Drug Monograph
Fluvoxamine
fluvoxamine maleate · Brand: Luvox
Pharmacokinetic Profile
Half-Life
~15.6 h (steady state, 100 mg/day)
Metabolism
Hepatic oxidative demethylation & deamination; CYP2D6 substrate (partial)
Protein Binding
~80%
Bioavailability
53%
Volume of Distribution
~25 L/kg
Clinical Information
Drug Class
SSRI
Available Doses
25, 50 (scored), 100 mg (scored) tablets
Route
Oral (bedtime dosing; BID if >100 mg)
Renal Adjustment
No accumulation in CrCl 5–45 mL/min
Hepatic Adjustment
Yes — clearance decreased ~30%; start low, titrate slowly
Pregnancy
No established teratogenicity; risk of PPHN and neonatal adaptation syndrome (3rd trimester)
Lactation
Present in breast milk; monitor infant
Schedule
Prescription only (not scheduled)
Generic Available
Yes
Black Box Warning
Suicidality in children, adolescents & young adults
Key CYP Inhibition
Potent CYP1A2 inhibitor; also inhibits CYP2C9, CYP3A4, CYP2C19
Indications
| Indication | Approved Population | Therapy Type | Status |
|---|---|---|---|
| Obsessive Compulsive Disorder (OCD) | Adults | Monotherapy | FDA Approved |
| Obsessive Compulsive Disorder (OCD) | Children & adolescents (ages 8–17) | Monotherapy | FDA Approved |
Fluvoxamine is FDA-approved exclusively for OCD in the United States. It was the first SSRI approved by the FDA specifically for OCD (1994) and the first SSRI approved for paediatric OCD (1997). Unlike most other SSRIs, fluvoxamine does not carry an FDA indication for major depressive disorder in the US, although it is widely approved for MDD internationally. Its clinical niche is defined by its potent CYP1A2 inhibition, which creates a unique drug interaction profile among the SSRIs.
Off-Label Uses
Major depressive disorder: Approved for MDD in many countries outside the US; extensively studied. Evidence quality: High (multiple RCTs).
Social anxiety disorder: Approved in Japan and some other countries; RCT evidence supports efficacy. Evidence quality: High.
Panic disorder: Evidence quality: Moderate (RCTs).
Post-traumatic stress disorder: Evidence quality: Moderate.
Dosing
Adult Dosing by Clinical Scenario
| Clinical Scenario | Starting Dose | Maintenance Dose | Maximum Dose | Notes |
|---|---|---|---|---|
| OCD — initial treatment | 50 mg at bedtime | 100–300 mg/day | 300 mg/day | Increase by 50 mg every 4–7 days as tolerated. Doses >100 mg should be given in two divided doses (larger dose at bedtime) Therapeutic range typically 100–300 mg/day in clinical trials |
| OCD — elderly patient | 25–50 mg at bedtime | Titrate slowly | 300 mg/day | Clearance decreased ~50% in elderly (Cmax 40% higher, t½ up to 25.9 h vs 15.6 h) Start lower, titrate more slowly |
| OCD — hepatic impairment | 25 mg at bedtime | Titrate slowly with monitoring | Individualise | Clearance decreased ~30% Low start, slow titrate, careful monitoring |
| Depression (off-label, international use) | 50 mg at bedtime | 100–200 mg/day | 300 mg/day | Not FDA-approved for MDD in the US; approved internationally Same titration schedule as OCD |
Paediatric Dosing (OCD, ages 8–17)
| Clinical Scenario | Starting Dose | Maintenance Dose | Maximum Dose | Notes |
|---|---|---|---|---|
| OCD — children (8–11 years) | 25 mg at bedtime | 50–200 mg/day | 200 mg/day | Increase by 25 mg every 4–7 days. Doses >50 mg should be divided BID Plasma levels 2–3× higher than adolescents; female children have higher exposure |
| OCD — adolescents (12–17 years) | 25 mg at bedtime | 50–200 mg/day | 300 mg/day | May need adult-range doses (up to 300 mg) for therapeutic benefit Steady-state levels similar to adults at 300 mg/day |
Clinical Pearl: Bedtime Dosing and BID Schedule
Fluvoxamine is unique among SSRIs in recommending bedtime dosing and a twice-daily schedule at higher doses. The shorter half-life (~15.6 hours) necessitates divided dosing above 100 mg (adults) or 50 mg (children) to maintain therapeutic levels throughout the day. The initial bedtime dose leverages sedation as a therapeutic advantage for the many OCD patients who experience insomnia. When dividing doses, the larger portion should be given at bedtime. Smokers metabolise fluvoxamine 25% faster than non-smokers, which may affect dose requirements.
