rivastigmine

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Rivastigmine

<table class="infobox infobox-therapeutic">
<tr>
<th class="infobox-header" colspan="2">rivastigmine</th>
</tr>
<tr>
<td class="label">Bioavailability</td>
<td>~36%</td>
</tr>
<tr>
<td class="label">T_max</td>
<td>1.0–1.4 hours</td>
</tr>
<tr>
<td class="label">Protein binding</td>
<td>~40%</td>
</tr>
<tr>
<td class="label">C_max (steady state)</td>
<td>~21.6 ng/mL (6 mg BID)</td>
</tr>
<tr>
<td class="label">Volume of distribution</td>
<td>~1.8–2.7 L/kg</td>
</tr>
<tr>
<td class="label">Adverse Effect</td>
<td>Oral (12 mg/day)</td>
</tr>
<tr>
<td class="label">Nausea</td>
<td>47%</td>
</tr>
<tr>
<td class="label">Vomiting</td>
<td>31%</td>
</tr>
<tr>
<td class="label">Diarrhea</td>
<td>19%</td>
</tr>
<tr>
<td class="label">Anorexia</td>
<td>17%</td>
</tr>
<tr>
<td class="label">Dizziness</td>
<td>13%</td>
</tr>
<tr>
<td class="label">Weight loss</td>
<td>3–7%</td>
</tr>
<tr>
<td class="label">Headache</td>
<td>13%</td>
</tr>
<tr>
<td class="label">Feature</td>
<td>Rivastigmine</td>
</tr>
<tr>
<td class="label">AChE inhibition</td>
<td>Yes (pseudo-irreversible)</td>
</tr>
<tr>
<td class="label">BuChE inhibition</td>
<td>Yes</td>
</tr>
<tr>
<td class="label">Nicotinic receptor modulation</td>
<td>No</td>
</tr>
<tr>
<td class="label">CYP metabolism</td>
<td>No (esterase hydrolysis)</td>
</tr>
<tr>
<td class="label">FDA approval: AD</td>

...

Rivastigmine

Introduction

Rivastigmine is an important component in the neurobiology of neurodegenerative diseases. This page provides detailed information about its structure, function, and role in disease processes.

Overview

Rivastigmine (brand name Exelon) is a carbamate-derived, pseudo-irreversible cholinesterase inhibitor used for the symptomatic [@jann2002]
treatment of mild-to-moderate dementia in [alzheimers](/diseases/alzheimers-disease) (AD) and [parkinsons](/diseases/parkinsons-disease) dementia (PDD). Uniquely among the approved [@jann2000]
[cholinesterase-inhibitors](/entities/cholinesterase-inhibitors), rivastigmine inhibits both acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE), and is available in a [@fda2000]
transdermal patch formulation that offers improved tolerability over oral dosing [@coreybloom1998] [@emre2004]
</a>[@jann2002] [@winblad2007]
</a>. It [@cummings2010]
remains a first-line symptomatic therapy for dementia and is the only cholinesterase inhibitor with FDA [@baron2002]
approval for PDD. [@colovi2013]

History and Development

Rivastigmine was originally synthesized by Marta Weinstock-Rosin at the Department of Pharmacology, Hebrew University of Jerusalem. The compound was licensed to Sandoz (later Novartis) through Yissum, the technology transfer company of Hebrew University. The molecule was selected for development based on its high affinity for brain AChE relative to peripheral forms of the enzyme, a property that suggested favorable CNS selectivity [@jann2000]. [@francis1999]

Key regulatory milestones include: [@greig2005]

2000: FDA approval of oral rivastigmine (Exelon capsules and oral solution) for mild-to-moderate [alzheimers](/diseases/alzheimers-disease) [@fda2000]
2006: FDA approval for [parkinsons](/diseases/parkinsons-disease) dementia, following the EXPRESS trial [@emre2004]
2007: FDA approval of the transdermal patch (Exelon Patch), following the IDEAL trial [@winblad2007]
2013: Expanded indication for the 13.3 mg/24h patch to treat severe [alzheimers](/diseases/alzheimers-disease) [@cummings2010]

Generic formulations became available following patent expiration, and rivastigmine is now widely available worldwide. [@lefvre2008]

