Rasator 0.5/Rasator 1 Mechanism of Action

Dopaminergic Agent (Monoamine Oxidase Inhibitor).
Pharmacology: Pharmacodynamics: Mechanism of Action: Rasagiline is a selective irreversible inhibitor of MAO type B, the enzyme, 80% defining MAO activity in the brain and dopamine metabolism. Rasagiline is 30-80 times more active with regard to MAO-B, than to another type of this enzyme - MAO-A. As a result of inhibiting MAO-B, Rasagiline may cause an increase in dopamine levels in CNS, reducing formation of toxic free radicals, which are excessive in Parkinson's disease patients. Rasagiline was also shown to have neuroprotective effect. Unlike non-selective MAO inhibitors, Rasagiline at the indicated dose does not block the metabolism of dietary intake of biogenic amines (e.g., tyramine), therefore not causing tyramine-caused hypertensive syndrome ("cheese effect").
Pharmacokinetics: Absorption: After oral administration, Rasagiline is rapidly absorbed, reaching peak plasma concentration (Cmax) in approximately 0.5 hours. The absolute bioavailability of a single rasagiline dose is about 36%. Food does not affect the Tmax of rasagiline, although Cmax and exposure (AUC) are decreased by approximately 60% and 20%, respectively, when the medicinal product is taken with a high fat meal.
Distribution and Metabolism: Rasagiline pharmacokinetics are linear with dose over the range of 0.5-2 mg. Plasma protein binding is approximately 60 to 70%. Rasagiline undergoes almost complete biotransformation in the liver prior to excretion. The metabolism of rasagiline proceeds through two main pathways: N-dealkylation and/or hydroxylation to yield: 1-aminoindan, 3-hydroxy-N-propargyl-1 aminoindan and 3-hydroxy-1-aminoindan. Both routes of rasagiline metabolism are dependent on cytochrome P450 system, with CYP1A2 being the major iso-enzyme involved in rasagiline metabolism.
Elimination: Rasagiline elimination occurs primarily via urine (>60%) and secondarily via faeces (>20%). Less than 1% of rasagiline is excreted as unchanged product in urine. Its terminal half-life is 0.6-2 hours.
Special Populations: Renal impairment: Rasagiline's pharmacokinetics characteristics in subjects with mild and moderate renal impairment were similar to healthy subjects.
Hepatic impairment: In subjects with mild hepatic impairment, AUC and Cmax were increased by 80% and 38%, respectively. In subjects with moderate hepatic impairment, AUC and Cmax were increased by 568% and 83%, respectively.
Elderly: Rasagiline can be administered at the recommended dose in the elderly (≥65 years) since age has little influence on rasagiline pharmacokinetics.
Pediatric Population: Use of rasagiline in patients below 18 years of age has not been established.
Gender: The pharmacokinetic profile of rasagiline is similar in men and women.