Galectin Therapeutics Inc. (OTC: GALT), the leader in developing carbohydrate-based therapeutic compounds to inhibit galectin proteins, today announced that it presented a poster at the European Association for the Study of the Liver (EASL) Special Conference on Liver Transplantation in Lisbon, Portugal. The data show that galectin inhibitor candidate GR-MD-02 reversed fibrosis in mouse models of steatohepatitis and prevented collagen deposits in groups treated before fibrotic cells were present. The data suggest that patients with non-alcoholic steatohepatitis (NASH), also referred to as fatty liver disease, may benefit from galectin inhibition and that GR-MD-02 could drive in a reduction of steatosis, necrosis, inflammation and collagen deposits. Currently, liver transplantation is the only option for patients afflicted with liver fibrosis or cirrhosis, and many times the condition recurs in the patient’s new liver, creating the need for a safer and more efficacious treatment. The data presented provide promising evidence for advancing GR-MD-02 into clinical studies for the treatment of NASH.

“Galectin Therapeutics has previously demonstrated the robust ability of our galectin inhibitor compounds to arrest and reverse liver fibrosis in preclinical studies,” said Dr. Peter G. Traber, President, Chief Executive Officer and Chief Medical Officer, Galectin Therapeutics. “We have now expanded that data to include promising results in preclinical models of NASH, offering hope that a new treatment option could be on the horizon and expanding the potential indications for Galectin Therapeutics to pursue in the clinic. The broad effect of GR-MD-02 on all parameters of NASH liver injury, including fat deposition, liver cell death, inflammation, and fibrosis makes this a particularly attractive drug candidate.”

The data presented at EASL Special Conference highlight two carbohydrate-based galectin inhibitors, GM-CT-01 and GR-MD-02, in preclinical mouse models of steatohepatitis. Mice are injected with streptozotocin to induce diabetes and then fed a high fat diet. Subsequently, these mice develop fatty liver (steatosis), liver cell death, inflammation between 5 weeks of age, and then, fibrosis by 9 weeks of age. To assess the ability of galectin inhibitors to prevent or reduce fibrosis, mice were separated into early or late treatment groups. Early treatment groups began receiving either GM-CT-01 or GR-MD-02 twice daily at 6 weeks of age, or before fibrosis is evident, until 9 weeks of age. Late treatment groups received either GM-CT-01 or GR-MD-02 twice daily at 9 weeks of age, or when fibrosis is established, until 12 weeks of age. GR-MD-02 demonstrated greater improvements in steatosis, hepatocellular degeneration and inflammation. In the early treatment group, GR-MD-02 prevented the development of collagen deposition, or fibrosis, and was able to completely reverse fibrosis in the late treatment group back to levels of normal mice. GM-CT-01 did show a moderate effect on reducing collagen deposition. Importantly, GR-MD-02 was able to reverse steatohepatitis and fibrosis without having an effect on the diabetic condition of the mice. To view the complete poster presentation, please go to the Galectin Therapeutics’ web site at

About NASH

NASH is a common disease of the liver, affecting 9 to 15 million people in the United States and is characterized by the presence of fat in the liver along with inflammation and damage in people who drink little or no alcohol. Over time, patients with NASH can develop fibrosis, or scarring of the liver, that can lead to cirrhosis, a severe liver disease where transplantation is the only current treatment available. Galectin Therapeutics is developing drug candidates as an alternative to transplantation and lead candidates have reversed fibrosis in preclinical disease models.

About Galectin Therapeutics

Galectin Therapeutics (OTC: GALT) is developing promising carbohydrate-based therapies for fibrotic liver disease and cancer based on the Company’s unique understanding of galectin proteins, key mediators of biologic function. We are leveraging extensive scientific and development expertise as well as established relationships with external sources to achieve cost effective and efficient development. We are pursuing a clear development pathway to clinical enhancement and commercialization for our lead compounds in liver fibrosis and cancer. Additional information is available at

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