| Class | Melatonin receptor agonist |
|---|---|
| Chemistry |
Acetamide |
| Routes of administration |
Oral only |
| Absorption |
Well absorbed (78%), with terrible bioavailability (less than 5%) |
| Solubility |
pKa 15.6; minimally water-soluble |
| Distribution |
VOD=30L/kg; 95% protein-bound |
| Metabolism |
Hepatic metabolism by 7-O-demethylation and hydroxylation; all metabolites are inactive at MT receptors |
| Elimination |
About 80% of the metabolites are eliminated in the urine, and the rest in the bile |
| Time course of action |
Elimination half-life is about 2.3 hours; duration of activity is much longer |
| Target receptor |
Melatonin MT1 and MT2 receptors, which are G-protein coupled receptors |
| Mechanism of action |
Mechanism of action is thought to be related to the regulation of dopamine release by melatonin receptor activation (i.e. the efefct of agomelatine, as an MT1 and MT2 agonist, is to increase the concentration of dopamine). |
| Clinical effects |
Both sedation and insomnia have been reported as side effects, but generally the incidence of side effects seems to be no greater than placebo |
| Literature reference |
Zupancic et al (2006) |
| CICM details of understanding | Not specifically listed in the CICM syllabus |
| Mentioned around Deranged Physiology | |
| Related SAQs |