Kymera Therapeutics, Inc. · NASDAQ:KYMR
Kymera Therapeutics — Investor Presentation (September 2026)
72 slides from Kymera Therapeutics's investor presentation, September 2026
Slide 1: Revolutionizing Immunology with Oral Medicines
Revolutionizing Immunology with Oral Medicines September 2026
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
Slide 3: 2016-2026: A Decade of Discovery and Progress in Motion
2016-2026: A Decade of Discovery and Progress in Motion 2016-2020: PIONEERING A NEW MODALITY Establishing TPD into a reproducible innovation engine Unlocked highly validated, undrugged targets with unmatched capabilities 2021-2026: DEMONSTRATING EARLY PROOF OF CONCEPT Advanced six new first-in-class
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
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%)
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
Slide 7: Targeted Protein Degradation: Achieving Biologics-like Activity with Oral Medicines
Targeted Protein Degradation: Achieving Biologics-like Activity with Oral Medicines Targeted Protein Degradation (TPD) Mechanism of Action Degraders Enable Continuous, Complete Pathway Blockade Harnessing the E3 Ubiquitin Proteasome System Superior to Traditional Small Molecule Inhibitors 1 2 3 4 Sm
Slide 8: Unique Target Selection Strategy Drives Best-In-Class 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
Slide 9: 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: By year-end 2026 AD, Asthma, COPD, KT-621 – AD Ph2b Asthma Data: STAT6 EoE, CRSwNP,
Slide 10: First-in-Class Oral STAT6 Degrader Program
First-in-Class Oral STAT6 Degrader Program Dupilumab-like activity in a pill 10
Slide 11: KT-621 Summary
KT-621 Summary Dupilumab-like Activity in a Pill KT-621 is the first • In preclinical in vitro and • Phase 1b AD data showed deep STAT6 degradation in highly selective, in vivo studies, it is equal blood and skin, robust reductions in disease-relevant Type potent, oral STAT6 or superior to dupilumab
Slide 12: 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 IL-4R⍺ IL-4R⍺ IL-13R⍺1 across multiple Type 2 dise
Slide 13: Unlocking the Full Market Potential in Type 2 Disease
Unlocking the Full Market Potential in Type 2 Disease Barriers Built Into the Current Treatment Paradigm • Do not address underlying drivers of Type >140M Local Therapies 2 disease, only manage symptoms Diagnosed (e.g., topicals, inhalers) > • Insufficient for most moderate/severe patients with pati
Slide 14: KT-621: Potential to Transform Type 2 Inflammatory Diseases
KT-621: Potential to Transform Type 2 Inflammatory Diseases KT-621 has the potential to be a novel oral medicine capable of delivering biologics-like efficacy and safety KT-621 PARADIGM SHIFT >90% ✓ Differentiated approach to address currently treated with an underlying disease biology injectable wo
Slide 15: 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
Slide 16: KT-621 Development Plan Enables Efficient Path to Registration Across All Type 2 Diseases
KT-621 Development Plan Enables Efficient Path to Registration Across All Type 2 Diseases PHASE 3 OPPORTUNITIES Atopic Dermatitis (initiate by mid-2027) Eosinophilic Esophagitis Ph2b AD Dose Ranging Chronic Spontaneous Urticaria DERMATOLOGY & GI Enrollment complete Prurigo Nodularis Data expected by
Slide 17: KT-621 Data Provide Validation and Derisk Future Clinical Trials
KT-621 Data Provide Validation and Derisk Future Clinical Trials Preclinical In Humans Relieves allergic rhinitis 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
Slide 18: KT-621: BROADEN2 Phase 2b Trial
KT-621: BROADEN2 Phase 2b Trial Accelerated Timeline, KT-621 Program Six Months Ahead of Schedule 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 extension safety in
Slide 19: 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 • 52-week open label extension safety in
Slide 20: 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 20
