Drug Monograph

Galantamine (Razadyne)

galantamine hydrobromide
Cholinesterase Inhibitor + Nicotinic Receptor Modulator · Oral (ER Capsule, IR Tablet, Solution)
Pharmacokinetic Profile
Half-Life
~7 h
Metabolism
CYP2D6, CYP3A4, glucuronidation
Protein Binding
18%
Bioavailability
~90%
Volume of Distribution
175 L
Clinical Information
Drug Class
AChE inhibitor + allosteric nicotinic receptor modulator
Available Doses
ER caps: 8, 16, 24 mg; IR tabs: 4, 8, 12 mg; Soln: 4 mg/mL
Route
Oral
Renal Adjustment
CrCl 9–59: max 16 mg/day; CrCl <9: not recommended
Hepatic Adjustment
Moderate (CP 7–9): max 16 mg/day; Severe: not recommended
Pregnancy
May cause fetal harm based on animal data; no adequate human studies
Lactation
Unknown if excreted in human milk
Schedule
Rx only (not scheduled)
Generic Available
Yes
Rx

Galantamine Indications

IndicationApproved PopulationTherapy TypeStatus
Mild-to-moderate dementia of the Alzheimer’s typeAdultsMonotherapy or adjunctive with memantineFDA Approved

Galantamine is distinguished from other cholinesterase inhibitors by its dual mechanism: competitive, reversible inhibition of acetylcholinesterase combined with allosteric potentiation of nicotinic acetylcholine receptors. This dual action may enhance cholinergic neurotransmission beyond simple enzyme inhibition by increasing presynaptic acetylcholine release through nicotinic receptor activation. Galantamine has demonstrated consistent efficacy across five randomised, placebo-controlled trials in patients with mild-to-moderate Alzheimer’s disease, with the effective dose range being 16–24 mg/day. It is not FDA-approved for Parkinson’s disease dementia, vascular dementia, or mild cognitive impairment (MCI).

Off-Label Uses

Dementia with Lewy bodies (DLB): Open-label studies and small RCTs suggest galantamine may improve cognition and behavioural symptoms in DLB. Evidence quality: Moderate.

Vascular dementia and mixed dementia (AD + cerebrovascular disease): The GAL-INT-6 trial showed cognitive benefits in patients with vascular dementia or AD with cerebrovascular disease. Evidence quality: Moderate.

Mild cognitive impairment (MCI): Not recommended. Two 2-year MCI trials showed no efficacy benefit and a mortality signal (13 deaths on galantamine vs 1 on placebo), attributed to various vascular causes. This indication was not approved by the FDA.

Dose

Galantamine Dosing

Dosing by Clinical Scenario

Clinical ScenarioStarting DoseMaintenance DoseMaximum DoseNotes
Alzheimer’s dementia — ER capsule initiation8 mg once daily (AM)16 mg once daily24 mg once dailyIncrease to 16 mg after minimum 4 weeks; then to 24 mg after another 4 weeks if tolerated
Administer with food; ensure adequate fluid intake
Alzheimer’s dementia — IR tablet initiation4 mg BID8 mg BID12 mg BID (24 mg/day)Increase by 4 mg/dose every 4 weeks; give with morning and evening meals
IR and ER are interchangeable at the same total daily dose
Switching from IR tablets to ER capsulesSame total daily dose (e.g., 8 mg BID IR → 16 mg once daily ER)24 mg/dayTake last IR tablet in the evening; start ER capsule the next morning
Treatment interruption — restart8 mg/day (ER) or 4 mg BID (IR)Re-titrate to target24 mg/dayIf interrupted >3 days, restart at lowest dose and re-escalate
Abrupt withdrawal does not increase adverse event frequency
Combination with memantineStandard galantamine titration16–24 mg/day24 mg/dayMemantine does not alter galantamine pharmacokinetics; no dose adjustment needed
Combination commonly used in moderate AD (FDA PI)

Special Population Adjustments

Clinical ScenarioStarting DoseMaintenance DoseMaximum DoseNotes
Moderate hepatic impairment (Child-Pugh 7–9)8 mg/day16 mg/day16 mg/dayClearance ~25% lower; do not exceed 16 mg/day
Severe hepatic impairment (Child-Pugh 10–15)Not recommendedNo clinical data available; substantially reduced clearance expected
Moderate renal impairment (CrCl 9–59 mL/min)8 mg/day16 mg/day16 mg/dayAUC increased by 37–67% depending on severity; cap at 16 mg/day
Severe renal impairment (CrCl <9 mL/min)Not recommendedInsufficient safety data for this population
CYP2D6 poor metabolizers or concurrent strong CYP2D6/3A4 inhibitor8 mg/dayTitrate cautiously16–24 mg/day per tolerabilityCYP2D6 poor metabolizers have ~50% higher exposure (ER); paroxetine increases bioavailability ~40%; titrate based on tolerability
Clinical Pearl: ER vs IR Formulation

