Drug/Small Molecule:
fluoxetine

PharmGKB contains no dosing guidelines for this drug/small molecule. To report known genotype-based dosing guidelines, or if you are interested in developing guidelines, click here.

PharmGKB gathers information regarding PGx on FDA drug labels from the FDA's "Table of Pharmacogenomic Biomarkers in Drug Labels", and from FDA-approved FDA and EMA-approved (European Medicines Agency) EMA labels brought to our attention. Excerpts from the label and downloadable highlighted label PDFs are manually curated by PharmGKB.

Please note that some drugs may have been removed from or added to the FDA's "Table of Pharmacogenomic Biomarkers in Drug Labels" without our knowledge. We periodically check the table for additions to this table and update PharmGKB accordingly.

There is currently no such list for European drug labels - we are working with the EMA to establish a list of European Public Assessment Reports (EPAR)s that contain PGx information. We are constructing this list by initially searching for drugs for which we have PGx-containing FDA drug labels - of these 44 EMA EPARs were identified and are being curated for pgx information.

We welcome any information regarding drug labels containing PGx information approved by the FDA, EMA or other Medicine Agencies around the world - please contact feedback.



last updated 10/25/2013

FDA Label for fluoxetine and CYP2D6

This label is on the FDA Biomarker List
Informative PGx

Summary

Fluoxetine is a selective serotonin reuptake inhibitor (SSRI). Fluoxetine is indicated for the treatment of major depressive disorder, obsessive compulsive disorder, bulimia nervosa, and panic disorder. Fluoxetine is metabolized by several cytochrome P450 enzymes with CYP2D6 being a major contributor. At the same time, fluoxetine is an inhibitor of CYP2D6 mediated reactions.

Annotation

Fluoxetine is a selective serotonin reuptake inhibitor (SSRI). Fluoxetine is indicated for the treatment of major depressive disorder, obsessive compulsive disorder, bulimia nervosa, and panic disorder. Fluoxetine is metabolized by several cytochrome P450 enzymes with CYP2D6 being a major contributor. At the same time, fluoxetine is an inhibitor of CYP2D6 mediated reactions.

Excerpts from the Fluoxetine drug label:

Drugs Metabolized by CYP2D6: Fluoxetine is a potent inhibitor of CYP2D6 enzyme pathway.

Fluoxetine inhibits the activity of CYP2D6, and may make individuals with normal CYP2D6 metabolic activity resemble a poor metabolizer. Coadministration of fluoxetine with other drugs that are metabolized by CYP2D6, including certain antidepressants (e.g., TCAs), antipsychotics (e.g., phenothiazines and most atypicals), and antiarrhythmics (e.g., propafenone, flecainide, and others) should be approached with caution. Therapy with medications that are predominantly metabolized by the CYP2D6 system and that have a relatively narrow therapeutic index (see list below) should be initiated at the low end of the dose range if a patient is receiving fluoxetine concurrently or has taken it in the previous 5 weeks. Thus, his/her dosing requirements resemble those of poor metabolizers. If fluoxetine is added to the treatment regimen of a patient already receiving a drug metabolized by CYP2D6, the need for decreased dose of the original medication should be considered. Drugs with a narrow therapeutic index represent the greatest concern (e.g., flecainide, propafenone, vinblastine, and TCAs). Due to the risk of serious ventricular arrhythmias and sudden death potentially associated with elevated plasma levels of thioridazine, thioridazine should not be administered with fluoxetine or within a minimum of 5 weeks after fluoxetine has been discontinued.

Because fluoxetine's metabolism, like that of a number of other compounds including TCAs and other selective serotonin reuptake inhibitors (SSRIs), involves the CYP2D6 system, concomitant therapy with drugs also metabolized by this enzyme system (such as the TCAs) may lead to drug interactions.

For the complete drug label text with sections containing pharmacogenetic information highlighted, see the Fluoxetine drug label.

*Disclaimer: The contents of this page have not been endorsed by the FDA and are the sole responsibility of PharmGKB.

Genes and/or phenotypes found in this label


last updated 12/17/2013

FDA Label for fluoxetine, olanzapine and CYP2D6

Informative PGx

Summary

Symbyax, a drug mixture of fluoxetine and olanzapine, is used for the treatment of bipolar disorder and treatment resistant depression and, due to its potent CYP2D6 inhibition as a result of fluoxetine, exhibits drug interactions with other medications also metabolized by CYP2D6. Coadministration with other drugs that are metabolized by CYP2D6 should be approached with caution.

Annotation

Symbyax is a drug mixture of fluoxetine and olanzapine used for the treatment of bipolar disorder and treatment resistant depression. Fluoxetine is a selective serotonin reuptake inhibitor and is metabolized by several cytochrome P450 enzymes with CYP2D6 being a major contributor (see Fluoxetine Pathway and CYP2D6 VIP for more details). Olanzapine is an atypical antipsychotic metabolized by CYP1A2. Clearance of olanzapine is influenced by smoking (see CYP1A2 VIP for additional information).

