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Biomira Selects PX-866 as Clinical Development Candidate and,Presents Promising Preclinical Data at AACR

of programmed cell death, was observed and PX-866 also inhibited invasive and angiogenic capabilities of cultured glioma cells. In animals, PX-866 inhibited subcutaneous tumor growth by 84 percent after 4 weeks of oral dosing and increased median survival of animals with intracranial tumors. The authors conclude that PX-866 is a highly promising PI3 kinase inhibitor in glioblastomas and other tumors with aberrant PTEN/PI3K expression, which include advanced ovarian, breast and prostate cancers, as well as lung and head and neck cancers.

Dr. Koul and colleagues at MDACC conducted the studies in collaboration with Dr. Lynn Kirkpatrick, Biomira's Chief Scientific Officer, under a grant from the U.S. National Institutes of Health.

About PX-866

PX-866 is an inhibitor of the phosphatidylinositol-3-kinase (PI3 kinase)/PTEN/AKT pathway, an important survival signaling pathway that is activated in many types of human cancer. PI3 kinase is overexpressed in a number of human cancers, especially ovarian, colon, head and neck, urinary tract, and cervical cancers, where it leads to increased proliferation and inhibition of apoptosis (programmed cell death). In preclinical studies, PX-866 has been shown to induce prolonged inhibition of tumor PI3 kinase signaling following both oral and intravenous administration. The compound also has been shown to have good in vivo anti-tumor activity in tumor models of human ovarian and lung cancer, as well as intracranial glioblastoma.

About Biomira

Biomira is a biotechnology company specializing in the development of innovative therapeutic products for the treatment of cancer. Biomira's goal is to develop and commercialize novel synthetic vaccines and targeted small molecules that have the potential to improve the lives and outcomes of cancer patients.

Forward-Looking Statements

This press release contains forward-looking statements, including, without limitation, statements related to the pre-
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