Abstract:Introduction: Activation of complement (C) constitutes an important effector mechanism of monoclonal antibodies in cancer therapy. Unmodified IgG1 antibodies against the epidermal growth factor receptor (EGFR), a well-validated tumor target, lack the capacity to induce complement-dependent cytotoxicity (CDC) as single agents. Recently, significantly improved CDC was demonstrated after antigen-bound IgG molecules formed hexameric structures through intermolecular Fc-Fc contacts. Single point mutations (E345K or… Show more
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