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for educational and safety purposes
Rasagiline and Clorgyline both come up in the same conversations. Rasagiline: Rasagiline is a prescription tablet for Parkinson's disease that permanently switches off monoamine oxidase B, the enzyme that breaks down dopamine in the brain; the effect is to make what dopamine remains last longer. Clorgyline: Clorgyline (also spelled clorgiline) is an irreversible and selective inhibitor of monoamine oxidase A (MAO-A), an enzyme that breaks down neurotransmitters such as serotonin and noradrenaline [1][2].
Rasagiline is a prescription tablet for Parkinson's disease that permanently switches off monoamine oxidase B, the enzyme that breaks down dopamine in the brain; the effect is to make what dopamine remains last longer. Four large placebo-controlled trials show a real but modest symptom benefit, whether taken alone in early disease or added to levodopa later, where it removes roughly one hour per day of the time when levodopa is not working. Whether it actually slows the disease itself is unsettled; in the ADAGIO trial the 1 mg dose met all three of its targets while the 2 mg dose failed them, and that contradiction was never resolved. Trials in multiple system atrophy and in ALS were negative, and no evidence supports rasagiline as a cognitive enhancer in healthy people.
Clorgyline (also spelled clorgiline) is an irreversible and selective inhibitor of monoamine oxidase A (MAO-A), an enzyme that breaks down neurotransmitters such as serotonin and noradrenaline [1][2]. Developed in the 1960s and studied as a possible antidepressant, it was never brought to market and is used today chiefly as a research tool [1]. It is historically important because its ability to block one form of monoamine oxidase while sparing another helped scientists establish that the enzyme exists in two distinct types [1][2].
both fingerprints on one instrument; where the marks line up the two compounds work the same lever, where a slot goes dark only one of them touches it. read straight from each entry's affinity table; nothing here is invented.
Irreversible inhibition
Proposed anti-apoptotic and neurotrophic actions attributed to the propargylamine moiety rather than to MAO inhibition. Preclinical only; not demonstrated in humans.
Weak off-target inhibitor. Selectivity for B over A is the whole safety argument for the drug; it is preserved at 0.5 to 1 mg/day but is not absolute, and is lost at higher exposures.
Irreversible covalent inhibitor; the propargylamine group forms an adduct with the enzyme's FAD cofactor, so activity returns only as new enzyme is synthesised (weeks), not as drug clears (plasma half-life is a few hours).
Modulation
Blocking MAO-B slows the oxidative breakdown of dopamine in the basal ganglia, raising and prolonging dopamine availability. This is the accepted explanation for the symptomatic benefit and for the levodopa-sparing effect.
Irreversible inhibition
strengths are the entries' qualitative ratings (strong / moderate / weak); Ki and EC50 figures appear where an entry records them.
easiest to source: Rasagiline is currently listed by more trusted vendors (1), so it's the simpler one to get hold of. for effects and safety, read each full entry; this is educational, not medical advice.