Fibrosis

When an internal organ is exposed to chronic disease, one of the responses is that scar tissue is laid down in the organ. Fibrosis is the development of this excess fibrous connective tissue, such as collagen and other proteins plus cellular elements like myofibroblasts, in an organ. The longer the disease affects the organ, the more fibrous tissue is deposited and this ultimately results in the failure of the organ.

This chronic fibrosis of organs may occur in the liver, lung, kidney, heart as well as others and, as a result, fibrosis of organs has been estimated to account for as much as 45 percent of all mortality. One of the exciting scientific findings of the last few years is that the galectin-3 protein is critically important in this fibrotic process in multiple organs.

Galectin Therapeutics’ drug candidates provide a promising and exciting new approach for the treatment of fibrotic diseases. When the fibrotic tissue becomes confluent, it obliterates the cellular architecture, leading to scarring and dysfunction of the underlying organ.


Liver fibrosis



We believe that our drug candidates have the potential to treat nonalcoholic steatohepatitis (NASH, or fatty liver disease) and other forms of liver fibrosis. Scientific evidence strongly suggests that galectin-3 is essential for the development of liver fibrosis in animals. Published data show that mice lacking the galectin-3 gene, and thus unable to produce galectin-3, are incapable of developing liver fibrosis in response to toxic insult to the liver (Henderson 2006) and in fatty liver disease (Iacobini 2010).

Read more about liver fibrosis and Galectin Therapeutics’ data in liver fibrosis, including fatty liver disease and toxin-induced liver fibrosis.


Lung fibrosis



Galectin Therapeutics believes that our drug candidates may play a role in the treatment of lung fibrosis, and in particular Idiopathic Pulmonary Fibrosis in humans. Preclinical studies have examined the effects of galectin-3 protein in pulmonary fibrosis, and have identified galectin-3 as an important regulator of lung fibrosis (MacKinnon 2012).

Read more about lung fibrosis and Galectin Therapeutics’ data in lung fibrosis.


Kidney fibrosis



We believe our drug candidate GR-MD-02 may have therapeutic effects on kidney fibrosis, particularly in reversing diabetic nephropathy.

Read more about kidney fibrosis and Galectin Therapeutics’ data in kidney fibrosis.