| Indication |
For the treatment of mild to moderate dementia associated with Parkinson's disease or of the Alzheimer's type. |
| Pharmacodynamics |
Rivastigmine is a parasympathomimetic and a reversible
cholinesterase inhibitor. An early pathophysiological feature of
Alzheimer's disease that is associated with memory loss and cognitive
deficits is a deficiency of acetylcholine as a result of selective loss
of cholinergic neurons in the cerebral cortex, nucleus basalis, and
hippocampus. Tacrine is postulated to exert its therapeutic effect by
enhancing cholinergic function. While the precise mechanism of
rivastigmine's action is unknown, it is postulated to exert its
therapeutic effect by enhancing cholinergic function. This is
accomplished by increasing the concentration of acetylcholine through
reversible inhibition of its hydrolysis by cholinesterase. If this
proposed mechanism is correct, rivastigmine's effect may lessen as the
disease progresses and fewer cholinergic neurons remain functionally
intact. |
| Mechanism of action |
Rivastigmine is a carbamate derivative that is structurally
related to physostigmine, but not to donepezil and tacrine. The precise
mechanism of rivastigmine has not been fully determined, but it is
suggested that rivastigmine binds reversibly with and inactivates
chlolinesterase (eg. acetylcholinesterase, butyrylcholinesterase),
preventing the hydrolysis of acetycholine, and thus leading to an
increased concentration of acetylcholine at cholinergic synapses. The
anticholinesterase activity of rivastigmine is relatively specific for
brain acetylcholinesterase and butyrylcholinesterase compared with those
in peripheral tissues. |
| Absorption |
Not Available |
| Volume of distribution |
|
| Protein binding |
40% |
| Metabolism |
Rivastigmine is rapidly metabolized by cholinesterase-mediated hydrolysis. |
| Route of elimination |
Rivastigmine is extensively metabolized primarily via
cholinesterase-mediated hydrolysis to the decarbamylated metabolite
NAP226-90. Renal excretion of the metabolites is the major route of
elimination. Less than 1% of the administered dose is excreted in the
feces. |
| Half life |
1.5 hours |
| Clearance |
|
| Toxicity |
Not Available |
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