| Class | Acetylcholinesterase inhibitor |
|---|---|
| Chemistry |
Aryl carbamate |
| Routes of administration |
Oral or transdermal |
| Absorption |
Completely absorbed, 40% oral bioavailability |
| Solubility |
pKa = 8.85, good solubility in both water and lipid |
| Distribution |
VOD = 1.8-2.7 L/kg, minimally protein bound |
| Metabolism |
Rapidly hydrolysed by esterases, with minimal involvement by the liver |
| Elimination |
minimal renal elimination |
| Time course of action |
Half-life 1.4-1.7 hrs (duration of effect is closer to 10 hours) |
| Target receptor |
Acetylcholinesterase |
| Mechanism of action |
By binding to acetylcholinesterase, rivastigmine 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 |
Colovic et al, 2013 |
| CICM details of understanding | Not specifically listed in the CICM syllabus |
| Mentioned around Deranged Physiology | |
| Related SAQs |