There is accumulating evidence that tumour necrosis factor (TNF) plays a major 
role in the pathogenesis of rheumatoid arthritis (RA). Recent biotechnological 
advances have allowed for the development of agents that directly target TNF, a 
pro-inflammatory cytokine. In the last 2 years, the US FDA and the EU's 
Commission of the European Communities have approved two biological agents for 
the treatment of refractory RA, etanercept and infliximab. Etanercept is a 
fusion protein, composed of the Fc portion of IgG1 and the extracellular domain 
of the TNF receptor (p75). Infliximab is a chimeric monoclonal antibody (mAb) 
composed of murine variable and human constant regions. In placebo-controlled 
trials, both agents have proven to be effective and well-tolerated in RA 
patients. This review evaluates the available TNF inhibitors, summarises 
pertinent clinical trials and underscores differences between the two agents in 
terms of molecular structure, efficacy, safety data, antigenicity and 
pharmacokinetics.