Excerpt from the Fluoxetine and Olanzapine (Symbyax) drug label:

A subset (about 7%) of the population has reduced activity of the drug metabolizing enzyme CYP2D6. Such individuals are referred to as "poor metabolizers" of drugs such as debrisoquin, dextromethorphan, and the tricyclic antidepressants (TCAs). In a study involving labeled and unlabeled enantiomers administered as a racemate, these individuals metabolized S-fluoxetine at a slower rate and thus achieved higher concentrations of S-fluoxetine. Consequently, concentrations of S-norfluoxetine at steady state were lower.

Because the metabolism of fluoxetine, like that of a number of other compounds including TCAs and other selective serotonin antidepressants, involves the CYP2D6 system, concomitant therapy with drugs also metabolized by this enzyme system (such as the TCAs) may lead to drug interactions.

Fluoxetine inhibits the activity of CYP2D6 and may make individuals with normal CYP2D6 metabolic activity resemble a poor metabolizer. Coadministration of fluoxetine with other drugs that are metabolized by CYP2D6... should be approached with caution.

For the complete drug label text with sections containing pharmacogenetic information highlighted, see the Fluoxetine and Olanzapine drug label.

*Disclaimer: The contents of this page have not been endorsed by the FDA and are the sole responsibility of PharmGKB.

Full label available at DailyMed

Genes and/or phenotypes found in this label

  • Bipolar Disorder
    • Indications & usage section, Dosage & administration section, Adverse reactions section, Clinical studies section, Use in specific populations section, Warnings and precautions section
    • source: FDA Label
  • Depression
    • Indications & usage section, Dosage & administration section, Adverse reactions section, Clinical studies section, Use in specific populations section, Warnings and precautions section
    • source: FDA Label
  • CYP1A2
    • Drug interactions section, Clinical pharmacology section, dosage, metabolism/PK
    • source: FDA Label
  • CYP2D6
    • Contraindications section, Drug interactions section, Clinical pharmacology section, Warnings and precautions section, dosage, metabolism/PK
    • source: FDA Label
  • CYP3A
    • Drug interactions section, metabolism/PK
    • source: FDA Label

PharmGKB contains no Clinical Variants that meet the highest level of criteria.

To see more Clinical Variants with lower levels of criteria, click the button at the bottom of the page.

Disclaimer: The PharmGKB's clinical annotations reflect expert consensus based on clinical evidence and peer-reviewed literature available at the time they are written and are intended only to assist clinicians in decision-making and to identify questions for further research. New evidence may have emerged since the time an annotation was submitted to the PharmGKB. The annotations are limited in scope and are not applicable to interventions or diseases that are not specifically identified.

The annotations do not account for individual variations among patients, and cannot be considered inclusive of all proper methods of care or exclusive of other treatments. It remains the responsibility of the health-care provider to determine the best course of treatment for a patient. Adherence to any guideline is voluntary, with the ultimate determination regarding its application to be made solely by the clinician and the patient. PharmGKB assumes no responsibility for any injury or damage to persons or property arising out of or related to any use of the PharmGKB clinical annotations, or for any errors or omissions.

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This is a non-comprehensive list of genetic tests with pharmacogenetics relevance, typically submitted by the manufacturer and manually curated by PharmGKB. The information listed is provided for educational purposes only and does not constitute an endorsement of any listed test or manufacturer.

A more complete listing of genetic tests is found at the Genetic Testing Registry (GTR).

