Amplia shows positive data in pancreatic cancer

Biotech News: An Australian company developing new approaches for the treatment of cancer and fibrosis, Amplia Therapeutics, announced its new data from the collaboration with Professor Paul Timpson of the Garvan Institute of Medical Research.

The new data show that Amplia’s Focal Adhesion Kinase (FAK) inhibitor AMP945 is able to improve the anticancer activity of combined gemcitabine and Abraxane in an animal model of aggressive pancreatic cancer.

Gemicitabine (original brand of Gemzar from Eli Lilly) and Abraxane (Specialised Therapeutics Australia) is a widely used first-line treatment for patients with pancreatic cancer. The new data shows that adding intermittent doses of Amplia’s AMP945 to this standard-of-care therapy increases survival by 27% in the aggressive KPC pancreatic cancer animal model.

This follows previous work showing that AMP945 enhances the activity of chemotherapy by increasing cell death and reducing cancer cell proliferation. The latest study shows that these effects translate into a survival benefit in an animal model of pancreatic cancer.

Commenting on the results, Professor Timpson noted “The pancreatic cancer cells used in this experiment are extremely aggressive, so showing any beneficial effect on survival is very encouraging. A 25% improvement in survival in this model is very impressive and a level of improvement that we rarely see.”

Dr. John Lambert, CEO of Amplia said “These data further underpin the rationale for our planned Phase 2 clinical trial in pancreatic cancer. Earlier data told us that adding AMP945 to gemcitabine and Abraxane increased cancer cell death and reduced proliferation, and this new data tells us that those effects actually translate into prolonged survival in this model. We are strongly encouraged by these results.”

Amplia is currently using recently raised capital for a range of essential activities required to initiate the Phase 2 clinical trial in pancreatic cancer patients towards the end of this year.