The extended-release capsule provides bioequivalent exposure (AUC) to the twice-daily tablet formulation, with a lower peak concentration (~25% lower Cmax) and delayed Tmax (~4.5–5 h vs ~1 h). The smoother pharmacokinetic profile of the ER capsule, combined with once-daily dosing, may improve caregiver adherence and reduce peak-related GI side effects. Most clinicians now prefer ER as the default formulation for new starts.

PK

Pharmacology

Mechanism of Action

Galantamine is a tertiary alkaloid originally isolated from snowdrop (Galanthus) species. It exerts its therapeutic effect through two complementary mechanisms. First, it acts as a competitive, reversible inhibitor of acetylcholinesterase (AChE), increasing the synaptic concentration of acetylcholine. Peak AChE inhibition of approximately 40% is achieved about one hour after a single 8 mg oral dose. Second, galantamine is an allosteric potentiating ligand at nicotinic acetylcholine receptors (nAChRs), binding to an allosteric site that enhances the receptor’s response to acetylcholine without directly activating it. This nicotinic modulation may amplify cholinergic neurotransmission by promoting presynaptic acetylcholine release and may also modulate the release of other neurotransmitters such as glutamate. Unlike rivastigmine, galantamine does not inhibit butyrylcholinesterase. There is no evidence that galantamine alters the underlying neurodegenerative disease process.

ADME Profile

ParameterValueClinical Implication
AbsorptionRapid and complete; Tmax ~1 h (IR), ~4.5–5 h (ER); bioavailability ~90%; food reduces Cmax by 25% and delays Tmax by 1.5 h but does not affect AUCHigh bioavailability ensures reliable drug delivery; administer with food to reduce GI side effects without compromising total exposure
DistributionVd 175 L; plasma protein binding 18%; blood-to-plasma ratio 1.2; 52.7% distributed to blood cellsLow protein binding minimises displacement interactions; large Vd indicates extensive tissue distribution
MetabolismHepatic via CYP2D6 (O-demethylation) and CYP3A4 (N-oxidation); also undergoes glucuronidation; ~20% excreted unchanged; linear PK over 8–32 mg/day rangeMultiple metabolic pathways provide redundancy; CYP2D6 poor metabolizers have ~50% higher exposure; strong CYP2D6 or CYP3A4 inhibitors increase galantamine levels modestly (30–40%)
Eliminationt½ ~7 h; ~95% urine, ~5% faeces; renal clearance ~65 mL/min; total plasma clearance ~300 mL/min; ~20% excreted unchanged in urine within 24 hRelatively short half-life supports once-daily ER dosing; significant renal component necessitates dose capping in moderate–severe renal impairment
SE

Side Effects

Adverse effects are predominantly cholinergic in origin and dose-related. Data below are from pooled placebo-controlled clinical trials (FDA PI Table 1, n = 3,956 galantamine vs n = 2,546 placebo). The majority of adverse reactions occurred during the dose-escalation period; the median duration of nausea was 5–7 days.