PGx Test Variants Assayed Gene?
Roche AmpliChip CYP450 Test CYP2D6*1, CYP2D6*10A, CYP2D6*10B, CYP2D6*11, CYP2D6*15, CYP2D6*17, CYP2D6*19, CYP2D6*20, CYP2D6*29, CYP2D6*2A, CYP2D6*2B, CYP2D6*2D, CYP2D6*3, CYP2D6*40, CYP2D6*41, CYP2D6*4A, CYP2D6*4B, CYP2D6*4D, CYP2D6*4J, CYP2D6*4K, CYP2D6*5, CYP2D6*6A, CYP2D6*6B, CYP2D6*6C, CYP2D6*7, CYP2D6*8, CYP2D6*9 , CYP2D6*1XN , CYP2D6*2XN , CYP2D6*4XN , CYP2D6*10XN , CYP2D6*17XN , CYP2D6*35XN , CYP2D6*41XN , *35 , *36
DMET Plus (Affymetrix, Inc) Variant in CYP2D6
VeraCode ADME Core Panel (Illumina, Inc) Variant in CYP2D6
TaqMan Drug Metabolism Genotyping Assay Sets (Applied Biosystems, Inc) Variant in CYP2D6
Laboratory Corporation of America Variant in CYP2D6
Quest Diagnostics, Inc Variant in CYP2D6
iPLEX ADME PGx (Sequenom, Inc) CYP2D6*11, CYP2D6*12, CYP2D6*14A, CYP2D6*14B, CYP2D6*15, CYP2D6*17, CYP2D6*18, CYP2D6*19, CYP2D6*1A, CYP2D6*20, CYP2D6*21A, CYP2D6*21B, CYP2D6*3, CYP2D6*30, CYP2D6*38, CYP2D6*4, CYP2D6*40, CYP2D6*41, CYP2D6*42, CYP2D6*44, CYP2D6*4M, CYP2D6*56A, CYP2D6*56B, CYP2D6*58, CYP2D6*6, CYP2D6*64, CYP2D6*69, CYP2D6*7, CYP2D6*8, CYP2D6*9 , Indistinguishable haplotypes with the current ADME core SNP: (CYP2D6*2A,CYP2D6*31,CYP2D6*51), (CYP2D6*2L,CYP2D6*35,CYP2D6*71), (CYP2D6*10,CYP2D6*36,CYP2D6*37,CYP2D6*47,CYP2D6*49,CYP2D6*52,CYP2D6*54,CYP2D6*57,CYP2D6*65,CYP2D6*72), CNV Assay: CYP2D6*5, CYP2D6*NxN (Haplotypes are identified manually)
Luminex xTAG CYP2D6 Assay CYP2D6*1, CYP2D6*10, CYP2D6*11, CYP2D6*15, CYP2D6*17, CYP2D6*2, CYP2D6*29, CYP2D6*3, CYP2D6*4, CYP2D6*41, CYP2D6*5, CYP2D6*6, CYP2D6*7, CYP2D6*8, CYP2D6*9 , CYP2D6*XN , *35
Cytochrome P450 2D6 (CYP2D6) CYP2D6*2, CYP2D6*5, CYP2D6*8 , rs28371725 , rs5030867 , rs5030656 , rs35742686 , rs3892097 , rs5030865 , rs5030655 , rs61736512 , rs28371706 , rs5030862 , rs1065852
INFINITI CYP450 2D6I (AutoGenomics, Inc) CYP2D6*10, CYP2D6*12, CYP2D6*17, CYP2D6*2, CYP2D6*29, CYP2D6*3, CYP2D6*4, CYP2D6*41, CYP2D6*5, CYP2D6*6, CYP2D6*7, CYP2D6*8, CYP2D6*9 , rs28371725 , rs5030867 , rs5030656 , rs35742686 , rs3892097 , rs5030865 , rs5030655 , rs61736512 , rs28371706 , rs5030862 , rs1065852 , CYP2D6*XN , *14

The table below contains information about pharmacogenomic variants on PharmGKB. Please follow the link in the "Variant" column for more information about a particular variant. Each link in the "Variant" column leads to the corresponding PharmGKB Variant Page. The Variant Page contains summary data, including PharmGKB manually curated information about variant-drug pairs based on individual PubMed publications. The PMIDs for these PubMed publications can be found on the Variant Page.

The tags in the first column of the table indicate what type of information can be found on the corresponding Variant Page.

Links in the "Gene" column lead to PharmGKB Gene Pages.