Pharmacology
Mechanism of Action
Fluvoxamine is a potent and selective inhibitor of the serotonin reuptake transporter (SERT), with no clinically significant affinity for histaminergic, adrenergic (α or β), muscarinic cholinergic, or dopaminergic receptors. This clean receptor profile contributes to its generally favourable side effect profile compared to tricyclic antidepressants. Fluvoxamine also demonstrates sigma-1 receptor agonist activity, which is unique among SSRIs and has been hypothesised to contribute to its anxiolytic and potentially neuroprotective properties. Unlike paroxetine or fluoxetine, fluvoxamine is only a weak inhibitor of CYP2D6. However, it is a potent inhibitor of CYP1A2 and also significantly inhibits CYP2C9, CYP3A4, and CYP2C19, making it the SSRI with the broadest and most clinically consequential cytochrome P450 inhibition profile.
ADME Profile
| Parameter | Value | Clinical Implication |
|---|---|---|
| Absorption | Bioavailability 53%; Tmax 3–8 h at steady state; food does not significantly affect absorption; nonlinear PK at 100–300 mg (disproportionately higher levels at higher doses) | Nonlinear kinetics mean dose increases produce greater-than-expected rises in plasma levels; can be taken with or without food |
| Distribution | Vd ~25 L/kg; ~80% protein-bound (mainly albumin, across 20–2000 ng/mL) | Extensive tissue distribution; moderate protein binding reduces displacement interaction risk |
| Metabolism | Extensive hepatic oxidative demethylation and deamination; 9 metabolites identified; main metabolite (fluvoxamine acid) and N-acetylated analogue account for ~60% of urinary excretion; metabolites 1–2 orders of magnitude less potent; ~2% excreted unchanged; partially metabolised by CYP2D6 (PM: Cmax +52%, AUC +200%, t½ +62%) | Potent CYP1A2 inhibitor is the dominant clinical concern; CYP2D6 PM status significantly increases exposure; hepatic impairment reduces clearance by ~30% |
| Elimination | t½ ~15.6 h (young adults at 100 mg/day); 94% recovered in urine within 71 h; steady state in ~1 week; elderly: t½ 17.4–25.9 h, clearance decreased ~50%; smokers: 25% increased metabolism | Shortest half-life among SSRIs; necessitates BID dosing at higher doses; elderly require lower starting dose and slower titration; smoking status affects dose requirements |
Side Effects
≥10%Very Common
| Adverse Effect | Incidence | Clinical Note |
|---|---|---|
| Nausea | 40% vs 14% placebo | Highest GI rate among SSRIs; dose-related; usually improves over 1–2 weeks; a leading cause of discontinuation (9%) |
| Headache | 22% vs 20% placebo | Similar to placebo; usually transient |
| Somnolence | 22% vs 8% placebo | Bedtime dosing leverages this as a therapeutic advantage; caution with driving |
| Insomnia | 21% vs 10% placebo | Paradoxical given somnolence; may represent disrupted sleep architecture |
| Asthenia | 14% vs 6% placebo | May be more pronounced in OCD-only trials |
| Dry mouth | 14% vs 10% placebo | Despite absence of muscarinic receptor activity; encourage oral hygiene |
| Nervousness | 12% vs 5% placebo | More common early in treatment; distinguish from akathisia |
| Diarrhoea | 11% vs 7% placebo | Serotonergic GI effect; generally mild |
| Dizziness | 11% vs 6% placebo | Usually resolves with continued treatment |
| Constipation | 10% vs 8% placebo | Marginally above placebo |
| Dyspepsia | 10% vs 5% placebo | Taking with food may help |
1–10%Common
| Adverse Effect | Incidence | Clinical Note |
|---|---|---|
| URTI | 9% vs 5% placebo | May be coincidental; comparable across SSRI trials |
