Dizal announced that it will present research findings on two of its first-in-class hematologic oncology assets?golidocitinib and DZD8586?at the 2025 European Hematology Association (EHA) Annual Congress and the 18th International Conference on Malignant Lymphoma (ICML). These include long-term follow-up data on golidocitinib as a maintenance therapy in peripheral T-cell lymphoma (PTCL) after first-line systemic therapy and pooled analysis results for DZD8586 in chronic lymphocytic leukemia /small lymphocytic lymphoma (CLL/SLL), both selected for oral presentations at ICML. olidocitinib Shows Potential to Significantly Improve Patient Outcomes in PTCL: PTCL patients who achieved tumor response with first-line standard therapy will relapse.
Approximately 40% of patients with complete response and 80% with partial response experienced disease progression within 2 years after initial tumor response, and the prognosis of these relapsed patients was very poor. The 24-month follow-up results from JACKPOT26, a prospective, multicenter Phase 2 clinical study of golidocitinib will be unveiled at EHA and featured as an oral presentation at ICML. The data suggest that golidocitinib showed promising efficacy in maintaining and enhancing tumor response with an acceptable and manageable safety profile in patients with PTCLs post first-line therapies.
In Cohort 1 (patients with complete response), the 24-month disease-free survival (DFS) rate reached 74.2%, with consistent efficacy observed across different subtypes. In Cohort 2 (patients with partial response), the complete response rate (CRR) was 50.0%, the median duration of response (DoR) was 23.9 months, and the median progression-free survival (PFS) was 17.4 months, with the longest PFS reaching 35.9 months and the patient was still responding. In addition, golidocitinib has shown encouraging antitumor activities and favorable safety profiles in combination with CHOP in 1st line PTCL patients, as well as in rare T-cell lymphoma subtypes, including relapsed/refractory T-cell large granular lymphocytic leukemia (r/r T-LGLL) and monomorphic epitheliotropic intestinal T-cell lymphoma (MEITL).
Further studies are warranted to validate the results. DZD8586 Overcomes Multi-Drug Resistance in CLL and other B-NHL: A pooled analysis of two phase I/II studies of DZD8586 in CLL/SLL patients previously treated with covalent/non-covalent Bruton's Tyrosine Kinase (BTK) inhibitors and BTK degraders was presented in an oral session at the 2025 American Society of Clinical Oncology (ASCO) Annual Meeting and will be presented at EHA. Subgroup analyses will be presented as an oral presentation at ICML.
In heavily pretreated CLL/SLL, DZD8586 achieved an ORR of 84.2%. Tumor response with a manageable safety profile was observed irrespective of prior covalent/non-covalent BTKi, BTK degrader, or BCL-2 inhibitor treatment, and in patients with classic BTK resistance mutations (C481X) as well as other BTK mutations, including kinase-dead mutations. No drug-related bleeding, atrial fibrillation, or major cardiac events observed.
A Phase II study of DZD8586 monotherapy in relapsed/refractory diffuse large B-cell lymphoma (r/r DLBCL) will also be presented at EHA and ICML. Clinical activities from small molecule targeted drugs such as BTK inhibitors have been less than desired for the treatment of DLBCL. Compensatory or redundant pathway activation could be one of the main escape mechanisms. DZD8586, a novel LYN/BTK dual inhibitor, is designed to overcome these limitations by blocking both BTK and LYN signaling pathways, and thus potentially improve therapeutic outcomes.
At recommended phase 2 doses (RP2Ds) of 50 mg and 75 mg QD, DZD8586 monotherapy demonstrated promising anti-tumor activity in r/r DLBCL. The majority of patients showed target lesion shrinkage, with a CRR of 35.5%. Complete responders showed durable responses, with 81.8% of patients remaining in response and the median DoR was not reached.
Notably, it showed efficacy in both GCB and non-GCB subtypes, supporting its broad therapeutic potential.
