Compare Acorda Therapeutics vs Nuon Therapeutics
Customers evaluate the quality of Acorda Therapeutics's products using the following success metrics.
Acorda Therapeutics is 29 yrs old and is based in United States.
Acorda Therapeutics, a biotechnology company, is developing therapies for spinal cord injury (SCI and related neurological conditions, including multiple sclerosis (MS. The Companyƒ-s lead product, Fampridine-SR, is in Phase 3 clinical trials for chronic SCI and Phase 2 for MS. Acordaƒ-s technology platform includes two remyelinating agents in preclinical development for MS. They include M1, a class of human monoclonal antibodies, and GGF2, a product of the neuregulin 1 gene. Both agents have been shown to restore myelin in the brain and spinal cord in animal models of MS. Additionally, Acorda is developing multiple approaches to regeneration and repair of the spinal cord and brain. In 2002, Acorda was the recipient of the National Spinal Cord Injury Associationƒ-s L. W. Freeman Award for scientific research. Nasdaq: ACOR
Nuon Therapeutics is 22 yrs old and is based in United States.
Nuon Therapeutics discovers novel uses for marketed drugs. The advantage of this approach is that the development program for the marketed indication will have investigated the compounds toxicity and established its tolerability. This makes it possible to proceed directly to clinical trials once the efficacy of the compound has been established in animal models. The costs and risks involved in the drug development process are greatly reduced. Tranilast is under development for the treatment of patients with multiple sclerosis. The only drugs available for the treatment of patients with relapsing-remitting and secondary- progressive multiple sclerosis are interferon-beta, glatiramer acetate and mitoxantrone which reduce the number of relapses and the rate of disease progression. Tysabri is a monoclonal antibody for the treatment of patients with relapsing forms of multiple sclerosis. There is an urgent need for new therapies which can be orally administered and are more cost effective. Tranilast inhibits antigen-specific T cell proliferation, skews a TH1-type T cell response to TH2 and suppresses the activation of antigen presenting cells by interfering with signal transducer and activator of transcription (STAT) pathways. The oral administration of Tranilast reverses paralysis in mice with established experimental autoimmune encephalomyelitis.
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