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Fluvoxamine seriously affects the ] of ] and increases the intensity and duration of its effects. Because of the potentially hazardous consequences, the concomitant use of ] with fluvoxamine, or other potent inhibitors of ], should be avoided.<ref>{{cite journal | vauthors = Granfors MT, Backman JT, Neuvonen M, Ahonen J, Neuvonen PJ | title = Fluvoxamine drastically increases concentrations and effects of tizanidine: a potentially hazardous interaction | journal = Clinical Pharmacology and Therapeutics | volume = 75 | issue = 4 | pages = 331–341 | date = April 2004 | pmid = 15060511 | doi = 10.1016/j.clpt.2003.12.005 | s2cid = 25781307 }}</ref> Fluvoxamine seriously affects the ] of ] and increases the intensity and duration of its effects. Because of the potentially hazardous consequences, the concomitant use of ] with fluvoxamine, or other potent inhibitors of ], should be avoided.<ref>{{cite journal | vauthors = Granfors MT, Backman JT, Neuvonen M, Ahonen J, Neuvonen PJ | title = Fluvoxamine drastically increases concentrations and effects of tizanidine: a potentially hazardous interaction | journal = Clinical Pharmacology and Therapeutics | volume = 75 | issue = 4 | pages = 331–341 | date = April 2004 | pmid = 15060511 | doi = 10.1016/j.clpt.2003.12.005 | s2cid = 25781307 }}</ref>


