Osimertinib mesylate

Preclinical data for EO1001 an orally bioavailable, irreversible pan-ErbB inhibitor targeting EGFR extracellular domain (ECD) mutant solid tumors. Preclinical data for EO4426 (tezacitabine), an orally bioavailable brain-penetrant, dual inhibitor of DNA polymerase alpha (Pol α) and ribonucleotide reductase (RNR), targeting CDA-mediated resistance in solid tumors and mesenchymal GBM. Presentations’ highlight – Edison Oncology’s expanding precision oncology pipeline focused on biomarker-directed therapies for molecularly-defined patient populations with significant unmet need. MENLO PARK, CA / ACCESS Newswire / March 18, 2026 / Edison Oncology Holding Corp. (“Edison Oncology” or the “Company”) today announced the presentation of two posters at the upcoming American Association for Cancer Research (AACR) Annual Meeting 2026, taking place April 17-22, in San Diego, California. The presentations showcased Edison Oncology’s advancements in precision oncology, including EO1001, an irreversible pan-ErbB TKI with CNS penetration, and EO4426, a brain-penetrant dual inhibitor of DNA polymerase alpha (Pol α) and ribonucleotide reductase (RNR). “We are pleased to present these two programs at the AACR Annual Meeting, which together reflect Edison Oncology’s focus on developing biomarker-directed oncology targeted therapies for molecularly-defined patient populations with significant unmet need,” said Jeffrey A. Bacha, Chief Executive Officer, Edison Oncology Holding Corp. “EO1001 addresses the critical gap in treatment for EGFR extracellular domain mutant cancers and is currently being evaluated in clinical studies, while EO4426 targets the CDA-mediated resistance mechanisms that limit the efficacy of current cytidine-based therapies.” EO1001 EGFR extracellular domain (ECD) mutations, including EGFRvIII, A289 substitutions, R108 variants, and related structural alterations, drive ligand-independent EGFR activation and highly aggressive tumor biology. These mutations occur in head and neck, lung, and gastrointestinal cancers and glioblastoma (GBM), where they are associated with therapeutic resistance and poor patient outcomes. EGFR-ECD mutations are generally resistant to approved EGFR TKIs, including osimertinib, erlotinib, gefitinib, and afatinib, because the structural alterations lie outside the ATP-binding pocket and may preserve receptor signaling despite drug engagement. EO1001 is an orally bioavailable, irreversible pan-ErbB inhibitor designed to inhibit signaling from both wild-type and structurally altered ErbB receptors. Early signals of clinical activity in EGFR-ECD mutant GBM patients have been observed in an ongoing Phase 1-2a study (ANZCTR: ACTRN12620000583943), underscoring the need for mechanistic validation. To further investigate this, Edison Oncology initiated a focused, preclinical program assessing EO1001 activity in patient derived xenograft (PDX) tumor models harboring clinically relevant EGFR-ECD variants. Preliminary preclinical data from the program will be presented at the AACR Annual Meeting. This preclinical program will further explore mechanisms of EO1001’s activity in EGFR-ECD mutant cancers, providing support for biomarker-guided clinical development. EO4426 EO4426 (tezacitabine) is a novel brain-penetrant, deamination-resistant, cytidine analog that exhibits dual inhibition of both DNA polymerase-α (Polα) and ribonucleotide reductase (RNR), resulting in depletion of deoxynucleotide pools, replication-fork collapse, and accumulation of DNA damage in rapidly proliferating tumor cells. Unlike gemcitabine and hydroxyurea, EO4426 resists cytidine deaminase (CDA)-mediated inactivation. Tumors with high CDA expression such as mesenchymal GBM, TNBC, NSCLC, and ovarian cancer are predicted to exhibit heightened dependence on Polα/RNR function and may therefore be particularly susceptible to dual-targeting strategies. Prior nonclinical studies demonstrate that EO4426 retains activity in CDA-high tumor environments and is less susceptible to rapid deamination than gemcitabine. Historically, EO4426 has been evaluated in multiple third-party Phase I and Phase II trials, demonstrating a generally manageable safety profile with reversible myelosuppression reported as the principal dose-limiting toxicity and evidence of clinical activity in heavily pretreated solid-tumor populations. New data are being developed to support further investigation of EO4426 in biomarker guided clinical development strategies for CDA-high solid tumors. Preliminary results of these ongoing non-clinical studies will be presented at the meeting. Additional details on key presentations at AACR are available below and further