1.
Bioorg Med Chem Lett
; 22(22): 6821-4, 2012 11 15.
Artigo
em Inglês
| MEDLINE
| ID: mdl-23083981
RESUMO
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.
Assuntos
Artrite Reumatoide/tratamento farmacológico , Imidazóis/farmacologia , Fator de Necrose Tumoral alfa/antagonistas & inibidores , Administração Oral , Animais , Artrite Reumatoide/induzido quimicamente , Colágeno , Relação Dose-Resposta a Droga , Imidazóis/administração & dosagem , Camundongos , Camundongos Endogâmicos BALB C , Estrutura Molecular , NF-kappa B/antagonistas & inibidores , Transdução de Sinais/efeitos dos fármacos , Relação Estrutura-Atividade , Fator de Necrose Tumoral alfa/metabolismo
2.
Bioorg Med Chem Lett
; 22(14): 4816-9, 2012 Jul 15.
Artigo
em Inglês
| MEDLINE
| ID: mdl-22682057
RESUMO
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.