Date: 2012-02-17
Type of information: Presentation of results at a congress
phase: preclinical
Announcement: novel preclinical data
Company: 4SC (Germany)
Product: Vidofludimus
Action
mechanism: The therapeutic efficacy of vidofludimus is based on a dual principle. Vidofludimus inhibits the expression of selected pro-inflammatory cytokines, including interleukin-17 (IL-17A and IL-17F) and IFN-gamma that have crucial pathogenic roles in a variety of autoimmune diseases. Vidofludimus also inhibits dihydroorotate dehydrogenase (DHODH), a key enzyme of the pyrimidine biosynthesis, thereby halting the proliferation of activated T and B cells which are involved in the pathology of autoimmune disorders.
Disease: inflammatory bowel disease
Therapeutic area: Inflammatory diseases
Country:
Trial details:
Latest
news: 4SC AG has presented novel preclinical data of its lead autoimmune compound vidofludimus demonstrating its dual anti-inflammatory mode of action. The data will be presented in two poster presentations at the 7th ECCO IBD conference of the European Crohn\'s and Colitis Organisation in Barcelona on 17 February 2012 and will be available for poster download under: http://www.4sc.de/product-pipeline/publications-posters/vidofludimus.
Last year, 4SC has announced final data of Phase IIa clinical study with vidofludimus in inflammatory bowel disease (See http://biopharmanalyses.fr/clinical-trails/?pageid=69). The presented data further encourage the planned Phase IIb clinical study, which the company is currently preparing in discussions with regulatory authorities and potential partners.
The data of the first ECCO IBD presentation \'Vidofludimus inhibits IL-17 and improves hapten-induced colitis in young rats by a unique dual mode of action\' show that vidofludimus considerably improves colonic inflammation in an animal model of induced colitis. The data further suggest that the anti-inflammatory effect of vidofludimus in this colitis model is caused by the compound\'s dual mode of action, namely inhibition of T-cell proliferation and suppression of pro-inflammatory cytokines including IL-17. The data of the second presentation \'Vidofludimus induces p53-mediated apoptosis in activated T-cells and inhibits IL-17A and IL-17F expression decoupled from lymphocyte proliferation\' demonstrate that vidofludimus strongly inhibits IL-17A and IL-17F production and induces apoptosis of activated T cells. T cell activation and IL17-A and IL17-F production are strongly related to autoimmune diseases and chronic inflammation such as IBD. Thus , these findings not only confirm the dual mode of action of vidofludimus but also the clinical rationale to further develop vidofludimus as a novel treatment of autoimmune diseases.
