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Cylene Selected to Present CK2 Inhibitor Multiple Myeloma Data at American Society of Hematology Meeting

December 6, 2010 By Bio-Medicine.Org

SAN DIEGO, Dec. 6, 2010 /PRNewswire/ — Cylene
Pharmaceuticals, Inc. has been selected to present data describing
the activity of their first-in-class CK2 inhibitor at the 52nd
Annual Meeting of the American Society of Hematology (ASH), to be
held on December 4-7 in Orlando, FL, the company announced today.
 Kenna Anderes, VP Cancer Biology at Cylene, will discuss
research on targeting CK2, a protein kinase that is essential for
the progression of multiple myeloma but that has not been
previously exploited as an anticancer target.  As the only CK2
inhibitor to have entered clinical trials, Cylene’s pioneering
compound, CX-4945, represents a promising new therapeutic approach
to the treatment of this life-threatening blood cancer.

“The data from Kenna’s lab demonstrates the importance of CK2 as
a target for cancer therapeutics, validating our decision to move
CX-4945 into humans.  We take pride both in being the first to
take a CK2 compound into the clinic and in the recognition by ASH
of the importance of this groundbreaking research,” commented
William G. Rice, PhD, President and CEO of Cylene Pharmaceuticals.
 “The recently initiated trial in multiple myeloma is being
conducted by Farnoush Abar, MD and Richard Maziarz, MD at the
Oregon Health & Science University Knight Cancer Institute and
by investigators who are part of the US Oncology Research
nationwide network.  This trial is designed both to treat
patients and simultaneously to expand our understanding of the
precise role of CK2 in myeloma.  Molecular level
characterization of patient samples alongside their response to
CX-4945 will increase the likelihood that targeted treatment with
CX-4945 will address this large unmet medical need.”

The presentation schedule is:

Monday, December 6, 2010: 4:30 PM

Title: CX-4945, a Selective and Orally Biovailable
Inhibitor of Protein Kinase CK2 Inhibits PI3K/Akt, JAK-STAT and
NF-_

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SOURCE

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