Gene ? Variant?
(138)
Alternate Names / Tag SNPs ? Drugs ? Alleles ?
(+ chr strand)
Function ? Amino Acid?
Translation
No VIP available No VIP available VA CYP2C19 *1 N/A N/A N/A
No VIP available No VIP available VA CYP2C19 *2 N/A N/A N/A
No VIP available No VIP available VA CYP2C19 *3 N/A N/A N/A
No VIP available No VIP available VA CYP2C19 *17 N/A N/A N/A
No VIP available No VIP available VA CYP2C9 *1 N/A N/A N/A
No VIP available No VIP available VA CYP2C9 *2 N/A N/A N/A
No VIP available No VIP available VA CYP2C9 *3 N/A N/A N/A
VIP CA VA CYP2D6 *1 N/A N/A N/A
No VIP available CA VA CYP2D6 *1XN N/A N/A N/A
VIP No VIP available VA CYP2D6 *2 N/A N/A N/A
No VIP available CA VA CYP2D6 *2XN N/A N/A N/A
VIP CA VA CYP2D6 *3 N/A N/A N/A
VIP CA VA CYP2D6 *4 N/A N/A N/A
No VIP available CA VA CYP2D6 *5 N/A N/A N/A
VIP CA VA CYP2D6 *6 N/A N/A N/A
VIP No VIP available No VIP available CYP2D6 *9 N/A N/A N/A
VIP No VIP available VA CYP2D6 *10 N/A N/A N/A
VIP No VIP available VA CYP2D6 *17 N/A N/A N/A
VIP No VIP available No VIP available CYP2D6 *29 N/A N/A N/A
VIP No VIP available VA CYP2D6 *41 N/A N/A N/A
No VIP available No VIP available VA SLC6A4 HTTLPR long form (L allele) N/A N/A N/A
No VIP available No VIP available VA SLC6A4 HTTLPR short form (S allele) N/A N/A N/A
No VIP available No Clinical Annotations available VA
CYP2D6 poor metabolizer N/A N/A N/A
No VIP available No Clinical Annotations available VA
rs10008257 19904049G>A, 95356328G>A
G > A
Not Available
No VIP available No Clinical Annotations available VA
rs1045642 208920T>A, 208920T>C, 25171488A>G, 25171488A>T, 3435T>A, 3435T>C, 87138645A>G, 87138645A>T, ABCB1*6, ABCB1: 3435C>T, ABCB1: C3435T, ABCB1: c.3435C>T, ABCB1:3435C>T, Ile1145=, Ile1145Ile, MDR1 3435C>T, MDR1 C3435T, PGP C3435T, c.3435C>T, mRNA 3853C>T
A > T
A > G
Synonymous
Ile1145Ile
rs1065852 100C>T, 21917263G>A, 42526694G>A, 5190C>T, CYP2D6:100C>T, Pro34Ser, part of CYP2D6*4 and CYP2D6*10
G > A
Missense
Pro34Ser
No VIP available No Clinical Annotations available VA
rs1109866 117G>A, 220083279C>T, 5434G>A, 70292697C>T, Leu39=
C > T
Synonymous
Leu39Leu
No VIP available No Clinical Annotations available VA
rs1109867 -58C>A, 220083453G>T, 5260C>A, 70292871G>T
G > T
5' UTR
No VIP available No Clinical Annotations available VA
rs1360780 106-2636A>G, 35547571T>C, 35607571T>C, 93790A>G
T > C
Intronic
No VIP available No Clinical Annotations available VA
rs1374385 -1099G>C, 239149645C>G, 5095904C>G
C > G
5' Flanking
No VIP available No Clinical Annotations available VA
rs1386494 24918T>C, 34495849T>C, 608+9108T>C, 72352543T>C
T > C
Intronic
No VIP available CA VA
rs153549 112236297A>G, 20550169A>G, 351+1780T>C
A > G
Intronic
No VIP available CA VA
rs153560 112254377G>A, 20568249G>A, 212+2483C>T
G > A
Intronic
VIP No Clinical Annotations available No Variant Annotations available
rs16947 21914512A>G, 42523943A>G, 733C>C, 7941C>C, 886C>C, Arg245=, Arg296=, CYP2D6:2850C>T
A > G
Not Available
No VIP available CA VA
rs1799889 -817_-816insA, -817_-816insG, 100769710_100769711insA, 100769710_100769711insG, 38802553_38802554insA, 38802553_38802554insG, 4332_4333insA, 4332_4333insG
A > G
5' Flanking
No VIP available CA VA
rs1800532 17987816G>T, 18047816G>T, 19520C>A, 803+221C>A
G > T
Intronic
No VIP available No Clinical Annotations available VA
rs1805054 19992513C>T, 267C>T, 6672601C>T, Tyr89=
C > T
Not Available
No VIP available No Clinical Annotations available VA
rs182694 43698815A>G, 522+1760A>G, 579+1760A>G, 588+1760A>G, 594+1760A>G, 621+1760A>G, 693256A>G
A > G
Intronic
No VIP available No Clinical Annotations available VA
rs2032582 186947T>A, 186947T>G, 25193461A>C, 25193461A>T, 2677A, 2677G, 2677T, 2677T>A, 2677T>G, 3095G>T/A, 87160618A>C, 87160618A>T, 893 Ala, 893 Ser, 893 Thr, ABCB1*7, ABCB1: 2677G>T/A, ABCB1: 2677T/A>G, ABCB1: A893S, ABCB1: G2677T/A, ABCB1: c.2677G>T/A, ABCB1:2677G>A/T, ABCB1:2677G>T/A, ABCB1:A893T, Ala893Ser/Thr, MDR1, MDR1 G2677T/A, Ser893Ala, Ser893Thr, mRNA 3095G>T/A, p.Ala893Ser/Thr
A > C
A > T
Missense
Ser893Ala
Ser893Thr
No VIP available CA VA
rs2227631 -989A>G, 100769538A>G, 38802381A>G, 4160A>G
A > G
5' Flanking
No VIP available CA VA
rs242941 -404-1310A>C, -404-1310A>G, -404-1310A>T, 122-1310A>C, 122-1310A>G, 122-1310A>T, 122-6202A>C, 122-6202A>G, 122-6202A>T, 35892C>C, 35892C>G, 35892C>T, 43892520A>C, 43892520A>G, 43892520A>T, 9166672A>C, 9166672A>G, 9166672A>T, 975003G>A, 975003G>C, 975003G>G, CRHR1:rs242941
G > T
Intronic
No VIP available No Clinical Annotations available VA
rs2433320 19918526G>A, 95370805G>A
G > A
