK1 • CCNE is often overexpressed or amplified in HGSOC and CDK4/6i CDK1 is essential for resistant breast cancers, driving uncontrolled cell p

  70. Slide 70: Abbreviations

    Abbreviations EoE EU Eosinophilic Esophagitis European Union IgE IHS4 Immunoglobulin E International Hidradenitis Suppurativa Ab Antibody Severity Score FDA Food and Drug Administration AD Atopic Dermatitis IL Interleukin FeNO Fractional Exhaled Nitric Oxide AIA Antigen-Induced Arthritis IND Investi

  71. Slide 71: Abbreviations

    Abbreviations Ph Phase SMI Small Molecule Inhibitor PK/PD Pharmacokinetics/Pharmacodynamics SOC Standard of Care pM Picomolar SSc Systemic Sclerosis PN Prurigo Nodularis STAT Signal Transducer and Activator of Transcription POC Proof-of-Concept STAT6 Signal Transducer and Activator of Transcription

Kymera Therapeutics — Q4 2025 Earnings Presentation on 6ix