Chemistry and Pharmacology

Chemical Structure

Rivastigmine is chemically designated as (S)-N-ethyl-N-methyl-3-1-(dimethylamino)ethyl-phenyl carbamate hydrogen-(2R,3R)-tartrate. Its [@lefvre2007]
molecular formula is C₁₄H₂₂N₂O₂ (free base), with a molecular weight of 250.34 g/mol. The pharmacophore is its carbamate moiety, which [@polinsky1998]
undergoes a covalent reaction with the active-site serine of cholinesterases, producing a carbamylated enzyme intermediate that is slow to [@rsler1999]
regenerate [@baron2002] [@farlow2013]
</a>[@colovi2013] [@schmitt2010]
</a>. [@poewe2006]

Mechanism of Action

Rivastigmine enhances cholinergic neurotransmission by inhibiting the enzymatic hydrolysis of [acetylcholine](/entities/acetylcholine) ([ACh](/entities/acetylcholine)). In [alzheimers](/diseases/alzheimers-disease), progressive loss of cholinergic [neurons](/entities/neurons) in the [nucleus-basalis-of-meynert](/nucleus-basalis-of-meynert) leads to reduced ACh] levels in the [cortex](/brain-regions/cortex) and [hippocampus](/brain-regions/hippocampus), contributing to cognitive decline. Rivastigmine acts to restore ACh] availability in these regions [@francis1999]. [@mckeith2000]

The inhibition mechanism is distinct from other cholinesterase inhibitors: [@ballard2008]

Pseudo-irreversible binding: Rivastigmine carbamylates the catalytic serine residue at the active site of AChE and BuChE. The resulting carbamylated enzyme is slow to regenerate (half-life of decarbamylation ~10 hours), producing sustained inhibition despite the drug's short plasma half-life of ~1.5 hours [@baron2002]

</a>[@colovi2013] [@devos2014]
</a>. [@fda2015]

Dual AChE/BuChE inhibition: Unlike [donepezil](/therapeutics/donepezil), which selectively inhibits AChE, rivastigmine inhibits both AChE and BuChE with comparable potency. At therapeutic doses (12 mg/day oral), brain AChE and BuChE are inhibited by approximately 61.7% and 61.8%, respectively [@jann2000]

</a>[@greig2005] [@tariot2004]
</a>. This dual inhibition is clinically relevant because BuChE activity increases progressively in AD brains as AChE-producing [neurons](/entities/neurons) degenerate, and BuChE may assume a greater role in ACh hydrolysis as disease advances [@greig2005] [@agrawal2023]
</a>. [@mohamed2019]

G1 isoform selectivity: Rivastigmine preferentially inhibits the G1 enzymatic form of AChE, which predominates in the AD brain, and is a more potent inhibitor of cortical and hippocampal AChE than of peripheral forms [@jann2000].

CNS Selectivity

Rivastigmine demonstrates favorable brain-over-periphery selectivity. Studies show approximately 40% inhibition of central AChE compared to only 10% inhibition of peripheral BuChE at therapeutic doses, indicating that the drug preferentially targets the CNS cholinergic system [@jann2000]. This selectivity may contribute to a somewhat lower incidence of peripheral cholinergic side effects relative to the degree of central AChE inhibition achieved. [@neurodegenerative]

Pharmacokinetics

Absorption and Distribution

The transdermal patch provides significantly smoother pharmacokinetic profiles, with lower peak-to-trough fluctuations. The C_max with the
9.5 mg/24h patch is approximately 60% lower than with equivalent oral doses, while maintaining comparable overall drug exposure (AUC)
[@lefvre2008]
</a>[@lefvre2007]
</a>. Patch absorption is highest when applied to the upper back, chest, or
upper arm;
abdominal and thigh application results in 20–30% lower exposure [@lefvre2007].

Metabolism and Elimination

Rivastigmine is primarily metabolized by target-mediated hydrolysis at the cholinesterase active site, yielding the decarbamylated
metabolite NAP226-90, which has minimal pharmacological activity. Critically, rivastigmine does not undergo significant hepatic
metabolism via cytochrome P450 (CYP) enzymes, distinguishing it from [donepezil](/therapeutics/donepezil) (CYP2D6/3A4) and
[galantamine](/therapeutics/galantamine) (CYP2D6/3A4) [@jann2002][@polinsky1998].