≥10%Very Common
Adverse EffectIncidenceClinical Note
Nausea20.7% (vs 5.5% placebo)Most common reason for discontinuation (6.2%); dose-related; improves during maintenance; median duration 5–7 days
Vomiting10.5% (vs 2.3% placebo)Primarily during titration; administer with food to reduce; second most common discontinuation reason
1–10%Common
Adverse EffectIncidenceClinical Note
Dizziness7.5% (vs 3.4%)Central cholinergic effect; advise caution with driving
Decreased appetite7.4% (vs 2.1%)Monitor weight at each visit; may compound disease-associated malnutrition
Diarrhea7.4% (vs 4.9%)Cholinergic-mediated increase in GI motility; usually self-limiting
Headache7.1% (vs 5.5%)Mild and transient; no specific management required
Decreased weight4.7% (vs 1.5%)Track body weight regularly; consider nutritional supplementation if progressive
Fall3.9% (vs 3.0%)May be related to dizziness and syncope; assess gait and fall risk
Abdominal pain3.8% (vs 2.0%)Related to increased gastric acid secretion; consider antacid if persistent
Depression3.6% (vs 2.3%)Distinguish from disease-related apathy; screen at follow-up visits
Fatigue3.5% (vs 1.8%)May limit functional activities; dose-related
Abdominal discomfort2.1% (vs 0.7%)Encourage taking with food and adequate fluid
Asthenia2.0% (vs 1.5%)General weakness; may overlap with fatigue and malaise
Tremor1.6% (vs 0.7%)Cholinergic origin; relevant when co-existing with parkinsonian features
Syncope1.4% (vs 0.6%)Dose-related: 0.4% at 8 mg/day, 1.3% at 16 mg/day, 2.2% at 24 mg/day (FDA PI)
Somnolence1.5% (vs 0.8%)Warn about driving and machinery operation
Bradycardia1.0% (vs 0.3%)Vagotonic effect on SA/AV nodes; ECG if symptomatic
Dyspepsia1.5% (vs 1.0%)Increased gastric acid secretion; consider PPI or H2-blocker if persistent
Lethargy1.3% (vs 0.4%)Central cholinergic sedation; may overlap with somnolence and fatigue
Muscle spasms1.2% (vs 0.5%)Cholinergic effect on skeletal muscle; usually mild and self-limiting
Malaise1.1% (vs 0.5%)Non-specific; may relate to GI intolerance or anorexia
Laceration1.1% (vs 0.5%)Likely related to falls and dizziness; assess fall risk and home safety
SeriousSerious Adverse Effects (Regardless of Frequency)
Adverse EffectEstimated FrequencyTypical OnsetRequired Action
Stevens-Johnson syndrome / AGEPVery rare (post-marketing)Days to weeks after initiationDiscontinue at first appearance of rash; do not rechallenge; seek emergency dermatological care
Complete AV blockRare (post-marketing)Any time during therapyImmediate ECG; temporary or permanent pacing may be required; discontinue galantamine
Bradycardia / syncope1–2.2% (dose-related)Any time; risk increases with doseECG monitoring; reduce dose or discontinue; assess cardiac conduction status
SeizuresRare (post-marketing)Any timeDifferentiate from AD-related seizure activity; hold galantamine and evaluate
GI haemorrhageRareAny time; higher risk with NSAIDsMonitor for occult bleeding; discontinue if active bleed; gastroprotection with NSAIDs
Hepatitis / elevated liver enzymesRare (post-marketing)VariableCheck LFTs; discontinue if hepatitis confirmed
Cholinergic crisis (overdose)Very rareWithin hours of ingestionIV atropine sulphate 0.5–1 mg titrated to effect; supportive care; QT prolongation and torsades de pointes reported in overdose
DiscontinuationDiscontinuation Rates
Double-Blind Trials (Pooled)
10.6% vs 2.2% placebo
N = 3,956 galantamine, 2,546 placebo. Top reasons: nausea (6.2%), vomiting (3.3%), decreased appetite (1.5%), dizziness (1.3%)
Open-Label Extension Studies
7.1%
N = 1,454. Top reasons: nausea (3.0%), vomiting (1.6%), decreased appetite (0.9%), headache (0.8%)
Reason for DiscontinuationIncidence (Galantamine)Context
Nausea6.2%vs 0.7% placebo; primarily during titration phase
Vomiting3.3%vs <0.5% placebo; more common in women
Decreased appetite1.5%Often accompanied by weight loss
Dizziness1.3%Central cholinergic mechanism
Diarrhea0.8%Usually self-limiting during dose escalation
Headache0.7%Mild; placebo DC rate not reported at this threshold
Decreased weight0.7%Often related to anorexia and GI intolerance
Managing GI Side Effects

Always administer galantamine with food and ensure adequate fluid intake. The 4-week minimum titration interval (vs weekly escalation used in early trials) was specifically adopted to reduce GI intolerance. If side effects develop, hold for several doses and restart at the same or lower dose. The ER formulation produces a lower Cmax than IR tablets and may be better tolerated in GI-sensitive patients.

Int

Drug Interactions

Unlike rivastigmine, galantamine is metabolised by hepatic CYP enzymes (CYP2D6 and CYP3A4), making it susceptible to pharmacokinetic interactions with enzyme inhibitors. However, galantamine itself does not inhibit any major CYP isoform, so it does not increase levels of co-administered drugs. No pharmacokinetic interaction was observed with warfarin, digoxin, or memantine in dedicated studies.