When a beta-blocker is required, ],<ref name="pmid7988100">{{cite journal | vauthors = Perucca E, Gatti G, Spina E | title = Clinical pharmacokinetics of fluvoxamine | journal = Clinical Pharmacokinetics | volume = 27 | issue = 3 | pages = 175–190 | date = September 1994 | pmid = 7988100 | doi = 10.2165/00003088-199427030-00002 | s2cid = 22472247 }}</ref> ]<ref name="pmid11543734">{{cite journal | vauthors = Zanardi R, Serretti A, Rossini D, Franchini L, Cusin C, Lattuada E, Dotoli D, Smeraldi E | display-authors = 6 | title = Factors affecting fluvoxamine antidepressant activity: influence of pindolol and 5-HTTLPR in delusional and nondelusional depression | journal = Biological Psychiatry | volume = 50 | issue = 5 | pages = 323–330 | date = September 2001 | pmid = 11543734 | doi = 10.1016/s0006-3223(01)01118-0 | s2cid = 22692759 }}</ref><ref>{{cite journal | vauthors = Sluzewska A, Szczawinska K | title = The effects of pindolol addition to fluvoxamine and buspirone in chronic mild stress model of depression. | journal = Behavioural Pharmacology | date = May 1996 | volume = 7 | pages = 105 }}</ref><ref name="pmid9817627">{{cite journal | vauthors = Mundo E, Guglielmo E, Bellodi L | title = Effect of adjuvant pindolol on the antiobsessional response to fluvoxamine: a double-blind, placebo-controlled study | journal = International Clinical Psychopharmacology | volume = 13 | issue = 5 | pages = 219–224 | date = September 1998 | pmid = 9817627 | doi = 10.1097/00004850-199809000-00005 | s2cid = 23946424 }}</ref> and, possibly, ]<ref name="pmid9681670">{{cite journal | vauthors = Belpaire FM, Wijnant P, Temmerman A, Rasmussen BB, Brøsen K | title = The oxidative metabolism of metoprolol in human liver microsomes: inhibition by the selective serotonin reuptake inhibitors | journal = European Journal of Clinical Pharmacology | volume = 54 | issue = 3 | pages = 261–264 | date = May 1998 | pmid = 9681670 | doi = 10.1007/s002280050456 | s2cid = 28105445 }}</ref><ref name="pmid8904628">{{cite journal | vauthors = Xu ZH, Xie HG, Zhou HH | title = In vivo inhibition of CYP2C19 but not CYP2D6 by fluvoxamine | journal = British Journal of Clinical Pharmacology | volume = 42 | issue = 4 | pages = 518–521 | date = October 1996 | pmid = 8904628 | pmc = 2042705 | doi = 10.1046/j.1365-2125.1996.45319.x }}</ref><ref name=":0"/><ref>{{cite journal | vauthors = Belpaire FM, Wijnant P, Tammerman A, Bogaert M, Rasmussen B, Brosen K | title = Inhibition of the oxidative metabolism of metoprolol by selective serotonin reuptake inhibitors in human liver microsomes. | journal = Fundamental and Clinical Pharmacology | date = 1997 | volume = 2 | issue = 11 | pages = 147 }}</ref> may be safer choices than ], as the latter's metabolism is seriously, potentially dangerously, inhibited by fluvoxamine.<ref name="pmid8846617">{{cite journal | vauthors = van Harten J | title = Overview of the pharmacokinetics of fluvoxamine | journal = Clinical Pharmacokinetics | volume = 29 | issue = Suppl 1| pages = 1–9 | date = 1995 | pmid = 8846617 | doi = 10.2165/00003088-199500291-00003 | s2cid = 71812133 }}</ref> Indeed, fluvoxamine may increase propranolol blood-levels by five-fold.<ref name="pmid22311403">{{cite journal | vauthors = Muscatello MR, Spina E, Bandelow B, Baldwin DS | title = Clinically relevant drug interactions in anxiety disorders | journal = Human Psychopharmacology | volume = 27 | issue = 3 | pages = 239–253 | date = May 2012 | pmid = 22311403 | doi = 10.1002/hup.2217 | s2cid = 11592004 }}</ref> When a beta-blocker is required, ]<ref name="pmid7988100">{{cite journal | vauthors = Perucca E, Gatti G, Spina E | title = Clinical pharmacokinetics of fluvoxamine | journal = Clinical Pharmacokinetics | volume = 27 | issue = 3 | pages = 175–190 | date = September 1994 | pmid = 7988100 | doi = 10.2165/00003088-199427030-00002 | s2cid = 22472247 }}</ref> and ]<ref name="pmid11543734">{{cite journal | vauthors = Zanardi R, Serretti A, Rossini D, Franchini L, Cusin C, Lattuada E, Dotoli D, Smeraldi E | display-authors = 6 | title = Factors affecting fluvoxamine antidepressant activity: influence of pindolol and 5-HTTLPR in delusional and nondelusional depression | journal = Biological Psychiatry | volume = 50 | issue = 5 | pages = 323–330 | date = September 2001 | pmid = 11543734 | doi = 10.1016/s0006-3223(01)01118-0 | s2cid = 22692759 }}</ref><ref>{{cite journal | vauthors = Sluzewska A, Szczawinska K | title = The effects of pindolol addition to fluvoxamine and buspirone in chronic mild stress model of depression. | journal = Behavioural Pharmacology | date = May 1996 | volume = 7 | pages = 105 }}</ref><ref name="pmid9817627">{{cite journal | vauthors = Mundo E, Guglielmo E, Bellodi L | title = Effect of adjuvant pindolol on the antiobsessional response to fluvoxamine: a double-blind, placebo-controlled study | journal = International Clinical Psychopharmacology | volume = 13 | issue = 5 | pages = 219–224 | date = September 1998 | pmid = 9817627 | doi = 10.1097/00004850-199809000-00005 | s2cid = 23946424 }}</ref> may be safer choices than ], as the latter's metabolism is seriously, potentially dangerously, inhibited by fluvoxamine.<ref name="pmid8846617">{{cite journal | vauthors = van Harten J | title = Overview of the pharmacokinetics of fluvoxamine | journal = Clinical Pharmacokinetics | volume = 29 | issue = Suppl 1| pages = 1–9 | date = 1995 | pmid = 8846617 | doi = 10.2165/00003088-199500291-00003 | s2cid = 71812133 }}</ref> Indeed, fluvoxamine may increase propranolol blood-levels by five-fold.<ref name="pmid22311403">{{cite journal | vauthors = Muscatello MR, Spina E, Bandelow B, Baldwin DS | title = Clinically relevant drug interactions in anxiety disorders | journal = Human Psychopharmacology | volume = 27 | issue = 3 | pages = 239–253 | date = May 2012 | pmid = 22311403 | doi = 10.1002/hup.2217 | s2cid = 11592004 }}</ref>


Anecdotally, more has been spoken about or (rightfully) assumed regarding the mutual compatibility of fluvoxamine and ] but the case may be similar with the other-two beta-blockers mentioned herein, also. This may be especially promising in the case of ], when patients with ] especially, a principal indication for fluvoxamine, need a beta-blocker for hypertensive/cardiac reasons or may benefit from it for additional augmentation. Anecdotally, more has been spoken about or (rightfully) assumed regarding the mutual compatibility of fluvoxamine and ] but the case may be similar with the other-two beta-blockers mentioned herein, also. This may be especially promising in the case of ], when patients with ] especially, a principal indication for fluvoxamine, need a beta-blocker for hypertensive/cardiac reasons or may benefit from it for additional augmentation.

