Infliximab is a recombinant chimeric IgG1κ monoclonal antibody which
binds specifically to TNFα, thereby blocking interaction of TNFα with
the p55 and p75 surface TNF receptors. Infliximab binds to both soluble
and cell-surface bound forms of TNFα, and is administered as an intravenous infusion.
TNFα is a central mediator of inflammation and is known to be dysregulated in a range of autoimmune diseases. TNFα blockers are thought to provide effective immunosuppression through a variety of mechanisms: neutralization of soluble and/or membrane-bound TNFα, direct cellular toxicity via complement-mediated lysis and/or antibody-dependent cytotoxicity, and induction of apoptosis or other downregulatory effects.
Infliximab was first licensed for use in Crohn's disease in 1998. Since then, additional indications have expanded to include rheumatoid arthritis, psoriatic arthritis, severe chronic plaque psoriasis, and ankylosing spondylitis. Adverse reactions are similar to those for other TNFα blockers, although recent post-licensing surveillance has noted a potentially increased incidence of hepatosplenic T-cell lymphomas associated with comcomitant 6-mercaptopurine or azathioprine use.rheumatoid arthritis;
ankylosing spondylitis;
psoriatic arthritis;
severe chronic plaque psoriasis;
Crohn's disease;
ulcerative colitis
| Source | Link | Revision Date | Access Date |
| Remicade Prescribing Information | http://www.remicade.com/remicade/glo...cp/hcp_pi.html | 2007-April | 2008-June-05 |
| Wong M, Ziring D, et al. TNFalpha blockade in human diseases: mechanisms and future directions. Clin Immunol. 2008 Feb;126(2):121-36 | http://www.pubmedcentral.nih.gov/art...medid=17916444 | 2008-June-05 |
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