Not Available
No VIP available No Clinical Annotations available VA
rs2452600 -266+2338C>T, 20044603C>T, 291+2338C>T, 292-212C>T, 407C>T, 41C>T, 95496882C>T, Ser136Phe, Ser14Phe
C > T
Intronic
Ser14Phe
No VIP available CA VA
rs25531 -1936A>G, 28564346T>C, 3301340T>C, 3609A>G
T > C
5' Flanking
rs28371706 21916341G>A, 320C>T, 42525772G>A, 6112C>T, CYP2D6:1023 C>T, Thr107Ile
G > A
Missense
Thr107Ile
rs28371725 21914374C>T, 42523805C>T, 8079G>A, 832+39G>A, 985+39G>A, CYP2D6*41, CYP2D6:2988G>A, part of CYP2D6*41
C > T
Intronic
No VIP available CA VA
rs28401781 199237G>A, 25181171C>T, 2927+314G>A, 87148328C>T
C > T
Intronic
No VIP available CA VA
rs334558 -1001T>C, -1195A>G, 119813282A>G, 26308428A>G, 4983T>C, GSK3B: -50 T>C
A > G
5' Flanking
rs35742686 -1793delT, -1830delT, -1940delT, 23418678delT, 40+2664delT, 42128242delT, 50569delT, 50583delT, 598delA, 622delA, 6750delA, 775delA, Arg200Glyfs, Arg208Glyfs, Arg259Glyfs
T > -
Not Available
Arg208Gly
No VIP available No Clinical Annotations available VA
rs3731885 *700C>T, -1074C>T, 220084469G>A, 4244C>T, 70293887G>A
G > A
5' Flanking
No VIP available No Clinical Annotations available VA
rs3747802 -440T>C, 25375429A>G, 458+2615A>G, 4979T>C, 509+2615A>G, 87342586A>G
A > G
5' UTR
No VIP available No Clinical Annotations available VA
rs3755047 *305C>T, -1469C>T, 220084864G>A, 3849C>T, 70294282G>A
G > A
5' Flanking
No VIP available No Clinical Annotations available VA
rs3800373 *1136G>T, 158885G>T, 35482476C>A, 35542476C>A
C > A
3' UTR
rs3892097 21915516C>T, 353-1G>A, 42524947C>T, 506-1G>A, 6937G>A, CYP2D6*4, CYP2D6:1846G>A, part of CYP2D6*4
C > T
Acceptor
No VIP available CA VA
rs4148739 186516A>G, 2482-236A>G, 25193892T>C, 87161049T>C
T > C
Intronic
No VIP available No Clinical Annotations available VA
rs4680 1-5G>A, 19951271G>A, 27009G>A, 3103421G>A, 322G>A, 472G>A, COMP: Val158Met, COMT:Val108Met, Val108Met, Val158Met
G > A
5' Flanking
Val158Met
No VIP available CA VA
rs4713916 -20+18122T>C, 31378T>C, 35609983A>G, 35669983A>G
A > G
Intronic
No VIP available CA VA
rs495794 112201094A>G, 20514966A>G, 225+665A>G, 229+665A>G, 301+665A>G
A > G
Intronic
rs5030655 -1098delA, -1563delA, -951delA, -988delA, 23419520delA, 277delT, 353-140delT, 40+3506delA, 42129084delA, 454delT, 51411delA, 51425delA, 5908delT, CYP2D6*6, CYP2D6:1707 del T, Trp152Glyfs, Trp93Glyfs, part of CYP2D6*6
A > -
Not Available
Trp152Gly
rs5030656 21914745_21914747delCTT, 42524176_42524178delCTT, 688_690delAAG, 7706_7708delAAG, 841_843delAAG, Lys230del, Lys281del
CTT > -
CTT > TTC
Non-synonymous
No VIP available No Clinical Annotations available VA
rs56294817 -424G>T, 239148970C>A, 5095229C>A
C > A
5' Flanking
No VIP available CA VA
rs57098334 GGGTGGGCT, SLC6A4:
C > 12
C > 10
C > (CCCACCCGA)9
Not Available
VIP No Clinical Annotations available No Variant Annotations available
rs59421388 1012G>A, 21914179C>T, 3271G>A, 42523610C>T, 8274G>A, 859G>A, CYP2D6: 3183G>A, Val287Met, Val338Met
G > T
G > C
Missense
Val287Met
rs61736512 1747G>A, 21915703C>T, 353-188G>A, 406G>A, 42525134C>T, 6750G>A, CYP2D6: 1659G>A, Val136Met
G > T
G > C
Intronic
Val136Met
No VIP available CA VA
rs61888800 -1325C>A, -22+18780C>A, -22+19615C>A, -22+19698C>A, -22+19913C>A, -22+250C>A, -22+566C>A, -422+240C>A, -571C>A, -589C>A, -59+240C>A, -696C>A, -77C>A, 26328C>A, 27662278G>T, 27722278G>T, 3+20681C>A, 66+240C>A
G > T
Intronic
No VIP available CA VA
rs6265 196G>A, 220G>A, 241G>A, 27619916C>T, 27679916C>T, 283G>A, 434C>T, 442G>A, 503C>T, 68690G>A, BDNF:Val66Met, Val148Met, Val66Met, Val74Met, Val81Met, Val95Met
C > T
Missense
Val66Met
No VIP available No Clinical Annotations available VA
rs6295 1-1019C>G, 1-1019G>C, 13852924C>C, 13852924C>G, 4555G>C, 4555G>G, 63258565C>C, 63258565C>G, HTR1A: -1019C/G
C > G
5' Flanking
No VIP available No Clinical Annotations available VA
rs6311 -1438, -510G>A, -998G>A, 28451478C>T, 4692G>A, 47471478C>T, G>A, HTR2A c.-1438G>A, HTR2A:, HTR2A: -1438G/A, HTR2A:-1438G>A
C > T
5' Flanking
No VIP available No Clinical Annotations available VA
rs6313 102C>T, 160+869C>T, 28449940G>A, 47469940G>A, 6230C>T, HTR2A:102C>T, HTR2A:T102C, Ser34=
G > A
Intronic
Ser34Ser
No VIP available No Clinical Annotations available VA
rs6946119 25161708T>C, 87128865T>C
T > C
Not Available
No VIP available No Clinical Annotations available VA
rs7997012 28391985A>G, 362-2211T>C, 47411985A>G, 5-HTR2A intron 2 variant, 614-2211T>C, 64185T>C
A > G
Intronic
Alleles, Functions, and Amino Acid Translations are all sourced from dbSNP 138
2D structure from PubChem
provided by PubChem

