AI Article Synopsis
- The discovery of the MYD88 (L265P) mutation prompted studies into BTK inhibitors for treating Waldenström macroglobulinemia (WM).
- Ibrutinib was the first BTK inhibitor approved following positive results from a phase II trial for patients who had relapsed or were refractory to treatment.
- The iNNOVATE study tested the effectiveness of ibrutinib with rituximab versus rituximab alone in various patient groups, while the ASPEN trial compared zanubrutinib with ibrutinib specifically in patients with the MYD88 mutation.
Article Abstract
The discovery of MYD88 (L265P) mutation led to investigating BTK inhibitors in Waldenström macroglobulinemia (WM). Ibrutinib, the first-in-class agent, was approved based on a phase II trial in relapsed/refractory patients. In the phase III iNNOVATE study, the combination of rituximab and ibrutinib was compared with rituximab and placebo in treatment-naïve and relapsed/refractory patients. Second-generation BTK inhibitor, zanubrutinib, was compared with Ibrutinib in MYD88-mutated WM patients in the phase III ASPEN trial, whereas acalabrutinib was investigated in a phase II trial. Here, we discuss the role of BTK inhibitors in treatment-naïve patients with WM based on currently available evidence.
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| http://dx.doi.org/10.1016/j.hoc.2023.04.005 | DOI Listing |
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