INN monograph
Fluvoxamine
Therapeutic agent (verify pharmacological class) · POM
Verified · Updated 01 Aug 2026 · Source: Local active-ingredient clinical extract; FDA drug label via OpenFDA/DailyMed; Professional class pharmacology (Therapeutic agent (verify pharmacological class))
Kenya market
Wholesale / list prices where loaded
Risk first
Contraindications
- thioridazine, tizanidine, pimozide, alosetron, or ramelteon with fluvoxamine maleate extended-release capsules is contraindicated ( see WARNINGS AND PRECAUTIONS [ 5.4 - 5.8 ] ) .
- Coadministration of thioridazine, tizanidine, pimozide, alosetron, or ramelteon ( 4 ).
- Serotonin Syndrome and MAOIs: Do not use MAOIs intended to treat psychiatric disorders with fluvoxamine maleate extended-release capsules or within 14 days of stopping treatment with fluvoxamine maleate extended-release capsules.
- Do not use fluvoxamine maleate extended-release capsules within 14 days of stopping an MAOI intended to treat psychiatric disorders.
- In addition, do not start fluvoxamine maleate extended-release capsules in a patient who is being treated with linezolid or intravenous methylene blue ( 4.1 ). 4.1 Monoamine Oxidase Inhibitors (MAOIs) The use of MAOIs intended to treat psychiatric disorders with fluvoxamine maleate extended-release capsules or within 14 days of stopping treatment with fluvoxamine maleate extended-release capsules is contraindicated because of an increased risk of serotonin syndrome.
- The use of fluvoxamine maleate extended-release within 14 days of stopping an MAOI intended to treat psychiatric disorders is also contraindicated (see DOSAGE AND ADMINISTRATION [ 2.5 ] and WARNINGS AND PRECAUTIONS [ 5.2 ] ) .
- Starting fluvoxamine maleate extended-release in a patient who is being treated with MAOIs such as linezolid or intravenous methylene blue is also contraindicated because of an increased risk of serotonin syndrome (see DOSAGE AND ADMINISTRATION [ 2.6 ] and WARNINGS AND PRECAUTIONS [ 5.2 ] ).
Precautions
- Risk: Monitor for clinical worsening of suicidal thoughts/behaviors especially during the initial months of therapy and at times of dose changes ( 5.1 ).
- Bipolar Disorder: Screen for bipolar disorder ( 5.1 ).
- Serotonin Syndrome: Serotonin syndrome has been reported with SSRIs and SNRIs, including fluvoxamine maleate extended-release capsules, both when taken alone, but especially when co-administered with other serotonergic agents.
- If such symptoms occur, discontinue fluvoxamine maleate extended-release capsules and serotonergic agents and initiate supportive treatment.
- If concomitant use of fluvoxamine maleate extended-release capsules with other serotonergic drugs is clinically warranted, patients should be made aware of a potential increased risk for serotonin syndrome, particularly during treatment initiation and dose increases ( 5.2 ).
- Angle Closure Glaucoma: Angle closure glaucoma has occurred in patients with untreated anatomically narrow angles treated with antidepressants ( 5.3 ).
- Other Potentially Important Drug Interactions: Benzodiazepines : Use with caution.
- Coadministration with diazepam is generally not advisable ( 5.9 ).
- Clozapine: Clozapine levels may be increased and produce orthostatic hypotension or seizures ( 5.9 ).
- Methadone: Coadministration may produce opioid intoxication.
- Discontinuation of fluvoxamine may produce opioid withdrawal ( 5.9 ).
- Mexiletine: Monitor serum mexiletine levels ( 5.9 ).
