Rituximab
Better Known as: Rituxan
Mechanism of ActionChronic Lymphocytic Leukemia & Rheumatoid Arthritis are diseases associated with B-cell dysfunction. B-cells play a key role in the humoral immune system by acting as antigen-presenting cells (which activate T-cells) and by eventually producing antibodies against invading antigens.[1] Although the function of B-Lymphocyte Antigen CD20 has not yet been determined, and in fact knockout mice which do not produce CD20 are healthy, CD20 is expressed on almost all normal and malignant B-cells. Since it is not expressed on other plasma cells or normal tissues, it is an ideal target for passive immunotherapy.[2] A number of studies have demonstrated that the binding of monoclonal antibodies to CD20 results in recruitment of immunological devices that trigger cytotoxic events, such as compliment-dependent cytotoxicity (CDC). CDC is the major natural immune response in the body triggered by antibody binding, used to eliminate invading or dysfunctional pathogenic cells.[3] Rituximab is an anti-CD20 chimeric monoclonal antibody which binds its target epitope with exceptional specificity. Numerous studies have indicated that residues Ala 170 and Pro 172 on human CD20 are critical determinants for effective binding. Several other interactions effectively fine tune and strengthen the bond between Rituximab and the epitope peptide.[4] See also Rituximab Fab (UMass Chem 423 Student Projects 2011-2).
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