On April 1, 2025 Dizal (SSE:688192), a biopharmaceutical company committed to developing novel medicines for the treatment of cancer and immunological diseases, reported that results of its investigational drug candidates DZD8586 and DZD6008, have been selected for presentation at the 2025 American Society of Clinical Oncology (ASCO) (Free ASCO Whitepaper) Annual Meeting, taking place May 30 – June 3, 2025, in Chicago (Press release, Dizal Pharma, APR 1, 2025, View Source [SID1234651733]).
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Oral and poster presentations of its DZD8586 study results in chronic lymphocytic leukemia (CLL) and diffuse large B-cell lymphoma (DLBCL) are selected by ASCO (Free ASCO Whitepaper) Scientific Program Committee. In addition, Dizal will present its 4th generation EGFR TKI clinical data in non-small cell lung cancer (NSCLC) during the conference.
About DZD8586
DZD8586 is a first-in-class, non-covalent, LYN/BTK dual inhibitor with full blood-brain barrier (BBB) penetration, designed as a potential treatment option for B-cell non-Hodgkin lymphoma (B-NHL).
While Bruton’s Tyrosine Kinase (BTK) inhibitors have been approved for the treatment of B-NHL, resistance can arise through two major mechanisms: the BTK C481X mutation and BTK-independent BCR signaling pathway activation. Currently, there is no targeted therapy available to address both resistance mechanisms, posing an urgent clinical challenge. Although BTK degraders have shown encouraging efficacy in early clinical studies, mutation-related resistance has been reported, and degrader-related toxicities may affect long-term clinical application.
DZD8586 has high selectivity against other TEC family kinases (TEC, ITK, TXK and BMX). By targeting BTK and LYN, it blocks both BTK-dependent and -independent BCR-signaling pathways, effectively inhibiting tumor growth of B-NHLs in cell lines and in animal models. Phase I clinical trial suggests that DZD8586 exhibits favorable PK properties, good central nervous system (CNS) permeability, complete blockade of BCR signaling, and encouraging anti-tumor efficacy with good safety and tolerability in patients with B-NHL.
About DZD6008
DZD6008, is a novel, highly selective, full-BBB penetrant EGFR TKI, designed as a potential treatment option for advanced EGFR mutation positive (EGFRm) NSCLC.
Non-small cell lung cancer is the leading cause of cancer death in the world. Epidermal growth factor receptor (EGFR) gene is one of the most common driver genes for NSCLC. Multiple agents can be used to treat patients with EGFR mutated NSCLC who develop resistance to EGFR tyrosine kinase inhibitors (TKIs), but the clinical outcome was not satisfactory. Brain metastases (BM) are a leading cause of death and disease progression for NSCLC. Approximately 23%-30% of NSCLC patients are synchronous BM at their initial diagnosis. Previous studies reported that the 3-year cumulative rate of BMs ranges from 29.4% to 60.3% in patients with mutated EGFR.
Currently, the clinical benefits of existing treatments for third-generation EGFR TKI-resistant NSCLC are limited and DZD6008 is expected to fill the unmet medical needs. DZD6008 effectively inhibits EGFR-mutated tumor growth in cell lines and in animal models. Previous clinical studies have validated the design concept of the molecule and suggest that DZD6008 demonstrates good safety and efficacy in NSCLC patients with brain metastases who had failed third-generation EGFR TKI therapy or multiple lines of pre-treatments.