
Q2 Company Update June 2026

Disclaimer Any statements made in this presentation that are not statements of historical fact, including statements about our beliefs and expectations, are forward-looking statements and should be evaluated as such. Forward-looking statements include information concerning the strategy, initiation, cost, timing, progress, and results of our preclinical studies and clinical trials for our product candidates; our ability to leverage our technology platform to enable more informed drug research and development; estimates of the number of patients with certain diseases and conditions we intend to treat, the number of patients that we plan to enroll in our clinical trials, and the size and nature of the market opportunity for our product candidates, expected milestones and business objectives for 2026 and beyond; and our ability to maintain our current license agreements and collaborations, including our ability to comply with our financial obligations pursuant to the terms of such agreements, and our ability to identify and enter into future license agreements and collaborations. These statements often include words such as "anticipate," "expect," "suggests," "plan," "believe," "intend," "estimates," "targets," "projects," "should," "could," "would," "may," "will," "forecast" and other similar expressions. These forward-looking statements are contained throughout this presentation. We have based these forward-looking statements on our current expectations, plans and assumptions that we have made in light of our experience in the industry, as well as our perceptions of historical trends, current conditions, expected future developments and other factors we believe are appropriate under the circumstances at such time. As you read and consider this presentation, you should understand that these statements are not guarantees of future performance or results. The forward-looking statements are subject to and involve risks, uncertainties and assumptions, and you should not place undue reliance on these forward-looking statements. Although we believe that these forward-looking statements are based on reasonable assumptions at the time they are made, you should be aware that many factors could affect our actual results or results of operations and could cause actual results to differ materially from those expressed in the forward-looking statements. Factors that may materially affect such forward-looking statements include: our limited operating history; our significant net losses incurred since inception and the likelihood of incurring additional losses for the foreseeable future; our need for substantial additional funding; the early stage of development of our product candidates and any future product candidates and the possibility they may fail in development; our dependence on the success of our current product candidates; legal and regulatory risks; intellectual property-related risks; and the other important factors described in the Annual Report on Form 10-K that we have filed with the Securities and Exchange Commission. These cautionary statements should not be construed by you to be exhaustive and are made only as of the date of this presentation. We undertake no obligation to update or revise any forward-looking statements, whether as a result of new information, future events, or otherwise, except as required by applicable law. You should, therefore, not rely on these forward-looking statements as representing our views as of any date subsequent to the date of this presentation. Certain information contained in this presentation and statements made orally during this presentation relate to or are based on studies, publications and other data obtained from third-party sources as well as our own internal estimates and research. While we believe these third-party sources to be reliable as of the date of this presentation, we have not independently verified, and make no representation as to the adequacy, fairness, accuracy or completeness of, any information obtained from third party sources. In addition, estimates involve a number of assumptions and limitations and you are cautioned not to give undue weight to such estimates. This presentation contains references to our trademarks and service marks and to those belonging to other entities. Solely for convenience, trademarks and trade names referred to in this presentation may appear without the® or TM symbols, but such references are not intended to indicate in any way that we will not assert, to the fullest extent under applicable law, our rights or the rights of the applicable licensor to these trademarks and tradenames. We do not intend our use or display of other entities' trade names, trademarks or service marks to imply a relationship with, or endorsement or sponsorship of us by, any other entity.

Advancing breakthrough therapeutics through the purposeful integration of science and engineering © 2026 | 3 Innovative Discovery Machine Learning & Advanced Engineering Experienced Leadership Clinical-Stage Pipeline Eikon is a late-stage clinical biopharmaceutical company

1This Phase 2/3 trial is designed to proceed to completion, subject to interim analysis by a data monitoring committee, and to form the basis for registration; 2 Phase 2 safety and efficacy study nearing completion; United States Food and Drug Administration, or FDA, has allowed us to proceed with the Phase 2/3 registrational trial; 3 NSQ = Non-squamous cohort, SQ = Squamous cohort, Phase 2 readout for NSQ cohort presented at ASCO 2026; 4 Greater China: China, Hong Kong, Macau, Taiwan. Note: Readouts are contingent on acceptance for presentation at one of several major medical conferences Eikon’s pipeline includes multiple indications addressing significant unmet medical needs We are also actively pursuing additional discovery research in oncology and neurodegeneration Melanoma1 NSCLC2 EIK1005 WRN EIK1003 PARP1 EIK1001 TLR7/8 Candidate/ Program Pre-Clinical Phase 1 Phase 2 Phase 3 Target Indication(s) Ownership Next Anticipated Milestone EIK1004 PARP1 (CNS Penetrant) Wholly owned Ovarian, Breast, Prostate, Pancreatic Solid Tumors with and without Brain Metastases MSI-high Tumors Global exclusive license excluding Greater China4 Global exclusive license excluding Greater China4 Target EIK1006 AR Wholly owned Prostate Cancer Phase 2/3 First Patient Dosed, 2H 2026 First Interim Analysis, 2H 2026 Phase 1 First Patient Dosed, Q1 2026 IND Submission, End of 2026 1A and 1C Data Readouts, 2H 2026 Completion of Phase 1/2 Dose Escalation, 2H 2026 Phase 2 Data (NSQ SQ)3 Readout, 2H 2026 Global exclusive license Milestone achieved ✽ ✽ ✽ ✽

