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Myrexis Presents Key Findings From Its Cancer Metabolism Inhibitor, MPC-9528

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). 

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