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CureFAKtor Pharmaceuticals Featured at University of Florida Innovation Showcase 2011

BUFFALO, N.Y., April 19, 2011 /PRNewswire/ -- Today, H. Shep Wild, President and Chief Executive Officer of CureFAKtor Pharmaceuticals, LLC, a privately-held biopharmaceutical company focused on the research and development of Focal Adhesion Kinase (FAK) inhibitors for cancer, provided a company overview to venture capital, pharmaceutical and biotechnology industry leaders at the Celebration of Innovation Showcase 2011 hosted by the University of Florida Office of Technology Licensing at the Hilton University of Florida Conference Center Gainesville.

The University of Florida Celebration of Innovation lets select start-up companies in life sciences, medical sciences and information technology present licensing, commercialization and investment opportunities generated as a result of the $678 million in research conducted at UF.

CureFAKtor's proprietary FAK technology platform may represent a significant breakthrough in the treatment of most solid tumors in that its unique mechanism of action disrupts the signaling of FAK in tumors by targeting specific protein to protein bindings.  CureFAKtor scientists first discovered FAK in human tumors approximately 20 years ago.  FAK is much like a force field that cocoons cancer cells and allows them to survive the effects of chemotherapy, radiation and other natural processes designed to execute aberrant cancer cells.  Since FAK is over-expressed in virtually all solid tumors, the technology has broad applicability in oncology.

More than 40 compounds have been identified that target FAK signaling sites.  In pre-clinical studies, lead compound CFAK-C4 demonstrated efficacy in a number of cancers including pancreatic, breast, advanced melanoma and neuroblastoma. The Company's second product candidate, CFAK-Y15 is being investigated for the treatment of lung, breast, pancreatic, neuroblastoma and colon cancer. The Company has promising results with CFAK-Y15 in vitro in lung cancer and glioblastoma.

CureFAKtor recently received Orphan Drug Designation by the U.S. Food and Drug Administration (FDA) for CFAK-C4 in combination with gemcitabine for the treatment of pancreatic cancer, a disease with the lowest survival rate of any cancer and limited patient treatment options, and is planning a Phase I clinical study in 2012.

"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 and metastasis," said H. Shep Wild.  "We have strong ties to the University of Florida Shands Cancer Center and we look forward to progressing this important research in order to help cancer patients."

CureFAKtor CFAK-C4 Research Results

CureFAKtor recently presented preclinical 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.  

In a poster presentation, CureFAKtor 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.

About Focal Adhesion Kinase (FAK)

Focal adhesion Kinase (FAK) is substantially over-expressed in many solid tumors. FAK operates by placing itself at the contact points between tumor cells and the extra cellular matrix that surrounds them. Studies by CureFAKtor and others found that in this role, FAK is an important facilitator for signals that cause tumor cells to survive, grow, and produce new blood vessels to sustain growth and travel to distant places within the body where they may establish new tumor sites. It also cocoons the tumor cells to protect them from the body's natural signaling mechanisms that would cause deviant tumor cells to be eliminated. In a similar fashion, FAK protects tumors from chemotherapeutic drugs and radiation, allowing the tumor cells to resist these therapies.

About CureFAKtor Pharmaceuticals

CureFAKtor Pharmaceuticals is a biopharmaceutical company focused on the research and development of Focal Adhesion Kinase therapies to prevent or treat cancer. CureFAKtor's investigational and combination therapy products target pancreatic, breast, colon, melanoma, lung and brain oncology disorders. CureFAKtor research is conducted at the Roswell Park Cancer Institute.  CureFAKtor is planning a Phase I clinical study of CFAK-C4 in combination with gemcitabine chemotherapy, the current standard of care for pancreatic cancer, in 2012.  Additional information about the company may be found at

Forward-Looking Safe Harbor Statement:

This press release contains forward-looking statements for CureFAKtor Pharmaceuticals that involve risks and uncertainties that could cause the Company's actual results to differ materially from the anticipated results and expectations expressed in these forward-looking statements. These statements are based on current expectations, forecasts and assumptions that are subject to risks and uncertainties, which could cause actual outcomes and results to differ materially from these statements.  

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SOURCE CureFAKtor Pharmaceuticals, LLC
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