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Data from In Vivo Disease Models on Taligen Therapeutics' Pipeline Candidates to be Presented at the XXII International Complement Workshop
Date:9/25/2008

Presentations Include Proof-of-Concept Animal Data on Previously Disclosed Fusion Protein TT30 and New Molecules TT32 and mAb171

CAMBRIDGE, Mass., Sept. 25 /PRNewswire/ -- Taligen Therapeutics Inc. today announced that data from in vivo disease models on several of the company's pipeline candidates will be presented next week at the XXII International Complement Workshop in Basel, Switzerland.

The data, which will be presented in eight oral and poster presentations, are the results of research conducted by the laboratories of Michael Holers, M.D., chief scientific officer of Taligen, and the company's academic collaborators in the complement research community. Five studies testing the company's fusion protein TT30 and two new compounds, a fusion protein TT32 and a monoclonal antibody mAb171, in animal models are highlighted below. These data further support Taligen's approach that targeting the alternative complement pathway can impact complement-mediated inflammatory disease processes.

Poster Presentations:

TT30

Targeted inhibition of the alternative pathway by CR2-fH fusion protein ameliorates progression of renal disease in MRL/lpr mice

Hideharu Sekine*, Gary Gilkeson, Stephen Tomlinson

Oct. 1, 2008, Posters - 10:30 a.m. - noon, Session 2, Poster 174

Alternative complement pathway signaling in a mouse model of choroidal neovascularisation

Barbel Rohrer*, Qin Long, Brooks Wilson, Beth Coughlin, Yuxiang Huang, Fei Qiao, Peter Tang, Kannan Kunchithapautham, Gary Gilkeson, Stephen Tomlinson

Oct. 1, 2008, Posters - 10:30 a.m. - noon, Session 2, Poster 202

TT30 and TT32

Targeted complement-inhibitory proteins CR2-Crry and CR2-fH ameliorate allergen-induced airway hyperresponsiveness and inflammation

Joshua Thurman*, Katsuyuki Takeda, Stephen Tomlinson, Erwin Gelfand, V. Michael Holers

Oct. 1, 2008, Posters - 10:30 a.m. - noon, Session 2, Poster 171

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SOURCE Taligen Therapeutics Inc.
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