EIK1001 – TLR7/8 Dual-Agonist

EIK1001: Eikon’s TLR7/8 dual-agonist has potential to complement checkpoint inhibition TLR7 and TLR8 activate innate and adaptive anti-tumor immunity TLR7/8 dual-agonist activates both innate and adaptive immune responses Orthogonal mechanism to checkpoint inhibition, a prerequisite for successful combination Established biology cutaneous administration of resiquimod1 (EIK1001) shown to provoke responses in lymphomas and basal cell carcinoma Monotherapy activity observed in phase 1 studies with EIK1001 doi.org/10.1016/j.medidd.2022.100122; 1doi: 10.1182/blood-2015-02-630335; doi: 10.3390/pharmaceutics14102076

NSCLC standard of care established in KEYNOTE studies of pembrolizumab + chemotherapy vs chemotherapy alone Source(s): DOI(s): 10.1056/NEJMoa1810865; 10.1056/NEJMoa1801005; 10.1200/JCO.22.01989; 10.1200/JCO.22.01990 || NEJM ITT population and JCO, all responses from NEJM are reported as based on the investigator review in the original publication Trial Regimen N ORR DCR DOR (months) KEYNOTE 189 (Non-Squamous) Pembro + chemo vs. Chemo 616 43% vs. 19% 81% vs. 70% Median: 12.6 vs. 7.6 KEYNOTE 407 (Squamous) Pembro + chemo vs. Chemo 559 55% vs. 32% 84% vs. 76% Median: 7.3 vs. 4.9 Investigator-based assessment from established standard of care

Data as of May 4, 2026; Safety, exposure, and disposition data cutoff: March 17, 2026; Presented at ASCO 2026 ALL (NSQ + SQ) N = 65 | 72 (Efficacy Evaluable | Total) % (95% CI) ORR (CR+PR) 63.1% (50.2%, 74.7%) DCR (CR+PR+SD) 90.8% (81.0%, 96.5%) Responses are based on RECIST 1.1 EIK1001-005 study fully enrolled: NSQ data updated at ASCO 2026, SQ data still maturing NSQ N = 36 | 39 (Efficacy Evaluable | Total) % (95% CI) ORR (CR+PR) 55.6% (38.1%, 72.1%) DCR (CR+PR+SD) 83.3% (67.2%, 93.6%) Median Follow Up, mo. 13.6 (range: 7.9-25.3) SQ N = 29 | 33 (Efficacy Evaluable | Total) % (95% CI) ORR (CR+PR) 72.4% (52.8%, 87.3%) DCR (CR+PR+SD) 100% (86.3%, 100%) Median Follow Up, mo. 8.8 (range: 2.8-21.4) Objective responses were observed across all PD-L1 TPS (Tumor Proportion Score) subgroups Study continues to perform at the high end of company expectations All Participants Nonsquamous Squamous

Data as of May 4, 2026; Safety, exposure, and disposition data cutoff: March 17, 2026; Presented at ASCO 2026 Responses are based on RECIST 1.1 EIK1001-005 is observed to be generally well tolerated, permitting administration in out-patient setting *Consolidated terms Drug-related: events determined by Investigator to be related to treatment regimen; TEAE = treatment-emergent adverse event; TRAE = treatment-related adverse event; SAE = serious adverse event; NSQ = non-squamous; SQ = squamous. Adverse events are shown for preferred terms occurring in ≥2 participants overall. No DLTs were observed during the safety run-in phase (N=13) High-grade treatment-related AEs were generally consistent with toxicities expected with pembrolizumab/platinum-based chemotherapy No Grade 3 or higher Cytokine Release Syndrome (CRS) events NSQ N=39 SQ N=33 All N=72 Grade ≥ 3 TRAEs: N(%) N(%) N(%) Neutropenia* 13(33.3%) 9(27.3%) 22(30.6%) Anemia* 6(15.4%) 1(3.0%) 7(9.7%) Thrombocytopenia* 6(15.4%) 1(3.0%) 7(9.7%) Fatigue* 4(10.3%) 1(3.0%) 5(6.9%) Colitis 1(2.6%) 2(6.1%) 3(4.2%) Febrile Neutropenia 2(5.1%) None 2(2.8%) Lymphopenia 1(2.6%) 1(3.0%) 2(2.8%) Grade ≥ 3 TRAE Occurring in ≥ 2 Subjects TEAEs: N % Any TEAE 72 100% Grade ≥ 3 TEAE 57 79.2% Grade ≥ 3 drug-related TEAE 35 48.6% SAE 36 50.0% TEAEs leading dose to: Death 9 12.5% Discontinuation 14 19.4% Modification 17 23.6% Overall Safety Summary

Data as of May 4, 2026; Presented at ASCO 2026 Responses are based on RECIST 1.1 EIK1001-005 study fully enrolled: NSQ data updated at ASCO 2026 Time on Study Participants Time Since Initiation of Treatment (months) Target Lesion Waterfall Participants Best (%) Change from Baseline Months in Response Duration of Response, % Number at Risk Median DOR > 11 months (as of May 4, 2026)

Data as of May 4, 2026; Presented at ASCO 2026 Responses are based on RECIST 1.1 EIK1001-005 NSQ summary EIK1001 + SOC demonstrated encouraging antitumor activity in the NSQ cohort Tumor reductions were observed in most response-evaluable participants Median DOR was greater than 11 months at the efficacy data cutoff of May 4, 2026 Response follow-up was ongoing, with several responders remaining on treatment or in response

