Randomised double-blind comparison of chimeric monoclonal antibody to tumour necrosis factor α (cA2) versus placebo in rheumatoid arthritis

  title={Randomised double-blind comparison of chimeric monoclonal antibody to tumour necrosis factor $\alpha$ (cA2) versus placebo in rheumatoid arthritis},
  author={Michael J. Elliott and Ravinda Nath Maini and Marc Feldmann and Joachim Robert Kalden and C E Antoni and J. S. Smolen and B. Leeb and Ferry C Breedveld and J. D. Macfarlane and J. A. Bijl and James N. Woody},
  journal={The Lancet},
Treatment of rheumatoid arthritis with a recombinant human tumor necrosis factor receptor (p75)-Fc fusion protein.
In this three-month trial TNFR:Fc was safe, well tolerated, and associated with improvement in the inflammatory symptoms of rheumatoid arthritis.
Efficacy of a novel PEGylated humanized anti-TNF fragment (CDP870) in patients with rheumatoid arthritis: a phase II double-blinded, randomized, dose-escalating trial.
CDP870 is effective, was very well tolerated in this small study, and has an extended duration of action following one or more intravenous doses.
Adalimumab, a fully human anti-tumor necrosis factor alpha monoclonal antibody, for the treatment of rheumatoid arthritis in patients taking concomitant methotrexate: the ARMADA trial.
The addition of adalimumab at a dosage of 20 mg, 40 mg, or 80 mg administered subcutaneously every other week to long-term MTX therapy in patients with active RA provided significant, rapid, and sustained improvement in disease activity over 24 weeks compared with MTX plus placebo.
Long term safety of infliximab.
  • T. Schaible
  • Medicine
    Canadian journal of gastroenterology = Journal canadien de gastroenterologie
  • 2000
While infections were reported more frequently overall in the patients given infliximab, there was no increased risk of serious infections and drug-induced lupus was seen in less than 1%, with these cases resolving upon discontinuation of the drug.
Infliximab: a review of its use in the management of rheumatoid arthritis.
If preliminary results indicating that infliximab is able to arrest joint destruction in patients with rheumatoid arthritis are corroborated, the drug will likely become an integral component of future management strategies for this difficult-to-treat condition.
Effects of treatment with a fully human anti-tumour necrosis factor α monoclonal antibody on the local and systemic homeostasis of interleukin 1 and TNFα in patients with rheumatoid arthritis
Blocking TNFα in RA results in down regulation of IL1β mRNA at the systemic level and in reduction of the endogenous antagonists for IL1 and TNF and of other cytokines related to the acute phase response, such as IL6, within days.
Randomized double-blind comparison of chimeric monoclonal antibody to tumor necrosis factor alpha (infliximab) versus placebo in active spondylarthropathy.
Tumor necrosis factor alpha blockade with infliximab in patients with active SpA was well tolerated and resulted in significant clinical and laboratory improvements in this short-term, placebo-controlled study.


Treatment of rheumatoid arthritis with chimeric monoclonal antibodies to tumor necrosis factor alpha.
Preliminary results support the hypothesis that TNF alpha is an important regulator in RA, and suggest that it may be a useful new therapeutic target in this disease.
A randomized, double-blind, placebo-controlled study of CD4 monoclonal antibody therapy in early rheumatoid arthritis.
Analysis of clinical parameters revealed no changes in arthritis activity in the groups that received CD4 MAb or the placebo group, and no difference between the groups, in either in the first or the second part of the study.
New directions for biological therapy in rheumatoid arthritis.
It is shown that the early promise displayed by anti-CD4 monoclonal antibodies in open clinical trials has not been sustained in controlled studies, providing a challenge to the concept that CD4+ T cells are of prime importance in RA, and prompts a search for alternative therapeutic targets.
Anti-tumor necrosis factor ameliorates joint disease in murine collagen-induced arthritis.
The capacity of the antibody to reduce the clinical score, paw swelling, and the histological severity of disease even when injected after the onset of clinical arthritis was found, which has implications for possible modes of therapy of human arthritis.
TNF-alpha in rheumatoid arthritis and prospects of anti-TNF therapy.
In preliminary trials in rheumatoid patients anti-TNF appears to have an impressive effect on indices of disease activity including C-reactive production and serum amyloid-A production, thereby suggesting that TNF has the potential for autocrine and paracrine activity in the joint.
DAB486IL-2 fusion toxin in refractory rheumatoid arthritis.
Preliminary evidence is provided for a potential therapeutic effect of DAB486IL-2 in RA, with an acceptable safety profile, and repeat courses were associated with less transaminase elevation and were clinically effective despite induction of anti-DT antibodies.
Analysis of improvement in individual rheumatoid arthritis patients treated with disease-modifying antirheumatic drugs, based on the findings in patients treated with placebo. The Cooperative Systematic Studies of Rheumatic Diseases Group.
The proposed index appears to be useful in estimating the probability that an RA patient will improve if taking a placebo during a DMARD trial, and may be a useful tool for analysis of DMARD studies.
Chronic exposure to tumor necrosis factor (TNF) in vitro impairs the activation of T cells through the T cell receptor/CD3 complex; reversal in vivo by anti-TNF antibodies in patients with rheumatoid arthritis.
It is demonstrated that persistent expression of TNF in vitro and in vivo impairs cell-mediated immune responses, and cell- mediated immunity in patients with active rheumatoid arthritis is studied.