Sept. 5, 2012
/PRNewswire/ - Oncothyreon Inc. (Nasdaq: ONTY) today announced that an ongoing Phase 2 trial of PX-866 in patients with recurrent or metastatic castration-resistant prostate cancer will be expanded to include an additional group of up to 25 patients whose disease has begun to progress while receiving abiraterone (Zytiga®) and prednisone. PX-866 is Oncothyreon's small molecule compound designed to inhibit the activity of phosphatidylinositol-3-kinase (PI-3K), a component of an important cell survival signaling pathway.
The open label Phase 2 trial is being conducted by the NCIC Clinical Trials Group (NCIC CTG), Queen's University in
. The initial part of this trial (Part A) has enrolled approximately 36 of a planned 40 patients with progressive castration-resistant prostate cancer who have received no prior chemotherapy. Part A included an interim efficacy analysis after enrollment of the first 23 patients, which was met. Enrollment of Part B of the trial will commence following full enrollment in Part A. Part B will enroll patients who demonstrate disease progression while receiving abiraterone as evidenced by a rising prostate specific antigen (PSA). PX-866 will be administered in addition to continuing treatment with abiraterone and prednisone. The primary endpoint of each part of this single-arm screening trial is the proportion of patients with lack of disease progression at 12 weeks from the initiation of therapy with PX-866.
"We appreciate the support and interest of the NCIC CTG in PX-866, our novel, irreversible PI-3K inhibitor, as demonstrated by the expansion of this Phase 2 trial in prostate cancer," said
Robert L. Kirkman
, M.D., President and CEO of Oncothyreon. "This trial is an important component of our broad Phase 2 program for PX-866, intended to provide significant information to guide later stage development of this product candidate."
PX-866 is an irreversible pan inhibitor of the PI-3K/PTEN/AKT pathway, a critical cell signaling pathway that is activated in many types of human cancer. Aberrant activation and regulation of PI-3K is implicated in a large proportion of human cancers, where it leads to increased proliferation and inhibition of apoptosis (programmed cell death).