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Reduction In Lung Fibrosis With The Anti-Galectin Drug GR-MD-02 Revealed In Preclinical Data

NORCROSS, Ga., Aug. 5, 2013 (GLOBE NEWSWIRE) -- Galectin Therapeutics (Nasdaq:GALT), the leading developer of therapeutics that target galectin proteins to treat fibrosis and cancer, today announced new preclinical data on the efficacy of anti-galectin therapy for lung fibrosis using a model that simulates the human disease idiopathic pulmonary fibrosis. In this model, treatment with GR-MD-02 showed a robust effect in reducing lung fibrosis, with somewhat lesser effect of GM-CT-01.

"These data extend the potential therapeutic use of our galectin inhibitors, and in particular GR-MD-02, into idiopathic pulmonary fibrosis, a chronic progressive disorder resulting in lung scarring and ultimately lung failure," said Peter G. Traber, MD, President, Chief Executive Officer and Chief Medical Officer, Galectin Therapeutics Inc. "These findings, taken together with others, show the broad potential of GR-MD-02 for treating organ fibrosis, which positions us to now develop partnerships with companies focused on idiopathic pulmonary fibrosis, while we continue our focus on development for the treatment of liver fibrosis."

"The galectin inhibitor GR-MD-02 had a robust effect on reducing lung fibrosis in this mouse model," said Dr. Gregory Lyng, Director of Research, Biomodels, LLC. "The treatment effects observed with GR-MD-02 are greater than those typically reported with commercially available pirfenidone and similar to the magnitude of response observed with anti-TGF-b antibody therapy in similar pre-clinical studies."

In the preclinical studies, lung fibrosis was induced in mice by the intra-tracheal instillation of bleomycin, a standard model in the pharmaceutical industry for simulating human disease and testing potential therapeutic agents. The two preclinical studies were performed in collaboration with Biomodels in Watertown, Mass., which has extensive experience with this mouse model of lung fibrosis. After induction of lung fibrosis, treatment with two anti-galectin drugs, GM-CT-01 and GR-MD-02, was started either immediately after (prevention study) or ten days after (treatment study) intra-tracheal instillation of bleomycin. In the prevention study, both drugs markedly reduced lung weight and hydroxyproline content, with reduction of histological evidence of inflammation and fibrosis when compared to vehicle-treated bleomycin mice. In the treatment study, GR-MD-02 was more effective than GM-CT-01. These results suggest that further studies are warranted to evaluate taking GR-MD-02 into clinical development for the indication of idiopathic pulmonary fibrosis.

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