Point of care
Dosing
Adult
Adults: Recommended starting dose is 100 mg at bedtime, with weekly increases of 50 mg as tolerated to maximum effect, not to exceed 300 mg/day ( 2.1 ) . Pediatric patients naïve to fluvoxamine maleate: The lowest available dose of fluvoxamine maleate extended-release capsules may not be appropriate ( 2.2 ) . Hepatically impaired: Decreased clearance may require modified dose and titration ( 2.3 ) . Extended treatment: Adjust dose to maintain lowest effective dose; reassess patients periodically ( 2.4 ) . Discontinuation: Gradual dose reduction is recommended ( 2.7 , see Warnings and Precautions [ 5.10 ] ). 2.1 OCD (Obsessive Compulsive Disorder) The recommended starting dose is 100 mg at bedtime, with weekly increases of 50 mg as tolerated to maximum therapeutic benefit, not to exceed 300 mg per day. Capsules should not be crushed or chewed. 2.2 Pediatric Patients Naïve to Fluvoxamine Maleate Physicians should consider that the lowest available dose of fluvoxamine maleate extended-release capsules may not be appropriate for pediatric patients naïve to fluvoxamine maleate. 2.3 Dosage for Elderly or Hepatically Impaired Patients Elderly patients and those with hepatic impairment have been observed to have a decreased clearance of fluvoxamine maleate. Consequently, it may be appropriate to titrate slowly following the initial dose of 100 mg in these patient groups. 2.4 Maintenance/Continuation of Extended Treatment Although the efficacy of fluvoxamine maleate extended-release capsules beyond 12 weeks of dosing has not been documented in controlled trials, OCD is a chronic condition, and it is reasonable to consider continuation for a responding patient. The benefit of maintaining patients with OCD on immediate-release fluvoxamine maleate tablets after achieving a response for an average duration of about 4 weeks in a 10-week single-blind phase during which patients were titrated to effect was demonstrated in a controlled trial ( see CLINICAL TRIALS [ 14.2 ] ).Dosage adjustments should be made to maintain the patient on the lowest effective dosage, and patients should be periodically reassessed to determine the need for continued treatment. 2.5 Switching a Patient To or From a Monoamine Oxidase Inhibitor (MAOI) Intended to Treat Psychiatric Disorders At least 14 days should elapse between discontinuation of an MAOI intended to treat psychiatric disorders and initiation of therapy with fluvoxamine maleate extended-release capsules. Conversely, at least 14 days should be allowed after stopping fluvoxamine maleate extended-release capsules before starting an MAOI intended to treat psychiatric disorders ( see CONTRAINDICATIONS [ 4.1 ] ). 2.6 Use of Fluvoxamine Maleate Extended-Release Capsules with Other MAOIs such as Linezolid or Methylene Blue Do not start fluvoxamine maleate extended-release capsules in a patient who is being treated with linezolid or intravenous methylene blue because there is an increased risk of serotonin syndrome. In a patient who requires more urgent treatment of a psychiatric condition, other interventions, including hospitalization, should be considered ( see CONTRAINDICATIONS [ 4.1 ] ) . In some cases, a patient already receiving fluvoxamine maleate extended-release therapy may require urgent treatment with linezolid or intravenous methylene blue. If acceptable alternatives to linezolid or intravenous methylene blue treatment are not available and the potential benefits of linezolid or intravenous methylene blue treatment are judged to outweigh the risks of serotonin syndrome in a particular patient, fluvoxamine maleate extended-release should be stopped promptly, and linezolid or intravenous methylene blue can be administered. The patient should be monitored for symptoms of serotonin syndrome for two weeks or until 24 hours after the last dose of linezolid or intravenous methylene blue, whichever comes first. Therapy with fluvoxamine maleate extended-release capsules may be resumed 24 hours after the last dose of linezolid or intravenous methylene blue ( see WARNINGS AND PRECAUTIONS [ 5.2 ] ) . The risk of administering methylene blue by non-intravenous routes (such as oral tablets or by local injection) or in intravenous doses much lower than 1 mg/kg with fluvoxamine maleate extended-release is unclear. The clinician should, nevertheless, be aware of the possibility of emergent symptoms of serotonin syndrome with such use ( see WARNINGS AND PRECAUTIONS [ 5.2 ] ) . 2.7 Discontinuation of Treatment with Fluvoxamine Maleate Extended-Release Capsules Symptoms associated with discontinuation of other SSRIs or SNRIs have been reported ( see WARNINGS AND PRECAUTIONS [ 5.10 ] ).Patients should be monitored for these symptoms when discontinuing treatment. A gradual reduction in the dose rather than abrupt cessation is recommended whenever possible. If intolerable symptoms occur following a decrease in the dose or upon discontinuation of treatment, then resuming the previously prescribed dose may be considered. Subsequently, the health care provider may continue decreasing the dose but at a more gradual rate.
