Bruton tyrosine kinase inhibitor ibrutinib (PCI-32765)

JA Burger, JJ Buggy - Leukemia & lymphoma, 2013 - Taylor & Francis
JA Burger, JJ Buggy
Leukemia & lymphoma, 2013Taylor & Francis
Over the past 3 years, ibrutinib (PCI-32765) has emerged as a breakthrough in targeted
therapy for patients with certain types of B cell malignancies. Early stage clinical trials found
ibrutinib to be particularly active in chronic lymphocytic leukemia (CLL) and mantle cell
lymphoma (MCL), providing the rationale for ongoing phase 3 trials. In contrast to
conventional chemo-immunotherapy, ibrutinib is not myelosuppressive, and responses are
not affected by disease features that predict failure to respond to or short remission durations …
Abstract
Over the past 3 years, ibrutinib (PCI-32765) has emerged as a breakthrough in targeted therapy for patients with certain types of B cell malignancies. Early stage clinical trials found ibrutinib to be particularly active in chronic lymphocytic leukemia (CLL) and mantle cell lymphoma (MCL), providing the rationale for ongoing phase 3 trials. In contrast to conventional chemo-immunotherapy, ibrutinib is not myelosuppressive, and responses are not affected by disease features that predict failure to respond to or short remission durations after chemo-immunotherapy, such as del17p. In CLL, ibrutinib characteristically causes an early redistribution of tissue-resident CLL cells into the blood, with rapid resolution of enlarged lymph nodes, along with a surge in lymphocytosis. Later, after weeks to months of continuous ibrutinib therapy, the growth- and survival-inhibitory activities of ibrutinib result in the normalization of lymphocyte counts and remissions in a majority of patients. This review discusses the discovery, preclinical and clinical development of ibrutinib, its pathophysiological basis, and outlines perspectives for future use of ibrutinib.
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