Cookies on this website
We use cookies to ensure that we give you the best experience on our website. If you click 'Continue' we'll assume that you are happy to receive all cookies and you won't see this message again. Click 'Find out more' for information on how to change your cookie settings.

Tumor necrosis factor-alpha (TNF) has been unequivocally validated as a therapeutic target in a number of immune-mediated inflammatory disorders (IMIDs). There is now increasing choice of biologic agents within the class all of which successfully neutralize sTNF. But approaches to TNF inhibition differ and currently include mAbs (infliximab, adalimumab, and golimumab), either chimeric or human in sequence, a PEGylated Fab' fragment (certolizumab), and an IgG1-TNFR2 fusion protein (etanercept). It is emerging that the pharmacological properties of these three anti-TNF subtypes differ with respect to Fc function, binding of tmTNF and the possible consequences of this, as well as the ability to form complexes. The mode of administration of each agent, clearance and the local tissue concentrations achieved may also confer unique characteristics of relevance with respect to efficacy and safety.

Original publication

DOI

10.1016/j.coph.2010.01.005

Type

Journal article

Journal

Current opinion in pharmacology

Publication Date

06/2010

Volume

10

Pages

308 - 315

Addresses

The Kennedy Institute Division, Faculty of Medicine, Imperial College School of Medicine, 65 Aspenlea Road, London W6 8LH, United Kingdom. peter.c.taylor@imperial.ac.uk

Keywords

Animals, Humans, Arthritis, Rheumatoid, Chronic Disease, Inflammation, Tumor Necrosis Factor-alpha, Anti-Inflammatory Agents, Antirheumatic Agents, Immunologic Factors, Antibodies, Monoclonal, Drug Delivery Systems