| Abnormal ejaculation (males) | 8% vs 1% placebo | Primarily delayed ejaculation; lower rate than paroxetine; enquire proactively |
| Sweating | 7% vs 3% placebo | May persist with chronic use |
| Anorexia | 6% vs 2% placebo | Monitor weight, especially in paediatric patients |
| Tremor | 5% vs 1% placebo | Fine postural tremor; dose-related |
| Vomiting | 5% vs 2% placebo | Part of the high GI burden; usually early and transient |
| Anxiety | 5% vs 3% placebo | May represent initial activation |
| Flatulence | 4% vs 3% placebo | Mild; GI tract serotonergic effect |
| Taste perversion | 3% vs 1% placebo | Usually self-limiting |
| Palpitations | 3% vs 2% placebo | No important ECG changes vs placebo in premarketing studies |
| Urinary frequency | 3% vs 2% placebo | Generally self-limiting |
| Decreased libido | 2% vs 1% placebo | Lower rate than paroxetine; likely underreported |
| Impotence (males) | 2% vs 1% placebo | Enquire proactively |
| Anorgasmia | 2% vs 0% placebo | Both sexes; likely underreported |
SeriousSerious Adverse Effects
| Adverse Effect | Estimated Frequency | Typical Onset | Required Action |
|---|---|---|---|
| Suicidal thoughts/behaviours | 14 per 1,000 (<18 y); 5 per 1,000 (18–24 y) | First weeks to months | Close monitoring at initiation and dose changes; daily observation by caregivers recommended |
| Serotonin syndrome | Rare | Hours to days, especially with co-serotonergic drugs | Discontinue all serotonergic agents; supportive care; hospital admission |
| Mania/hypomania | ~1% (adults); 4% (paediatric OCD) | Days to weeks | Discontinue; psychiatric reassessment for bipolar disorder |
| Seizures | 0.2% | Any time | Discontinue; avoid in unstable epilepsy |
| Hyponatraemia (SIADH) | Uncommon; Na <110 mmol/L reported | Days to weeks; elderly at higher risk | Check sodium; discontinue; medical management |
| Abnormal bleeding | Uncommon | Any time; increased with anticoagulants/NSAIDs | Assess source; caution with concurrent anticoagulants |
| Angle-closure glaucoma | Rare | Any time | Ophthalmological emergency; discontinue |
| Stevens-Johnson syndrome / TEN | Very rare (postmarketing) | Days to weeks | Immediate discontinuation; dermatology referral |
DiscontinuationDiscontinuation Rates
Adults (OCD + Depression Trials)
22% discontinued due to adverse events (N=1,087)
Top reasons: Nausea (9%), insomnia (4%), somnolence (4%), headache (3%), asthenia (2%), vomiting (2%), nervousness (2%), agitation (2%), dizziness (2%)
Discontinuation Syndrome Risk
Moderate short t½ increases risk
Shortest half-life among SSRIs (~15.6 h); gradual taper recommended. Symptoms: dysphoric mood, irritability, dizziness, paresthesia, anxiety, confusion, insomnia
Managing Nausea (Leading Cause of Discontinuation)
Fluvoxamine’s nausea rate (40%) is the highest among SSRIs and is the most common reason for early discontinuation (9%). Strategies include: starting at the lower 50 mg dose (or 25 mg in sensitive patients), slow titration (every 4–7 days), bedtime dosing to sleep through peak GI effects, taking with food, and temporary use of an antiemetic if needed. Most patients who persist through the first 1–2 weeks will see substantial improvement in nausea.
Drug Interactions
Fluvoxamine has the most extensive CYP inhibition profile of any SSRI, acting as a potent inhibitor of CYP1A2 and a significant inhibitor of CYP2C9, CYP3A4, and CYP2C19. This makes drug interaction management the central challenge of prescribing fluvoxamine. It is a relatively weak CYP2D6 inhibitor. Any drug with a narrow therapeutic index that is metabolised by CYP1A2, CYP2C9, CYP3A4, or CYP2C19 requires careful evaluation before co-prescribing.
