In 2003 Teva partnered with Eisai, giving Eisai the right to jointly market the drug for Parkinsons in the US, and to co-develop and co-market the drug for Alzheimers and other neurological diseases.It was approved by the European Medicines Agency for Parkinsons in 2005 and in the US in 2006.: 255

Research
Rasagiline was tested for efficacy in people with multiple system atrophy in a large randomized, placebo-controlled, double-blind disease-modification trial; the drug failed.Teva conducted clinical trials attempting to prove that rasagiline did not just treat symptoms, but was a disease-modifying drug - that it actually prevented the death of the dopaminergic neurons that characterize Parkinsons disease and slowed disease progression. They conducted two clinical trials, called TEMPO and ADAGIO, to try to prove this. The FDA advisory committee rejected their claim in 2011, saying that the clinical trial results did not prove that rasagiline was neuroprotective. The main reason was that in one of the trials, the lower dose was effective at slowing progression, but the higher dose was not, and this made no sense in light of standard dose-response pharmacology. See also
Selegiline
Ladostigil

References
External links
"Rasagiline". Drug Information Portal. U.S. National Library of Medicine. "Rasagiline mesylate". Drug Information Portal. U.S. National Library of Medicine.
During a CIS, there is a subacute attack suggestive of demyelination but the patient does not fulfill the criteria for diagnosis of multiple sclerosis. Treatment with interferons after an initial attack decreases the risk of developing clinical definite MS.

Relapsing-remitting MS
Medications are modestly effective at decreasing the number of attacks in relapsing-remitting multiple sclerosis and in reducing the accumulation of brain lesions, which is measured using gadolinium-enhanced magnetic resonance imaging (MRI). Interferons reduce relapses by approximately 30% and their safe profile make them the first-line treatments. Nevertheless, not all the patients are responsive to these therapies. It is known that 30% of MS patients are non-responsive to Beta interferon. They can be classified in genetic, pharmacological and pathogenetic non-responders. One of the factors related to non-respondance is the presence of high levels of interferon beta neutralizing  antibodies. Interferon therapy, and specially interferon beta-1b, induces the production of  neutralizing  antibodies, usually in the second 6 months of treatment, in 5 to 30% of treated patients. Moreover, a subset of RRMS patients with specially active MS, sometimes called "rapidly worsening MS" are normally non-responders to interferon beta-1b.While more studies of the long-term effects of the drugs are needed,  some data on the effects of interferons indicate that early-initiated long-term therapy is safe and it is related to better outcomes. More recent data suggest that interferon betas does not hasten disability.Interferon-β exacerbates Th17-mediated inflammatory disease. Commercial formulations
Betaferon/Betaseron is marketed today by Bayer Pharma.