EIK1001: Current program(s) status Currently conducting multiple clinical trials: EIK1001-005 Phase 2 exploratory/tolerability study in NSCLC of triplet (chemo + EIK1001 + pembrolizumab), initiated in Q1 2024 EIK1001-006 Phase 2/3 registrational trial in melanoma of combination (EIK1001 + pembrolizumab), initiated in Q2 2025 EIK1001-008 Phase 2/3 registrational trial in NSCLC (chemo + EIK1001 + pembrolizumab), initiated in Q1 2026 Anticipated 2026 milestone(s): 2H2026 Phase 2 data readout NSQ and SQ 2H2026 First Interim Analysis 2H2026 First Patient Dosed ✽ Milestone achieved ✽

EIK1003/EIK1004: PARP1-Selective Inhibitors for Treatment of Malignancy

HRRD = Sensitive Selective EIK1003: Eikon’s PARP1 selective inhibitor has potential to overcome current limitations and expand usage setting PARP1 inhibition and subsequent trapped PARP1 leads to DNA double strand breaks and anti-tumor activity in HR deficient cells EIK1003 is designed to be highly selective for PARP1 over PARP2, in contrast to currently approved agents PARP2 activity is thought to be a major driver of hematotoxicity, limiting current therapies to maintenance setting A differentiated PARP1 selective inhibitor could potentially be used in combination and beyond the maintenance setting 1: AstraZeneca FY 2024 results; HR: homologous recombination; HRRD: HRR deficient

Target Lesion Waterfall Participants Best (%) Change from Baseline EIK1003: Tumor responses observed in Phase 1/2 trial as monotherapy. Results from the fully-enrolled dose-escalation trial. Note: CA125 Response: reduction of over 50% in serum CA-125 levels from a high pre-treatment baseline, maintained for at least 28 days Data as of May 4, 2026; Safety data as of February 27th, 2026; Presented at ASCO 2026 Responses are based on RECIST 1.1, PARPi: PARP inhibitor Monotherapy Time on Study Participants Time Since Initiation of Treatment (months)

EIK1003: Summary of observed responses and safety profile as monotherapy (Cohort 1A) (CR+PR)/Evaluable ORR % Total 7/49 14.3% Tumor Type Breast 2/16 12.5% Ep. Ovarian 4/27 14.8% Prostate 1/1 100% Pancreatic 0/5 0% PARPi Naïve 4/15 26.7% Monotherapy Key Endpoints Data as of May 4, 2026; Safety data as of February 27th, 2026; Presented at ASCO 2026 Responses are based on RECIST 1.1, PARPi: PARP inhibitor N (Total = 65) % TEAEs: All 63 96.9% Grade ≥ 3 29 44.6% Anemia 6 9.2% Neutropenia 5 7.7% Ascites 5 7.7% Thrombocytopenia 1 1.5% TEAEs leading dose to: Interruption 22 33.8% Reduction 7 10.8% Discontinuation 6 9.2% Monotherapy Safety Summary 4 out of 6 participants who developed Grade ≥ 3 anemia had Grade 1-2 anemia at baseline There were no treatment-related AEs (TRAEs) that led to death All 7 responses were PRs (5 confirmed, 2 unconfirmed) Median duration of response (DOR) in confirmed responders: 7.8 months (range: 6.0-15.9+) Disease control rate (DCR: CR+PR+SD): 38.8% TEAE: treatment emergent adverse event; TRAE: treatment related adverse event; ORR: objective response rate; DCR: disease control rate; DOR: duration of response

Target Lesion Waterfall Participants Best (%) Change from Baseline EIK1003: Tumor responses observed in Phase 1/2 trial in combination with paclitaxel. Results from fully enrolled dose escalation trial. Note: CA125 Response: reduction of over 50% in serum CA-125 levels from a high pre-treatment baseline, maintained for at least 28 days Data as of May 4, 2026; Safety data as of February 27th, 2026; Presented at ASCO 2026 Responses are based on RECIST 1.1, PARPi: PARP inhibitor Cohort 1C Time on Study Participants Time Since Initiation of Treatment (months)

EIK1003: Summary of observed responses and safety profile in combination with paclitaxel (Cohort 1C) (CR+PR)/Evaluable ORR % Total 13/53 24.5% Tumor Type Breast 5/26 19.2% Ep. Ovarian 8/27 29.6% Prior Taxane 12/13 92% Paclitaxel Combo. Key Endpoints Data as of May 4, 2026; Safety data as of February 27th, 2026; Presented at ASCO 2026 Responses are based on RECIST 1.1, PARPi: PARP inhibitor N (Total = 60) % TEAEs: All 60 100% Grade ≥ 3 in at least 10% 45 75% Anemia 8 13.3% Neutropenia 30 50% TEAEs leading dose to: Interruption 50 83.3% Reduction 15 25% Discontinuation* 11 18.3% Paclitaxel Combo. Safety Summary Dose-limiting toxicities of febrile neutropenia and tachycardia (1 participant each) occurred at the highest dose level tested (EIK1003 60 mg) All 8 participants who developed Grade ≥ 3 anemia had Grade 1-2 anemia at baseline There were no treatment-related AEs (TRAEs) that led to death 1 CR (confirmed), 12 PR (8 confirmed, 4 unconfirmed) Prior taxane exposure by tumor type: 100% (8/8) ovarian cancer; 80% (4/5) breast cancer DOR range in confirmed responders: 1.5+ - 11.4 months. The response remains ongoing for 3 responders Disease control rate (DCR: CR+PR+SD): 79.2% *discontinuation of either or both drugs TEAE: treatment emergent adverse event; TRAE: treatment related adverse event; ORR: objective response rate; DCR: disease control rate; DOR: duration of response