Overview

Generic Names
  • Fluoxetina [INN-Spanish]
  • Fluoxetina [Spanish]
  • Fluoxetine Hcl
  • Fluoxetine Hydrochloride
  • Fluoxetinum [INN-Latin]
Trade Names
  • Adofen
  • Animex-On
  • Deprex
  • Eufor
  • Fluctin
  • Fluoxeren
  • Fluval
  • Fontex
  • Foxetin
  • Portal
  • Prozac
  • Prozac Weekly
  • Pulvules
  • Reneuron
  • Sarafem
Brand Mixture Names

PharmGKB Accession Id:
PA449673

Description

Fluoxetine hydrochloride is the first agent of the class of antidepressants known as selective serotonin-reuptake inhibitors (SSRIs). Despite distinct structural differences between compounds in this class, SSRIs possess similar pharmacological activity. As with other antidepressant agents, several weeks of therapy may be required before a clinical effect is seen. SSRIs are potent inhibitors of neuronal serotonin reuptake. They have little to no effect on norepinephrine or dopamine reuptake and do not antagonize alpha- or beta-adrenergic, dopamine D 2 or histamine H 1 receptors. During acute use, SSRIs block serotonin reuptake and increase serotonin stimulation of somatodendritic 5-HT 1A and terminal autoreceptors. Chronic use leads to desensitization of somatodendritic 5-HT 1A and terminal autoreceptors. The overall clinical effect of increased mood and decreased anxiety is thought to be due to adaptive changes in neuronal function that leads to enhanced serotonergic neurotransmission. Side effects include dry mouth, nausea, dizziness, drowsiness, sexual dysfunction and headache. Side effects generally occur within the first two weeks of therapy and are usually less severe and frequent than those observed with tricyclic antidepressants. Flouxetine may be used to treat major depressive disorder (MDD), moderate to severe bulimia nervosa, obsessive-compulsive disorder (OCD), premenstrual dysphoric disorder (PMDD), panic disorder with or without agoraphobia, and in combination with olanzapine for treatment-resistant or bipolar I depression. Fluoxetine is the most anorexic and stimulating SSRI.

Source: Drug Bank

Indication

Labeled indication include: major depressive disorder (MDD), moderate to severe bulimia nervosa, obsessive-compulsive disorder (OCD), premenstrual dysphoric disorder (PMDD), panic disorder with or without agoraphobia, and combination treatment with olanzapine for treatment-resistant or bipolar I depression. Unlabeled indications include: selective mutism, mild dementia-associated agitation in nonpsychotic patients, post-traumatic stress disorder (PTSD), social anxiety disorder, chronic neuropathic pain, fibromyalgia, and Raynaud's phenomenon.

