Ann: ATX FAK Inhibitors Reduce Fibrosis in Animal Model of NASH, page-3

AMPLIA’S FAK INHIBITORS REDUCE FIBROSIS IN ANIMAL MODEL OF NASH
• AMP945 produces a statistically significant reduction in liver fibrosis
• Further evidence of broad-spectrum antifibrotic action of Amplia’s FAK inhibitors
• New data is expected to support Amplia’s future development and partnering programs
Melbourne, Australia: Amplia Therapeutics Limited (ASX: ATX), (“Amplia” or the “Company”, a
company developing new drugs for the treatment of cancer and fibrosis, is pleased to announce it has
received data from a successful pre-clinical study showing that both of Amplia’s proprietary Focal
Adhesion Kinase (FAK) inhibitors, AMP886 and AMP945, reduce fibrosis arising from the liver disease,
Non-Alcoholic Steatohepatitis (NASH). These data highlight the key role that FAK plays in the
underlying pathophysiology of multiple fibrotic diseases and is expected to open up new development
and partnering opportunities for the Company in the future.
NASH occurs when an accumulation of fat in the liver (called Non-Alcoholic Fatty Liver Disease, or
NAFLD) causes inflammation. This inflammation eventually leads to the build-up of fibrotic scar tissue
throughout the liver that can then lead to cirrhosis, and then primary liver cancer (HCC, or
hepatocellular carcinoma). It is estimated that approximately 5% of adults in the United States have
NASH. However, despite this significant unmet need, attempts to develop an effective therapeutic for
NASH have met with little success to date.
Both Amplia’s FAK inhibitors, AMP886 and AMP945, were tested by SMC Laboratories Inc (“SMC”,
Tokyo, Japan) using their proprietary STAM™ mouse model for NASH. This model replicates the
progression from fatty liver, to fibrotic liver, and then to liver cancer, and is considered to be the
animal disease model that best recapitulates the pathological attributes of NASH. Consequently, the
STAM™ model has been used by a number of companies trialling new therapeutic approaches to
treat NASH.
The Figure below shows that AMP945 delivered a statistically significant reduction in liver fibrosis. In
addition, both AMP886 and AMP945 produced a significant reduction in ER-TR7 and Alpha-SMA, two
key activators of liver fibrosis. Mice were treated with a negative control (vehicle), AMP886 or
AMP945, or a positive control drug called Telmisartan. ER-TR7 is a marker for fibroblasts which are the
cells that lay down collagen in fibrotic tissue. Alpha-SMA is a marker for the activation of fibroblasts