Hollis-Eden’s cancer treatment promising in preclinical study

The report demonstrates that the drug, HE3235, significantly inhibited tumor growth in a preclinical model of hormone-independent prostate cancer utilizing human tumor cells. Mechanism of action data was presented showing that HE3235 lowers the expression of the anti-apoptotic gene BCL2 and induces apoptosis (cell death) in LNCaP cells.

The induction of apoptosis appears to be independent of endogenous hormones that may induce tumor cell proliferation. The data suggest that the activity of HE3235 is due, at least in part, to its ability to kill tumor cells.

The results of the study showed that HE3235 significantly inhibited the rate of tumor growth in comparison to untreated tumors by the third week of the study (p=0.038), with a greater difference in the rate of growth achieved between the HE3235 treatment and control groups during week four (p=0.005).

The company considers this LuCaP 35V data to be particularly exciting because it extends the activity of HE3235 beyond the previously described activity in models of hormone sensitive tumors to a model of hormone-independent tumors, which are associated with late-stage prostate cancer disease.

Richard Hollis, chairman and CEO of the company, said: “With these exciting data and our IND filing planned for the first quarter of 2008, we are rapidly advancing our cancer program and driving our product pipeline into the clinic along with our other opportunities in metabolic disorders and diseases of inflammation.”