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 arthritis in BALB/c mice.
Department of Chemistry, Michigan State University, East Lansing, MI, USA.
Theresa A
TA
Lansdell
Sandra
S
O'Reilly
Tracey
T
Woolliscroft
Lauren M
LM
Azevedo
Daljinder K
DK
Kahlon
Stacy
S
Hovde
J Justin
JJ
McCormick
R William
RW
Henry
Joseph A
JA
Cornicelli
Jetze J
JJ
Tepe
D000284:Administration, Oral; D000818:Animals; D001172:Arthritis, Rheumatoid / Q000139:chemically induced / Q000188:drug therapy*; D003094:Collagen; D004305:Dose-Response Relationship, Drug; D007093:Imidazoles / Q000008:administration & dosage / Q000494:pharmacology*; D051379:Mice; D008807:Mice, Inbred BALB C; D015394:Molecular Structure; D016328:NF-kappa B / Q000037:antagonists & inhibitors; D015398:Signal Transduction / Q000187:drug effects; D013329:Structure-Activity Relationship; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors* / Q000378:metabolism
D007093:Imidazoles; D016328:NF-kappa B; C000593813:TCH-013; D014409:Tumor Necrosis Factor-alpha; D003094:Collagen