MajorSuccinylcholine & depolarising NM blockers
MechanismCholinesterase inhibition prolongs neuromuscular blockade
EffectExaggerated and prolonged muscle relaxation during anaesthesia
ManagementInform anaesthetist; consider non-depolarising agents or dose reduction of succinylcholine
FDA PI
MajorAnticholinergic drugs
MechanismDirect pharmacodynamic antagonism of cholinesterase inhibition
EffectReduced efficacy of galantamine; negates cognitive benefits
ManagementAvoid concurrent use; audit anticholinergic burden at each visit (oxybutynin, diphenhydramine, amitriptyline)
FDA PI
ModerateParoxetine (strong CYP2D6 inhibitor)
MechanismInhibits CYP2D6-mediated O-demethylation of galantamine
EffectIncreases galantamine oral bioavailability by ~40%
ManagementTitrate galantamine cautiously; monitor for increased GI and CNS side effects; consider alternative SSRI (e.g., sertraline, citalopram)
FDA PI (PK study)
ModerateKetoconazole (strong CYP3A4 inhibitor)
MechanismInhibits CYP3A4-mediated N-oxidation of galantamine
EffectIncreases galantamine AUC by ~30%
ManagementMonitor for increased side effects; dose reduction may be needed; applies to other strong CYP3A4 inhibitors (itraconazole, clarithromycin)
FDA PI (PK study)
ModerateFluoxetine, fluvoxamine, quinidine, amitriptyline
MechanismCYP2D6 inhibition reducing galantamine clearance by 25–33%
EffectModest increase in galantamine exposure
ManagementMonitor for GI tolerability; dose adjustment seldom required unless poor CYP2D6 metaboliser genotype is also present
FDA PI (Pop PK, n=852)
MinorErythromycin (moderate CYP3A4 inhibitor)
MechanismModerate CYP3A4 inhibition
EffectMinimal AUC increase (~10%)
ManagementNo dose adjustment needed; short-course macrolides are unlikely to be clinically significant
FDA PI (PK study)
MinorWarfarin
MechanismNo pharmacokinetic interaction; galantamine does not inhibit CYP2C9
EffectNo effect on R- or S-warfarin levels or prothrombin time
ManagementNo dose adjustment; routine INR monitoring as standard of care
FDA PI (Healthy volunteer study)
MinorMemantine
MechanismNo pharmacokinetic interaction at steady state
EffectNo change in galantamine pharmacokinetics
ManagementSafe to co-administer; commonly used combination in moderate AD
FDA PI
Mon

Monitoring

  • Cognitive functionBaseline, then every 3–6 months
    Routine
    Use MMSE, MoCA, or ADAS-cog to track treatment response. If no stabilisation after 3–6 months at 16–24 mg/day, reassess continuation.
  • Body weightEach visit during titration, then every 3 months
    Routine
    Weight loss (4.7% incidence) can worsen frailty and nutritional status in elderly patients. Consider dietitian referral if progressive.
  • GI tolerabilityEach visit during titration
    Routine
    Assess nausea, vomiting, diarrhea, and appetite at each dose step. Consider switching to ER formulation or reducing dose if persistent.
  • Heart rate & ECGBaseline; as clinically indicated
    Trigger-based
    Vagotonic effects may cause bradycardia and AV block even in patients without known conduction disease. Obtain ECG if syncope, dizziness, or palpitations develop. Syncope risk is dose-related (2.2% at 24 mg/day).
  • SkinAt each visit
    Trigger-based
    Stevens-Johnson syndrome and AGEP have been reported post-marketing. Advise patients to discontinue at first sign of rash and seek medical evaluation.
  • Renal functionBaseline, then annually or if clinical change
    Routine
    Dose capped at 16 mg/day if CrCl 9–59 mL/min; not recommended if CrCl <9. Reassess if renal function declines.
  • Hepatic functionBaseline in at-risk patients
    Trigger-based
    Dose capped at 16 mg/day for moderate impairment; not recommended for severe. Post-marketing hepatitis reports warrant vigilance.
CI

Contraindications & Cautions

Absolute Contraindications

  • Known hypersensitivity to galantamine hydrobromide or any excipient in the formulation

Relative Contraindications (Specialist Input Recommended)

  • Sick sinus syndrome or AV block: Vagotonic effects may worsen bradycardia; cardiology input required before initiation
  • Active peptic ulcer disease or GI bleeding: Increased gastric acid secretion may worsen mucosal injury
  • Severe hepatic impairment (Child-Pugh 10–15): Use is not recommended; no dosing data available
  • Severe renal impairment (CrCl <9 mL/min): Use is not recommended

