Abstract
Rituximab is a mouse/human chimeric IgG1kappa monoclonal antibody that targets the CD20 antigen found on the surface of malignant and normal B-lymphocytes. The mechanisms of action of rituximab involve complement-dependent cytotoxicity (CDC), complement-dependent cellular cytotoxicity (CDCC), antibody dependent cellular cytotoxicity (ADCC) and induction of apoptosis. Pharmacokinetic issues, tumor and molecular related factors mediate resistance to rituximab. Optimizing rituximab treatment requires a therapeutic project that might ideally be individualized and that includes enhancing of ADCC and CDC mechanisms, acting over apoptosis-regulating proteins and using synergistic conventional chemotherapeutic agents. Pharmacokinetic favourable schedules in specific diseases alone or associated to chemotherapeutic agents are not well known, therefore studies focusing on these issues are warranted. New information regarding targeting the lymphoma microenvironment and rituximab effects is the focus of current research.
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