Hollis-Eden Commences Phase I/II Clinical Trial with APOPTONE™ in Late-Stage Prostate Cancer Patients

Hollis-Eden Pharmaceuticals, Inc. has announced that it has commenced a Phase I/II clinical trial with its oral drug candidate APOPTONE™ (HE3235) in late-stage prostate cancer patients who have failed hormone therapy and at least one round of chemotherapy treatment.

The Phase I/II open-label dose ranging study, being conducted with the Prostate Cancer Clinical Trial Consortium (PCCTC), will evaluate the safety, tolerance, pharmacokinetics and potential activity of APOPTONE when administered twice daily for 28 days in up to 44 late-stage prostate cancer patients.

Potential activity of the compound will be measured by standard prostate-specific antigen (PSA) tests and effect on well-established markers of progression free survival (PFS).

In addition, in conjunction with Memorial Sloan-Kettering Cancer Center, the clinical trial will evaluate circulating tumor cell (CTC) enumeration as a marker for effectiveness for tumor treatment. Previous studies have shown that metastatic prostate cancer patients with less than 5 CTCs per 7.5 ml of blood have statistically better survival than patients with greater than 5 CTCs.

APOPTONE has been tested in a number of preclinical cancer models and has been shown to date to be active in controlling the incidence, growth and development of new tumors.

Hollis-Eden believes that APOPTONE may be directly inducing apoptosis, or cell death, in tumor cells, as opposed to traditional hormone blockade therapies directed at simply interrupting either the synthesis or the signaling of the tumor cell growth through the androgen or estrogen receptor. While hormone blockade therapy can effectively control prostate cancer for a period of time, it will eventually fail and the cancer can continue to grow and spread.

Analysis of gene expression from tumor cells in preclinical studies conducted to date indicate APOPTONE appears to act as an apoptotic agent, down-regulating genes that protect tumor cells from apoptosis, such as Bcl-2, while increasing the expression of pro-apoptotic genes such as caspases.