Revision as of 14:58, 5 December 2023

SSRI antidepressant drug Not to be confused with Fluoxetine.

Pharmaceutical compound
Fluvoxamine
Clinical data
Trade namesLuvox, Faverin, others
AHFS/Drugs.comMonograph
MedlinePlusa695004
License data
Pregnancy
category
  • AU: C
Routes of
administration		By mouth
Drug classSelective serotonin reuptake inhibitor (SSRI)
ATC code
Legal status
Legal status
Pharmacokinetic data
Bioavailability53% (90% confidence interval: 44–62%)
Protein binding77–80%
MetabolismLiver (primarily O-demethylation)
Major: CYP1A2
Minor: CYP3A4
Minor: CYP2C19
Elimination half-life12–13 hours (single dose), 22 hours (repeated dosing)
ExcretionKidney (98%; 94% as metabolites, 4% as unchanged drug)
Identifiers
IUPAC name
  • 2-{ pentylidene}amino]oxy}ethanamine
CAS Number
PubChem CID
IUPHAR/BPS
DrugBank
ChemSpider
UNII
KEGG
ChEBI
ChEMBL
CompTox Dashboard (EPA)
ECHA InfoCard100.125.476 Edit this at Wikidata
Chemical and physical data
FormulaC15H21F3N2O2
Molar mass318.340 g·mol
3D model (JSmol)
SMILES
  • FC(F)(F)c1ccc(\C(=N\OCCN)CCCCOC)cc1
InChI
  • InChI=1S/C15H21F3N2O2/c1-21-10-3-2-4-14(20-22-11-9-19)12-5-7-13(8-6-12)15(16,17)18/h5-8H,2-4,9-11,19H2,1H3/b20-14+
  • Key:CJOFXWAVKWHTFT-XSFVSMFZSA-N
  (what is this?)  (verify)

Fluvoxamine, commonly sold under the brand names Luvox and Faverin, is an antidepressant of the selective serotonin reuptake inhibitor (SSRI) class. It is primarily used to treat major depressive disorder and obsessive–compulsive disorder (OCD), but is also used to treat anxiety disorders such as panic disorder, social anxiety disorder, and post-traumatic stress disorder.

Fluvoxamine's side-effect profile is very similar to other SSRIs: constipation, gastrointestinal problems, headache, anxiety, irritation, sexual problems, dry mouth, sleep problems and a risk of suicide at the start of treatment by lifting the psychomotor inhibition, but these effects appear to be significantly weaker than with other SSRIs (except gastrointestinal side-effects). Although the many drug-drug interactions of fluvoxamine can be problematic (and may temper enthusiasm for its prescribing, advocation and usage to some), its tolerance-profile itself is actually superior in some respects to other SSRIs (particularly with respect to cardiovascular complications), despite its age. Compared to escitalopram and sertraline, indeed, fluvoxamine's gastrointestinal profile may be less intense, often being limited to nausea. Mosapride has demonstrated efficacy in treating fluvoxamine-induced nausea. It is also advised practice to divide total daily doses of fluvoxamine greater than 100 milligrams, with the higher fraction being taken at bedtime (e.g., 50 mg at the beginning of the waking day and 200 mg at bedtime). In any case, high starting daily doses of fluvoxamine rather than the recommended gradual titration (starting at 50 milligrams and gradually titrating, up to 300 if necessary) may predispose to nauseous discomfort.

It is on the World Health Organization's List of Essential Medicines.

Fluvoxamine is related to clovoxamine, a proposed SNRI which has been subject to a certain amount of investigative research but was never marketed.

Medical uses

In many countries (e.g., Australia, the UK, and Russia) it is commonly used for major depressive disorder. Fluvoxamine is also approved in the United States for obsessive–compulsive disorder (OCD), and social anxiety disorder. In Japan, it is also approved to treat OCD, social anxiety disorder and major depressive disorder. Fluvoxamine is indicated for children and adolescents with OCD. The NICE guidelines in the United Kingdom have, as of 2005, authorised its use for obsessive-compulsive disorder in adults and adolescents of any age and children over the age of 7.

