Reprint of BMCL_19101

The pathogenesis of rheumatoid arthritis is mainly driven by NF-κB-mediated production of cytokines, such as TNF-α. We report herein that the orally available imidazoline-based NF-κB inhibitor, TCH-013, was found to significantly reduce TNF-α signaling and attenuate collagen antibody induced arthrit...

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Bibliographic Details
Published inBioorganic & medicinal chemistry letters Vol. 22; no. 22; pp. 6821 - 6824
Main Authors Lansdell, Theresa A., O’Reilly, Sandra, Woolliscroft, Tracey, Azevedo, Lauren M., Kahlon, Daljinder K., Hovde, Stacy, McCormick, J. Justin, Henry, R. William, Cornicelli, Joseph A., Tepe, Jetze J.
Format Journal Article
LanguageEnglish
Published England Elsevier Ltd 15.11.2012
Subjects
Administration, Oral
Animals
Arthritis, Rheumatoid - chemically induced
Arthritis, Rheumatoid - drug therapy
chemistry
Collagen
Cytokines
Dose-Response Relationship, Drug
Imidazoles - administration & dosage
Imidazoles - pharmacology
Imidazolines
Inflammation
Mice
Mice, Inbred BALB C
Molecular Structure
NF-kappa B - antagonists & inhibitors
NF-κB
pathogenesis
Rheumatoid arthritis
Signal Transduction - drug effects
Structure-Activity Relationship
transcription factor NF-kappa B
tumor necrosis factor-alpha
Tumor Necrosis Factor-alpha - antagonists & inhibitors
Tumor Necrosis Factor-alpha - metabolism
NF-κB
Imidazolines
Inflammation
Cytokines
Rheumatoid arthritis
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Summary:The pathogenesis of rheumatoid arthritis is mainly driven by NF-κB-mediated production of cytokines, such as TNF-α. We report herein that the orally available imidazoline-based NF-κB inhibitor, TCH-013, was found to significantly reduce TNF-α signaling and attenuate collagen antibody induced arthritis in BALB/c mice.
Bibliography:http://dx.doi.org/10.1016/S0960-894X(12)01341-8
ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0960-894X
1464-3405
DOI:10.1016/S0960-894X(12)01341-8