MajorTizanidine
MechanismPotent CYP1A2 inhibition; Cmax increased 12-fold (range 5–32), AUC increased 33-fold (range 14–103)
EffectSevere hypotension (systolic −35 mmHg, diastolic −20 mmHg), excessive sedation, psychomotor impairment
ManagementContraindicated. Must not be co-administered
FDA PIMajorThioridazine
MechanismCYP1A2 inhibition; thioridazine and metabolite levels increased 3-fold
EffectQTc prolongation, torsade de pointes, sudden death risk
ManagementContraindicated
FDA PIMajorAlosetron
MechanismCYP1A2 inhibition; AUC increased ~6-fold, t½ ~3-fold
EffectMarkedly elevated alosetron exposure
ManagementContraindicated
FDA PIMajorPimozide
MechanismCYP3A4 inhibition; increased pimozide levels expected
EffectQT prolongation, ventricular arrhythmia risk
ManagementContraindicated
FDA PIMajorMAOIs (linezolid, IV methylene blue)
MechanismDual serotonergic enhancement
EffectSerotonin syndrome (potentially fatal)
ManagementContraindicated. ≥14 days washout in either direction
FDA PIMajorRamelteon
MechanismCYP1A2 inhibition; AUC increased ~190-fold, Cmax ~70-fold
EffectExtreme ramelteon overexposure
ManagementShould not be used together
FDA PIMajorTheophylline
MechanismCYP1A2 inhibition; theophylline clearance decreased ~3-fold
EffectTheophylline toxicity (seizures, arrhythmias, nausea)
ManagementReduce theophylline dose to one-third of usual; monitor levels
FDA PIMajorWarfarin
MechanismCYP1A2 and CYP2C9 inhibition; warfarin levels increased 98%, PT prolonged
EffectMajor bleeding risk
ManagementMonitor PT/INR closely; expect to reduce warfarin dose substantially
FDA PIModerateAlprazolam
MechanismCYP3A4 inhibition; AUC doubled, clearance reduced ~50%
EffectIncreased sedation; impaired psychomotor and memory function
ManagementHalve initial alprazolam dose; titrate to lowest effective dose
FDA PIModerateDiazepam
MechanismCYP inhibition; diazepam clearance reduced 65%; active metabolite unmeasurably low
EffectSubstantial accumulation of diazepam and metabolites
ManagementGenerally not advisable to co-administer; use lorazepam, oxazepam, or temazepam instead (glucuronidated, not affected)
FDA PIModeratePropranolol / Metoprolol
MechanismCYP1A2/CYP2D6 inhibition; propranolol levels increased 5-fold (range 2–17)
EffectBradycardia, hypotension; reported cases with metoprolol
ManagementReduce beta-blocker dose; titrate cautiously; atenolol (renally cleared) not affected
FDA PIModerateTCAs (amitriptyline, clomipramine, imipramine)
MechanismCYP inhibition; significantly increased plasma TCA levels
EffectTCA toxicity (QT prolongation, seizures, anticholinergic effects)
ManagementMonitor TCA levels; reduce TCA dose as needed
FDA PIModerateClozapine
MechanismCYP1A2 inhibition; elevated clozapine levels
EffectDose-related seizure risk and orthostatic hypotension
ManagementClose monitoring; reduce clozapine dose; monitor clozapine levels
FDA PIModerateMethadone
MechanismCYP inhibition; significantly increased methadone levels
EffectOpioid intoxication reported; opioid withdrawal on fluvoxamine discontinuation
ManagementMonitor closely; adjust methadone dose as needed
FDA PIMonitoring
- Mood & SuicidalityWeekly for 4 weeks, biweekly for 8 weeks, then per judgement
RoutineEspecially important in paediatric patients (approved for ages 8–17); daily observation by caregivers recommended per FDA PI - Drug InteractionsAt every prescription change
RoutineReview the medication list for CYP1A2, CYP2C9, CYP3A4, and CYP2C19 substrates at every visit; fluvoxamine has the broadest CYP inhibition of any SSRI - Weight & GrowthBaseline, then every 3 months (paediatric)
RoutineDecreased appetite and weight loss observed with SSRIs in children; regular monitoring recommended per FDA PI for long-term paediatric treatment - Sodium (Na+)Baseline in at-risk; recheck 2–4 weeks
Trigger-basedAt-risk: elderly, diuretic users, volume-depleted. Na <110 mmol/L reported - Sexual FunctionBaseline, then each visit
RoutineFDA PI specifically advises routine enquiry; rates likely underestimated - Smoking StatusAt initiation and if changes
Trigger-basedSmokers metabolise fluvoxamine 25% faster; starting or stopping smoking may require dose adjustment - Theophylline LevelsIf co-prescribed
Trigger-basedClearance reduced 3-fold; dose must be cut to one-third; monitor levels closely - INR (if on warfarin)At initiation and dose changes
Trigger-basedWarfarin levels increased 98%; expect substantial dose reduction needed
Contraindications & Cautions
Absolute Contraindications
- Concurrent tizanidine — CYP1A2 inhibition causes 33-fold AUC increase with life-threatening hypotension