There is some evidence that fluvoxamine is effective for generalised social anxiety in adults, though the results may be compromised by having been funded by pharmaceutical companies.

There is tentative evidence that fluvoxamine may reduce the overall morbidity of COVID-19 and complications thereof.

Fluvoxamine is also effective for treating a range of anxiety disorders in children and adolescents, including generalized anxiety disorder, social anxiety disorder, panic disorder and separation anxiety disorder.

The drug works long-term, and retains its therapeutic efficacy for at least one year. It has also been found to possess some analgesic properties in line with other SSRIs and tricyclic antidepressants.

The average therapeutic dose for fluvoxamine is 100 to 300 mg/day, with 300 mg being the upper daily limit normally recommended. Obsessive-compulsive disorder, however, often requires higher doses; doses of up to 450 mg/day may be prescribed in this case. In any case with fluvoxamine, treatment is generally begun at 25 or 50 mg and increased in 50 mg increments every 4 to 7 days until a therapeutic optimum is reached.

Adverse effects

Fluvoxamine's side-effect profile is very similar to other SSRIs, with gastrointestinal side effects more characteristic of those receiving treatment with fluvoxamine.

Common

Common side effects occurring with 1–10% incidence:

Uncommon

Uncommon side effects occurring with 0.1–1% incidence:

  • Arthralgia
  • Confusional state
  • Cutaneous hypersensitivity reactions (e.g. oedema , rash, pruritus)
  • Extrapyramidal side effects (e.g. dystonia, parkinsonism, tremor, etc.)
  • Hallucination
  • Orthostatic hypotension

Rare

Rare side effecs occurring with 0.01–0.1% incidence:

  • Abnormal hepatic (liver) function
  • Galactorrhoea (expulsion of breast milk unrelated to pregnancy or breastfeeding)
  • Mania
  • Photosensitivity (being abnormally sensitive to light)
  • Seizures

Unknown frequency

Interactions

Luvox (fluvoxamine) 100 mg film-coated scored tablets

Fluvoxamine inhibits the following cytochrome P450 enzymes:

By so doing, fluvoxamine can increase serum concentration of the substrates of these enzymes.

Fluvoxamine may also elevate plasma levels of olanzapine by approximately two times. Combined olanzapine and fluvoxamine, which may cause increased sedation, should be used cautiously and controlled clinically and by therapeutic drug monitoring to avoid olanzapine induced adverse effects and/or intoxication.

The plasma levels of oxidatively metabolized benzodiazepines (e.g., triazolam, midazolam, alprazolam and diazepam) are likely to be increased when co-administered with fluvoxamine. However, the clearance of benzodiazepines metabolized by glucuronidation (e.g., lorazepam; oxazepam, which is coincidentally a metabolite of diazepam; temazepam) are not affected by fluvoxamine and may be safely taken alongside fluvoxamine should concurrent treatment with a benzodiazepine be necessary. Additionally, it appears that benzodiazepines metabolized by nitro-reduction (clonazepam, nitrazepam) may also, in a somewhat similar vein, be unlikely to be affected by fluvoxamine. Concurrent use of diazepam (Valium) is generally inadvisable and should probably not be done.

Using fluvoxamine and alprazolam together can increase alprazolam plasma concentrations. If alprazolam is coadministered with fluvoxamine, the initial alprazolam dose should be reduced to the lowest effective dose.

Fluvoxamine and ramelteon coadministration is not indicated.

Fluvoxamine has been observed to increase serum concentrations of mirtazapine, which is mainly metabolized by CYP1A2, CYP2D6, and CYP3A4, by three- to four-fold in humans. Caution and adjustment of dosage as necessary are warranted when combining fluvoxamine and mirtazapine.

Fluvoxamine seriously affects the pharmacokinetics of tizanidine and increases the intensity and duration of its effects. Because of the potentially hazardous consequences, the concomitant use of tizanidine with fluvoxamine, or other potent inhibitors of CYP1A2, should be avoided.

When a beta-blocker is required, atenolol and pindolol may be safer choices than propranolol, as the latter's metabolism is seriously, potentially dangerously, inhibited by fluvoxamine. Indeed, fluvoxamine may increase propranolol blood-levels by five-fold.

