| Class | Acetylcholinesterase inhibitor |
|---|---|
| Chemistry |
Piperidine derivative |
| Routes of administration |
Oral or transdermal |
| Absorption |
100% oral bioavailability |
| Solubility |
pKa = 8.9, good solubility in both water and lipid |
| Distribution |
VOD=12L/kg, 96% protein bound |
| Metabolism |
Small fraction etabolised in the liver; mostly eliminated unchanged via the urine |
| Elimination |
50-70% is eliminated renally as unchanged drug |
| Time course of action |
Half-life ~ 80 hours |
| Target receptor |
Acetylcholinesterase |
| Mechanism of action |
By binding to acetylcholinesterase, donepezil acts as a competing substrate, replacing acetylcholine and decreasing acetylcholinesterase activity. The drug is metabolised much more slowly than acetylcholine, which means the enzyme is blocked for a sustained period. |
| Clinical effects | |
| Literature reference |
Wilkinson, 1999 |
| CICM details of understanding | Not specifically listed in the CICM syllabus |
| Mentioned around Deranged Physiology | |
| Related SAQs |