RESEARCH MONOGRAPH · KDC-MN-225
Rasagiline
Rasagiline (Azilect) is a second-generation MAO-B inhibitor from Teva, approved by the FDA in 2006 for Parkinson disease. It is structurally distinct from selegiline (built around an indane scaffold rather than a phenethylamine) and the key practical advantage is that the body does not break it down into amphetamine derivatives. That eliminates one of the more annoying features of selegiline and makes drug screening cleaner. Like selegiline it binds MAO-B irreversibly, so a single daily dose keeps the enzyme suppressed for weeks. The ADAGIO trial controversially suggested it might also slow disease progression rather than just treat symptoms, although that finding has not been universally accepted. Used as monotherapy in early Parkinson and as an add-on in advanced disease. Not stocked by Kodiac. This monograph is provided for research and educational reference.
Intrigue 0–100 blends mechanism novelty, evidence strength, and translational potential. Kodiac editorial, not peer-reviewed.
Selective irreversible MAO-B inhibitor (second-generation)
A second-generation propargyl MAO-B inhibitor lacking the amphetamine metabolites of selegiline.
Abstract
Rasagiline ((R)-N-(prop-2-yn-1-yl)-2,3-dihydro-1H-inden-1-amine; CAS 136236-51-6; molecular formula C12H13N; molecular weight 171.24) is a second-generation irreversible MAO-B inhibitor developed at Teva and approved by the FDA in 2006 under the trade name Azilect. Structurally distinct from selegiline by the indane scaffold replacing the phenethylamine, rasagiline does not yield amphetamine-class metabolites, simplifying its drug screening profile and avoiding the subjective stimulation associated with selegiline. MAO-B selectivity is approximately 14:1 over MAO-A at clinical dose (1 mg daily); the inhibition is irreversible and recovery requires de novo enzyme synthesis (approximately 14-day washout). Approved as monotherapy in early Parkinson disease and as adjunct to levodopa in advanced disease. The ADAGIO trial suggested possible disease-modifying effect for the 1 mg dose, though this remains debated. Tyramine restriction is not required at 1 mg daily; at higher experimental doses (2 mg) the cheese-effect risk emerges. Plasma half-life is approximately 3 hours, but the irreversible binding produces effective enzyme inhibition for weeks. Used as a reference second-generation MAO-B inhibitor in Parkinson research.
Mechanism of action
Irreversible MAO-B inhibition (selective at 1 mg). Indane scaffold avoids amphetamine metabolites of selegiline. Effective enzyme inhibition persists for weeks owing to irreversible binding.
Reported research dose ranges
Reported research dose ranges in the literature.
References
- Olanow CW, et al. A double-blind, delayed-start trial of rasagiline in Parkinson's disease. N Engl J Med 2009.
- Chen JJ, Swope DM. Pharmacotherapy for Parkinson's disease. Pharmacotherapy 2007.
- Lecht S, et al. Rasagiline - a novel MAO B inhibitor. CNS Drug Rev 2007.
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The full reference document is provided strictly for research use only. It reports research dose ranges from the published literature, not instructions for use in humans or animals.
FOR RESEARCH USE ONLY. Not for medical, diagnostic, or therapeutic purposes. Not for human consumption. All information is provided for research and educational purposes only.