| Class | Monoamine oxidase inhibitor |
|---|---|
| Chemistry |
Benzamide
|
| Routes of administration |
Oral only |
| Absorption |
Rapidly and completely absorbed; bioavailability is about 50%
|
| Solubility |
pKa 10.6; poor water solubility
|
| Distribution |
VOD = 2L/kg; 50% protein-bound
|
| Metabolism |
Hepatic metabolism; oxidation of the morpholine ring moiety, aromatic hydroxylation and deamination; multiple inactive metabolites
|
| Elimination |
Renal clearance accounts for very little total clearance, and appears to be unimportant
|
| Time course of action |
Half-life is only about 2 hours, but the duration of MAO-I effect is much greater
|
| Target receptor |
Monoamine oxidase A |
| Mechanism of action |
By binding to just MAO-A monoamine oxidase enzymes (reversibly), moclobemide increases the availability of catecholamine neurotransmitters (i.e. mainly noradrenaline and dopamine) |
| Clinical effects |
Hypertension, restlessness, agitation, nausea, insominia (i.e. features of sympathomimetic effect) |
| Literature reference |
Nair et al (1993) |
| CICM details of understanding | Not specifically listed in the CICM syllabus |
| Mentioned around Deranged Physiology | |
| Related SAQs |