Anti-TNF- therapies: they are all the same (aren't they?)

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Abstract
The development of anti-tumour necrosis factor α (TNF-α) therapy has been a milestone in the treatment of rheumatoid arthritis (RA) and is proving equally important in other inflammatory-mediated conditions [1–3 ]. The three currently licensed biological anti-TNF-α drugs, etanercept, infliximab and adalimumab, have all been clearly shown to suppress disease activity in RA. They all target the same molecule—but are they really just more of the same and, indeed, are all three needed? As uptake of anti-TNF-α therapy increases around the world, these questions are becoming increasingly posed. However, it is also becoming clear that these drugs possess significant differences, both in vitro and clinically. Understanding these differences is of course important for the clinic, but equally important is the appreciation that these drugs provide new tools to investigate the pathogenesis of RA and other inflammatory disorders and inform the development of newer generations of anti-inflammatory drugs.

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