PDA

View Full Version : Ariad begins cancer study of AP23573


eric
04-28-2005, 05:52 AM
Ariad begins cancer study of AP23573 (http://www.datamonitor.com/~db266ae1ab854d7795574c959b17e173~/industries/news/article/?pid=FC4570EA-E820-48AE-B085-1037EA4A855C&type=NewsWire)

Ariad Pharmaceuticals has initiated patient enrollment for clinical trials of its novel mTOR inhibitor, AP23573. Advanced cancer patients will receive AP23573 as an adjunct to the widely used chemotherapeutic agents, paclitaxel or capecitabine.

These non-randomized, dose-escalation studies will evaluate the safety and tolerability, pharmacokinetics, and anticancer activity of AP23573 in combination with paclitaxel or capecitabine.

The primary goal of these studies is to determine the optimal dosing regimen for AP23573 when used in combination with each of these cytotoxic drugs, predominantly in patients with progressive breast, ovarian, non-small-cell lung, and prostate cancers, as well as certain sarcomas. Up to approximately 110 cancer patients will be enrolled in the two trials at three to five centers in Italy and Switzerland.

Despite advances in cancer therapy, prolonged cancer remission remains difficult to achieve in many types of solid tumors. Additional treatment options are needed for patients whose cancer is progressing and unresponsive to currently available therapies. Combining novel molecularly targeted agents, such as AP23573 with traditional cytotoxic agents may prove to be a more effective treatment for patients with advanced cancers.

The initiation of the new studies sees the beginning of the European phase of the company's global development plan for AP23573, according to chairman and CEO of Ariad, Harvey Berger.

The drug, which has already been fast-tracked by the FDA for the treatment of soft-tissue and bone sarcomas, works by starving cancer cells and shrinks tumors by inhibiting the critical cell-signaling protein, mTOR, which regulates the response of tumor cells to nutrients and growth factors, and controls tumor blood supply and angiogenesis through effects on Vascular Endothelial Growth Factor (VEGF) in tumor and endothelial cells.

Source: Datamonitor