Use with Caution

  • Asthma or COPD: Cholinergic stimulation may cause bronchoconstriction; monitor respiratory function
  • Bladder outflow obstruction: Cholinomimetics may exacerbate urinary retention
  • History of seizures: Cholinesterase inhibitors have theoretical proconvulsant potential
  • Concurrent NSAID use: Monitor for GI bleeding; gastroprotection recommended
  • Planned surgery requiring anaesthesia: Inform anaesthetist; galantamine may potentiate succinylcholine-type muscle relaxants
  • Concurrent strong CYP2D6 or CYP3A4 inhibitors: Monitor for increased galantamine side effects
FDA Safety Warning Mortality Signal in Mild Cognitive Impairment (MCI) Trials

In two 2-year, placebo-controlled MCI trials, 13 patients on galantamine (n = 1,026) and 1 patient on placebo (n = 1,022) died. Deaths were due to various causes including myocardial infarction, stroke, and sudden death. The mortality imbalance was statistically significant. Galantamine is not approved for MCI and should not be used in this population. This mortality signal was not replicated in Alzheimer’s disease trials where the placebo mortality rate numerically exceeded the galantamine rate.

FDA Safety Warning Serious Skin Reactions

Post-marketing reports of Stevens-Johnson syndrome (SJS) and acute generalised exanthematous pustulosis (AGEP) have been received. Therapy should be discontinued at the first appearance of any skin rash, unless it is clearly unrelated to the drug. If signs or symptoms suggest a serious skin reaction, galantamine should not be resumed and alternative therapy should be considered.

Pt

Patient Counselling

Purpose of Therapy

Galantamine is prescribed to help preserve memory, thinking ability, and the capacity to manage daily activities in people with Alzheimer’s disease. It works by increasing levels of a chemical messenger called acetylcholine in the brain and by enhancing the activity of certain brain receptors (nicotinic receptors). It does not cure the underlying disease but may slow the rate of cognitive decline. Caregivers play a central role in ensuring the medication is taken correctly and in monitoring for side effects.

How to Take

ER capsules: Take once daily in the morning with food. Swallow whole; do not crush or chew. IR tablets: Take twice daily with morning and evening meals. Oral solution: Measure dose using the provided syringe; may be mixed with a small glass of water, juice, or soda. Ensure adequate fluid intake throughout the day.

Nausea & Vomiting
Tell patientStomach upset is most common during the first few weeks at each dose increase and usually improves within a week. Always take with food and drink plenty of fluids. If you vomit repeatedly, stop the medicine and contact your doctor before restarting.
Call prescriberIf vomiting persists beyond 24 hours, if unable to keep fluids down, or if treatment has been missed for more than 3 days.
Weight Loss & Appetite
Tell patientReduced appetite is a known effect. Try small, frequent, nutrient-dense meals. Caregivers should weigh the patient regularly.
Call prescriberIf weight loss exceeds 5% of body weight or if the patient refuses most meals for several days.
Dizziness, Fainting & Heart Rate
Tell patientThis medicine may slow the heart rate and cause dizziness or fainting. Rise slowly from sitting or lying down. Avoid driving until you know how galantamine affects you.
Call prescriberIf fainting occurs, if you feel your heart beating unusually slowly, or if dizziness does not improve.
Skin Rash
Tell patientRare but serious skin reactions have been reported. If you develop any rash, blistering, or skin peeling, stop the medicine immediately and seek medical attention.
Call prescriberImmediately at the first sign of any skin rash, even if it seems mild.
Treatment Interruptions
Tell patientIf you miss doses for more than 3 days for any reason, do not restart at your previous dose. Contact your doctor for instructions to re-titrate from the lowest dose.
Call prescriberWhenever treatment has been interrupted for more than 3 days, including during hospitalisation.
Surgery
Tell patientInform your anaesthetist or surgeon that you are taking galantamine, as it can interact with muscle relaxants used during surgery.
Call prescriberBefore any planned procedure requiring general anaesthesia.
Ref

