Adamis' APC-300 inhibits growth of prostate cancer cells

Adamis Pharmaceuticals Corporation (OTCBB: ADMP) announced today that in addition to activity in pancreatic cancer and its multiple modes of action, APC-300 significantly inhibits the growth of prostate cancer cells.

In 2010, the American Cancer Society reported that 217,730 men in the U.S. were diagnosed with prostate cancer and 32,050 were projected to die from the disease. While treatment with surgery and/or radiation is often successful, about one-third of patients will experience disease recurrence. Despite the initial success of androgen deprivation therapy (castration), prostate cancer continues to progress from androgen-dependent prostate cancer (ADPC) to castrate-resistant prostate cancer (CRPC) in most of these patients within a matter of years. More and more data point to the fact that androgen receptor (AR) plays a central role in both ADPC and CRPC. Therefore, identifying inhibitors of AR signaling which can act independent of hormonal status is of prime importance. These types of inhibitors could prove to be very important in the treatment of prostate cancer and thereby prevent or delay ADPC from progressing to CRPC. Based on the most recent information, APC-300 could very well be a molecule that acts independent of hormonal status.

A study published in Clinical Cancer Research (June 28, 2011) and authored by Dr. Mohammad Saleem and his associates from the Hormel Institute, University of Minnesota and the Mayo Clinic showed that APC-300 inhibits AR signaling and activation in prostate cancer in both ADPC and CRPC. Agents that have the potential to combat prostate cancer under both conditions (androgen and non-androgen responsive environments) are rare, but obviously desirable. APC-300 has been shown to have this desired activity. The results of the current study are significant because they demonstrate that APC-300, while sparing normal cells, preferentially inhibits the growth and proliferation of heterogeneous prostate cancer cells representing differential androgen sensitivity and AR expression status. Also, the observation that APC-300 sensitized highly aggressive CRPC cells to bicalutamide (currently used to treat ADPC) has high clinical relevance.

Additionally, APC-300 was shown to decrease messenger RNA and protein expression of the AR-target gene, PSA (biomarker for prostate cancer) in ADPC and CRPC cells. This translated into APC-300 showing a decrease in the secreted levels of PSA in a concentration dependent manner and a decrease in the growth of prostate cancer cells in vitro and in vivo. The data provide good evidence that APC-300 has the potential to decrease the AR transcriptional activity of ADPC and CRPC cells by blocking the AR occupancy on AR-responsive elements in target genes. The data also show that APC-300 had a significant effect on reducing the growth of ADPC and CRPC and reducing the levels of PSA in the mouse tumor model. Taken together, these data suggest that APC-300 may very well play a significant role in the treatment of prostate cancer.

Dennis J. Carlo, Ph.D., President and CEO of Adamis, states that, "We continue to build upon our prostate cancer franchise. New independent published data validate the importance of our three compounds (APC-100, 200, 300) for the treatment of prostate and pancreatic cancer. We will continue to focus and aggressively move these compounds into the clinic. Molecules such as APC-300 could very well work alone, but also just as important, APC-300 may enhance the activity of compounds already marketed and used for the treatment of prostate cancer."