EIK1003/EIK1004: Current program(s) status Currently conducting multiple clinical trials: EIK1003-001 (Part 1): Cohort 1A: Monotherapy Cohort 1B: Combo with abiraterone Cohort 1C: Combo with paclitaxel Cohort 1D: Combo with platinum-based therapy and paclitaxel EIK1003-001 (Part 2): Ph 2 Monotherapy dose optimization study EIK1004-001 (Part 1): Dose escalation safety study Anticipated 2026 milestone(s): 1H 2026 Read out at ASCO 2026 2H 2026 Read out 1H 2026 Read out at ASCO 2026 1H 2026 Study initiated 1H 2026 First patient dosed 2H 2026 Complete dose escalation Milestone achieved ✽ ✽ ✽ ✽ ✽

EIK1005: WRN Inhibitor for Treatment of MSI-High Cancers

EIK1005: Eikon’s WRN inhibitor for the treatment of microsatellite instability high cancers MSI-high cancers rely on WRN helicase activity to resolve secondary DNA structures WRN inhibition blocks DNA repair leading to fragmented DNA and cell death in sensitive cells Unmet need exists for cancers that are primary refractory or relapse from currently available therapies PD-L1 combinations could potentially enhance the anti-tumor activity of a WRN inhibitor

EIK1005: WRN inhibitor clinical program initiated based on favorable results in tumor xenograft studies, starting dose established 23 subjects were dosed in a two-part study (P1 N=15; P2 N=8) at 50mg (P1 & P2) and 100mg (P1) doses All subjects competed the study and all AEs were unrelated and mild with the exception of a single moderate AE with no clinically significant events T 1/2 was 9.4 days, EIK1005 exposure increased in a dose related manner and no clinically significant food effect was observed Findings supported a starting dose of 50mg for EIK1005-002 trial (NCT#007262619) Tumor volume decrease observed at multiple dose levels in preclinical studies Early clinical data presented at ASCO 2026 HCT116 Xenograft WRNi EIK1005EIK1005 EIK1005 P1: Part 1; P2: Part 2 Presented at ASCO 2026

Eikon Technology Provides Novel Scientific Insights and Permits Rapid Lead Optimization

Single molecule tracking captures the real-time dynamics of individual proteins at scale 0.0 2.5 5.0 7.5 10 Fast Slow Diffusion Coefficient (mm2/s) Membranes | DNA | Target Protein © 2026 | 24

WRN trapping and degradation upon inhibition revealed by Eikon SMT VCP proteasome WRN WRN Findings led to elucidation of key contributors to WRN inhibitor-driven degradation mechanism slow WRN upon inhibition Shift from fast to slower proteins is quantifiable WRN

AI/ML + Physics-Based Models Docking vs ML Antagonist Deprioritize Prioritize Predicted AR Antagonism pIC50 Predicted AR Agonism pEC50 Predicted AR Antagonism pEC50 Protein-Ligand Docking Score Agonist Explore, Interactions Not Captured by ML Explore, Unfavorable Protein-Ligand Interactions ML Guided Compound Prioritization Predicted Lipophilic Efficiency (LipE = pEC50 – LogD) LipE=6 5 4 3 2 1 Machine learning and computational chemistry guide Eikon’s AR antagonist designs Protein-Ligand Docking Predicted AR Antagonism pEC50 Ligand AR Protein ML Models R2 Caco-2 Permeability 0.77 Chrom LogD 0.86 Kinetic Solubility 0.59 EPSA 0.87 Microsomal Stability (HLM, MLM) 0.62, 0.49 Stability in Hepatocytes (hHep,mHep) 0.39, 0.64 AR SMT Antagonist 0.61 AR SMT Agonist 0.64 Local ML Models Developed for AR

Eikon’s AR programs aim to address limitations of current therapies EIK1006 (AR clinical candidate) observed to inhibit tumor growth, reduce PSA levels and alter AR gene expression in preclinical models Observed activity across a range of emerging resistant variants EIK1006 declared clinical candidate in November 2025; preclinical studies now tracking ahead of schedule, expected to enable IND submission by the end of 2026

Conclusion

Meaningful progress expected across all of our development efforts EIK1001 (TLR 7/8) EIK1003 (PARP1) EIK1004 (PARP1) (CNS-penetrant) EIK1005 (WRN) Phase 2 Non-Squamous NSCLC data readout First interim analysis to choose dose for melanoma study Full Phase 2 NSCLC data readout First patient dosed in NSCLC registration enabling trial Full read out of Phase 1/2 study Read out of EIK1003 + abiraterone study Read out of EIK1003 + paclitaxel study Initiation of study start-up of EIK1003 + platinum-based therapy + paclitaxel study Completion of Phase 1/2 study dose escalation First patient dosed in Phase 1 study EIK1006 (AR) IND submission(Submission projected by end of 2026) Completed and Upcoming for 2026 Milestone achieved ✽ ✽ ✽ ✽ ✽

