BTK inhibitor PCI-32765 induces durable responses in relapsed or refractory chronic lymphocytic leukaemia/small lymphocytic lymphoma

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Published: 9 Jan 2012
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Prof Susan O’Brien - University of Texas MD Anderson Cancer Center, Houston

ASH 2011 Press conference: The Bruton’s Tyrosine Kinase (BTK) Inhibitor PCI-32765 Induces Durable Responses in Relapsed or Refractory (R/R) Chronic Lymphocytic Leukaemia/Small Lymphocytic Lymphoma (CLL/SLL): Follow-up of a Phase Ib/II Study

A recent update of a multicenter Phase Ib/II clinical trial concludes that the novel Bruton’s Tyrosine Kinase (BTK) inhibitor PCI-32765 may be an important new targeted treatment approach for patients with chronic lymphocytic leukemia (CLL). 

Tyrosine kinase enzymes are important targets for cancer research because they function as “on/off switches” in many cell functions and can signal cells to either maintain normal functioning or to grow uncontrollably, leading to cancer. BTK in particular is largely responsible for the signaling that drives normal B-cell development, making it a primary target for research on B-cell malignancies such as non-Hodgkin lymphoma (NHL). 

PCI-32765 is an orally-administered BTK inhibitor that induces apoptosis, or programmed cell suicide, and inhibits function of malignant B-cells. Earlier promising studies of PCI-32765 have shown that the compound may be highly active and tolerable in patients with CLL. 

The current analysis summarizes results of an ongoing study using PCI-32756 as a treatment for patients with relapsed CLL. Two cohorts of CLL patients were treated with PCI-32765 at doses of either 420 mg (n=27) or 840 mg (n=34) daily for 28-day cycles until they showed signs of disease progression. Nearly three-fourths (72%) of participating patients had at least one high-risk feature, indicating that they may not respond well to treatment.