Paediatric
8.4 Pediatric Use Fluvoxamine maleate extended-release capsules have not been evaluated in pediatric patients (see BOXED WARNING ). The efficacy of fluvoxamine maleate administered as immediate-release tablets for the treatment of OCD was demonstrated in a 10 week multicenter placebo-controlled study with 120 outpatients ages 8 to 17. In addition, 99 of these outpatients continued open-label fluvoxamine maleate treatment for up to another one to three years, equivalent to 94 patient years. The adverse reaction profile observed in that study was generally similar to that observed in adult studies with immediate-release fluvoxamine maleate tablets (see ADVERSE REACTIONS [ 6.3 ]). Decreased appetite and weight loss have been observed in association with the use of fluvoxamine as well as other SSRIs. Consequently, regular monitoring of weight and growth should be performed in children and adolescents treated with an SSRI such as fluvoxamine maleate extended-release capsules. The risks, if any, that may be associated with fluvoxamine’s extended use in children and adolescents with OCD have not been systematically assessed. The prescriber should be mindful that the evidence relied upon to conclude that fluvoxamine is safe for use in children and adolescents derives from relatively short-term clinical studies and from extrapolation of experience gained with adult patients. In particular, there are no studies that directly evaluate the effects of long-term fluvoxamine use on the growth, cognitive behavioral development, and maturation of children and adolescents. Although there is no affirmative finding to suggest that fluvoxamine possesses a capacity to adversely affect growth, development, or maturation, the absence of such findings is not compelling evidence of the absence of the potential of fluvoxamine to have adverse effects in chronic use (see WARNINGS AND PRECAUTIONS–Clinical Worsening and Suicide Risk [ 5.1 ] ). Safety and effectiveness in the pediatric population other than pediatric patients with OCD have not been established (see BOXED WARNING and WARNINGS AND PRECAUTIONS–Clinical Worsening and Suicide Risk [ 5.1 ] ). Anyone considering the use of fluvoxamine maleate extended-release capsules in a child or adolescent must balance the potential risks with the clinical need.
Renal
Review renal impairment dosing; many agents need CrCl/eGFR adjustment.
- CrCl 0–120: Confirm renal dosing in product SmPC / primary label.
Hepatic
Review hepatic impairment dosing; monitor LFTs if agent is hepatically cleared or hepatotoxic.
Safety
Drug interactions
- Professional use: confirm indication, dose, duration, monitoring and patient counselling points against current Kenya STG / EML and the product SmPC.
- Document allergy status and key interactions.
Safety
Adverse effects
- conditions, adverse reaction rates observed in the clinical trials of a drug cannot be directly compared to rates in the clinical trials of another drug and may not reflect the rates observed in clinical practice.
- Most common reactions in controlled trials with OCD patients and patients from another studied population (incidence ≥5% and at least twice that for placebo) were abnormal ejaculation, anorexia, anorgasmia, asthenia, diarrhea, nausea, somnolence, sweating and tremor ( 6.2 ) .
- The following additional reactions occurred: anxiety, decreased libido, myalgia, pharyngitis, and vomiting in the OCD population
- and dyspepsia, dizziness, insomnia, and yawning in another studied population.
- To report SUSPECTED ADVERSE REACTIONS, contact Ajanta Pharma USA Inc., at 855-664-7744 or FDA at 1-800-FDA-1088 or www.fda.gov/medwatch. 6.1 Clinical Trial Data Sources Fluvoxamine maleate extended-release capsules were studied in one 12-week controlled trial in patients with OCD (N = 124
- mean exposure 66.6 days) and in two 12-week controlled trials for another condition (N = 279
- mean exposure 59.2 days).
- Patients in these trials were initiated on 100 mg/day and were titrated in 50 mg increments over the first 6 weeks to within a range of 100 mg/day to 300 mg/day.
- The reactions listed in Table 2 show reactions from the two populations separately.