Led by world-renowned drug developers Eikon Therapeutics highlights Technology platform, centered around proprietary single-molecule tracking (SMT) Clinical-stage programs have generated early signs of encouraging clinical activity Internally identified and strategically tailored product candidates advancing into clinical investigation 1 2 3 4

Appendix

Eikon’s leadership team delivers proven depth and experience to bring novel therapies to market Roger Perlmutter CEO & Board Chair Roy D. Baynes CMO Freddie Bowie CFO Barbara Howes CPO Benjamin Thorner CBO & GC Russ Berman CTO Michael Klobuchar COO Executive Team Board of Directors Kenneth C. Frazier Former CEO, Merck; current Chairman, General Catalyst’s Health Assurance initiatives Leon Chen, Ph. D.Partner, The Column Group; Venture Partner, OrbiMed Advisors Robbie HuffinesFormer Global Chairman of Investment Banking, JP Morgan Joshua WolfeCo-Founder & Managing Partner, Lux Capital David W. MelineFormer CFO, Moderna; Former CFO, Amgen; Former CFO, 3M


Deep R&D expertise coupled with proprietary technology combine to develop innovative medicines Eikon key strengths Leadership team that has supervised 100+ new drug approvals In-house clinical development expertise and executional excellence Proprietary technology to pursue difficult or historically undruggable targets Drug development approach EIK1005 WRN EIK1003 PARP1 EIK1001 TLR7/8 EIK1004 PARP1 (CNS Penetrant) EIK1006 AR Discovery Pipeline assets In License Discovery

Our oncology drug development strategy – potential assets Immuno-responsive cancers requiring enhanced immune stimulation Advanced cancers with DNA repair abnormalities Hormonally responsive cancers Androgen receptor (AR) antagonists (EIK1006) Checkpoint inhibitor foundation + TLR7/8 dual-agonist (EIK1001) Brain and non-brain penetrant PARP-1 selective agents (EIK1003 and 1004) Werner helicase inhibitor (EIK1005)

EIK1001 – TLR7/8 Dual-Agonist

JReview data as of Oct 27, 2025; data is not fully cleaned All (N=53) n % (95% CI) ORR (CR+PR) 32 60%(46%, 74%) DCR (CR+PR+SD) 47 89%(77%, 96%) Responses are based on RECIST 1.1 Target Lesion Best % Change from Baseline Time on Study EIK1001-005 study fully enrolled: NSQ + SQ as of October 27th, 2025 Subject Subject Time Since Initiation of Treatment Best (%) Change from Baseline

EIK1001 introduces a systemic proinflammatory signal which may complement traditional checkpoint inhibitor-based regimens Dual agonism stimulates innate and adaptive responses Orthogonal mechanism of action to checkpoint inhibitors Cutaneous administration of resiquimod (EIK1001) has been shown to provoke responses in cutaneous T-cell lymphoma and basal cell carcinoma1 Monotherapy activity observed in Phase 1 study Observed to be generally well-tolerated when dosed systemically in Eikon’s large (>400) patient-exposure database Differentiation of EIK1001 EIK1001 is designed to be an Active Anti-Neoplastic Agent EIK1001 TLR7/8 Field 1doi: 10.1182/blood-2015-02-630335; doi: 10.3390/pharmaceutics14102076

EIK1001 squamous data shows especially encouraging disease control (data to be updated at ASCO 2026) Squamous (N=17) n % (95% CI) ORR (CR+PR) 12 71% (44%, 90%) DCR (CR+PR+SD) 17 100% (80%, 100%) Subject Best (%) Change from Baseline Target Lesion Best % Change from Baseline JReview data as of Oct 27, 2025; data is not fully cleaned Responses are based on RECIST 1.1; DCR: disease control rate;

EIK1003/EIK1004: PARP1-Selective Inhibitors for Treatment of Malignancy

Improved PARP1 selectivity may mitigate liabilities of currently approved agents Normal Hematopoiesis Anemia (reduced red blood cells), neutropenia (low neutrophils) and thrombocytopenia (reduction in platelets) are all associated with the use of non-selective PARP inhibitors 1. Smith MR et al Lancet Oncol 2022; 2.Litton JK et al NEJM 2018; 3. Abida W et al J Clin Oncology 2020; 4. Robson ME et al Ann Oncology 2019; 5.Yap TA et al AACR 2024 Neutrophils 1st generation PARP inhibitors, characterized by both PARP1 and PARP2 activity, exhibit hematological toxicities1-4 2nd generation PARP inhibitors although more selective, have not completely solved the problem5 Eikon’s PARP inhibitors are observed to have ~600x – 850x biochemical potency selectivity and ~20000x – 50000x PARP1 trapping selectivity over PARP2

