Exelixis

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Overview

To view the corporate site Click Here

To Contact:

Exelixis Inc.,

210 East Grand Avenue

P.O. Box 511

So. San Francisco, CA 94083-0511

(650) 837-7000 phone

(650) 837-8300 fax

Image:Exelixis - Scangos 01.jpg George SCANGOS of Exelixis

Articles

25-Oct-2007 - Exelixis presents encouraging data for renal cancer drug

Exelixis presents encouraging data for renal cancer drug

By Staff Writer

Biotechnology company Exelixis has reported encouraging results from an ongoing multi-center open-label Phase II trial of XL880, an inhibitor of MET and VEGFR2 kinases, in patients with papillary renal cell carcinoma.

The data shows that significant majority of patients on study have experienced tumor shrinkage with prolonged duration of stable disease, highlight the potential utility of drug and its potent effects in modulating both MET and VEGFR2 in the clinical setting.

Of 19 patients with measurable disease evaluable for tumor responses, 15 (79%) have had a decrease in tumor size (4-33%), including one patient with a partial response. All 19 evaluable patients with at least one post-baseline tumor assessment have had stable disease for at least three months, including 12 patients with stable disease for six months to 15+ months. Results of preliminary analyses of plasma biomarkers and tumor samples are consistent with inhibition of angiogenesis and proliferation and an increase in apoptosis.

Preliminary pharmacodynamic analyses in 11 patients show statistically significant changes in PIGF, VEGF-A, sVEGFR2 and EPO, markers of anti-angiogenic activity, following administration of inhibitor of MET and VEGFR2 kinases (XL880). XL880 also demonstrated growth inhibition and induction of apoptosis comparing pre- and post-XL880 tumor biopsies from one patient. Preliminary pharmacokinetic analyses were consistent with results from the Phase I trial.

Michael Morrissey, Exelixis's president of R&D, said: "The Phase II trial of XL880 in PRC was supported both by the biology of the disease, which frequently is associated with activating mutations or amplifications in MET, and the favorable responses observed in patients with PRC in the reported Phase I study of the compound. We are excited about the potential therapeutic utility of modulating these targets in a variety of solid tumor types."

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