- Table 3 shows reactions from the three controlled studies combined. 6.2 Adverse Reactions Observed in Controlled Trials Adverse Reactions Associated with Discontinuation of Treatment : Of the 124 patients with OCD and 279 patients in other studies treated with fluvoxamine maleate extended-release capsules in controlled clinical trials, 19% and 26% discontinued treatment due to an adverse reaction.
- The most common reactions (≥1%) associated with discontinuation and considered to be drug related (i.e., those reactions associated with dropout at a rate at least twice that of placebo) were anorexia (including, but not limited to, loss of appetite and decreased appetite) (1%), anxiety (3%), asthenia (3%), diarrhea (2%), dizziness (4%), headache (2%), insomnia (5%), nausea (7%), nervousness (1%), somnolence (5%), and thinking abnormal (1%).
- Commonly Observed Adverse Reactions: Fluvoxamine maleate extended-release capsules have been studied in one controlled trial in patients with OCD (N = 124) and two controlled trials for another condition (N = 279).
- In general, adverse reaction rates were similar in the two data sets as well as in a study of pediatric patients with OCD treated with immediate-release fluvoxamine maleate tablets.
- The most commonly observed treatment-emergent adverse reactions associated with the use of fluvoxamine maleate extended-release capsules and likely to be drug- related (incidence of 5% or greater and at least twice that for placebo) and derived from Table 2 were: abnormal ejaculation, anorexia, anorgasmia, asthenia, diarrhea, nausea, somnolence, sweating, and tremor .
Use
Indications
- 1 INDICATIONS AND USAGE Fluvoxamine maleate extended-release capsules is a selective serotonin reuptake inhibitor (SSRI) indicated for the treatment of obsessive compulsive disorder (OCD) ( 1 ).
- Efficacy was demonstrated in: One 12-week study fluvoxamine maleate extended-release capsules in adults ( 14.1 ).
- Two 10-week studies with immediate-release (IR) fluvoxamine tablets in adults and one 10-week study with IR fluvoxamine tablets in children and adolescents ( 14.1 , 14.3 ).
- One maintenance study with IR fluvoxamine tablets ( 14.2 ). 1.1 Obsessive Compulsive Disorder Fluvoxamine maleate extended-release capsules are indicated for the treatment of obsessive compulsive disorder (OCD), as defined in the DSM-IV.
- Obsessive compulsive disorder is characterized by recurrent and persistent ideas, thoughts, impulses, or images (obsessions) that are ego-dystonic and/or repetitive, purposeful, and intentional behaviors (compulsions) that are recognized by the person as excessive or unreasonable.
- The obsessions or compulsions cause marked distress, are time-consuming, or significantly interfere with social or occupational functioning.
- The efficacy of fluvoxamine maleate extended-release capsules was demonstrated in one 12-week trial in adults with fluvoxamine maleate extended-release capsules as well as in two 10-week trials in adults and in one 10-week trial in children and adolescents (ages 8 years to 17 years) with immediate-release fluvoxamine tablets in outpatients with the diagnosis of OCD as defined in DSM-IV or DSM-III-R (see CLINICAL STUDIES [ 14.1 , 14.3 ]).
- The efficacy of fluvoxamine for long-term use was established in one maintenance study in adults with immediate-release fluvoxamine tablets (see CLINICAL STUDIES [ 14.2 ]).
- The health care provider who elects to prescribe fluvoxamine maleate extended-release capsules for extended periods should periodically re-evaluate the long-term usefulness of the drug for the individual patient (see DOSAGE AND ADMINISTRATION [ 2.4 ]).
Pharmacology
Mode of action
neurons.
Full mechanism text
neurons. Fluvoxamine has been shown to be a potent inhibitor of the serotonin reuptake transporter in preclinical studies, both in vitro and in vivo . Mechanism is agent-specific. At receptor, enzyme, ion channel, transporter or microbial target level, the drug alters a physiological or pathological pathway to produce its therapeutic effect. Confirm precise molecular mechanism in current SmPC / pharmacology reference for this INN before high-stakes decisions.