EIK1003: Tumor responses observed in Phase 1/2 trial as monotherapy. Results from the fully-enrolled dose-escalation trial to be updated at ASCO 2026. Monotherapy Key Endpoints Adverse Event Summary: Total TEAEs: 96.9% Grade 3 AEs: 43.1% SAEs: 23.1% Treatment Related SAEs: 6.2% Leading to Death: 0% Leading to treatment discontinuation: 9.2% (CR+PR)/Evaluable ORR (95% CI) Total 7/49 14.3% (5.9, 27.2) Tumor Type Breast 2/16 12.5% (1.6, 38.3) Ep. Ovarian 4/27 14.8% (4.2, 33.7) Prostate 1/1 - Pancreatic 0/5 - PARPi Naïve 5/16 31.2% (11.0, 58.7) Note: CA125 Response: reduction of over 50% in serum CA-125 levels from a high pre-treatment baseline, maintained for at least 28 days Best (%) Change from Baseline JReview data as of Oct 27, 2025; data is not fully cleaned; Responses are based on RECIST 1.1, PARPi: PARP inhibitor Subject Cohort 1A – Tumor Type Epithelial Ovarian Breast Pancreatic Prostate Other Best Overall Response Complete Response Confirmed PR Partial Response Stable Disease Progressive Disease CA125 Response PARPi Naive Monotherapy

EIK1003 monotherapy provided encouraging preliminary data regarding durability of responses (data to be updated at ASCO 2026) JReview data as of Oct 27, 2025; data is not fully cleaned Responses are based on RECIST 1.1 Time on Study Subject Time Since Initiation of Treatment (months)

Encouraging preliminary tolerability and disease control observed for EIK1003 in combination with paclitaxel (data to be updated at ASCO 2026) JReview data as of Oct 27, 2025; data is not fully cleaned; * “Other” subject in the right plot was identified as a breast cancer patient after Oct 27, 2025; Additional “other” subject in the left plot has no confirmed information at this time Responses are based on RECIST 1.1; 3 confirmed PRs, 1 unconfirmed PR, and 1 confirmed CR Combination Therapy By Tumor Type Target Lesion Best % Change from Baseline Time on Study Subject Subject Best (%) Change from Baseline CA125 Response Time Since Initiation of Treatment (months)

Eikon Technology Provides Novel Scientific Insights and Permits Rapid Lead Optimization

MAKE TEST ANALYZE DESIGN Eikon’s approach: designed to accelerate drug discovery both conceptually, and through advanced technology ROBOTICS & AUTOMATION SYSTEMS BIOLOGY SINGLE MOLECULE TRACKING AI/ML-ENHANCED DATA ANALYSIS

Eikon’s discovery platform advanced WRN program (EIK1005) from tool compound to clinical candidate in under 18 months JAN 2023 Tool compounds targeting WRN helicase identified and synthesized JAN 2023 Eikon identifies novel WRN degradation MOA through SMT platform APR 2023 Eikon generates co-crystal structure of WRN and an inhibitor AUG 2023 Hit-to-Lead status declared, supported by SMT assay NOV 2023 Definitive efficacy studies begin DEC 2023 Eikon pre-print on WRN MOA1 manuscript; WRN Lead-Op declaration Biochemical and Cellular Assay Development Efficacy and MOA Studies Conducted Eikon nominates clinical candidate May 2024; preclinical studies begin 1Published in Nature Communications, July 2024

Androgen receptor overview Androgens drive proliferation of prostate cancer cells Anti-Androgens block proliferation Two resistance variant mechanisms evade current therapies

