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Biomira selects PX-866 as clinical development candidate and presents promising preclinical data at AACR
Biomira selects PX-866 as clinical development candidate and presents promising preclinical data at AACR.
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[{"type":"text","content":"\n\n\n\n-IND filing expected by end of 2007-\n\n\nEDMONTON, April 16 /CNW/ - Biomira Inc. (Nasdaq: BIOM) (TSX: BRA) today\nannounced that it has selected PX-866 as its next clinical development\ncandidate. PX-866 is an inhibitor of the phosphatidylinositol-3-kinase (PI3\nkinase)/ PTEN/AKT pathway, an important survival signaling pathway that is\nactivated in many types of human cancer, including glioblastoma. Preclinical\ndata presented this past weekend at the American Association of Cancer\nResearch (AACR) annual meeting demonstrate that PX-866 has activity in an\nintracranial model of glioma.\n\n\n"The preclinical data for PX-866, including those presented at AACR, are\nvery promising and warrant advancing this small molecule compound to clinical\ndevelopment," said Robert L. Kirkman, M.D., President and Chief Executive\nOfficer of Biomira. "The data presented this weekend are particularly\ncompelling, as they provide evidence of PX-866 activity in an intracranial\nmodel of glioma, a disease that accounts for 77 percent of all malignant brain\ncancers and is refractory to conventional therapies. We are in the process of\ncompleting preclinical studies designed to support the expected filing of an\ninvestigational new drug (IND) application for PX-866 later this year.\nExpanding and advancing our clinical pipeline is a key priority for Biomira,\nand we are on track to have four programs in clinical development by the end\nof 2007."\n\n\nPreclinical data presented at AACR by Dr. Dimpy Koul of The University of\nTexas M. D. Anderson Cancer Center (MDACC) (Abstract No.278) showed that\nPX-866 treatment resulted in growth inhibition in three different glioma cell\nlines. The magnitude of the inhibition depended on the status of PTEN in the\ncell lines, with PTEN-negative cells showing greater sensitivity to PX-866.\nTreatment with PX-866 inhibited activation of AKT and other downstream targets\nof PI3K. A dose-dependent increase in autophagy, a type of programmed cell\ndeath, was observed and PX-866 also inhibited invasive and angiogenic\ncapabilities of cultured glioma cells. In animals, PX-866 inhibited\nsubcutaneous tumor growth by 84 percent after 4 weeks of oral dosing and\nincreased median survival of animals with intracranial tumors. The authors\nconclude that PX-866 is a highly promising PI3 kinase inhi...