information on the AACR Annual Meeting 2026 is available here. Title: Preclinical evaluation of EO1001 in EGFR-ECD mutant solid tumor models: Toward biomarker-directed therapy Date/Time: Tuesday April 21, 2026, 2:00-5:00PM PT Session: Poster, Experimental and Molecular Therapeutics, Tyrosine Kinase, Phosphatase, and Other Inhibitors Abstract Number: 5889 Title: Overcoming cytidine deaminase (CDA) mediated resistance via EO4426 dual DNA-replication targeting: Implications for CDA-high solid tumors and mesenchymal GBM Date/Time: Wednesday April 22, 2026, 9:00AM – noon PT Session: Poster, Experimental and Molecular Therapeutics, Novel Antitumor Agents Abstract Number: 7102 About Edison Oncology Holding Corp. 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 Edison Oncology 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. Contact Hayden IR Brett Maas (646) 536-7331 brett@haydenir.com or James Carbonara (646)-755-7412 james@haydenir.com SOURCE: Edison Oncology Holding Corp. View Original Press Release Here Edison Oncology to Present Two Posters at the 2026 AACR Annual Meeting Society for NeuroOncology: EO-4426: A Brain-Penetrant Dual DNA Polymerase α and Ribonucleotide Reductase Inhibitor for High-Grade Gliomas and Other Aggressive Cancers

California-based EpiBiologics has posted details of a Phase I clinical trial (NCT07462377) for EPI-326, a tissue-selective bispecific antibody targeting EGFR in patients with locally advanced or metastatic EGFR-mutant non-small cell lung cancer (NSCLC) and head and neck squamous cell carcinoma (HNSCC). EPI-326 is designed to trigger lysosomal degradation of EGFR rather than block its activity. The antibody binds EGFR and a second cell-surface receptor enriched in tumor tissue, promoting internalization and breakdown of the receptor. EpiBiologics describes the approach as extracellular targeted protein degradation, an antibody-based strategy intended to remove disease-driving proteins from the cell surface. The molecule was developed using the company’s EpiTAC platform, which traces to work from UCSF chemist Jim Wells. EpiBiologics raised USD 107 million in Series B financing in 2026, co-led by GV and Johnson & Johnson Innovation. The open-label, multicenter, sequential dose-escalation study plans to enroll approximately 110 adults with confirmed NSCLC harboring any documented EGFR mutation, or pathologically confirmed HNSCC. Disease must be locally advanced or metastatic. The study, set to initiate in Q2 2026, will assess safety, dose-limiting toxicities, PK/PD, and aim to establish maximum dosing. Primary completion is estimated for Q3 2029. Sites include MD Anderson Cancer Center in Houston, Sarah Cannon Research Institute in Nashville, START centers in San Antonio and Los Angeles, and Astera Cancer Care in New Jersey. Research context EPI-326’s mechanism diverges from existing EGFR-directed therapies in two respects. First, by inducing degradation of the EGFR protein rather than inhibiting its enzymatic function, the molecule eliminates both kinase-dependent and kinase-independent survival signaling, a limitation of small-molecule TKIs such as osimertinib, erlotinib, and afatinib. Second, the bispecific format engages a second receptor that is enriched in tumor tissue, which in principle confines EGFR degradation to malignant cells and spares normal epithelia in skin and gut, the tissues responsible for the rash and diarrhea that constrain dosing of every approved EGFR-targeting agent. The EpiTAC platform from which EPI-326 emerged traces to academic work on engineered bispecific constructs that co-opt surface receptors for targeted degradation. EGFR-mutant NSCLC remains one of the most intensively targeted areas of oncology drug development. AstraZeneca’s osimertinib (Tagrisso) remains the leading first-line therapy, while Johnson & Johnson’s amivantamab (Rybrevant) targets both EGFR and MET signaling using a bispecific antibody approach. Other programs are exploring alternative strategies, including antibody-drug conjugates such as patritumab deruxtecan, which targets HER3, and next-generation EGFR inhibitors designed to overcome resistance mutations. In head and neck cancer, the EGFR-directed pipeline is smaller. Cetuximab remains the only approved anti-EGFR antibody, while newer bispecific antibodies such as Merus’s petosemtamab are being tested in late-stage trials. If successful, EPI-326 could represent a different approach by eliminating EGFR protein rather than inhibiting its signaling, potentially offering activity across multiple EGFR mutation types. Leave a Reply Cancel reply Your email address will not be published. Required fields are marked * Comment * Name * Email * Website