Anecdotally, more has been spoken about or (rightfully) assumed regarding the mutual compatibility of fluvoxamine and atenolol but the case may be similar with the other-two beta-blockers mentioned herein, also. This may be especially promising in the case of pindolol, when patients with obsessive-compulsive disorder especially, a principal indication for fluvoxamine, need a beta-blocker for hypertensive/cardiac reasons or may benefit from it for additional augmentation.

Clomipramine increases fluvoxamine levels and, conversely-likewise, fluvoxamine increases clomipramine levels (thereby its serotoninergic potential) and inhibits its metabolism to its strongly-noradrenergic metabolite, norclomipramine. Although the two drugs can certainly be prescribed and taken concurrently quite safely, and often are in the case of certain characteristic obsessional complexes, the inter-pharmacology between these two drugs is rather complex and caution is needed in doing this (often necessitating a lower dose of one or the other) to keep blood-levels of the two agents within acceptable levels and avoid serotonin-toxicity. Even-greater caution is needed when combining clomipramine with drugs which inhibit CYP2D6 (e.g., fluoxetine, paroxetine), if it has to be done at all, as CYP2D6-inhibition may do the opposite of fluvoxamine and increase desmethylclomipramine levels to an uncomfortable extent.

Pharmacology

Receptor affinity profile
Site Ki (nM)
SERTTooltip Serotonin transporter 2.5
NETTooltip Norepinephrine transporter 1,427
5-HT2C 5,786
α1-adrenergic 1,288
σ1 36

Fluvoxamine is a potent selective serotonin reuptake inhibitor with around 100-fold affinity for the serotonin transporter over the norepinephrine transporter. It has negligible affinity for the dopamine transporter or any other site, with the sole exception of the σ1 receptor. It behaves as a potent agonist at this receptor and has the highest affinity (36 nM) of any SSRI for doing so. This may contribute to its antidepressant and anxiolytic effects and may also afford it some efficacy in treating the cognitive symptoms of depression. Unlike some other SSRIs, fluvoxamine's metabolites are pharmacologically neutral.

History

Fluvoxamine was developed by Kali-Duphar, part of Solvay Pharmaceuticals, Belgium, now Abbott Laboratories, and introduced as Floxyfral in Switzerland in 1983. It was approved by the U.S. Food and Drug Administration (FDA) in 1994, and introduced as Luvox in the US. In India, it is available, among several other brands, as Uvox by Abbott. It was one of the first SSRI antidepressants to be launched, and is prescribed in many countries to patients with major depression. It was the first SSRI, a non-TCA drug, approved by the U.S. FDA specifically for the treatment of OCD. At the end of 1995, more than ten million patients worldwide had been treated with fluvoxamine. Fluvoxamine was the first SSRI to be registered for the treatment of obsessive compulsive disorder in children by the FDA in 1997. In Japan, fluvoxamine was the first SSRI to be approved for the treatment of depression in 1999 and was later in 2005 the first drug to be approved for the treatment of social anxiety disorder. Fluvoxamine was the first SSRI approved for clinical use in the United Kingdom. Manufacturers include BayPharma, Synthon, and Teva, among others.

Research directions

While early studies have suggested potential benefits for fluvoxamine as an anti-inflammatory agent and a possible impact on reducing cytokine storms, further studies did not confirm this expected benefit on COVID-19 patients. A cytokine storm refers to an excessive immune response characterized by a release of large amounts of pro-inflammatory cytokines.

In May 2022, based on a review of available scientific evidence, the U.S. Food and Drug Administration (FDA) chose not to issue an emergency use authorization covering the use of fluvoxamine to treat COVID-19, saying that, at the time, the data was not sufficient to conclude that fluvoxamine may be effective in treating non-hospitalized people with COVID-19 to prevent serious illness or hospitalization. The agency stated that study results suggest that further clinical trials may be warranted.

A large double-blind randomized controlled trial called ACTIV-6, published in 2023 in JAMA, revealed that taking 200 mg of fluvoxamine every day for about two weeks was not significantly better than placebo at shortening the duration of mild or moderate COVID-19 symptoms.

Environment

Fluvoxamine is a common finding in waters near human settlement. Christensen et al. 2007 finds it is "very toxic to aquatic organisms" by European Union standards.

References

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