Abstract: P1122
Type: Poster
Abstract Category: Pathology and pathogenesis of MS - Biomarkers
Backgrounds: Although interferon-beta (IFN-β) is the first-line therapy in relapsing-remitting multiple sclerosis (RRMS), one-third of patients are poor responders to IFN-β therapy. Currently, other disease-modifying drugs (DMDs) such as Fingolimod, Natalizumab, and BG12 become available. However, the problem is that there are no suitable biomarkers for the selection of treatment of MS. We previously reported that immune semaphorin Sema4A is increased in the sera of MS patients and those with high Sema4A do not respond well to IFN-β therapy. We also reported that recombinant Sema4A inhibits the therapeutic effect of IFN-β in experimental autoimmune encephalomyelitis (EAE). However, it remains unknown whether other DMDs are effective for patients with high Sema4A or not.
Objective: The purpose of this study is to investigate whether patients with high Sema4A respond to Fingolimod or not.
Methods: Fifty-six patients with MS who have been treated with Fingolimod were investigated. The levels of serum Sema4A were assayed with a sandwich ELISA, and the association between Sema4A levels and clinical characteristics including responsiveness to Fingolimod treatment was analyzed. We also investigated the efficacy of Fingolimod in EAE mice given Sema4A-Fc.
Results: The serum Sema4A titer was 2877 ± 5469. The ratio of patients with high Sema4A levels (≧2500) was 30.3%. The levels of Sema4A were not changed by Fingolimod treatment. Fingolimod reduced the relapse rates of patients both with low and high Sema4A. Fingolimod also ameliorated the severity of mice with EAE given Sema4A-Fc.
Conclusions: Fingolimod is more suitable for patients with high Sema4A levels than IFN-β
Disclosure: There is nothing to disclose.
Abstract: P1122
Type: Poster
Abstract Category: Pathology and pathogenesis of MS - Biomarkers
Backgrounds: Although interferon-beta (IFN-β) is the first-line therapy in relapsing-remitting multiple sclerosis (RRMS), one-third of patients are poor responders to IFN-β therapy. Currently, other disease-modifying drugs (DMDs) such as Fingolimod, Natalizumab, and BG12 become available. However, the problem is that there are no suitable biomarkers for the selection of treatment of MS. We previously reported that immune semaphorin Sema4A is increased in the sera of MS patients and those with high Sema4A do not respond well to IFN-β therapy. We also reported that recombinant Sema4A inhibits the therapeutic effect of IFN-β in experimental autoimmune encephalomyelitis (EAE). However, it remains unknown whether other DMDs are effective for patients with high Sema4A or not.
Objective: The purpose of this study is to investigate whether patients with high Sema4A respond to Fingolimod or not.
Methods: Fifty-six patients with MS who have been treated with Fingolimod were investigated. The levels of serum Sema4A were assayed with a sandwich ELISA, and the association between Sema4A levels and clinical characteristics including responsiveness to Fingolimod treatment was analyzed. We also investigated the efficacy of Fingolimod in EAE mice given Sema4A-Fc.
Results: The serum Sema4A titer was 2877 ± 5469. The ratio of patients with high Sema4A levels (≧2500) was 30.3%. The levels of Sema4A were not changed by Fingolimod treatment. Fingolimod reduced the relapse rates of patients both with low and high Sema4A. Fingolimod also ameliorated the severity of mice with EAE given Sema4A-Fc.
Conclusions: Fingolimod is more suitable for patients with high Sema4A levels than IFN-β
Disclosure: There is nothing to disclose.