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TargeGen Announces Planned Initiation of Clinical Trial of JAK2 Inhibitor TG101348 in Myeloproliferative Disease Patients, and Presentations at ASH
Date:12/6/2007

SAN DIEGO, Dec. 6 /PRNewswire/ -- TargeGen, Inc. today announced that the Company's recently submitted IND for TG101348 is now active and the Company plans to initiate a multi-center clinical trial of TG101348, an internally discovered, oral, potent, and highly selective JAK2 inhibitor in January, 2008. Additionally, TargeGen announced that a series of presentations related to TG101348 will be made at the 2007 ASH Conference (Atlanta, December 8-11, 2007) by Company scientific staff and outside academic collaborators.
(Logo: http://www.newscom.com/cgi-bin/prnh/20030430/TARGEGENLOGO)

Scheduled ASH presentations include:

-- Catriona Jamieson -- Selective Inhibition of JAK2 Driven Erythroid

Differentiation of Polycythemia Vera

-- Animesh Pardanani & Ayalew Tefferi -- Primary Cell Experiments with

TG101348, A JAK2 Selective Small Molecule Inhibitor, in the Presence of

Myeloproliferative Disorder-Associated JAK2V617F, MPLW515K, or Exon 12

Mutations

-- Gerlinde Wernig & Gary Gilliland -- Efficacy of TG101348, a Selective

JAK2 Inhibitor, in Treatment of a Murine Model of JAK2V617F-Induced

Polycythemia Vera, Session Type

-- Betty Tam -- TG101348: A Dual Acting JAK2/FLT3 Small Molecule Kinase

Inhibitor for the Treatment of AML

-- John Hood -- Prospective Identification of Resistance Mutants to the

JAK2 Inhibitor TG101348

The V617F mutation of JAK2 is implicated in the pathogenesis of certain myeloproliferative diseases, including polycythemia vera (PV), essential thrombocytopenia (ET) and primary myelofibrosis (PMF). In preclinical models of myeloproliferative diseases, TG101348, administered orally, was shown to reduce to reduce V617F expressing cell populations in a dose-dependant manner without adversely impacting normal hematopoeisis. The reduction of V
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SOURCE TargeGen, Inc.
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