Source: Drug Bank

Other Vocabularies

Information pulled from DrugBank has not been reviewed by PharmGKB.

Pharmacology, Interactions, and Contraindications

Mechanism of Action

Metabolized to norfluoxetine, fluoxetine is a selective serotonin-reuptake inhibitor (SSRI), it blocks the reuptake of serotonin at the serotonin reuptake pump of the neuronal membrane, enhancing the actions of serotonin on 5HT 1A autoreceptors. SSRIs bind with significantly less affinity to histamine, acetylcholine, and norepinephrine receptors than tricyclic antidepressant drugs.

Source: Drug Bank

Pharmacology

Fluoxetine, an antidepressant agent belonging to the selective serotonin reuptake inhibitors (SSRIs), is used to treat depression, bulimia nervosa, premenstrual dysphoric disorder, panic disorder and post-traumatic stress. According to the amines hypothesis, a functional decrease in the activity of amines, such as serotonin and norepinephrine, would result in depression; a functional increase of the activity of these amines would result in mood elevation. Fluoxetine's effects are thought to be associated with the inhibition of 5HT receptor, which leads to an increase of serotonin level.

Source: Drug Bank

Food Interaction

Avoid alcohol.|Take with food to reduce irritation and nausea.

Source: Drug Bank

Absorption, Distribution, Metabolism, Elimination & Toxicity

Biotransformation

Limited data from animal studies suggest that fluoxetine may undergo first-pass metabolism may occur via the liver and/or lungs. Fluoxetine appears to be extensively metabolized, likely in the liver, to norfluoxetine and other metabolites. Norfluoxetine, the principal active metabolite, is formed via N-demethylation of fluoxetine. Norfluoxetine appears to be comparable pharmacologic potency as fluoxetine. Fluoxetine and norfluoxetine both undergo phase II glucuronidation reactions in the liver. It is also thought that fluoxetine and norfluoxetine undergo O-dealkylation to form p-trifluoromethylphenol, which is then subsequently metabolized to hippuric acid.

Source: Drug Bank

Protein Binding

94.5%

Source: Drug Bank

Absorption

Well absorbed from the GI tract following oral administration. Oral bioavailability is estimated to be at least 60-80%. Peak plasma concentrations occur within 4-8 hours following oral administration of conventional dosage preparations.

Source: Drug Bank

Half-Life

1-3 days

Source: Drug Bank

Toxicity

Symptoms of overdose include agitation, restlessness, hypomania, and other signs of CNS excitation. LD 50=284mg/kg (orally in mice). The most frequent side effects include: nervous system effects such as anxiety, nervousness, insomnia, drowsiness, fatigue or asthenia, tremor, and dizziness or lightheadedness; GI effects such as anorexia, nausea, and diarrhea; vasodilation; dry mouth; abnormal vision; decreased libido; abnormal ejaculation; rash; and sweating. Withdrawal symptoms include flu-like symptoms, insomnia, nausea, imbalance, sensory changes and hyperactivity.

Source: Drug Bank

Route of Elimination

The primary route of elimination appears to be hepatic metabolism to inactive metabolites excreted by the kidney.

Source: Drug Bank

Volume of Distribution

  • 20-45 L/kg

Source: Drug Bank

Chemical Properties

Chemical Formula

C17H18F3NO

Source: Drug Bank

Isomeric SMILES

CNCCC(c1ccccc1)Oc2ccc(cc2)C(F)(F)F

Source: OpenEye

Canonical SMILES

CNCCC(OC1=CC=C(C=C1)C(F)(F)F)C1=CC=CC=C1

Source: Drug Bank

Average Molecular Weight

309.3261

Source: Drug Bank

Monoisotopic Molecular Weight

309.134048818

Source: Drug Bank

PharmGKB Curated Pathways

Pathways created internally by PharmGKB based primarily on literature evidence.

  1. Fluoxetine Pathway, Pharmacokinetics
    Representation of the candidate genes involved in the metabolism of fluoxetine.
  1. Selective Serotonin Reuptake Inhibitor Pathway, Pharmacodynamics
    Genes involved in serotonin synthesis, release, reuptake, and in mediation of the antidepressant effect of selective serotonin reuptake inhibitors (SSRI) in human brain.

External Pathways

Links to non-PharmGKB pathways.

PharmGKB contains no links to external pathways for this drug. To report a pathway, click here.

Genes that are associated with this drug in PharmGKB's database based on (1) variant annotations, (2) literature review, (3) pathways or (4) information automatically retrieved from DrugBank, depending on the "evidence" and "source" listed below.

Curated Information ?

