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Many clinical studies have reported the excellent clinical efficacy of infliximab (IFX), an antitumour necrosis factor α (anti-TNFα) monoclonal antibody, in the treatment of rheumatoid arthritis (RA).1 IFX is also reported to induce a rapid and marked reduction in circulating interleukin 6 (IL-6) levels, suggesting that its efficacy may result from the suppression of IL-6 as well as TNF.2,–,5 In the RISING Study (NCT00691028),6 ,7 we observed patients who showed no response to IFX therapy, despite maintaining a serum IFX level higher than the threshold level for clinical response. Here, we examined data on clinical response to better understand the mechanism of action of IFX.
In this study, patients with methotrexate-refractory RA treated with 3 mg/kg of IFX at weeks 0, 2 and 6 were randomly assigned to receive 3, 6 or 10 mg/kg of IFX every 8 weeks from week 14 to 46 in …
Funding Mitsubishi Tanabe Pharma Corporation sponsored this clinical trial and was responsible for the collection and analysis of data.
Patients consent Obtained.
Ethics approval This study was conducted with the approval of the local ethics committees of every participant centre.
Competing interests TT has received lecture fees from Abbott Japan, Bristol-Myers Squibb, Chugai Pharmaceutical, Eisai, Janssen Pharmaceutical, Mitsubishi Tanabe Pharma, Novartis, Pfizer Japan and Takeda Pharmaceutical. NM has received grant support from Abbott Japan, Astellas Pharma, Chugai Pharmaceutical, Daiichi Sankyo, Mitsubishi Tanabe Pharma and Takeda Pharmaceutical; and lecture fees from Benesis and Otsuka Pharmaceutical. YT, T Yano and T Yoshinari are employees of Mitsubishi Tanabe Pharma. TA has no conflicts of interest. TK has received lecture fees from Abbott Japan, Bristol-Myers Squibb, Chugai Pharmaceutical, Eisai, Mitsubishi Tanabe Pharma, Otsuka Pharmaceutical, Pfizer and Takeda Pharmaceutical.
Provenance and peer review Not commissioned; externally peer reviewed.
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