- Concurrent thioridazine — 3-fold increase in levels, QTc prolongation, torsade de pointes risk
- Concurrent alosetron — 6-fold AUC increase
- Concurrent pimozide — QT prolongation risk via CYP3A4 inhibition
- MAOIs — within 14 days, including linezolid and IV methylene blue; serotonin syndrome risk
Relative Contraindications (Specialist Input Recommended)
- Patients on multiple CYP1A2/CYP3A4 substrates with narrow therapeutic indices — complex interaction management; consider alternative SSRI
- Unstable epilepsy — avoid; seizures reported in 0.2%
- Undiagnosed bipolar disorder — mania risk ~1% (adults), 4% (paediatric)
Use with Caution
- Elderly patients — clearance decreased ~50%; Cmax 40% higher; start low, titrate slowly
- Hepatic impairment — clearance decreased ~30%; start low, slow titration with monitoring
- Patients on benzodiazepines metabolised by hepatic oxidation (alprazolam, midazolam, triazolam) — reduce benzodiazepine dose; lorazepam/oxazepam/temazepam preferred (glucuronidated)
- Late pregnancy — PPHN risk and neonatal adaptation syndrome
- Breastfeeding — present in breast milk; monitor infant for diarrhoea, vomiting, agitation, decreased sleep
- Anatomically narrow angles (untreated) — risk of angle-closure glaucoma
- CYP2D6 poor metabolisers — Cmax +52%, AUC +200%, t½ +62%; consider lower doses
- Smokers — 25% faster metabolism; dose may need to be higher; stopping smoking requires dose reduction
FDA Boxed Warning
Suicidality and Antidepressant Drugs
Antidepressants increased the risk of suicidal thinking and behaviour in children, adolescents, and young adults (ages 18–24) with MDD and other psychiatric disorders. Fluvoxamine is not approved for MDD or for paediatric use other than OCD (ages 8–17). All patients started on antidepressant therapy should be monitored closely for clinical worsening, suicidality, and unusual behavioural changes, especially during the initial months and at dose changes. Families and caregivers should be alerted to the need for daily observation.
Patient Counselling
Purpose of Therapy
Fluvoxamine works by increasing serotonin activity in the brain to help reduce obsessive thoughts and compulsive behaviours. Improvement may take several weeks and often requires dose adjustments to find the right balance between benefit and tolerability.
How to Take
Take fluvoxamine at bedtime initially. If your prescriber increases the dose above 100 mg/day, divide into two doses with the larger portion at bedtime. Tablets can be taken with or without food. Do not stop suddenly.
Nausea
Tell patientNausea is very common early in treatment (affects up to 4 in 10 patients) but usually improves within 1–2 weeks. Taking the medication with food or at bedtime can help.
Call prescriberIf nausea is severe, persistent beyond 2 weeks, or causes vomiting preventing fluid intake.
Drowsiness
Tell patientSleepiness is common and is why we recommend taking fluvoxamine at bedtime. Avoid driving or operating machinery until you know how the medication affects you.
Call prescriberIf drowsiness significantly interferes with daily activities and does not improve after 2–3 weeks.
Drug Interactions
Tell patientFluvoxamine interacts with many medications. Always inform every healthcare provider that you take fluvoxamine before starting any new prescription or over-the-counter medication. This includes sleep aids, pain medications, heart medications, and anti-anxiety drugs.
Call prescriberBefore taking any new medication, including herbal products such as St. John’s Wort.
Sexual Side Effects
Tell patientChanges in sexual function (delayed orgasm, reduced desire) can occur. Fluvoxamine generally has lower sexual side effect rates than some other SSRIs, but these effects should be discussed openly.
Call prescriberIf sexual side effects are distressing; alternatives can be considered.
Do Not Stop Suddenly
Tell patientBecause fluvoxamine has a shorter duration in your body than some similar medications, stopping abruptly can cause withdrawal symptoms including dizziness, tingling, irritability, and mood changes. Always taper under medical supervision.
Call prescriberIf you miss doses or experience withdrawal symptoms during any dose reduction.
Mood Changes & Suicidality
Tell patientRarely, this medication may cause new or worsening thoughts of self-harm, especially in the early weeks. A trusted person should watch for mood or behavioural changes.
Call prescriberImmediately if new suicidal thoughts, agitation, or unusual behaviour develops. Go to the emergency department if in immediate danger.