Slide 21: 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
Slide 22: 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
Slide 23: 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
Slide 24: 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 (
Slide 25: Robust Impact on All Disease-Relevant Biomarkers of Type 2 Inflammation in BroADen Phase 1b
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
Slide 26: KT-621 Significantly Downregulated Core Type 2 Inflammation Gene Set in Skin Lesions
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
Slide 27: 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
Slide 28: 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
Slide 29: 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
Slide 30: 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 Median % Change from Baseline Mean Point Change ACQ-5 Responders in FeNO (n=4) in ACQ-5 (n=4) (Improvement ≥ 0.5, n=4) 0.0 100 Median (Q1, Q3) Percent Change Baseline in ACQ-5 Score (Points) 60 Mean (±SE) Change from
Slide 31: 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
Slide 32: 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
Slide 33: 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
Slide 34: 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
Slide 35: First-in-Class Oral IRF5 Degrader Program
First-in-Class Oral IRF5 Degrader Program Drugging a Genetically Validated Transcription Factor with an Oral Degrader 35
Slide 36: KT-579 Overview
KT-579 Overview Potential First-in-Class Opportunity with Oral Small Molecule Profile KT-579 is • IRF5 has the potential • Human and mouse • IRF5 degradation in • KT-579 fully a first-in-class, to be the first broad genetics de-risk vivo leads to robust degrades IRF5 potent, anti-inflammatory to saf
Slide 37: A New Treatment Paradigm for Complex Autoimmune Diseases
A New Treatment Paradigm for Complex Autoimmune Diseases Complex diseases are driven by multiple IRF5 hyperactivation impacts multiple validated inflammatory pathways disease-defining pathways SLE, IBD, RA, others KT-579 IRF5 Type I Cytokines Autoantibodies IFNs (Myeloid/T Cells) (B cells) Type I Cy
Slide 38: 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
Slide 39: 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
Slide 40: 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
Slide 41: 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
Slide 42: 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
Slide 43: 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
Slide 44: KT-579 Effectively Blocks TLR Induced Pro-inflammatory Cytokines and Reduces Total IgG in SLE PBMC
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
Slide 45: KT-579 Superior Activity in the MRL/lpr Model of Lupus
KT-579 Superior Activity in the MRL/Ipr1 Model of Lupus Sustained Reduction All KT-579 Treated Mice Plasmablasts2 of Serum Anti-dsDNA Survived Length of Study (Units/mL) 1.5 2000 *p≤0.05 Serum(Units/mL) *p=0.04 SEM # Total Cells+ +SEM Treatment 1500 survival 1.0 CD45+Cells Vehicle 10/15 inSerum 1000
Slide 46: KT-579 Significantly Decreases IgG, Complement 3 (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 Vehicle Area + SEM % C3+ Area of Renal Cortex Area + SEM Total Kidney Lesion Score + SEM 8 KT-579 50
Slide 47: IRF5 Degradation Demonstrated Generally Better Outcomes than Approved or Clinically Active Drugs in NZBW Lupus Model
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 Anti-dsDNA Ab in Serum (Units/mL)
Slide 48: 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
Slide 49: KT-579 Reduces Disease Progression, Fibrosis, and Intestinal Damage in TNBS Mouse Model of IBD
KT-579 Reduces Disease Progression, Fibrosis, and Intestinal Damage in the Preclinical TNBS Mouse Model of IBD KT-579 Reduces Inflammatory Cytokines in the Colon H&E Pathological Scoring Sham Total Score (0-11) TNF-α IL-6 IL-1β 10 Concentration (pg/mg) Concentration (pg/mg) Concentration (pg/mg) 100