ADME
Pharmacokinetics & PD
| Onset | Product-specific |
|---|---|
| Duration | Product-specific |
| Route | See product SmPC |
| Absorption | of fluvoxamine. |
| Distribution | for fluvoxamine is approximately 25 L/kg, suggesting extensive tissue distribution. Approximately 80% of fluvoxamine is bound to plasma protein, mostly albumin, over a concentration range of 20 ng/mL to 2,000 ng/mL. |
| Metabolism | Fluvoxamine maleate is extensively metabolized by the liver; the main metabolic routes are oxidative demethylation and deamination. Nine metabolites were identified following a 5 mg radiolabelled dose of fluvoxamine maleate, constituting approximately 85% of the urinary |
| Elimination | products of fluvoxamine. The main human metabolite was fluvoxamine acid which, together with its N-acetylated analog, accounted for about 60% of the urinary excretion products. A third metabolite, fluvoxethanol, formed by oxidative deamination, accounted for about 10%. Fluvoxamin... |
| Half-life | of fluvoxamine in healthy male and female volunteers was 16.3 hours. Gender: In a study with 15 male and 13 female healthy volunteers who were administered fluvoxamine maleate extended-release capsules 100 mg, AUC and C max of fluvoxamine were increased by approximately 60% in fe... |
Full PK/PD text
12 CLINICAL PHARMACOLOGY 12.1 Mechanism of Action The mechanism of action of fluvoxamine maleate in obsessive compulsive disorder is presumed to be linked to its specific serotonin reuptake inhibition in brain neurons. Fluvoxamine has been shown to be a potent inhibitor of the serotonin reuptake transporter in preclinical studies, both in vitro and in vivo . 12.2 Pharmacodynamics In in vitro studies, fluvoxamine maleate had no significant affinity for histaminergic, alpha or beta adrenergic, muscarinic, or dopaminergic receptors. Antagonism of some of these receptors is thought to be associated with various sedative, cardiovascular, anticholinergic, and extrapyramidal effects of some psychotropic drugs. 12.3 Pharmacokinetics Bioavailability: A single-dose crossover study in 28 healthy subjects was conducted to compare the pharmacokinetics of fluvoxamine after administration of fluvoxamine maleate extended-release capsules and immediate-release fluvoxamine maleate tablets. In the single-dose crossover study, mean C max was 38% lower and relative bioavailability was 84% for fluvoxamine maleate extended-release capsules versus immediate-release fluvoxamine maleate tablets. In a multiple-dose proportionality study, fluvoxamine maleate extended-release capsules were administered over a dose range of 100 mg/day to 300 mg/day to 20 healthy volunteers. Steady-state plasma concentrations were achieved within a week of dosing. Mean maximum plasma concentrations were 47 ng/mL, 161 ng/mL, and 319 ng/mL, respectively, at the 100 mg, 200 mg, and 300 mg administered dose levels. Fluvoxamine exhibited nonlinear pharmacokinetics producing disproportionately higher concentrations over the dose range. The AUC and C max values increased 5.7-fold following the 3-fold increase in dose from 100 mg to 300 mg. Food caused the mean AUC and C max of fluvoxamine to increase only slightly; therefore, administration of fluvoxamine maleate extended-release capsules with food does not significantly affect the absorption of fluvoxamine. Distribution/Protein Binding : The mean apparent volume of distribution for fluvoxamine is approximately 25 L/kg, suggesting extensive tissue distribution. Approximately 80% of fluvoxamine is bound to plasma protein, mostly albumin, over a concentration range of 20 ng/mL to 2,000 ng/mL. Metabolism: Fluvoxamine maleate is extensively metabolized by the liver; the main metabolic routes are oxidative demethylation and deamination. Nine metabolites were identified following a 5 mg radiolabelled dose of fluvoxamine maleate, constituting approximately 85% of the urinary excretion products of fluvoxamine. The main human metabolite was fluvoxamine acid which, together with its N-acetylated analog, accounted for about 60% of the urinary excretion products. A third metabolite, fluvoxethanol, formed by oxidative deamination, accounted for about 10%. Fluvoxamine acid and fluvoxethanol were tested in an in vitro assay of serotonin and norepinephrine reuptake inhibition in rats; they were inactive except for a weak effect of the former metabolite on inhibition