Half-life: ~1.5 hours (oral), though pharmacological effect extends to ~10 hours due to pseudo-irreversible binding
Excretion: ~90% renal (as metabolites)
Drug interactions: Minimal CYP-mediated interactions; no clinically significant interactions with digoxin, warfarin, diazepam, or fluoxetine demonstrated in healthy volunteer studies [@polinsky1998]
Special populations: No dose adjustment required for mild-to-moderate hepatic impairment; contraindicated in severe hepatic impairment

Clinical Efficacy

Alzheimer's Disease

Multiple randomized controlled trials have demonstrated rivastigmine's efficacy in mild-to-moderate [alzheimers](/diseases/alzheimers-disease):

Pivotal Oral Trials: The B303 and B304 studies (Rösler et al., 1999; Corey-Bloom et al., 1998) enrolled over 1,400 patients and showed
statistically significant improvements in cognition (ADAS-Cog) and global function (CIBIC-Plus) with rivastigmine 6–12 mg/day versus placebo
over 26 weeks. Intent-to-treat analyses showed a mean treatment difference of 3–4 points on the ADAS-Cog [@coreybloom1998]
</a>[@rsler1999]
</a>.

IDEAL Trial (Investigation of transDermal Exelon in Alzheimer's Disease): This Phase 3, 24-week, double-blind study randomized 1,195
patients with mild-to-moderate AD to the rivastigmine 10 cm[@jann2002]
patch (9.5 mg/24h), 20 cm[@jann2002]
patch (17.4 mg/24h), oral capsules (12 mg/day), or
placebo. The 9.5 mg/24h patch demonstrated efficacy comparable to oral capsules on ADAS-Cog and ADCS-CGIC, with approximately two-thirds
fewer reports of nausea (7.2% vs 23.1%) and vomiting (6.2% vs 17.0%). The 20 cm[@jann2002] patch showed numerically superior cognitive scores with
tolerability similar to oral capsules [@winblad2007]. Two-thirds of
caregivers preferred the patch formulation.

ACTION Trial: The 48-week study compared the high-dose 13.3 mg/24h patch to the 9.5 mg/24h patch in patients with severe AD (MMSE 3–12).
The higher-dose patch showed significant cognitive benefits on the Severe Impairment Battery (SIB), supporting its use in advanced disease
[@cummings2010]
</a>[@farlow2013]
</a>.

Parkinson's Disease Dementia

EXPRESS Trial (EXelon in Parkinson's Disease dementia Study): This landmark 24-week, double-blind, placebo-controlled trial randomized 541 patients with PDD to rivastigmine 3–12 mg/day or placebo. Results demonstrated [@emre2004]:

Cognition: Mean improvement of 2.1 points on ADAS-Cog in the rivastigmine group vs. mean decline of 0.7 points with placebo (p < 0.001)
Global function: Clinically meaningful improvement on ADCS-CGIC in 19.8% of rivastigmine patients vs. 14.5% with placebo; clinically meaningful worsening in 13.0% vs. 23.1%
Executive function and attention: Significant benefits demonstrated in Parkinson's-relevant cognitive domains [@schmitt2010]
Activities of daily living: Significant improvement on the ADCS-ADL scale

A 24-week open-label extension showed that long-term treatment was well tolerated and provided sustained cognitive benefits at 48 weeks [@poewe2006].

The EXPRESS trial led to FDA approval of rivastigmine for PDD in 2006, making it the first and still the only cholinesterase inhibitor specifically approved for this indication.

Other Investigational Uses

Rivastigmine has been studied in several other conditions with cholinergic deficits:

[lewy-body-dementia](/diseases/lewy-body-dementia): Open-label and small controlled studies suggest benefits for cognitive and behavioral symptoms, particularly visual hallucinations [@mckeith2000]
[vascular-dementia](/diseases/vascular-dementia): The VantagE trial showed modest cognitive benefits [@ballard2008]
Post-operative delirium: Investigated for prevention in surgical populations, with mixed results
Apathy in [parkinsons](/diseases/parkinsons-disease): A randomized trial showed no significant benefit for apathy in non-demented PD patients [@devos2014]

Formulations and Dosing

Oral Capsules

Available doses: 1.5 mg, 3 mg, 4.5 mg, 6 mg
Titration: Start 1.5 mg twice daily; increase by 1.5 mg/dose every 2 weeks
Target dose: 6 mg twice daily (12 mg/day)
Administration: Take with food to reduce GI side effects

Oral Solution

2 mg/mL solution for patients with swallowing difficulties
Same dosing as capsules

Transdermal Patch (Preferred Formulation)

The transdermal patch is now considered the preferred formulation due to substantially better GI tolerability [@winblad2007]
</a>[@lefvre2008]
</a>:

