| Class | Monoamine oxidase inhibitor |
|---|---|
| Chemistry |
Substituted amphetamine
|
| Routes of administration |
Oral only |
| Absorption |
Rapidly and completely absorbed; bioavailability ~ 50%
|
| Solubility |
pKa 9.6; reasonably water-soluble
|
| Distribution |
VOD=1.75L/kg; probably highly protein-bound (eg. to MAO!)
|
| Metabolism |
Extensively metabolised, probably in the liver, into N-acetylated and ring-hydroxylated metabolites, which retain some limited MAO-inhibitory activity
|
| Elimination |
Minimum renal excretion (4% as unchanged drug)
|
| Time course of action |
Half-life is only about 2 hours, but this does not have any relationship to the duration of its effect
|
| Target receptor |
Monoamine oxidase A and B |
| Mechanism of action |
By binding to both kinds of monoamine oxidase enzymes (in a completely irreversible fashion) tranylcypramine increases the availability of catecholamine neurotransmitters (i.e. mainly noradrenaline and dopamine) |
| Clinical effects |
Hypertensive crises, hepatotoxicity, seizures, hypoglycaemia, mania, serotonin syndrome. Dangerous pharmacodynamic interactions with other antidepressants and monoaminergic drugs, as well as foods that act as catecholamine precursors |
| Literature reference |
Ulrich et al (2017) |
| CICM details of understanding | Not specifically listed in the CICM syllabus |
| Mentioned around Deranged Physiology | |
| Related SAQs |