Rivastigmine, sold under the brand name Exelon, is a cholinergic agent used to treat mild to moderate Alzheimer's dementia or dementia due to Parkinson's disease. The drug can be taken orally or by transdermal patch; the latter form reduces the incidence of side effects, including nausea and vomiting. The drug is excreted in the urine, and appears to have relatively few drug interactions. Rivastigmine was developed by Marta Weinstock-Rosin of the Department of Pharmacology at the Hebrew University of Jerusalem and sold to Novartis by Yissum Commercial Development. It is a semisynthetic derivative of physostigmine. It has been available in capsule and liquid formulations since 1997. In 2006 it became the first product approved worldwide for the treatment of mild to moderate dementia due to Parkinson's disease; in 2007, rivastigmine transdermal patches became the first patches for the treatment of dementia. Rivastigmine tartrate is a white, lipophilic, hydrophilic crystalline powder. It is available in several forms: capsules, solutions, and skin patches. Like any cholinesterase inhibitor, it requires a gradual increase in dose over several weeks, a phase called titration. Oral doses of rivastigmine should be titrated by 3 mg/day increments every 2-4 weeks. Oral administration begins with a dose of 1.5 mg twice daily followed by an increase in dose of 1.5 mg per dose after 4 weeks. The dose should be increased to the point where side effects are tolerable. Patients should always be reminded to take it with food. For transdermal patches, the initial dose is 4.6 mg/day and is increased to 9.5 mg per day after 4 weeks if side effects are tolerable for the patient. Patients should be reminded to change the patch daily and to change the sites of application. It is preferable to apply it to the upper back and trunk. Rivastigmine is category B for pregnancy, and there is insufficient information to monitor its risks for breastfeeding. In cases of overdose, atropine is given to treat bradycardia. Dialysis is ineffective because of the drug's half-life. Rivastigmine, a cholinesterase inhibitor, inhibits both butyriccholinesterase and acetylcholinesterase, meaning it works by inhibiting the cholinesterase enzymes that break down acetylcholine transporters in the brain. The U.S. Food and Drug Administration has approved rivastigmine in its various forms to treat mild to moderate Alzheimer's dementia and mild to moderate Parkinson's-related dementia. It has been used by approximately 6 million patients. Rivastigmine has shown significant therapeutic effects on cognitive, functional, and behavioral problems associated with Alzheimer's and Parkinson's dementia. The drug has shown real, satisfactory results in patients with both types of dementia by increasing their sense of independence, and these results have been particularly evident in the most severe cases. For example, the presence of hallucinations is an indication of a strong response to the drug in patients with Alzheimer's and Parkinson's. These effects reflect inhibition of butyric cholinesterase and suggest additional benefits over selective acetylcholinesterase inhibitors. Patients with multi-infarct dementia show modest improvements in executive and behavioral functions. In patients with schizophrenia, there is no strong evidence to support their use. Rivastigmine is similar in efficacy to donepezil and tarcine. Doses less than 6 mg/day may be ineffective. The effects of these drugs in various types of dementia, including Alzheimer's dementia, are modest, and it remains unclear which enzyme inhibitor is best for Parkinson's dementia, despite studies on rivastigmine. Side effects may include nausea, vomiting, decreased appetite, and weight loss. The strong effect of rivastigmine leads to more nausea and vomiting during the titration phase of the oral medication, which encourages taking the medication with food. However, rates of nausea and vomiting are significantly reduced when rivastigmine patches are used once daily. Patients and caregivers should be aware of the signs of potential toxicity and when to call their doctor. A rash can occur with both the skin patch and the oral medication, and a doctor should be contacted immediately. The patient should monitor for severe itching, redness, swelling, or blistering at the patch site. In this case, the patient should remove the patch, rinse the affected area, and call their doctor immediately. In a large clinical trial of rivastigmine patches in 1,195 patients with Alzheimer's disease, the target dose of the patches, which is 9.5 mg/24 hours, achieved similar results to the higher dose of rivastigmine capsules, but with one-third the risk of nausea and vomiting. The drug is well absorbed when given orally, with a bioavailability of 40% at a dose of 3 mg. The pharmacokinetics follow a linear dose relationship up to 3 mg/12 h and become nonlinear at higher doses. The drug is eliminated in the urine. The concentration of the drug in plasma reaches its peak in about 1 h, and in the cerebrospinal fluid within 1.4-3.8 h. When taken as a transdermal patch, its kinetics are smoother compared to capsules with a peak concentration and less fluctuations. The patches at a dose of 9.5 mg/24 h show a comparison of the amount of exposure to the drug between them and capsules that reach the maximum permissible dose of 12 mg/24 h. This compound cannot cross the blood-brain barrier, and its plasma protein binding reaches 40%. The main route of metabolism of the drug is via the degradation of the enzyme cholinesterase, and when eliminated, it avoids the liver and therefore cytochrome p450 is not affected by its presence. It has few drug interactions because it is not exposed to cytochrome P450, which is a metabolic pathway for many other drugs.