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Tragara Pharmaceuticals' Apricoxib Reverses EMT, a Key Process for Cancer Progression and Metastasis

Thu, 05/26/2011 - 10:33am
Bio-Medicine.Org

SAN DIEGO, May 26, 2011 /PRNewswire/ -- Tragara Pharmaceuticals, Inc. announced today that apricoxib (Capoxigem®, TG01), its novel COX-2 inhibitor in development for select cancer types, demonstrated reversal of the epithelial-mesenchymal transition (EMT) in xenograft models of several types of solid tumors. These data results were presented at the 2011 American Society for Clinical Oncology (ASCO) Gastrointestinal Cancers Symposium and the 2011 American Association for Cancer Research (AACR) Annual Meeting and demonstrate that apricoxib potently inhibits the activity of COX-2 and COX-2 derived prostaglandin E2 (PGE2), which in turn mediates EMT and the associated progression and metastasis of solid tumors.

"Reversal of EMT may provide several clinical benefits to patients with non-small cell lung cancer and pancreatic cancer," stated Sara Zaknoen, M.D., chief medical officer, Tragara Pharmaceuticals, Inc. "Patients may experience longer survival due to effects of EMT reversal on metastases and the cancer stem cell, and benefit from the reversal of resistance to drugs such as erlotinib."

Tragara has completed two phase II clinical trials of apricoxib. Results from the APRiCOT-L trial, a biomarker-based, phase II, randomized, placebo-controlled study of apricoxib in combination with erlotinib in non-small cell lung cancer, will be presented on June 6th at the ASCO meeting in Chicago. A second phase II study of apricoxib in combination with gemcitabine and erlotinib has completed enrollment and is currently being analyzed.

"COX-2 has been implicated in EMT, so we were gratified to see robust reversal of EMT resulting from apricoxib treatment in xenograft models of pancreatic, colon, and head and neck cancers," stated Francis Burrows, Ph.D., head of oncology biology, Tragara Pharmaceuticals, Inc.  "This effect was associated with profound inhibition of metastasis in orthotopic cancer models but, interestingly, apricoxib-mediated EMT re

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