For patients whose Chronic Lymphocytic Leukemia (CLL) has either returned or prior treatments stopped working, zanubrutinib a chemo-free BTK inhibitor treatment proved to be significantly better than one of the original BTK inhibitors ibrutinib at limiting cancer progression (progression-free survival (PFS)) and having fewer side effects (specifically fewer heart side effects that have been a common issue with ibrutinib).

This was also true for CLL patients that have the chromosome 17p deletion and/ or the TP53 mutation who typically struggle to find treatment success after other therapies have failed. Zanubrutinib is FDA approved for patient use. Jennifer R. Brown, MD, PhD, of the Dana-Farber Cancer Institute and Harvard University, presented the data from the ALPINE study sponsored by BeiGene during the recent American Society of Hematology (ASH) December 2022 conference. The data was also published in The New England Journal of Medicine. 

Patient health-related quality of life during treatment

At several intervals during the clinical trial, patients were provided surveys to assess their health-related quality of life status including physical and role functions as well as negative symptoms such as diarrhea, fatigue, nausea/vomiting, and pain. Patients taking zanubrutinib reported better health-related quality of life during treatment than those taking ibrutinib (jnccn230.org). 

More about the study

Starting in December 2020, 652 patients from 15 countries with relapsed or refractory CLL/SLL were divided into two groups to compare the effectiveness of BTK inhibitors zanubrutinib and ibrutinib. Half of the participants were given zanubrutinib orally at 160 mg twice daily and the other half were given ibrutinib orally at 420 mg once daily.

The below data is up to August 2022. PFS is progression-free survival meaning the cancer did not progress for patients during treatment. 

The study is ongoing and will wrap up in September 2023. The researchers are continuing to review CLL patient data including those with chromosome 17p deletion, TP53 mutation, complex karyotype, and other mutations.