Sources

Regulatory (PI / SmPC)
  1. Razadyne ER (galantamine extended-release capsules) — FDA-approved Prescribing Information. Janssen Pharmaceuticals. Revised September 2022. accessdata.fda.govPrimary source for ER capsule dosing, adverse reactions (Table 1, pooled n=3,956), pharmacokinetics, drug interactions, and MCI mortality warning.
  2. Razadyne/Razadyne ER (galantamine hydrobromide tablets, oral solution, ER capsules) — FDA-approved Prescribing Information. Revised 2017. accessdata.fda.govComprehensive label covering all formulations; source for IR tablet dosing and historical adverse event data.
Key Clinical Trials
  1. Raskind MA, Peskind ER, Wessel T, Yuan W. Galantamine in AD: A 6-month randomized, placebo-controlled trial with a 6-month extension (GAL-USA-1). Neurology. 2000;54(12):2261–2268. doi:10.1212/wnl.54.12.2261Pivotal 6-month RCT (n=636) demonstrating 3.8–3.9 point treatment effect on ADAS-cog at 24 and 32 mg/day; with 6-month open-label extension.
  2. Tariot PN, Solomon PR, Morris JC, Kershaw P, Lilienfeld S, Ding C. A 5-month, randomized, placebo-controlled trial of galantamine in AD (GAL-USA-10). Neurology. 2000;54(12):2269–2276. doi:10.1212/wnl.54.12.2269Key trial (n=978) using slow 4-week dose escalation; demonstrated 3.3–3.6 point ADAS-cog benefit at 16 and 24 mg/day with improved tolerability.
  3. Wilcock GK, Lilienfeld S, Gaens E; Galantamine International-1 Study Group. Efficacy and safety of galantamine in patients with mild to moderate Alzheimer’s disease: multicentre randomised controlled trial. BMJ. 2000;321(7274):1445–1449. doi:10.1136/bmj.321.7274.1445International 6-month trial (n=653) confirming ~3-point ADAS-cog treatment effect; demonstrated cognitive, functional, and global benefits.
  4. Rockwood K, Mintzer J, Truyen L, Wessel T, Wilkinson D. Effects of a flexible galantamine dose in Alzheimer’s disease: a randomised, controlled trial. J Neurol Neurosurg Psychiatry. 2001;71(5):589–595. doi:10.1136/jnnp.71.5.589Flexible-dose trial supporting the clinical utility of individually titrated galantamine; Goal Attainment Scaling was used as a secondary outcome.
  5. Raskind MA, Peskind ER, Truyen L, Kershaw P, Damaraju CV. The cognitive benefits of galantamine are sustained for at least 36 months: a long-term extension trial. Arch Neurol. 2004;61(2):252–256. doi:10.1001/archneur.61.2.25236-month open-label extension demonstrating sustained cognitive benefits on ADAS-cog/11 with continuous galantamine 24 mg/day.
  6. Burns A, Bernabei R, Bullock R, et al. Safety and efficacy of galantamine (Reminyl) in severe Alzheimer’s disease (the SERAD study): a randomised, placebo-controlled, double-blind trial. Lancet Neurol. 2009;8(1):39–47. doi:10.1016/S1474-4422(08)70261-3RCT in severe AD; showed some cognitive benefit but no significant functional improvement; extends safety data beyond mild-moderate population.
Guidelines
  1. National Institute for Health and Care Excellence (NICE). Dementia: assessment, management, and support for people living with dementia and their carers. NICE guideline [NG97]. 2018 (updated 2023). nice.org.uk/guidance/ng97UK guideline recommending AChE inhibitors (donepezil, galantamine, rivastigmine) as first-line pharmacotherapy for mild-to-moderate AD.
Mechanistic / Basic Science
  1. Samochocki M, Höffle A, Fehrenbacher A, et al. Galantamine is an allosterically potentiating ligand of neuronal nicotinic but not of muscarinic acetylcholine receptors. J Pharmacol Exp Ther. 2003;305(3):1024–1036. doi:10.1124/jpet.102.045773Establishes galantamine’s allosteric potentiating ligand activity at nicotinic receptors, the pharmacological basis for its dual mechanism.
Pharmacokinetics / Special Populations
  1. Huang F, Fu Y. A review of clinical pharmacokinetics and pharmacodynamics of galantamine, a reversible acetylcholinesterase inhibitor for the treatment of Alzheimer’s disease, in healthy subjects and patients. Curr Clin Pharmacol. 2010;5(2):115–124. doi:10.2174/157488410791110805Comprehensive PK review covering absorption, distribution, metabolism, elimination, and effects of CYP2D6 polymorphism on galantamine exposure.
  2. Farlow MR. Clinical pharmacokinetics of galantamine. Clin Pharmacokinet. 2003;42(15):1383–1392. doi:10.2165/00003088-200342150-00005Detailed PK characterisation including hepatic and renal impairment data, drug-drug interactions, and population pharmacokinetics.