Rivastigmine

250.34

250.34

1308068-626-2

PKI06M3IW0

DTXSID7023564

N06DA03|N - Nervous system

2924296000

32.8

2.3

Solid

1.038±0.06 g/cm3(Predicted)

316.2±34.0 °C(Predicted)

145℃

1.518

2.04e+00 g/L

-20°C

D20 -32.1° (c = 5 in ethanol)

165 Ų [M+H]+ [CCS Type: TW, Method: Major Mix IMS/Tof Calibration Kit (Waters)]

UN 2810 6.1 / PGIII

In large placebo controlled trials, rivastigmine therapy was not associated with an increased rate of serum enzyme elevations compared to placebo treatment and no instances of clinically apparent liver injury with jaundice were reported. Nevertheless, since its introduction into clinical use, rivastigmine (administered by transdermal patch) has been implicated in at least one report of clinically apparent hepatotoxicity with mild jaundice. The time to onset was 2 months and the serum enzyme elevations had a mildly hepatocellular pattern. Mild rash and eosinophilia were also present, but autoimmune features were not. Recovery was complete within 5 weeks of drug discontinuation.

40%

For the treatment of mild to moderate dementia associated with Parkinson's disease or of the Alzheimer's type.|FDA Label|Symptomatic treatment of mild to moderately severe Alzheimer's dementia.Symptomatic treatment of mild to moderately severe dementia in patients with idiopathic Parkinson's disease.|Symptomatic treatment of mild to moderately severe Alzheimer's dementia.|Treatment of dementia

Rivastigmine is an oral acetylcholinesterase inhibitor used for therapy of Alzheimer disease. Rivastigmine is associated with a minimal rate of serum enzyme elevations during therapy and is a rare cause of clinically apparent liver injury.

Alzheimer Disease Agents

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.

Drugs intended to prevent damage to the brain or spinal cord from ischemia, stroke, convulsions, or trauma. Some must be administered before the event, but others may be effective for some time after. They act by a variety of mechanisms, but often directly or indirectly minimize the damage produced by endogenous excitatory amino acids. (See all compounds classified as Neuroprotective Agents.)|Drugs that inhibit cholinesterases. The neurotransmitter ACETYLCHOLINE is rapidly hydrolyzed, and thereby inactivated, by cholinesterases. When cholinesterases are inhibited, the action of endogenously released acetylcholine at cholinergic synapses is potentiated. Cholinesterase inhibitors are widely used clinically for their potentiation of cholinergic inputs to the gastrointestinal tract and urinary bladder, the eye, and skeletal muscles; they are also used for their effects on the heart and the central nervous system. (See all compounds classified as Cholinesterase Inhibitors.)

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.|1.8 to 2.7 L/kg|renal cl=2.1-2.8 L/hr

Rivastigmine is rapidly metabolized by cholinesterase-mediated hydrolysis.

1.5 hours

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.

(S)-N-ethyl-3-((1-dimethyl-amino)ethyl)-N-methylphenylcarbamate

Human drugs -> Exelon -> EMA Drug Category|Psychoanaleptics -> Human pharmacotherapeutic group|Human drugs -> Prometax -> EMA Drug Category|Human drugs -> Rivastigmine Hexal -> EMA Drug Category|Human drugs -> Rivastigmine Sandoz -> EMA Drug Category|Human drugs -> Rivastigmine 1 A Pharma -> EMA Drug Category|Human drugs -> Rivastigmine Actavis -> EMA Drug Category|Human drugs -> Nimvastid -> EMA Drug Category|Human drugs -> Rivastigmine 3M Health Care Ltd -> EMA Drug Category|Psychoanaleptics, Anticholinesterases -> Human pharmacotherapeutic group|Human drugs -> Rivastigmine Teva -> EMA Drug Category|Anticholinesterases -> Human pharmacotherapeutic group|Human Drugs -> EU pediatric investigation plans|Human Drugs -> FDA Approved Drug Products with Therapeutic Equivalence Evaluations (Orange Book) -> Active Ingredients