Pharmacology of TNF blockade in rheumatoid arthritis and other chronic inflammatory diseases.

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 dif...

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Main Author: Taylor, P
Format: Journal article
Language:English
Published: 2010
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author Taylor, P
author_facet Taylor, P
author_sort Taylor, P
collection OXFORD
description 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.
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spelling oxford-uuid:f45e4e7f-5bff-42b0-8eee-9c9ca108f2462022-03-27T12:19:14ZPharmacology of TNF blockade in rheumatoid arthritis and other chronic inflammatory diseases.Journal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:f45e4e7f-5bff-42b0-8eee-9c9ca108f246EnglishSymplectic Elements at Oxford2010Taylor, PTumor 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.
spellingShingle Taylor, P
Pharmacology of TNF blockade in rheumatoid arthritis and other chronic inflammatory diseases.
title Pharmacology of TNF blockade in rheumatoid arthritis and other chronic inflammatory diseases.
title_full Pharmacology of TNF blockade in rheumatoid arthritis and other chronic inflammatory diseases.
title_fullStr Pharmacology of TNF blockade in rheumatoid arthritis and other chronic inflammatory diseases.
title_full_unstemmed Pharmacology of TNF blockade in rheumatoid arthritis and other chronic inflammatory diseases.
title_short Pharmacology of TNF blockade in rheumatoid arthritis and other chronic inflammatory diseases.
title_sort pharmacology of tnf blockade in rheumatoid arthritis and other chronic inflammatory diseases
work_keys_str_mv AT taylorp pharmacologyoftnfblockadeinrheumatoidarthritisandotherchronicinflammatorydiseases