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Myrexis To Provide Update On The Company's Cancer Metabolism Inhibitor At Upcoming Scientific Meetings

SALT LAKE CITY, Sept. 16, 2010 (GLOBE NEWSWIRE) -- Myrexis, Inc. (Nasdaq:MYRX), a biotechnology company focused on discovering, developing, and commercializing novel treatments for cancer, today announced it will present a poster at the Cancer and Metabolism: Pathways to the Future meeting in Edinburgh, Scotland, as well as two additional posters at the 22 nd European Organisation for Research and Treatment of Cancer (EORTC), National Cancer Institute (NCI) and American Association for Cancer Research (AACR) Symposium on "Molecular Targets and Cancer Therapeutics" November 16-19, 2010, in Berlin, Germany.

The posters will highlight key findings from Myrexis' cancer metabolism inhibitor (CMI) program, including the Company's potential best-in-class Nampt inhibitor, MPC-9528, which is currently in preclinical IND studies and has demonstrated flexible dosing and dramatic tumor regression across multiple tumor types.  

Cancer & Metabolism: Pathways to the Future; Edinburgh, Scotland
Title:  MPC-9528, a cancer metabolism inhibitor, 
  demonstrates improved efficacy in a Naprt1 deficient 
  cancer xenograft model with co-administration of
  efficacy in a Naprt1 deficient nicotinic acid.
Date & Time:  September 20, 2010; 9AM - 5PM British Time (BT)
Poster Number:  10
22 nd EORTC-NCI-AACR Symposium on "Molecular Targets and Cancer Therapeutics"; Berlin, Germany
Title:  Anti-Tumor Activity of MPC-9528, GMX1778, and 
  APO866: Nampt Inhibitors of Three Structural Classes
Date & Time:  Nov 17, 2010; 12 PM – 2 PM Central European Time
Poster Number:  6LB
Title:  The Nampt inhibitor MPC-9528 and the PARP
  inhibitor olaparib synergize in killing a BRCA--
  deficient cancer cell line
Date & Time:  Nov 17, 2010; 12 PM – 2 PM CET
Poster Number:  7LB

About MPC-9528

MPC-9528 is an orally-bioavailable, small molecule Cancer Metabolism Inhibitor (CMI) discovered by Myrexis that is currently in preclinical development for the treatment of a variety of cancers.  MPC-9528 potently and selectively inhibits nicotinamide phosphoribosyltransferase, or Nampt, an enzyme critical for converting nicotinamide into nicotinamide adenine dinucleotide (NAD). Cellular processes such as glucose metabolism, DNA repair and gene expression require and consume NAD. Cancer cells have increased NAD requirements and are highly sensitive to NAD depletion.  Blocking the Nampt-NAD pathway severely inhibits cancer cell metabolism, resulting in energy deprivation and ultimately cell death. In non-clinical models, MPC-9528 causes dramatic tumor regressions across multiple tumor types. 

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