Galectin Therapeutics (NASDAQ: GALT), the leading developer of therapeutics that target galectin proteins to treat fibrosis and cancer, today presented new preclinical data on the mechanism of action of GR-MD-02 at the American Association for the Study of Liver Disease (AASLD) Annual Meeting in Boston, MA. GR-MD-02 is the Company’s lead galectin inhibitor in development for the treatment of non-alcoholic steatohepatitis (NASH), or fatty liver disease. These new data help to further explain the mechanism of action of GR-MD-02, showing that this galectin inhibitor affects multiple pathways involved with both the prevention and reversal of fibrosis in NASH pathology.
“The data presented at AASLD further elucidate the mechanism of how galectin inhibition affects liver fibrosis in preclinical models of disease, resulting in the prevention and reversal of fibrosis,” said Peter G. Traber, MD, President, Chief Executive Officer and Chief Medical Officer, Galectin Therapeutics. “As we continue to advance GR-MD-02 for the treatment of NASH with advanced fibrosis, we are hopeful that galectin inhibition could provide patients with a novel treatment option, where liver transplantation is currently the only therapy available. GR-MD-02 is expected to enter the clinic in the first quarter of 2013.”
The presentation, entitled “Galectin-3 targeting drugs inhibit multiple pathological pathways leading to improvement of non-alcoholic steatohepatitis (NASH)”, was authored by Peter G. Traber and Eliezer Zomer. As previously demonstrated, GR-MD-02 treatment in a mouse model of NASH resulted in marked improvement in liver histology with significant reduction in steatosis, ballooning and inflammation, as well as fibrosis, determined by Sirius red staining. This disease improvement upon treatment with GR-MD-02 was seen when animals were treated early in disease (disease prevention) or after fibrosis had been established (disease reversal).
The new data show that Galectin-3 protein expression was markedly increased in animals with NASH, and those levels were dramatically reduced to barely detectable levels following treatment with GR-MD-02. Elevated expression of iNOS, an important inflammatory mediator, and CD36, a scavenger receptor involved in the pathogenesis of NASH, were markedly reduced following treatment with GR-MD-02. Alpha-smooth muscle actin, a marker used to identify activated cells that cause liver fibrosis, showed increased numbers of cells in control livers, which was markedly reduced in livers treated with GR-MD-02. Together, these data suggest that GR-MD-02 works to prevent or reverse fibrosis in NASH by reducing galectin-3, which is associated with multiple pathogenic effects.