of serotonin uptake (1 to 2 orders of magnitude less potent than the parent compound). Approximately 2% of fluvoxamine was excreted in urine unchanged (see DRUG INTERACTIONS [ 7 ] ). Elimination: Following a 14 C-labelled oral dose of fluvoxamine maleate (5 mg), an average of 94% of drug-related products was recovered in the urine within 71 hours . After administration of a 100 mg, single oral dose of fluvoxamine maleate extended-release capsules, the mean plasma half-life of fluvoxamine in healthy male and female volunteers was 16.3 hours. Gender: In a study with 15 male and 13 female healthy volunteers who were administered fluvoxamine maleate extended-release capsules 100 mg, AUC and C max of fluvoxamine were increased by approximately 60% in females compared to males. There were no differences in the elimination half-life between males and females. Elderly Subjects: In a study using immediate-release fluvoxamine maleate tablets at 50 mg and 100 mg and comparing elderly (ages 66 years to 73 years) and young subjects (ages 19 years to 35 years), mean maximum plasma concentrations in the elderly were 40% higher. The multiple-dose elimination half-life of fluvoxamine was 17.4 hours and 25.9 hours in the elderly compared to 13.6 hours and 15.6 hours in the young subjects at steady state for 50 mg and 100 mg doses, respectively. In elderly patients administered immediate-release fluvoxamine maleate tablets, the clearance of fluvoxamine was reduced by about 50%; therefore, fluvoxamine maleate extended-release capsules should be slowly titrated during initiation of therapy (see DOSAGE AND ADMINISTRATION [ 2.3 ] ). Pediatric Subjects: The pharmacokinetics of fluvoxamine maleate extended-release capsules have not been evaluated in pediatric patients. However, the multiple-dose pharmacokinetics of fluvoxamine were determined in male and female children (ages 6 to 11) and adolescents (ages 12 to 17). Steady-state plasma fluvoxamine concentrations were 2-fold to 3-fold higher in children than in adolescents. AUC and C max in children were 1.5-fold to 2.7-fold higher than that in adolescents (see Table 4). As in adults, both children and adolescents exhibited nonlinear multiple-dose pharmacokinetics. Female children showed significantly higher AUC (0-12) and C max compared to male children and, therefore, lower doses of immediate-release fluvoxamine maleate tablets may produce therapeutic benefit (see Table 5). No gender differences were observed in adolescents. Steady-state plasma fluvoxamine concentrations were similar in adults and adolescents at a dose of 300 mg/day, indicating that fluvoxamine exposure was similar in these two populations (see Table 4). Dose adjustment in adolescents (up to the adult maximum dose of 300 mg) may be indicated to achieve therapeutic benefit. TABLE 4:COMPARISON OF MEAN (SD) IMMEDIATE-RELEASE TABLET FLUVOXAMINE MALEATE PHARMACOKINETIC PARAMETERS BETWEEN CHILDREN, ADOLESCENTS, AND ADULTS Pharmacokinetic Parameter (body weight corrected) Dose = 200 mg/day (100 mg Twice Daily) Dose = 300 mg/day (150 mg Twice Daily) Children (n = 10) Adolescent (n = 17) Adolescent (n= 13) Adult (n = 16) AUC 0-12 (ng • h/mL/kg) 155.1 (160.9) 43.9 (27.9) 69.6 (46.6) 59.4 (40.9) C max (ng/mL/kg) 14.8 (14.9) 4.2 (2.6) 6.7 (4.2) 5.7 (3.9) C min (ng/mL/kg) 11.0 (11.9) 2.9 (2.0) 4.8 (3.8) 4.6 (3.2) TABLE 5:COMPARISON OF MEAN (SD) IMMEDIATE-RELEASE TABLET FLUVOXAMINE MALEATE PHARMACOKINETIC PARAMETERS BETWEEN MALE AND FEMALE CHILDREN (6 YEARS TO 11 YEARS) Pharmacokinetic Parameter (body weight corrected) Dose = 200 mg/day (100 mg Twice Daily) Male Children (n = 7) Female Children (n = 3) AUC 0-12 (ng • h/mL/kg) 95.8 (83.9) 293.5 (233.0) C max (ng/mL/kg) 9.1 (7.6) 28.1 (21.1) C min (ng/mL/kg) 6.6 (6.1) 21.2 (17.6) Hepatic and Renal Disease: A cross-study comparison (healthy subjects versus patients with hepatic dysfunction) using immediate-release fluvoxamine maleate tablets suggested a 30% decrease in fluvoxamine clearance in association with hepatic dysfunction. The mean minimum plasma concentrations in renally impaired patients (creatinine clearance of 5 mL/min to 45 mL/min) after 4 weeks and 6 weeks of treatment (50 mg given twice daily, N = 13) were comparable to each other, suggesting no accumulation of fluvoxamine in these patients (see WARNINGS AND PRECAUTIONS–Use in Patients with Concomitant Illness [ 5.15 ] ) .
