Cytotoxicity of bevacizumab is enhanced by {beta}-glucan in tumors expressing membrane-bound VEGF

3060 Background: Bevacizumab (B-Mab) is a murine-derived monoclonal antibody with human IgG1 framework against vascular endothelial growth factor (VEGF). Soluble PGG β -glucan functions with complement activation product iC3b to activate complement receptor 3 (CR3) and recruit neutrophils and macrophages leading to CR3 (iC3b-receptor)-dependent cytotoxicity of tumors coated with iC3b. In mouse xenograft models, PGG β-glucan has a synergistic effect with human anti-tumor antibodies. Consequently, we hypothesized that the IgG1 antibody B-Mab is capable of binding surface VEGF (sVEGF) on tumor cells thereby activating complement, and synergizing with PGG β-glucan to elicit CR3-dependent cytotoxicity. Methods: SCID mouse xenografts with SKOV-3 human ovarian carcinoma cells were established in groups treated intravenously as follows: PBS treated as control (C), PGG β-glucan alone (B), B-Mab alone (A) and combination PGG β-glucan + B-Mab (B+A), twice weekly for 4 weeks. After implantation, tumors were allowed t...