In the Phase I study the drug OGX-011* inhibited the production of clusterin, a protein that protects cell survival and is widely distributed in body tissue. Clusterin is implicated in a range of activities, including apoptosis (programmed cell death). When it is over-produced, as it is many major cancers, clusterin can stop cancer cells from dying and counters the effectiveness of chemotherapy, hormone treatment and radiotherapy.

Dr. Kim Chi, assistant professor of medicine at the University of British Columbia and medical oncologist at the BC Cancer Agency in Canada, told the EORTC-NCI-AACR[1] Symposium on Molecular Targets and Cancer Therapeutics in Geneva today (Wednesday 29 September) that the Phase I trial was unique in that the clinical research team was able to demonstrate that the target clusterin was inhibited by OGX-011 in patients' cancers in a dose dependent way.

"This means that the drug is doing what it is supposed to be doing something that we can't always say about targeted therapeutics and we were able to identify a biologically active dose," he said.

Antisense drugs work by inhibiting the production of a protein from a specifically targeted gene. As a second-generation antisense drug, OGX-011 is an advance on earlier ones in that the molecules have a longer tissue half life and are potentially more potent. Pre-clinical studies had shown that blocking the production of clusterin with OGX-011 impairs a cancer cell's survival mechanism and enhances the effectiveness of standard chemotherapy, radiation and hormone therapy.

Twenty-five patients with localised prostate cancer that was to be removed by surgery were given escalati
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Contact: Margaret Willson
m.willson@mwcommunications.org.uk
41-227-612-205
European Organisation for Research and Treatment of Cancer
29-Sep-2004