Kenya
Brands & prices
| Brand | Company | Pack | KES |
|---|---|---|---|
| Faverin | Abbott Laboratories | Standard Commercial Pack | — |
Special populations
Pregnancy & lactation
Pregnancy
8.1 Pregnancy Teratogenic Effects: When pregnant rats were given daily doses of fluvoxamine (60 mg/kg, 120 mg/kg, or 240 mg/kg) orally throughout the period of organogenesis, developmental toxicity in the form of increased embryofetal death and increased incidences of fetal eye abnormalities (folded retinas) was observed at doses of 120 mg/kg or greater. Decreased fetal body weight was seen at the high dose. The no effect dose for developmental toxicity in this study was 60 mg/kg (approximately 2 time the maximum recommended human dose [MRHD] on a mg/m 2 basis). In a study in which pregnant rabbits were administered doses of up to 40 mg/kg (approximately 2 times the MRHD on a mg/m 2 basis) orally during organogenesis, no adverse effects on embryofetal development were observed. In other reproduction studies in which female rats were dosed orally during pregnancy and lactation (5 mg/kg, 20 mg/kg, 80 mg/kg, or 160 mg/kg), increased pup mortality at birth was seen at doses of 80 mg/kg or greater and decreases in pup body weight and survival were observed at all doses (low effect dose approximately 0.1 times the MRHD on a mg/m 2 basis). Nonteratogenic Effects: Based on data from published observational studies, exposure to SSRIs, particularly in the month before delivery, has been associated with a less than 2-fold increase in the risk of postpartum haemorrhage [see Warnings and Precautions ( 5.11 ) and Clinical Considerations]. Neonates exposed to fluvoxamine maleate tablets and other SSRIs or serotonin and norepinephrine reuptake inhibitors (SNRIs) late in the third trimester have developed complications requiring prolonged hospitalization, respiratory support, and tube feeding. Such complications can arise immediately upon delivery. Reported clinical findings have included respiratory distress, cyanosis, apnea, seizures, temperature instability, feeding difficulty, vomiting, hypoglycemia, hypotonia, hypertonia, hyperreflexia, tremor, jitteriness, irritability and constant crying. These features are consistent with either a direct toxic effect of SSRIs or SNRIs or, possibly, a drug discontinuation syndrome. It should be noted that, in some cases, the clinical picture is consistent with serotonin syndrome (see WARNINGS AND PRECAUTIONS - Serotonin Syndrome [ 5.2 ] ). Infants exposed to SSRIs in pregnancy may have an increased risk for persistent pulmonary hypertension of the newborn (PPHN). PPHN occurs in 1-2 per 1,000 live births in the general population and is associated with substantial neonatal morbidity and mortality. Several recent epidemiologic studies suggest a positive statistical association between SSRI use (fluvoxamine maleate and fluvoxamine maleate extended-release are SSRIs) in pregnancy and PPHN. Other studies do not show a significant statistical association. Physicians should also note the results of a prospective longitudinal study of 201 pregnant women with a history of major depression, who were either on antidepressants or had received antidepressants less than 12 weeks prior to their last menstrual period, and were in remission. Women who discontinued antidepressant medication during pregnancy showed a significant increase in relapse of their major depression compared to those women who remained on antidepressant medication throughout pregnancy. When treating a pregnant woman with fluvoxamine, the physician should carefully consider both the potential risks of taking an SSRI, along with the established benefits of treating depression with an antidepressant. This decision can only be made on a case by case basis (see DOSAGE AND ADMINISTRATION [ 2.7 ] ). Maternal Adverse Reactions: Use of fluvoxamine maleate extended-release capsules in the month before delivery may be associated with an increased risk of postpartum hemorrhage [see Warnings and Precautions ( 5.11 )] .