Available doses: 4.6 mg/24h, 9.5 mg/24h, 13.3 mg/24h
Titration: Start with 4.6 mg/24h; increase to 9.5 mg/24h after ≥4 weeks; may increase to 13.3 mg/24h for moderate-to-severe disease
Application: Once daily to clean, dry, hairless skin on the upper back (preferred), upper arm, or chest
Rotation: Change application site daily; do not reuse the same site for 14 days

Switching from Oral to Patch

Patients on oral rivastigmine <6 mg/day may switch to the 4.6 mg/24h patch; those on 6–12 mg/day may switch to the 9.5 mg/24h patch. The first patch should be applied the day after the last oral dose [@polinsky1998].

Safety and Adverse Effects

Common Adverse Effects

The transdermal patch demonstrates a markedly improved GI tolerability profile compared to oral capsules, with nausea and vomiting rates comparable to placebo [@winblad2007].

Patch-Specific Effects

Application site reactions: Erythema, pruritus, dermatitis (8–12% of patients)
Mild skin irritation usually does not require discontinuation
Site rotation minimizes skin reactions

Serious Adverse Effects and Warnings

Bradycardia and heart block: Cholinomimetic effects may exacerbate sinus node disease or conduction abnormalities; use with caution in patients with cardiac disease
GI hemorrhage: Monitor for occult bleeding, especially in patients with peptic ulcer risk factors
Seizures: May lower seizure threshold through cholinergic activation
Bronchospasm: Use with caution in asthma and COPD
Urinary obstruction: Cholinergic stimulation may worsen obstructive uropathy
Tremor exacerbation: Particularly relevant in PDD patients (10.2% vs 3.9% with placebo in EXPRESS) [@emre2004]

Overdose and Application Errors

In 2015, the FDA issued a safety alert regarding rivastigmine patch application errors, including application of multiple patches simultaneously, which can cause overdose with severe nausea, vomiting, and potentially life-threatening cholinergic crisis [@fda2015].

Comparison with Other Cholinesterase Inhibitors

Rivastigmine's lack of CYP metabolism makes it particularly suitable for elderly patients on multiple medications, where drug–drug
interaction risk is a concern [@jann2002]
</a>[@polinsky1998]
</a>. Its dual AChE/BuChE inhibition may offer theoretical advantages in moderate-to-severe
disease when BuChE becomes
the predominant ACh-metabolizing enzyme [@greig2005].

Current Status and Future Directions

Rivastigmine remains a cornerstone of symptomatic treatment for [alzheimers](/diseases/alzheimers-disease) and [parkinsons](/diseases/parkinsons-disease) dementia. Current and emerging areas of investigation include:

Combination therapy: Rivastigmine plus [memantine](/therapeutics/memantine) is widely used clinically for moderate-to-severe AD, with evidence suggesting additive benefits on cognition and behavior [@tariot2004]
Novel delivery systems: Multi-day patches (twice-weekly application) are under investigation to improve adherence [@agrawal2023]
Biomarker-guided treatment: Research into predicting cholinesterase inhibitor response using [csf-biomarkers](/diagnostics/csf-biomarkers), cholinergic [neuroimaging](/diagnostics/neuroimaging), and genetic markers (e.g., [memantine](/therapeutics/memantine)

Background

The study of Rivastigmine has evolved significantly over the past decades. Research in this area has revealed important insights into the underlying mechanisms of neurodegeneration and continues to drive therapeutic development.

Historical context and key discoveries in this field have shaped our current understanding and will continue to guide future research directions.

Brain Atlas Resources

Allen Human Brain Atlas: [Rivastigmine expression search](https://human.brain-map.org/microarray/search/show?search_term=Rivastigmine)
Allen Mouse Brain Atlas: [Rivastigmine search](https://mouse.brain-map.org/search/index.html?query=Rivastigmine)
Allen Cell Type Atlas: [Transcriptomic cell type reference](https://portal.brain-map.org/atlases-and-data/rnaseq)
BrainSpan Developmental Transcriptome: [Rivastigmine developmental expression](https://www.brainspan.org/rnaseq/search/index.html?search_term=Rivastigmine)

External Links

[PubMed Search: Rivastigmine](https://pubmed.ncbi.nlm.nih.gov/?term=Rivastigmine)
[Google Scholar Search: Rivastigmine](https://scholar.google.com/scholar?q=Rivastigmine)

