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Priliximab is a human-mouse chimeric monoclonal antibody targeting the CD4 antigen on T cells. It was constructed from the antigen-binding variable region of the murine CD4 antibody M-T412 and the constant region of human IgG1 kappa immunoglobulin. Priliximab binds to CD4 on T-helper cells, leading to a profound and sustained decrease in circulating CD4+ T cells and downregulation of T-helper-inducer function. Its mechanism involves inhibition of T cell activation through blockade of CD4-mediated signaling pathways. The drug has been evaluated for several autoimmune and immune-mediated conditions including Crohn’s disease, multiple sclerosis, rheumatoid arthritis, heart transplant rejection (prevention), mycosis fungoides (cutaneous T-cell lymphoma), myasthenia gravis, and non-Hodgkin lymphoma. Clinical development reached phase I/II trials but no FDA approval has been granted[1][3][5][7]. The original developer was Centocor.
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