Lactation
8.3 Nursing Mothers Fluvoxamine is secreted in human breast milk. Because of the potential for serious adverse reactions in nursing infants from fluvoxamine maleate extended-release capsules, a decision should be made whether to discontinue nursing or discontinue the drug, taking into account the importance of the drug to the mother.
Diet
Food & alcohol
- Drug & food interactions (label) 7 DRUG INTERACTIONS Drug Interactions (not described in Contraindications or Warnings and Precautions) include the following: Drugs Inhibiting or Metabolized by Cytochrome P450: Fluvoxamine inhibits several cytochrome P450 isoenzymes (CYP1A2, CYP2C9, CYP3A4, and CYP2C19) ( 7.1 ) . Carbamazepine: Elevated carbamazepine levels and symptoms of toxicity with coadministration ( 7.2 ) . Sumatriptan: Rare postmarketing reports of weakness, hyperreflexia, and incoordination following use of an SSRI and sumatriptan. Monitor appropriately if concomitant treatment is clinically warranted ( 7.2 ) . Tacrine: Coadministration increased tacrine C max and AUC five-and eight-fold and caused nausea, vomiting, sweating, and diarrhea ( 7.2 ) . Tricyclic Antidepressants (TCAs): Coadministration significantly increased plasma TCA levels. Use caution; monitor plasma TCA levels; reduce TCA dose if indicated ( 7.2 ) . Tryptophan: Severe vomiting with coadministration ( 7.2 ) . Diltiazem: Bradycardia with coadministration ( 7.3 ) . Propranolol or Metoprolol: Reduce dose if coadministered with fluvoxamine and titrate more cautiously ( 7.3 ) . 7.1 Potential Interactions with Drugs that Inhibit or are Metabolized by Cytochrome P450 Isoenzymes Multiple hepatic cytochrome P450 isoenzymes are involved in the oxidative biotransformation of a large number of structurally different drugs and endogenous compounds. The available knowledge concerning the relationship of fluvoxamine and the cytochrome P450 isoenzyme system has been obtained mostly from pharmacokinetic interaction studies conducted in healthy volunteers, but some preliminary in vitro data are also available. Based on a finding of substantial interactions of fluvoxamine with certain of these drugs (see later parts of this section and also WARNINGS AND PRECAUTIONS [ 5 ] for details) and limited in vitro data for CYP3A4, it appears that fluvoxamine inhibits several cytochrome P450 isoenzymes that are known to be involved in the metabolism of other drugs such as: CYP1A2 (e.g., warfarin, theophylline, propranolol, tizanidine), CYP2C9 (e.g., warfarin), CYP3A4 (e.g., alprazolam), and CYP2C19 (e.g., omeprazole). In vitro data suggest that fluvoxamine is a relatively weak inhibitor of CYP2D6. Approximately 7% of the normal population has a genetic code that leads to reduced levels of activity of CYP2D6 enzyme. Such individuals have been referred to as “poor metabolizers” (PM) of drugs such as debrisoquin, dextromethorphan, and tricyclic antidepressants. While none of the drugs studied for drug interactions significantly affected the pharmacokinetics of fluvoxamine, an in vivo study of fluvoxamine single-dose pharmacokinetics in 13 PM subjects demonstrated altered pharmacokinetic properties compared to 16 “extensive metabolizers” (EM): mean C max , AUC, and half-life were increased by 52%, 200%, and 62%, respectively, in the PM compared to the EM group. This suggests that fluvoxamine is metabolized, at least in part, by CYP2D6.
Trust
Sources & disclaimer
Source: Local active-ingredient clinical extract; FDA drug label via OpenFDA/DailyMed; Professional class pharmacology (Therapeutic agent (verify pharmacological class))
Last reviewed: 01 Aug 2026
Decision support only — not a substitute for clinical judgment, product SmPC, or Kenya STG/EML.