| Class | Monoamine oxidase inhibitor |
|---|---|
| Chemistry |
Substituted amphetamine
|
| Routes of administration |
Oral only |
| Absorption |
Well absorbed (even better with food); only about 10% bioavailability due to extensive first pass effect
|
| Solubility |
pKa 8.6; highly lipid-soluble,
|
| Distribution |
VOD=about 25L/kg; highly protein-bound (96%)
|
| Metabolism |
Hepatic metabolism; rapidly metabolized by the microsomal enzymes to amphetamine, methamphetamine, and desmethyl-deprenyl
|
| Elimination |
Renal clearance is important: 86% of the active metabolites are recovered in the urine
|
| Time course of action |
Elimination half-life of the parent drug is only aout 1.5 hours, but it leaves behind active metabolites with longer periods of activity, and its MAO-I effect is long lasting
|
| Target receptor |
Monoamine oxidase A only |
| Mechanism of action |
By binding to just MAO-A monoamine oxidase enzymes (in a completely irreversible fashion) selegiline increases the availability of catecholamine neurotransmitters (i.e. mainly noradrenaline and dopamine) |
| Clinical effects |
Euphoria, insomnia, hypertension (i.e. the effects of amphetamine intoxication,it being one of the major metabolites) |
| Literature reference |
Magyar (2011) |
| CICM details of understanding | Not specifically listed in the CICM syllabus |
| Mentioned around Deranged Physiology | |
| Related SAQs |