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• W200737354 abstract "Blocking the binding of TNF to TNF receptor subtype 1 (TNFR1) is believed to be a promising strategy for the treatment of rheumatoid arthritis (RA). However, because of the unavailability of any TNFR1-selective antagonist, the therapeutic potency of this strategy still remains to be confirmed. To this end, we recently developed a novel TNFR1-selective antagonistic TNF mutant (R1antTNF) and reported that this agent efficiently inhibits TNF/TNFR1-mediated signaling in vitro. Here, the anti-inflammatory effects of R1antTNF on a murine collagen-induced arthritis (CIA) model have been investigated. To improve in vivo stability, polyethylene glycol-modified R1antTNF (PEG-R1antTNF) was prepared. Using site-specific PEGylation technology, the in vivo half-life of R1antTNF was improved without loss of antagonistic activity. In the CIA model, the clinical score of the mice given PEG-R1antTNF was improved effectively. Recently, there has been much concern over the increased susceptibility to pathogenic infection caused by TNF blockade. Therefore, we assessed whether PEG-R1antTNF and Etanercept had similar deleterious effects in adenoviral infection model. The data suggest that PEG-R1antTNF has less negative effects on viral clearance than Etanercept. We conclude that selective inhibition of TNF/TNFR1-mediated signaling could be effective in treating RA and that PEG-R1antTNF could serve as a novel anti-inflammatory drug for this purpose." @default.
• W200737354 created "2016-06-24" @default.
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• W200737354 date "2010-10-22" @default.
• W200737354 modified "2023-09-26" @default.
• W200737354 title "Anti-inflammatory Effects of a Novel TNFR1-Selective Antagonistic TNF Mutant on Established Murine Collagen-Induced Arthritis" @default.
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• W200737354 doi "https://doi.org/10.1007/978-1-4419-6612-4_51" @default.
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