AbstractPurpose: Androgen deprivation therapy (ADT) remains the cornerstone treatment for advanced prostate cancer despite being principally palliative in nature. New treatment strategies aimed at enhancing tumor immunogenicity and damaging tumor vasculature could potentially improve prostate cancer response to ADT. We recently showed that targeting phosphatidylserine by antibodies resulting in enhanced tumor immunogenicity and tumor vascular damage. Bavituximab, a chimeric version anti-phosphatidylserine antibody, is being tested in clinic trails for different cancers. Here we tested the hypothesis that the fully human anti-phosphatidylserine antibody 1N11 can enhance the antitumor properties of ADT in prostate cancerExperimental Design: Efficacy of ADT and 1N11 against prostate cancer was assessed in C57BL/6 mice bearing syngeneic RM1 prostate tumor by using castration and mouse chimeric 1N11(mch1N11). Effects on mouse survival were assessed. In vivo localization of 1N11,effects on immune cell infiltration, vasculature density were also estimated by histology.Results: Our data showed that castration of RM1 tumor bearing mice increased the percentage of tumor vessels with exposed phosphatidylserine from 60% to 93%. Castration, when combined with mouse chimeric 1N11, led to significant survival befit versus individual treatments. The mean survival time was 16 days with control antibody. The prolongation in survival was 15 days with the combination, as compared with 3 days with mch1N11, 5 days with castration alone. Toxicity to the mice was not observed. A dramatic enhancement of tumor infiltration by a variety of immune cells and disruption of vasculature implied the combination to be more immunostimulatory and antivasculitic.Conclusion: Combined treatment with 1N11 and ADT improves survival of mice bearing prostate cancer. These results provide the foundation for using ADT plus fully human 1N11, or bavituximab, to treat prostate cancer patients.Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 5330.