Paris, France, 25 May 2016 – MedDay, a biotechnology company focused on the treatment of nervous system disorders, announces that an oral presentation entitled “High doses of biotin in progressive multiple sclerosis: extension phase results of the MS-SPI trial” will be given by Professor Ayman Tourbah, Principal Investigator of the Phase 3 study, at the 2nd Congress of the European Academy of Neurology (EAN) in Copenhagen, Denmark. The oral Session “MS and related disorders 3” will take place on Sunday, 29 May 2016 from 14:45 to 16:15 CEST in Hall C.
The MS-SPI trial tested the efficacy of MD1003, a patented pharmaceutical-grade biotin administered at a dose of 300 mg per day, in the treatment of multiple sclerosis (MS) and particularly of the most difficult to treat “not-active progressive MS,” for which there is currently no approved drug. Data previously presented at the American Academy of Neurology Annual Meeting (AAN) in April 2015 showed that the MS-SPI study’s primary endpoint was met and that MD1003 is the first drug capable of reversing disease progression in patients with progressive MS. Extension phase data announced at AAN in 2016 demonstrated sustained efficacy for up to 2 years and reconfirmed a good safety profile of MD1003.
The management team from MedDay will be in attendance at the EAN congress and available at MedDay’s booth, C44.
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MedDay is a privately held biotechnology company developing new drugs for nervous system disorders. The company was founded in 2011 by Frédéric Sedel, MD, PhD (Chief Executive Officer); and Guillaume Brion, MD (Chief Operating Officer). The Company’s most advanced pipeline candidate is MD1003 for the treatment of primary and secondary progressive multiple sclerosis. MedDay is well funded by investors including Sofinnova Partners, InnoBio, Edmond de Rothschild Investment Partners and Bpifrance Large Venture. For more information, please see: medday-pharma.cdmail.biz.
About progressive MS
MS is the most common disabling neurological disease among young adults, with first symptoms typically manifesting between 20 and 40 years of age. In the majority (85%) of cases, patients experience an initial phase of relapsing-remitting neurological dysfunction (RRMS), which typically evolves into a secondary progressive disease at a later point in the clinical course (SPMS). Once MS is in the progressive phase, individuals experience a gradual worsening of neurological disability. Primary progressive MS (PPMS) characterized by disease progression from onset affects 10–15% of MS patients. Progressive disease (either SPMS or PPMS) can be further divided into active or not-active progressive disease based on the existence or not of superimposed inflammatory activity. Immunosuppressive and immunomodulatory drugs have been shown to decrease the frequency of relapses and CNS lesions in relapsing remitting MS. These drugs may also delay progression in the subgroup of patients with active progressive MS. However, there is currently no drug targeting non-active progressive MS, which represents the larger and most difficult to treat population.
In relapsing MS, lymphocytes and monocytes of the peripheral adaptive immune system infiltrate perivascular brain and spinal cord tissue causing focal inflammation that can be identified on imaging as acute contrast enhancing lesions. The histopathological hallmark of these lesions is injury to oligodendroglia cells that wrap axons in myelin, the cell membrane that enhances electrical resistance and allows saltatory conduction through the nervous system. Axons themselves are typically relatively spared. In contrast, progressive MS is mainly associated with progressive axonal degeneration, chronic demyelination and, usually, little or no inflammation. It is considered that axonal degeneration results from energy failure caused by chronic demyelination and mitochondrial dysfunction.
MD1003 is a patented, highly dosed pharmaceutical grade biotin that has already shown efficacy in patients with progressive multiple sclerosis. MD1003 has a unique mode of action which potentially acts on two targets related to progressive MS: (1) it activates the Krebs cycle, the main route for energy production that protects against axonal degeneration and (2) it potentially activates acetyl-CoA carboxylases (ACC1 and ACC2), the rate-limiting enzymes in the synthesis of fatty acids required for myelin repair. The drug is already commercialized in some European countries under early-access programs.
For more information, please contact:
Consilium Strategic Communications
Mary-Jane Elliott, Jonathan Birt, Laura Thornton
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