Sources
Regulatory (PI / SmPC)
- Fluvoxamine Maleate Tablets. Full Prescribing Information. ANI Pharmaceuticals, Inc. Revised August 2023. FDA LabelPrimary regulatory source for all dosing, adverse reaction rates, contraindications, CYP interaction data, and pharmacokinetics used in this monograph.
- LUVOX CR (fluvoxamine maleate) extended-release capsules. Full Prescribing Information. Revised 2017. FDA Label (CR)Extended-release formulation PI; cross-referenced for additional interaction data and comparative safety information.
Key Clinical Trials
- Goodman WK, Price LH, Rasmussen SA, et al. Efficacy of fluvoxamine in obsessive-compulsive disorder: a double-blind comparison with placebo. Arch Gen Psychiatry. 1989;46(1):36–44. DOIPivotal RCT establishing fluvoxamine efficacy in OCD using the Y-BOCS as primary outcome.
- Riddle MA, Reeve EA, Yaryura-Tobias JA, et al. Fluvoxamine for children and adolescents with obsessive-compulsive disorder: a randomized, controlled, multicenter trial. J Am Acad Child Adolesc Psychiatry. 2001;40(2):222–229. DOIKey paediatric OCD trial (ages 8–17) supporting FDA approval for this population.
- Hollander E, Allen A, Steiner M, et al. Acute and long-term treatment and prevention of relapse of obsessive-compulsive disorder with paroxetine. J Clin Psychiatry. 2003;64(9):1113–1121. DOIOCD relapse prevention study design referenced for the fluvoxamine maintenance trial methodology.
- Irons J. Fluvoxamine in the treatment of anxiety disorders. Neuropsychiatr Dis Treat. 2005;1(4):289–299. PMCReview of fluvoxamine efficacy across anxiety disorders including panic, social anxiety, and PTSD.
Guidelines
- American Psychiatric Association. Practice Guideline for the Treatment of Patients with Obsessive-Compulsive Disorder. Arlington, VA: APA; 2007. APAAPA guideline positioning SSRIs including fluvoxamine as first-line pharmacotherapy for OCD.
- National Institute for Health and Care Excellence (NICE). Obsessive-compulsive disorder and body dysmorphic disorder: treatment. Clinical guideline CG31. Updated 2021. NICEUK guideline including fluvoxamine among recommended SSRIs for OCD in adults and children over 8.
- Bandelow B, Allgulander C, Baldwin DS, et al. World Federation of Societies of Biological Psychiatry (WFSBP) guidelines for treatment of anxiety, obsessive-compulsive, and posttraumatic stress disorders. World J Biol Psychiatry. 2023;24(2):79–117. DOIInternational guideline with evidence-level ratings for fluvoxamine across OCD and anxiety disorders.
Mechanistic / Basic Science
- Hashimoto K. Sigma-1 receptor chaperone and brain-derived neurotrophic factor: emerging links between cardiovascular disease and depression. Prog Neurobiol. 2013;100:15–29. DOIElucidates fluvoxamine’s unique sigma-1 receptor agonist activity and potential neuroprotective mechanisms.
- Fisar Z, Hroudova J, Raboch J. Inhibition of monoamine oxidase activity by antidepressants and mood stabilizers. Neuro Endocrinol Lett. 2010;31(5):645–656.Comparative pharmacology of SSRIs; positions fluvoxamine’s receptor selectivity among class members.
Pharmacokinetics / Special Populations
- van Harten J. Clinical pharmacokinetics of selective serotonin reuptake inhibitors. Clin Pharmacokinet. 1993;24(3):203–220. DOIComparative PK review establishing fluvoxamine’s nonlinear kinetics, short half-life, and bioavailability data.
- Christensen M, Tybring G, Mihara K, et al. Low daily 10-mg and 20-mg doses of fluvoxamine inhibit the metabolism of both caffeine (cytochrome P4501A2) and omeprazole (cytochrome P4502C19). Clin Pharmacol Ther. 2002;71(3):141–152. DOIDemonstrates that even low fluvoxamine doses produce clinically significant CYP1A2 and CYP2C19 inhibition.
- Spigset O, Granberg K, Hagg S, et al. Non-linear fluvoxamine disposition. Br J Clin Pharmacol. 1998;45(3):257–263. DOICharacterises the dose-dependent nonlinear pharmacokinetics of fluvoxamine across the therapeutic range.