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Data Presented at AACR Meeting Show Peregrine's Bavituximab,Equivalent Can Generate Curative Immune Responses as Part of a,Vaccine-Like Regimen in Preclinical Models of Aggressive Brain,Cancer

s can fuel development of a lethal tumor. In addition, the researchers calculated that in order to achieve the long-term survival observed in the animals receiving the 2aG4 regimen, more than 99.99% of the glioma cells contained in the challenge dose would have had to have been destroyed by the immune system. These results indicate that the 2aG4 vaccine-like regimen resulted in a strong immune response to the cancer not seen in controls.

"These exciting data suggest a potential new application for bavituximab and our anti-PS antibody platform as part of a cancer vaccine regimen that aims to restore the ability of the patient's own immune system to recognize and fight cancer," said Steven W. King, president and CEO of Peregrine. "Based on these promising results, we are continuing our evaluation of these vaccine-like regimens containing bavituximab for potential application to a variety of cancers."

Study data further showed that administering the combination of 2aG4 and irradiated tumor cells to the glioma cell-challenged animals resulted in a robust immune response, including enhanced cross-presentation of tumor antigens, increased expression of inflammatory anti-cancer cytokines and enhanced recognition and phagocytosis of tumor cells by macrophages. A key result was the fact that inclusion of the bavituximab equivalent in the regimen appeared to reverse suppression by tumor cells of the ability of dendritic cells to "present" cancer cells for destruction by the immune system. In these studies, the animals receiving 2aG4-treated irradiated cells showed increased antigen presentation of PS positive tumor cells by dendritic cells, as well as an increase in the number of cytotoxic T cells enabling the animals' immune systems to attack the tumor cells directly. These results are key signs of a strong immune response.

"We believe that a key mechanism of action of our anti-PS agents is that they block the immune-suppressing effects of phosphatidylse
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