|1.||Björklund, Ulf: 2 articles (10/2015 - 08/2010)|
|2.||Israelsson, Charlotte: 1 article (10/2015)|
|3.||Kylberg, Annika: 1 article (10/2015)|
|4.||Ebendal, Ted: 1 article (10/2015)|
|5.||Frascaroli, Giada: 1 article (01/2011)|
|6.||Tammik, Charlotte: 1 article (01/2011)|
|7.||Söderberg-Nauclér, Cecilia: 1 article (01/2011)|
|8.||Varani, Stefania: 1 article (01/2011)|
|9.||Gredmark-Russ, Sara: 1 article (01/2011)|
|10.||Giusti, Pablo: 1 article (01/2011)|
|1.||Autoimmune Diseases (Autoimmune Disease)
01/01/2009 - "In this study we aimed to evaluate Rabeximod as a treatment for autoimmune diseases, using animal models. "
01/01/2009 - "In the present investigation we have evaluated Rabeximod as a treatment for autoimmune diseases using mouse models of RA and MS, ie, collagen-induced arthritis, collagen antibody induced arthritis and experimental autoimmune encephalomyelitis. "
01/01/2011 - "Rabeximod (9-chloro-2,3-dimethyl-6-(N,N-dimethylaminoethylamino-2-oxoethyl)-6H-indolo[2,3-b]quinoxaline) is a synthetic compound that is currently being developed for the treatment of rheumatoid arthritis (RA). "
08/01/2010 - "The novel small molecule 9-chloro-2,3-dimethyl-6-(N,N-dimethylaminoethylamino-2-oxoethyl)-6H-indolo[2,3-b] quinoxaline (Rabeximod) reduces severity of arthritis in rodent models of rheumatoid arthritis (RA) and multiple sclerosis (MS). "
08/01/2010 - "Rabeximod suppresses arthritis by preventing activation of inflammatory cells, most likely macrophages, in a time dependent fashion, downstream of TLR2 and TLR4 stimulation."
08/01/2010 - "Rabeximod reduces arthritis severity in mice by decreasing activation of inflammatory cells."
08/01/2010 - "In addition, it was found that the arthritis ameliorating effect of Rabeximod was time dependent, since inhibition of tumour necrosis factor alpha production from macrophages in vitro was more pronounced if administered close to stimulation. "
01/01/2009 - "Rabeximod efficiently prevented arthritis and encephalomyelitis in mice. "
08/01/2010 - "Rabeximod efficiently prevented arthritis during the time window when TLR2 or TLR4 ligands activate inflammatory macrophages. "