Eikon Therapeutics Presents Data on Clinical-Stage Programs at the 2026 Annual Meeting of the American Society of Clinical Oncology
•TeLuRide-005, a Phase 2 trial of EIK1001 in first-line patients with stage 4 NSCLC completed enrollment of both non-squamous and squamous cohorts and reports updated rates of response and disease control, strengthening the case for continued development
•Phase 1/2 trial of EIK1003 reports updated safety and efficacy monotherapy data and initial combination data with weekly paclitaxel in patients with advanced solid tumors
MILLBRAE, Calif., May 30, 2026 -- Eikon Therapeutics, Inc. (Nasdaq: EIKN) (Eikon), a late-stage clinical biopharmaceutical company dedicated to developing innovative medicines to address serious unmet medical needs, today announced presentations on several of its lead programs at the 2026 American Society of Clinical Oncology (ASCO) Annual Meeting in Chicago, including updated data for its EIK1001 trial in non-small cell lung cancer (NSCLC) and its highly selective PARP1 inhibitor EIK1003.
“We are pleased to present six abstracts at ASCO reflecting both the progress of our pipeline and the growing body of evidence supporting our lead programs,” said Roy Baynes, M.D., Ph.D., Chief Medical Officer of Eikon. “In our most advanced program, EIK1001 demonstrated encouraging response rates and durability in combination with standard of care in first-line NSCLC. We also observed meaningful clinical activity of EIK1003 both as a monotherapy and, potentially a first for the field, in combination with paclitaxel, including responses in heavily pretreated patients. Together, these data continue to reinforce the scientific rationale behind our programs and their potential to deliver meaningful benefit to people living with cancer.”
EIK1001 Clinical Update.
Updated data from our ongoing Phase 2 trial evaluating the safety and tolerability of EIK1001 in combination with both pembrolizumab and histology appropriate chemotherapy for the front-line treatment of patients with advanced NSCLC, also known as our TeLuRide-005 trial, provide evidence of a potentially durable effect of EIK1001 in combination with standard of care, and a preliminary tolerability profile supportive of systemic administration in an out-patient setting, a potential key differentiator of EIK1001 from previous TLR7/8 targeted therapies.
EIK1001 is an investigational, systemically administered dual-agonist of Toll-like receptors 7 and 8 designed to stimulate both innate and adaptive immune responses. In Phase 1 trials of EIK1001, single-agent activity was observed in patients with advanced malignancy. This mechanism may complement the antitumor immune response engendered by PD-(L)1 blockade.
TeLuRide-005 is our multicenter, open-label trial of once-weekly (QW) systemically administered EIK1001 in combination with standard of care, once every third week (Q3W) pembrolizumab and histology appropriate chemotherapy in first-line, treatment-naïve patients with stage 4 NSCLC. Enrollment completed in the first quarter of 2026.
As of enrollment cutoff, 72 participants with previously untreated stage 4 NSCLC received intravenous EIK1001 QW combined with standard of care pembrolizumab plus chemotherapy Q3W. After 8 cycles, EIK1001 administration was reduced to Q3W. The maximum treatment duration is 2 years (up to 35 cycles) for EIK1001 in combination with pembrolizumab, with pemetrexed continued at the discretion of the Investigator for non-squamous patients.
At the March 17, 2026 safety data cutoff, among the safety evaluable population (n=72: 39 non-squamous; 33 squamous), the combination of EIK1001 with pembrolizumab and chemotherapy was generally well tolerated, with an adverse event (AE) profile similar to standard of care alone. Most treatment-emergent adverse events (TEAEs) were Grade 1-2, and the most common Grade 3 or higher treatment-related adverse events (TRAEs) were neutropenia (30.6%), anemia (9.7%), and thrombocytopenia (9.7%). All cytokine release syndrome (CRS) AEs were Grade 1 and 2, and all CRS events occurred before Cycle 4 in all but one patient. This profile was sufficient to support administration in an out-patient setting during the ongoing trial.
Among the efficacy-evaluable population (n=65: 36 non-squamous; 29 squamous), EIK1001 treatment in combination with pembrolizumab and chemotherapy resulted in a 63.1% objective response rate (ORR) and 90.8% disease control rate (DCR) at the efficacy data cutoff of May 4, 2026. Among participants in the non-squamous cohort, an ORR of 55.6% and a DCR of 83.3% were observed, respectively, with a median follow-up of 13.6 months. The median duration of response (DOR) in the non-squamous cohort was greater than 11 months at the efficacy data cutoff. Among participants in the squamous cohort, for which the data set was still maturing at the data cutoff due to slower enrollment, an ORR of 72.4% and a DCR of 100% were observed, respectively, with a median follow-up of 8.8 months.
EIK1003 Clinical Update.
Updated data from EIK1003-001, our Phase 1/2 trial evaluating the safety and efficacy of EIK1003 as monotherapy or in combination with anti-cancer agents in participants with advanced solid tumors, demonstrate that EIK1003 monotherapy (Cohort 1A) was generally well-tolerated across multiple dose levels. In Cohort 1C, signals of antitumor activity were observed with EIK1003 in combination with weekly paclitaxel, with a combination safety profile consistent with paclitaxel’s known toxicities. These data support what appears to be a unique profile for EIK1003 in combination strategies within the evolving PARP inhibitor landscape.
EIK1003 is an investigational, highly-selective PARP1 inhibitor designed to leave PARP2 signaling intact. PARP2 inhibition may be a key driver of the hematological toxicity associated with first generation, non-selective PARP inhibitors.
Cohort 1A: Updated EIK1003 Monotherapy Data
As of the enrollment cutoff, 65 patients with breast, ovarian, prostate, or pancreatic cancer have been treated in Cohort 1A with EIK1003 monotherapy at doses ranging from 10mg to 160mg once daily (QD), using a Bayesian optimal interval dose-escalation design to assess for safety, tolerability, pharmacokinetics and antitumor activity. This represents an expansion of the dataset previously presented at ASCO 2025, with additional patients enrolled and longer follow-up.
At the February 27, 2026 safety data cutoff, the updated safety profile in Cohort 1A remained generally consistent with data previously presented at ASCO 2025. Treatment-emergent adverse events (TEAEs) were reported in 63 of 65 patients (96.9%). Grade 3 or higher TEAEs occurred in 29 patients (44.6%); the most common were anemia (9.2%), neutropenia (7.7%), and ascites (7.7%). 4 of the 6 patients who developed Grade 3 or higher anemia had Grade 1-2 anemia at study entry. TEAEs led to dose reductions in 7 patients (10.8%) and to treatment discontinuation in 6 patients (9.2%). No TRAEs leading to death were reported.
