Tumor necrosis factor (TNF-alpha) binding antibody (chimeric IgG1). It is composed of human constant and murine variable regions. Infliximab is produced by a recombinant cell line cultured by continuous perfusion
As described above, several reports have shown that patients treated with Enbrel or Remicade worsen their congestive heart failure and develop serious infection and sepsis, and increase exacerbations of multiple sclerosis and other central nervous system problems [15,16].
Infliximab (Remicade, Centocor Inc, Malvern, PA, Schering Plough SpA, Italy), 5 mg/kg, was administered by a two-hour intravenous infusion.
These investigations led to the development of several TNF and IL-1 inhibitors, two of which are currently licensed Remicade (chimeric anti-TNF antibody) and Enbrel (TNF-receptor fusion protein).
Today there are two main biologic agents targeting TNF-α: the chimeric monoclonal IgG1 antibody infliximab (Remicade) with human constant and murine variable regions and the recombinant 75-kD TNF receptor IgG1 fusion protein etanercept (Enbrel).
The success of antiTNF therapy of rheumatoid arthritis with infliximab (Remicade) and etanercept (Enbrel) has prompted us to seek other ways of inhibiting TNF production, and to seek to determine the cellular and molecular mechanisms underlying the excess and prolonged TNF synthesis in RA.