References

Unknown, Corey-Bloom J, Anand R, Veach J; for the ENA 713 B352 Study Group. A randomized trial evaluating the efficacy and safety of ENA 713 (rivastigmine tartrate], a new acetylcholinesterase inhibitor, in patients with mild to moderately severe alzheimers (1998)

[Unknown, Jann MW, Shirley KL, Small GW. Clinical pharmacokinetics and pharmacodynamics of cholinesterase inhibitors. Clin Pharmacokinet. 2002;41(10):719-739. [PMID:12162759 (2002)](https://pubmed.ncbi.nlm.nih.gov/12162759/)

[Unknown, Jann MW. Rivastigmine, a new-generation cholinesterase inhibitor for the treatment of Alzheimer's Disease. Pharmacotherapy. 2000;20(1):1-12. [PMID:10641971 (2000)](https://pubmed.ncbi.nlm.nih.gov/10641971/)

Unknown, FDA. Drug Approval Package: Exelon (Rivastigmine Tartrate NDA #20-823. [April 2000. [FDA) (2000)

[Emre M, Aarsland D, Albanese A, et al., Rivastigmine for dementia associated with Parkinson's Disease. N Engl J Med. 2004;351(24):2509-2518. [PMID:15590953 (2004)](https://pubmed.ncbi.nlm.nih.gov/15590953/)

[Winblad B, Cummings J, Andreasen N, et al., A six-month double-blind, randomized, placebo-controlled study of a transdermal patch in Alzheimer's Disease—rivastigmine patch versus capsule. Int J Geriatr Psychiatry. 2007;22(5):456-467. [PMID:17646619 (2007)](https://pubmed.ncbi.nlm.nih.gov/17646619/)

Cummings JL, Farlow MR, Meng X, Christensen DD, Yonan C, Rivastigmine transdermal patch skin tolerability and use in clinical practice (2010)

[Bar-On P, Millard CB, Harel M, et al., Kinetic and structural studies on the interaction of cholinesterases with the anti-Alzheimer drug rivastigmine. Biochemistry. 2002;41(11):3555-3564. [PMID:11888271 (2002)](https://pubmed.ncbi.nlm.nih.gov/11888271/)

[Unknown, Colović MB, Krstić DZ, Lazarević-Pašti TD, Bondžić AM, Vasić VM. Acetylcholinesterase inhibitors: pharmacology and toxicology. Curr Neuropharmacol. 2013;11(3):315-335. [PMID:24179466 (2013)](https://pubmed.ncbi.nlm.nih.gov/24179466/)

[Unknown, Francis PT, Palmer AM, Snape M, Wilcock GK. The cholinergic hypothesis of Alzheimer's Disease: a review of progress. J Neurol Neurosurg Psychiatry. 1999;66(2):137-147. [PMID:10071091 (1999)](https://pubmed.ncbi.nlm.nih.gov/10071091/)

[Greig NH, Utsuki T, Ingram DK, et al., Selective butyrylcholinesterase inhibition elevates brain acetylcholine, augments learning and lowers Alzheimer beta-amyloid peptide in rodent. Proc Natl Acad Sci USA. 2005;102(47):17213-17218. [PMID:16275899 (2005)](https://pubmed.ncbi.nlm.nih.gov/16275899/)

[Lefèvre G, Sédek G, Jhee SS, et al., Pharmacokinetics and pharmacodynamics of the novel daily rivastigmine transdermal patch compared with twice-daily capsules in Alzheimer's Disease patients. Clin Pharmacol Ther. 2008;83(1):106-114. [PMID:17522596 (2008)](https://pubmed.ncbi.nlm.nih.gov/17522596/)

[Lefèvre G, Sédek G, Huang HL, et al., Pharmacokinetics of a rivastigmine transdermal patch formulation in healthy volunteers: relative effects of body site application. J Clin Pharmacol. 2007;47(4):471-478. [PMID:17389556 (2007)](https://pubmed.ncbi.nlm.nih.gov/17389556/)

[Unknown, Polinsky RJ. Clinical pharmacology of rivastigmine: a new-generation acetylcholinesterase inhibitor for the treatment of Alzheimer's Disease. Clin Ther. 1998;20(4):634-647. [PMID:9737824 (1998)](https://pubmed.ncbi.nlm.nih.gov/9737824/)

