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Systematic (IUPAC) name
CAS number 1875-50-9
ATC code N04BD02
PubChem 3052776
Chemical data
Formula C12H13N 
Mol. mass 171.238 g/mol
Pharmacokinetic data
Bioavailability 36%
Protein binding 88 – 94%
Metabolism Hepatic (CYP1A2-mediated)
Half life 3 hours
Excretion Renal and fecal
Therapeutic considerations
Licence data


Pregnancy cat.


Legal status


Routes Oral

Rasagiline (trade name Azilect®) is a irreversible inhibitor of monoamine oxidase used as a monotherapy in early Parkinson's disease or as an adjunct therapy in more advanced cases. Adequate studies to determine if rasagline is selective for MAO-B have been conducted.[1] It was developed by Teva Neuroscience, initially investigated by Prof. Moussa Youdim and Prof. John Finberg of the Faculty of Medicine, Technion – Israel Institute of Technology.[2]


Mechanism of Action

Human cells contain two forms of monoamine oxidase, MAO-A and MAO-B. Both are found in the brain, but MAO-B is far more prevalent and is responsible for the breakdown of dopamine after its release into the synapse. Parkinson's disease is characterized by the death of cells that use dopamine to transmit their signals, this results in a decrease in synaptic signal strength and concommitant symptomology. By inhibiting the breakdown of dopamine in the synapse, rasagiline permits the signaling neurons to reabsorb more of it for reuse later, somewhat compensating for the diminished quantities manufactured.

Selegiline was the first MAO inhibitor approved for use in Parkinson's disease in the United States. It is chemically similar to methamphetamine and its metabolic breakdown path eventually yields l-methamphetamine derivatives that have been associated with cardiac and psychiatric effects in some patients. The chief metabolite of rasagiline is aminoindan which has no amphetamine characteristics. Some clinicians believe rasagiline will be better tolerated in sensitive patients for these reasons.

Laboratory studies show that rasagiline has in vitro and in vivo neuroprotective effects but its neuroprotective effect in Parkinson's disease patients is unknown at present. These studies show that MAO-B can, under some circumstances, create a harmful chemical called MPP+ that in turn creates free radicals. These studies show that amphetamines may block this neuroprotective effect; since rasagiline does not metabolize to amphetamines or their metabolites it may have superior neuroprotective properties when compared to selegiline. There is uncertainty because the mechanism of cell death in human PD may or may not involve the actions of free radicals, but there is suggestive evidence that the drug slows disease progression.


Rasagiline is broken down via CYP1A2, part of the cytochrome P450 metabolic path in the liver. It is probably contraindicated in patients with hepatic insufficiency and its use should be monitored carefully in patients taking other drugs that alter the normal effectiveness of this metabolic path. Examples include but are not limited to cimetidine, ciprofloxacin and omeprazole.


Monotherapy in Early PD

A study called TVP-1012 (an early name for rasagiline) in Early Monotherapy for Parkinson's Disease Outpatients (TEMPO) enrolled 404 patients. A double-blind, randomized, delayed start study, it evaluated patients for a year using a placebo and doses of 1mg and 2mg per day. The initial six-month placebo controlled part of the study yielded data that led organizers to conclude both rasagiline doses were superior to placebo. The evaluation compared patients' Unified Parkinson's Disease Rating Scale (UPDRS) scores. The UPDRS is a standard method of measuring PD severity. Starting at six months the placebo treated group received the higher dosage of rasagiline (2mg) until the conclusion of the study at twelve months and patients' UPDRS scores were compared again. Patients who had consistently received the higher dose had significantly better scores than patients who had received the placebo, and somewhat better scores than other groups. These data suggest but do not prove a neuroprotective effect. Some patients entered an open-label follow up study. About half of them did not require additional dopaminergic therapy two years later. Over a six and a half year period the mean deterioration in UPDRS scores for patients receiving some level of rasagiline therapy was 2-3 points. Other clinical studies of placebo treated patients with early PD reported a diminution of 8-12 points per year.

Adjunct Therapy in Advanced PD

An eighteen week double-blind placebo-controlled study called the Lasting Effect in Adjunct Therapy with Rasagiline Given Once Daily (LARGO) compared the drug to entacapone and a placebo in 687 patients experiencing motor fluctuations, a hallmark symptom of PD. Rasagiline at a 1mg dose significantly reduced daily off time (1.18 hours) compared to the placebo (0.4 hours) and increased on time without dyskinesia by 0.85 hours. This was approximately the same benefit granted by entacapone.

The Parkinson's Rasagiline: Efficacy and Safety in the Treatment of "OFF" (PRESTO) study monitored 472 patients treated with levodopa for motor fluctuations despite attempts to optimize dopaminergic therapy. PRESTO did not have an active comparison drug; its patients randomly received a 0.5mg dose, a 1mg dose, or a placebo. Patients receiving both doses of rasagiline experienced less significantly less off time (1.4 hours and 1.8 hours) than did those who received the placebo.

These studies suggest patients with advanced and fluctuating PD benefit in the short term from rasagiline therapy but do not comment on long term effects.


Between the TEMPO, LARGO and PRESTO studies 530 patients were treated with the recommended dosage of 1mg/day for a total of 212 patient-years. The number of patients who discontinued participation due to adverse symptoms was not significantly different between active drug and placebo.

Although rasagiline is an inhibitor of MAO-B, some concern still exists regarding possible drug interactions with medications that are normally considered contraindicated when taken with general MAO inhibitors since adequate studies to establish rasagiline's selectivity for MAO-B have not been conducted.[1] The concern revolves around a possible serotonin-syndrome effect, which was not known to occur during clinical trials despite patients being allowed to take certain antidepressant drugs that are normally contraindicated with general MAO inhibitors. Concern for a possible interaction between rasagiline and tyramine also exists, although no dietary restrictions were imposed during the TEMPO, PRESTO and LARGO studies and no hypertensive crises resulted due to the possible interaction of tyramine and rasagiline.

CAS# 136236-51-6


  1. ^ a b Prescribing Information. Teva Neurosciences (2005-06). Retrieved on 2007-03-20.
  2. ^ Lakhan SE. From a Parkinson's disease expert: Rasagiline and the Future of Therapy. Molecular Neurodegeneration 2007;2(13).
  • Chen JJ, Swope D. Clinical pharmacology of rasagiline: a novel, second-generation propargylamine for the treatment of Parkinson disease. J Clin Pharmacol 2005;45:878-94.
  • Fernandez, Hubert H., What Patients Need to Know About Rasagiline, Parkinson Report Summer 2006, National Parkinson Foundation, pp 15-17.
  • Oldfield V, Keating GM, Perry CM. Rasagiline: a review of its use in the management of Parkinson's disease. Drugs 2007;67(12):1725-47.
This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Rasagiline". A list of authors is available in Wikipedia.
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