SALT LAKE CITY, Sept. 20, 2010 (GLOBE NEWSWIRE) -- Myrexis, Inc. (Nasdaq:MYRX), a biotechnology company focused on discovering, developing, and commercializing novel treatments for cancer, today announced key findings from preclinical studies of the Company's novel cancer metabolism inhibitor (CMI), MPC-9528, at the Cancer and Metabolism: Pathways to the Future Symposium in Edinburgh, Scotland. Compelling preclinical evidence demonstrates that treatment with MPC-9528 results in significant tumor growth inhibition and that the co-administration of niacin improves the therapeutic index of MPC-9528. Additional data, from a large panel of tumor cell lines and primary human tumor tissue indicate that approximately 40% of all cancers may carry a biochemical defect making them respond well to the combination of niacin and MPC-9528 treatment. A simple companion diagnostic could be used to identify patients with such tumors. Key Findings: MPC-9528 is a potent and selective inhibitor In biochemical and cellular assays, MPC-9528 demonstrated picomolar potency for its target, Nampt (nicotinamide phosphoribosyltransferase). Tumoricidal activity is on target and effective against a wide rage of tumor cells. Co-administration of niacin (vitamin B3) improves MPC-9528's therapeutic index Myrexis demonstrated that co-administration of niacin (vitamin B3) could protect healthy cells from MPC-9528 activity, and that this protective effect was dependent on expression of the enzyme Naprt1. Niacin could not prevent MPC-9528-induced cell death in cancer cells that express little or no Naprt1. Expression of Naprt1 is deficient in approximately 40% of all cancers The Company evaluated 145 tumor cell lines across diverse cancer types and found Naprt1 deficiency to be common, affecting about 40% of the cell lines. MPC-9528 causes dramatic tumor regressions across multiple tumor types. In animal models, both Naprt1-proficient and Naprt1-deficient tumors responded to MPC-9528, demonstrating potent tumoricidal activity. However, greater tumor growth inhibition could be achieved in Naprt1-deficient tumors by adding niacin, which allowed MPC-9528 to be tolerated at doses greater than twice the typical maximum tolerated dose (MTD).