Slide 50: 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
Slide 51: 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 Primary • Safety & tolerability of Key Trial Aim Part A escalating single and Single Ascending Dose multiple doses of KT-579 Key trial aim is to show that KT-579 ca
Slide 52: Partnered Oral Degrader Programs
Partnered Oral Degrader Programs 52
Slide 53: IRAK4 Overview
IRAK4 Overview Combined Activity of Upstream Biologics (anti-IL-1/18/33/36) in a Pill KT-485, a second • KT-485 has increased • Learnings from the generation IRAK4 selectivity and potency over clinical studies of KT- degrader, is a highly KT-474 including absence of 474 will be applied to selective,
Slide 54: KT-485 (SAR447971): Phase 1 First-in-Human Trial
KT-485 (SAR447971): Phase 1 First-in-Human Trial SAD and MAD in Healthy Volunteers and Hidradenitis Suppurativa Patients Three Part Phase 1 Study Design • Safety & tolerability of Primary escalating single and multiple doses of KT-485 SAD MAD MAD • Pharmacokinetic ~46 ~48 ~20 measures Healthy Volunt
Slide 55: CDK2 Overview
CDK2 Overview Novel Oral Molecular Glue (MG) Degrader KT-200 is a • CDK2 is a master • Unlike inhibitors, • In preclinical testing, KT-200 first-in-class, regulator of the cell cycle CDK2 molecular glue demonstrated low-nanomolar oral CDK2 with strong genetic/ degraders selectively degradation of CD
Slide 56: Catalysts for Growth
Catalysts for Growth • Report BROADEN2 Phase 2b AD data by year-end 2026 KT-621 First-in-Class Oral • Initiate Phase 3 trials in AD by mid-2027 STAT6 Degrader • Advance BREADTH Phase 2b asthma study; report data in late-2027 KT-579 • Report Phase 1 healthy volunteer data in 4Q26 First-in-Class Oral
Slide 57: Thank You
Thank You NASDAQ: KYMR www.kymeratx.com For additional information contact: @KymeraTX investors@kymeratx.com media@kymeratx.com KYMERA THERAPEUTICS 500 North Beacon Street, 4th Floor Watertown, MA 02472
Slide 58: Appendix: First-in-Class Oral STAT6 Degrader Program
Appendix: First-in-Class Oral STAT6 Degrader Program 58
Slide 59: 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
Slide 60: Single Doses of KT-621 Achieved Rapid, Deep and Prolonged STAT6 Degradation in Blood
SAD Single Doses of KT-621 Achieved Rapid, Deep and Prolonged STAT6 Degradation in Blood Absolute STAT6 Levels1 Mean Percent Change from Baseline in STAT6 1.5 Placebo n=12 100 Placebo n=12 6.25 mg SD n=6 6.25 mg SD n=6 25 mg SD n=6 25 mg SD n=6 Change from Baseline in STAT6 75 mg SD n=6 75 mg SD n=6
Slide 61: Single Dose Administration of KT-621 Achieved >90% STAT6 Degradation in Blood
SAD Single Dose Administration of KT-621 Achieved >90% STAT6 Degradation in Blood Across All Dose Levels >95% Mean STAT6 Degradation Achieved at Doses of 75 mg or Greater 20 Placebo Mean (±SE) Percent Change from Baseline in STAT6 6.25 mg SD 0 25 mg SD -20 75 mg SD -40 200 mg SD 400 mg SD -60 800 mg
Slide 62: 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 TRAEs by Preferred Term: SAD Cohorts • No Serious Adverse Events SAD SAD • No Severe Adverse Events AE Term (severity) Placebo KT-621 (n=12) (n
Slide 63: 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.
Slide 64: 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
Slide 65: 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 SCORAD PPNRS 0 0 Percent Change fr
Slide 66: 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
Slide 67: 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
Slide 68: Appendix: Partnered Programs
Appendix: Partnered Programs 68
Slide 69: 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 the TLR Cytokines IL-1, IL-18, only approach to fully block the pathway Agonists IL-33, IL-36 TLRs IL-1R Human Genetics • Adult hu
Slide 70: 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
Slide 71: 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
Slide 72: 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 — Investor Presentation (September 2026) on 6ix