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CureFAKtor Pharmaceuticals Demonstrates that Novel Focal Adhesion Kinase (FAK) Inhibitors Targeted to Protein-Protein Binding Sites Inhibit Pancreatic Cancer Cells Growth
Date:1/21/2011

BUFFALO, N.Y., Jan. 21, 2011 /PRNewswire/ -- CureFAKtor Pharmaceuticals, LLC, a privately-held biopharmaceutical company focused on the research and development of Focal Adhesion Kinase (FAK) inhibitors for cancer, today presented research results at the American Society of Clinical Oncology (ASCO) Gastrointestinal Cancers Symposium in San Francisco demonstrating that novel FAK inhibitors targeting the binding site of vascular endothelial growth factor receptor 3 (VEGFR-3) reduced the growth of pancreatic cancer cells in vitro and in vivo.  The research was conducted by CureFAKtor scientists at the Roswell Park Cancer Institute in Buffalo, together with the University of Florida Shands Cancer Center.

In a poster presentation, CureFAKtor Chief Scientific Officer Dr. William Cance and Senior Scientist Dr. Elena Kurenova reported that the study pinpointed the site of interaction of VEGFR-3 and FAK to create small molecule drugs capable of disrupting signaling and causing death of pancreatic cancer cells.  CureFAKtor's lead compound, CFAK-C4, reduced tumor growth in vivo in mouse pancreatic cancer cells by up to 60 percent, and CFAK-C4 combined with chemotherapy drug gemcitabine had a synergistic effect and led to 80 percent pancreatic cancer tumor reduction.  

The study also found that CFAK-C4 combined with gemcitabine had a prolonged effect on pancreatic tumor growth.  Two weeks after treatment, the tumor size in the previously treated group was approximately 75 percent smaller than the tumor in the control group. The researchers concluded that targeting FAK with small molecule inhibitors can be effectively used to develop potential oral-based cancer therapies.

"Focal Adhesion Kinase protein binding inhibitors, such as CFAK-C4, represent a promising area of research as FAK is expressed at extremely high levels in solid cancer tumors and serves as a survival mechanism by signaling tumor growth, invasion
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SOURCE CureFAKtor Pharmaceuticals, LLC
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