Individuals experienced increases in PSA with stable disease. Plasma PSA increases are expected because the mechanism of action is believed to involve inhibition of tumor cell proliferation while the androgen receptor transcription element is engaged, independent of the androgen receptor. This results in an increase in tumor cell PSA expression followed by induction of apoptosis, which releases PSA into circulation. As tumor cell death occurs, the PSA is expected to decline or stabilize.

"Based on the encouraging responses and the tolerability profile we have seen in these end-stage patients, we are dose-escalating to 200 mg per day," commented Dr. Montgomery. "As we track time to progression through further treatment cycles, we expect that PSA levels will remain stable or continue to decline, consistent with the unique mechanism of this drug, which is distinct from other compounds in later-stage development for CRPC."

Howard Scher, M.D., Chief of the Genitourinary Oncology Service at the Sidney Kimmel Center for Urologic and Prostate Cancers at Memorial Sloan-Kettering and Principal Investigator of the PCCTC, added: "These data provide initial evidence of activity in late-stage prostate cancer. The next step will be to expand the subject eligibility criteria to include earlier-stage, chemotherapy-naive patients in a controlled Phase II trial."

SOURCE Hollis-Eden Pharmaceuticals, Inc.