Tezacitabine

Data highlight encouraging clinical activity of EO1001 and differentiated preclinical efficacy of EO‑4426 inhighly resistant, replication‑stress–driven tumors Menlo Park, CA — November 24, 2025 /Accessnewswire/ — Edison Oncology Holding Corp. (“EdisonOncology” or “the Company”) today announced the presentation of new clinical and preclinical data fortwo of its precision-oncology drug candidates—EO1001, an irreversible pan-ErbB inhibitor, and EO4426(tezacitabine), a dual DNA polymerase-α and ribonucleotide reductase inhibitor—at the 2025 Society forNeuro-Oncology (SNO) Annual Meeting. Together, the presentations underscore Edison Oncology’s leadership in developing differentiatedtherapies aimed at addressing major unmet needs in aggressive, treatment-resistant cancers, includingthose driven by complex genomic alterations and metabolic resistance mechanisms that limit theeffectiveness of current treatments. Interim results from the Phase 1 dose-escalation portion of the ongoing Phase 1–2a trial demonstratedthat EO1001 was generally well tolerated across dose levels from 2.5 mg to 90 mg once daily, withmostly Grade 1–2 gastrointestinal and dermatologic adverse events consistent with the ErbB inhibitorclass. Dose-limiting toxicities observed at higher dose levels were primarily gastrointestinal—specificallydiarrhea—aligned with the known safety profile of FDA-approved ErbB inhibitors. Pharmacokinetic datashowed dose-proportional exposure and identified 50 mg once daily as a biologically active dose alignedwith preclinical efficacy targets, and both the 50 mg and 70 mg dose levels are currently being evaluatedin an ongoing Phase 2a expansion cohort. Among patients treated at ≥50 mg daily, 10 of 14 evaluable participants achieved stable disease orpartial responses, including three partial responses. Several patients derived durable clinical benefit,with five continuing on therapy beyond six months in an extension protocol due to sustained tumorcontrol. Notably, patients with recurrent glioblastoma harboring EGFR extracellular domain mutations—includingEGFRvIII and A289 hotspot variants—experienced prolonged stable disease, consistent with preclinicalmodels showing rapid and efficient brain penetration with brain-to-plasma ratios exceeding 4:1 anddurable tumor retention. These data support the potential of EO1001 in genetically defined tumors withlimited effective treatment options. Edison Oncology is conducting the Phase 1–2a clinical trial under the terms of its collaboration andlicensing agreement with Apollomics, Inc., through which Apollomics is providing funding for the studywhile Edison retains responsibility for trial execution and oversight. Edison Oncology also presented new mechanistic and preclinical findings for EO4426, a next-generationcytidine analog designed to overcome cytidine deaminase (CDA)-mediated inactivation, a key metabolicresistance mechanism driving poor outcomes in multiple solid tumors. EO4426 retains activation bydeoxycytidine kinase and maintains its ability to inhibit both DNA polymerase-α and ribonucleotidereductase, sustaining replication-fork collapse even in highly resistant tumor environments. In comparative preclinical biochemical studies, EO4426 was shown to be ~30-fold more resistant to CDAmediated degradation than gemcitabine, enabling potent antitumor activity in CDA-high cancers such asnon-small cell lung cancer (NSCLC), triple negative breast cancer (TNBC), ovarian cancer, and head andneck squamous cell carcinoma. Across multiple intracranial and systemic tumor models—including GBM, neuroblastoma, and metastaticTNBC—EO4426 delivered significant survival extension, robust intracranial tumor control, and durablecomplete responses. In neuroblastoma models, EO4426 achieved up to 90% long-term survival,outperforming standard agents such as BCNU. Particularly compelling was the drug’s activity in mesenchymal (MES) GBM, a subtype associated withAPOBEC3G-driven replication stress and high metabolic turnover. EO4426’s brain penetration andresistance to CDA inactivation position it as a differentiated treatment option for tumors defined bygenomic instability, replication stress, and metabolic resistance, where standard chemotherapies oftenfail. Edison Oncology is undertaking a coordinated development strategy for both programs: EO1001 dose expansion at 50 mg and 70 mg daily is underway to refine the recommended Phase 2 dose and deepen evaluation of early clinical activity. EO4426 is advancing toward clinical re-initiation with GMP manufacture of drug product. Planning is ongoing for Phase 1b/2 trials targeting CDA-high metastatic tumors. Translational studies across both programs will integrate biomarker analyses and combinationtherapy strategies. “These data highlight the strength of our platform and the momentum behind our clinical and translational pipeline,” said Jeffrey A. Bacha, CEO of Edison Oncology. “EO1001 continues to show early signs of durable clinical activity, including in genomically defined glioblastoma subtypes that have been historically insensitive to ErbB inhibitors. EO4426, with its dual mechanism and resistance to CDA inactivation, represents a differentiated approach for tumors driven by extreme replication stress. Together, these programs are designed to address some of the most challenging and underserved segments of oncology.” Edison Oncology Holding Corp. is a clinical-stage biopharmaceutical company developing a pipeline of first-in-class, small-molecule, biomarker-driven therapies designed to overcome key resistance mechanisms and address critical unmet needs in aggressive and underserved cancers. Leveraging existing clinical data and a modern understanding of cancer biology, the company focuses on genetically defined cancers, advancing its programs through a capital-efficient combination of internal development and strategic partnerships while retaining meaningful development and commercial rights. To learn more, please visit https://www.edisononcology.com/ and follow us for updates on LinkedIn. Brett MaasHayden IR(646) 536-7331brett@haydenir.comJames CarbonaraHayden IR(646)-755-7412james@haydenir.com Download PDF here Society for NeuroOncology: EO-4426: A Brain-Penetrant Dual DNA Polymerase α and Ribonucleotide Reductase Inhibitor for High-Grade Gliomas and Other Aggressive Cancers Society for NeuroOncology: Phase 1 Dose Escalation of EO1001, an Oral Brain-Penetrating Pan-ErbB Inhibitor, in Advanced Cancer: Preliminary Results from an Ongoing Phase 1–2a Clinical Trial