Gilenya® data presenteras på ACTRIMS-ECTRIMS

* No evidence of disease activity’ (NEDA), the ultimate treatment goal in MS, is currently assessed by measuring relapses, MRI lesions and disability progression
* New Gilenya data will highlight importance of brain shrinkage as NEDA fourth key measure, giving physicians more complete assessment of MS disease in patients
* Separate analyses will confirm the clinical relevance of brain shrinkage based on its association with future long-term MS disability progression

Novartis announced today that new analyses to be presented at the Joint ACTRIMS-ECTRIMS Meeting in Boston, USA from September 10-13, 2014, will add to the growing evidence confirming the importance of redefining treatment goals in multiple sclerosis (MS). The goal of MS treatment is to have ’no evidence of disease activity’ or ’NEDA’, which is currently defined as no evidence of relapses, MRI lesions and disability progression. New data to be presented will reinforce the clinical relevance of brain shrinkage (brain volume loss) and highlight the benefit of including it as a fourth key measure of MS in the definition of NEDA[1],[2]. In addition, other analyses will show that patients treated with Gilenya® (fingolimod) were more likely to achieve NEDA based on assessment of these four key measures, including MS-related brain shrinkage, than those on placebo[3].

Everyone’s brain shrinks as they age, but people with MS experience brain shrinkage up to three to five times faster[4-7].  Brain shrinkage begins early in MS, even before symptoms occur[8-11], and is associated with a loss of physical and cognitive function[12].

New Gilenya analyses will show how brain shrinkage is associated with future long-term disability progression in patients with MS and that patients with relapsing MS treated with Gilenya had lower rates of brain shrinkage that importantly were sustained over time[3]. The findings will also provide further evidence of the high efficacy of Gilenya on MS disease activity across four key measures[3].

”The data at ACTRIMS-ECTRIMS will reinforce the role of brain shrinkage and its association with future long-term MS disability progression,” said Vasant Narasimhan, Global Head of Development at Novartis Pharmaceuticals, ”Novartis is committed to improving treatment outcomes for people with MS, and we believe that by including brain shrinkage as part of NEDA, clinicians can gain a more complete understanding of disease progression and treatment effects.”

Novartis MS portfolio highlights at the Joint ACTRIMS-ECTRIMS Meeting will include four oral presentations and 22 poster presentations on Gilenya, and two poster presentations on siponimod.

 

References
[1] Jeffrey D et al. Brain volume change by quartile and disability progression in multiple sclerosis: a 4-year analysis of the phase 3 FREEDOMS trial and its extension. Abstract presented at: 2014 Joint ACTRIMS-ECTRIMS Meeting; September 10-13, 2014; Boston, Massachusetts. Abstract 36. Free communication FC2.3.
[2]  Radue E.W. et al. Sustained low rate of brain volume loss under long-term fingolimod treatment in relapsing multiple sclerosis: Results from the LONGTERMS study. Abstract presented at: 2014 Joint ACTRIMS-ECTRIMS Meeting; September 10-13, 2014; Boston, Massachusetts. Abstract 1346. Poster 439.
[3]  Kappos L et al. Inclusion of brain volume loss in a revised measure of multiple sclerosis disease-activity freedom: the effect of fingolimod. Abstract presented at: 2014 Joint ACTRIMS-ECTRIMS Meeting; September 10-13, 2014; Boston, Massachusetts. Abstract 1570. Free communication FC1.5.
[4]  De Stefano N et al. Proportion of patients with BVL comparable to healthy adults in fingolimod phase 3 MS studies. Abstract presented at: 66th AAN Annual Meeting; April 26 – May 3, 2014; Philadelphia, Pennsylvania. Oral session S13:006.
[5]  Hedman AM et al. Human Brain Changes Across the Life Span: a review of 56 longitudinal magnetic resonance imaging studies. Human Brain Mapping 2012; 33: 1987-220
[6]  Barkhof F et al. Imaging outcomes for neuroprotection and repair in multiple sclerosis trials. Nat Rev Neurol. 2009;5(5):256-266.
[7]  Bermel RA & Bakshi R. The measurement and clinical relevance of brain atrophy in multiple sclerosis. Lancet Neurol. 2006;5(2):158-170.
[8]  Di Stefano N et al. Clinical Relevance of Brain Volume Measures in Multiple Sclerosis. CNS Drugs 2014; published online January 22, 2014.
[9]  Pérez-Miralles F et al. Clinical impact of early brain atrophy in clinically isolated syndromes. Mult Scler. Published online: May 7, 2013.
[10] Filippi M et al. Evidence for widespread axonal damage at the earliest clinical stage of multiple sclerosis. Brain. 2003;126(Pt 2):433-437.
[11] Filippi M et al. The contribution of MRI in assessing cognitive impairment in multiple sclerosis. Neurology 2010; 75: 2121-28.
[12] Popescu V. et al; on behalf of the MAGNIMS Study Group. Brain atrophy and lesion load predict long term disability in multiple sclerosis. J Neurol Neurosurg Psychiatry. Mar 23, 2013.
[13] http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001747/. Accessed August 2014.
[14] http://www.nationalmssociety.org/about-multiple-sclerosis/what-we-know-about-ms/symptoms/index.aspx. Accessed August 2014.
[15] http://www.msif.org/includes/documents/cm_docs/2013/m/msif-atlas-of-ms-2013-report.pdf?f=1. Accessed August 2014.
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[20] Cohen JA et al.; for TRANSFORMS Study Group. Oral fingolimod or intramuscular interferon for relapsing multiple sclerosis. N Engl J Med. 2010;362(5):402-415.
[21] Kappos L et al.; for FREEDOMS Study Group. A placebo-controlled trial of oral fingolimod in relapsing multiple sclerosis.
[22] Montalban et al. Long-term efficacy of fingolimod in patients with relapsing-remitting multiple sclerosis previously treated with interferon beta-1a or disease-modifying therapies: A Post-hoc analysis of the TRANSFORMS 4.5 year extension study. European Neurological Society, June 10, 2013 P539.
[23] Kappos L et al. Phase 3 FREEDOMS study extension: fingolimod (FTY720) efficacy in patients with relapsing-remitting multiple sclerosis receiving continuous or placebo-fingolimod switched therapy for up to 4 years. Poster presented at: 28th Congress of the European Committee for Treatment and Research in Multiple Sclerosis; October 10-13, 2012; Lyon, France. Poster P979.
[24] Chin PS et al. Early effect of fingolimod on clinical and MRI related outcomes in relapsing multiple sclerosis. Poster presented at: 28th Congress of the European Committee for Treatment and Research in Multiple Sclerosis; October 10-13, 2012; Lyon, France. Abstract P459.
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[27] Data on file. Novartis Pharmaceuticals.