BAY 43-9006 Shown to Delay Disease Progression in Phase III Study in Advanced Kidney Cancer Patients
Monday March 21, 2:00 am ET
Study met surrogate endpoint
WEST HAVEN, Conn. and EMERYVILLE, Calif., March 21 /PRNewswire-FirstCall/ -- Bayer Pharmaceuticals Corporation (NYSE: BAY - News) and Onyx Pharmaceuticals, Inc. (Nasdaq: ONXX - News) today announced that an independent data monitoring committee (DMC) has reviewed the safety and efficacy data from the companies' pivotal Phase III trial in patients with advanced kidney cancer. Based on its analysis, the DMC has concluded that the trial met its surrogate endpoint -- resulting in statistically significant longer progression-free survival in those patients administered BAY 43-9006 versus those patients administered placebo. As a result of this favorable outcome, Bayer and Onyx plan to prepare a New Drug Application for possible accelerated approval in the United States.
As previously agreed with the U.S. Food and Drug Administration (FDA), the two companies will continue the Phase III study as originally planned to its primary endpoint of overall survival. Bayer and Onyx also intend to submit data from the Phase III study for the upcoming American Society of Clinical Oncology meeting, May 13-17, in Orlando, Florida.
Phase III Summary
The multi-national, placebo-controlled Phase III study recently finished enrolling over 800 patients with advanced kidney cancer. The primary endpoint of the study is overall survival, with disease progression, overall response rate, and safety also being assessed. The pivotal trial was initiated in the fourth quarter of 2003 after a Special Protocol Assessment (SPA) was completed by the FDA.
About BAY 43-9006
BAY 43-9006, a novel investigational drug candidate, has demonstrated both anti-proliferative and anti-angiogenic properties -- two important anticancer activities. In preclinical models, BAY 43-9006 inhibited tumor cell proliferation by targeting the RAF/MEK/ERK signaling pathway at the level of RAF kinase. BAY 43-9006 also exerted an antiangiogenic effect by targeting the receptor tyrosine kinases VEGFR-2 and PDGFR and their associated signaling cascades. In addition, BAY 43-9006 also inhibited other tyrosine kinases, including FLT-3 and c-KIT.
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