Interim data from Hollis-Eden Pharmaceuticals' Apoptone Phase I/II clinical trial presented

Nov 16 2009

Hollis-Eden Pharmaceuticals, Inc. (Nasdaq: HEPH), today reported preliminary results of its ongoing Phase I/II clinical trial with Apoptone® (HE3235) for hormone-resistant prostate cancer (also called castrate-resistant prostate cancer or CRPC). Presented at the Molecular Targets and Cancer Therapeutics Conference, which is co-sponsored by the AACR, NCI and EORTC, the poster is titled: "Results of preclinical and clinical Phase I/II open-label dose-ranging trial with HE3235, a synthetic adrenal hormone, in Castrate Resistant Prostate Cancer (CRPC)." Apoptone (HE3235), a novel steroid that is an analog of a dihydrotestosterone metabolic pathway member, stimulates cell death (apoptosis) in hormone-dependent prostate tumors. Presenting the data is the lead investigator of the study, R. Bruce Montgomery, M.D., Associate Professor, Department of Medicine, Division of Oncology, University of Washington School of Medicine. The poster also included supportive preclinical data.

The interim results of the Phase I/II study, which is being conducted with participating member sites of the Prostate Cancer Clinical Trial Consortium (PCCTC), demonstrated that 47% of subjects who were radiographically evaluable for response had stable disease. With the assessment of progression every 56 days, the median time to progression was 107 days. Forty-three percent of the biochemically evaluable subjects experienced a drop in PSA during treatment, with 33% equal to or greater than a 50% decline.

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."