Tigris Pharmaceuticals Presents Results of Breast Cancer Research at AACR Annu...( BONITA SPRINGS Fla. April 30 /- Tigri...)

BONITA SPRINGS, Fla., April 30 /PRNewswire/ -- Tigris Pharmaceuticals, Inc., a privately held drug development company, announced that preclinical data were presented on its novel molecule, AFP-464, during the recent AACR 100th Annual Meeting 2009 in Denver. "This research represents a significant advancement in the treatment of Triple Negative Breast Cancer, one of the most aggressive forms of invasive breast cancer," stated Edmundo Muniz, M.D., Ph.D., President and Chief Executive Officer of Tigris.

Sponsored by Tigris, the research was led by Angelika Burger, Ph.D., director of the Translational Research Laboratory at the Barbara Ann Karmanos Cancer Institute and professor of Pharmacology at Wayne State University School of Medicine in Detroit. The research found that the luminal (ER-positive) and the triple negative (ER, PR, and HER-2 negative) breast cancer cell lines with the basal A gene profile subtype were very sensitive to AFP-464, while the triple negative cell lines with the basal B subtype were not. However, when the latter was pre-treated with a histone deacetylase inhibitor, such as the suberoylanilide hydroxamic acid (SAHA), also known as vorinostat (Zolinza(R), Merck & Co. Inc.), the cells became very sensitive to AFP-464. The mechanism in which this is achieved is believed to be the de-silencing of ER expression by the histone deacetylase inhibitor, followed by CYP1A1 induction and subsequent AFP metabolism into active species that covalently bind to DNA in these cancer cells and cause specific cell death.

Dr. Burger said the findings offer particular hope to those women battling triple-negative breast cancer. "We could now find a way to treat every kind of invasive, metastatic breast cancer, the ER-positive and ER-negative types with AFP-464," said Dr. Burger. "The synergism between AFP-464 and vorinostat in the triple negative breast cancer cell lines is very impressive."

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