Among efficacy-evaluable patients in Cohort 1A (n=49), ORR was 14.3% overall and 26.7% in PARP-naïve patients. Objective responses by tumor type were 14.8% (4/27) in ovarian cancer, 12.5% (2/16) in breast cancer, and one patient with prostate cancer. Median duration of response among confirmed responders (n=5) was 7.8 months at the efficacy data cutoff of May 4, 2026.
Cohort 1C: Initial Data on EIK1003 in Combination with Weekly Paclitaxel
As of the February 27, 2026 safety data cutoff, 60 patients with platinum-resistant ovarian cancer or HER2-negative breast cancer that failed chemotherapy or hormonal therapy have been treated in Cohort 1C with EIK1003 at doses ranging from 10mg to 60mg QD in combination with paclitaxel 80 mg/m2 IV QW. Dose-limiting toxicities of febrile neutropenia and tachycardia were reported in one patient each at the highest dose level tested, 60mg. TEAEs were reported in 60 out of 60 patients (100%). Grade 3 or higher TEAEs occurred in 45 patients (75%); the most common were neutropenia (50%) and anemia (13.3%). Neutropenia is a known and expected adverse event associated with weekly paclitaxel chemotherapy. All 8 patients who developed Grade 3 or higher anemia had Grade 1-2 anemia at study entry. TEAEs led to dose reductions in 15 patients (25%) and discontinuation of one or both study drugs in 11 patients (18.3%). No TRAEs leading to death were reported.
Among efficacy-evaluable patients in Cohort 1C (n=53), ORR was 24.5%; 12 of 13 responders (92%) had received prior taxane therapy. Objective responses by tumor type were 29.6% (8/27) in platinum-resistant ovarian cancer and 19.2% (5/26) in breast
cancer. Duration of response among confirmed responders (n=9) ranged from 1.5 to 11.4 months, with responses ongoing in 3 responders at the efficacy data cutoff of May 4, 2026.
2026 ASCO Abstract Titles.
EIK1001
Title: Efficacy, safety and cytokine profiling with addition of the toll-like receptor (TLR) 7/8 dual agonist EIK1001 to Standard of Care First-Line Therapy: the Phase 2 TeLuRide-005 trial in Stage 4 Non-Small Cell Lung Cancer
Title: Adaptive Phase 2/3 Study of EIK1001, a TLR7/8 Dual Agonist, in Combination with Pembrolizumab, as First-Line Therapy in Participants with Advanced Melanoma (TeLuRide-006)
Title: A Phase 2/3 Study of EIK1001 in Combination with Pembrolizumab and Chemotherapy in Participants with Stage 4 Non-Small Cell Lung Cancer (TeLuRide-008)
EIK1003
Title: EIK1003, a PARP1-selective inhibitor, in combination with paclitaxel (PTX): Initial combination and updated monotherapy results from a Phase 1/2 study EIK1003-001 in advanced solid tumors
EIK1005
Title: First-in-Human Study to Evaluate the Safety, Tolerability, and PK of EIK1005, a Novel WRN Inhibitor in Healthy Participants
Title: Phase 1/2 Study of the novel Werner helicase inhibitor EIK1005 as Monotherapy and in Combination with Pembrolizumab in Patients with Advanced Solid Tumors, including MSI-H or dMMR Tumors (Publication only)
Copies of the 2026 ASCO presentations will be made available on our website: www.eikontx.com under Scientific Papers & Publications.
About Eikon Therapeutics
Eikon is a late-stage clinical biopharmaceutical company dedicated to building a global, fully-integrated organization developing innovative medicines to address serious unmet medical needs. Eikon’s initial focus is oncology, where it is advancing a pipeline of drug candidates targeting areas of high unmet need that could eventually become critical medicines for the treatment of various cancers. Eikon deploys its technology platform, including its proprietary single molecule tracking system, to develop internally-derived novel therapies, while also leveraging the deep expertise of its management team to
in-license promising assets. Eikon’s vision is to become a generational leader, by purposefully integrating traditional biology research with advanced engineering to develop better medicines faster. For more information, visit www.eikontx.com.
Forward-Looking/Safe Harbor Statements
This press release contains forward-looking statements within the meaning of the “safe harbor” provisions of the Private Securities Litigation Reform Act of 1995. All statements in this press release that are not historical facts are hereby identified as forward-looking statements for this purpose. These statements may be identified by words such as “aims,” “anticipates,” “believes,” “could,” “estimates,” “expects,” “forecasts,” “goal,” “intends,” “may,” “plans,” “possible,” “potential,” “seeks,” “will” and variations of these words or similar expressions that are intended to identify forward-looking statements, although not all forward-looking statements contain these words. Forward-looking statements in this press release include, but are not limited to, statements regarding: the therapeutic potential, safety, and efficacy of Eikon’s product candidates; the timing for anticipated data readouts; expected milestones and business objectives for 2026 and beyond, including Eikon’s anticipated presentations at the ASCO Annual Meeting; and other statements regarding Eikon’s future operations, financial performance, financial position, prospects, objectives, strategies and other future events.
These forward-looking statements are based upon management’s current expectations and assumptions, and are subject to a number of risks, uncertainties and other factors that could cause actual results and events to differ materially and adversely from those indicated by such forward-looking statements including, among others: our limited operating history; our significant net losses incurred since inception and the likelihood of incurring additional losses for the foreseeable future; our need for substantial additional funding; the early stage of development of many of our product candidates and the possibility that our product candidates may fail in development; our dependence on the success of our current product candidates; our ability to leverage our technology platform to enable more informed drug research and development; legal and regulatory risks; intellectual property-related risks; and those risks, uncertainties and other factors discussed under the caption “Risk Factors” and elsewhere in Eikon’s Quarterly Report on Form 10-Q for the quarter ended March 31, 2026, filed with the Securities and Exchange Commission (“SEC”) on May 11, 2026, and in other public filings with the SEC in the future.
As a result, you should not place undue reliance on any forward-looking statements. The forward-looking statements made in this press release speak only as of the date of this press release, and Eikon undertakes no obligation to update such forward-looking statements, whether as a result of new information, future developments or otherwise, except as required by law.
Contacts:
Investors
Alfred “Freddie” Bowie, Ph.D., CFO
ir@eikontx.com
Media
Colin Sanford
colin@bioscribe.com