[Rösler M, Anand R, Cicin-Sain A, et al., Efficacy and safety of rivastigmine in patients with Alzheimer's Disease: international randomised controlled trial. BMJ. 1999;318(7184):633-638. [PMID:10066204 (1999)](https://pubmed.ncbi.nlm.nih.gov/10066204/)

[Unknown, Farlow MR, Grossberg GT, Sadowsky CH, Meng X, Somogyi M. A 24-week, randomized, controlled trial of rivastigmine patch 13.3 mg/24 h versus 4.6 mg/24 h in severe Alzheimer's dementia. CNS Neurosci Ther. 2013;19(10):745-752. [PMID:23870612 (2013)](https://pubmed.ncbi.nlm.nih.gov/23870612/)

[Unknown, Schmitt FA, Farlow MR, Meng X, Tekin S, Olin JT. Efficacy of rivastigmine on executive function in patients with Parkinson's Disease dementia. CNS Neurosci Ther. 2010;16(6):330-336. [PMID:20950329 (2010)](https://pubmed.ncbi.nlm.nih.gov/20950329/)

[Poewe W, Wolters E, Emre M, et al., Long-term benefits of rivastigmine in dementia associated with Parkinson's Disease: an active treatment extension study. Mov Disord. 2006;21(4):456-461. [PMID:16229010 (2006)](https://pubmed.ncbi.nlm.nih.gov/16229010/)

[McKeith I, Del Ser T, Spano P, et al., Efficacy of rivastigmine in dementia with Lewy bodies: a randomised, double-blind, placebo-controlled international study. Lancet. 2000;356(9247):2031-2036. [PMID:11145488 (2000)](https://pubmed.ncbi.nlm.nih.gov/11145488/)

[Ballard C, Sauter M, Scheltens P, et al., Efficacy, safety and tolerability of rivastigmine capsules in patients with probable Vascular Dementia: the VantagE study. Curr Med Res Opin. 2008;24(9):2561-2574. [PMID:18674407 (2008)](https://pubmed.ncbi.nlm.nih.gov/18674407/)

[Devos D, Moreau C, Maltête D, et al., Rivastigmine in apathetic but dementia and depression-free patients with Parkinson's Disease: a double-blind, placebo-controlled, randomised clinical trial. J Neurol Neurosurg Psychiatry. 2014;85(6):668-674. [PMID:24218528 (2014)](https://pubmed.ncbi.nlm.nih.gov/24218528/)

[FDA Drug Safety Communication: FDA warns about medication errors and skin reactions with Exelon Patch (rivastigmine transdermal system]. 2015, FDA Safety Communication (2015)

PMID: 14734594(https://pubmed.ncbi.nlm.nih.gov/14734594/)

[Agrawal A, Deore M, Vora LJ, et al, Comparative bioavailability study of a novel multi-day patch formulation of rivastigmine (twice weekly] with Exelon transdermal patch (daily] (2023)]([PMID:36869255)(https://pubmed.ncbi.nlm.nih.gov/36869255/))

Mohamed LA, Keller JN, Bhatt S, et al, Role of cholinesterase inhibitors in modulation of neuroinflammation (2019)

Unknown, - [Neurodegenerative Diseases (n.d.)

Unknown, - [Genes Index (n.d.)

Unknown, - [Mechanisms of Neurodegeneration (n.d.)

Unknown, - [Proteins Index## External Links (n.d.)

-, NCBI Gene (n.d.)

-, UniProt (n.d.)

Unknown, - (n.d.)

Pathway Diagram

The following diagram shows the key molecular relationships involving rivastigmine discovered through SciDEX knowledge graph analysis:

Mermaid diagram (expand to render)

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rivastigmine

Rivastigmine

Rivastigmine

Introduction

Overview

History and Development

Chemistry and Pharmacology

Chemical Structure

Mechanism of Action

CNS Selectivity

Pharmacokinetics

Absorption and Distribution

Metabolism and Elimination

Clinical Efficacy

Alzheimer's Disease

Parkinson's Disease Dementia

Other Investigational Uses

Formulations and Dosing

Oral Capsules

Oral Solution

Transdermal Patch (Preferred Formulation)

Switching from Oral to Patch

Safety and Adverse Effects

Common Adverse Effects

Patch-Specific Effects

Serious Adverse Effects and Warnings

Overdose and Application Errors

Comparison with Other Cholinesterase Inhibitors

Current Status and Future Directions

Background

Brain Atlas Resources

See Also

External Links

References

Pathway Diagram