Drug Targets

Gene Description
HTR2A (source: Drug Bank)
SLC6A4 (source: Drug Bank)

Drug Interactions

Drug Description
fluoxetine Increased risk of CNS adverse effects (source: Drug Bank)
fluoxetine Increased risk of CNS adverse effects (source: Drug Bank)
fluoxetine Fluoxetine increases the effect and toxicity of tricyclics (source: Drug Bank)
fluoxetine The SSRI, fluoxetine, may increase the serum concentration of the tricyclic antidepressant, amitriptyline, by decreasing its metabolism. Additive modulation of serotonin activity also increases the risk of serotonin syndrome. Monitor for development of serotonin syndrome during concomitant therapy. Monitor for changes in the therapeutic and adverse effects of amitriptyline if fluoxetine is initiated, discontinued or dose changed. (source: Drug Bank)
fluoxetine Fluoxetine increases the effect and toxicity of tricyclics (source: Drug Bank)
fluoxetine The SSRI, fluoxetine, may increase the serum concentration of the tricyclic antidepressant, amoxapine, by decreasing its metabolism. Additive modulation of serotonin activity also increases the risk of serotonin syndrome. Monitor for development of serotonin syndrome during concomitant therapy. Monitor for changes in the therapeutic and adverse effects of amoxapine if fluoxetine is initiated, discontinued or dose changed. (source: Drug Bank)
fluoxetine Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank)
fluoxetine Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank)
fluoxetine The CYP2D6 inhibitor could increase the effect and toxicity of atomoxetine (source: Drug Bank)
fluoxetine The CYP2D6 inhibitor could increase the effect and toxicity of atomoxetine (source: Drug Bank)
fluoxetine Fluoxetine increases the effect of carbamazepine (source: Drug Bank)
fluoxetine Fluoxetine increases the effect of carbamazepine (source: Drug Bank)
fluoxetine The SSRI increases the effect of the beta-blocker (source: Drug Bank)
fluoxetine The SSRI, fluoxetine, may increase the bradycardic effect of the beta-blocker, carvedilol. (source: Drug Bank)
fluoxetine Fluoxetine increases the effect of cilostazol (source: Drug Bank)
fluoxetine Possible serotoninergic syndrome with this combination (source: Drug Bank)
fluoxetine Possible serotoninergic syndrome with this combination (source: Drug Bank)
fluoxetine Fluoxetine increases the effect and toxicity of tricyclics (source: Drug Bank)
fluoxetine The SSRI, fluoxetine, may increase the serum concentration of the tricyclic antidepressant, clomipramine, by decreasing its metabolism. Additive modulation of serotonin activity also increases the risk of serotonin syndrome. Monitor for development of serotonin syndrome during concomitant therapy. Monitor for changes in the therapeutic and adverse effects of clomipramine if fluoxetine is initiated, discontinued or dose changed. (source: Drug Bank)
fluoxetine The antidepressant increases the effect of clozapine (source: Drug Bank)
fluoxetine The antidepressant increases the effect of clozapine (source: Drug Bank)
fluoxetine The antidepressant increases the effect and toxicity of cyclosporine (source: Drug Bank)
fluoxetine The antidepressant increases the effect and toxicity of cyclosporine (source: Drug Bank)
fluoxetine Possible antagonism of action (source: Drug Bank)
fluoxetine Possible antagonism of action (source: Drug Bank)
fluoxetine Fluoxetine increases the effect and toxicity of tricyclics (source: Drug Bank)
fluoxetine The SSRI, fluoxetine, may increase the serum concentration of the tricyclic antidepressant, desipramine, by decreasing its metabolism. Additive modulation of serotonin activity also increases the risk of serotonin syndrome. Monitor for development of serotonin syndrome during concomitant therapy. Monitor for changes in the therapeutic and adverse effects of desipramine if fluoxetine is initiated, discontinued or dose changed. (source: Drug Bank)
fluoxetine Risk of serotoninergic syndrome (source: Drug Bank)
fluoxetine Combination associated with possible serotoninergic syndrome (source: Drug Bank)
fluoxetine Combination associated with possible serotoninergic syndrome (source: Drug Bank)
fluoxetine Risk of serotoninergic syndrome (source: Drug Bank)
fluoxetine Possible ergotism and severe ischemia with this combination (source: Drug Bank)
fluoxetine Possible ergotism and severe ischemia with this combination (source: Drug Bank)
fluoxetine Fluoxetine increases the effect and toxicity of tricyclics (source: Drug Bank)
fluoxetine The SSRI, fluoxetine, may increase the serum concentration of the tricyclic antidepressant, doxepin, by decreasing its metabolism. Additive modulation of serotonin activity also increases the risk of serotonin syndrome. Monitor for development of serotonin syndrome during concomitant therapy. Monitor for changes in the therapeutic and adverse effects of doxepin if fluoxetine is initiated, discontinued or dose changed. (source: Drug Bank)
fluoxetine Increased risk of CNS adverse effects (source: Drug Bank)
fluoxetine Increased risk of CNS adverse effects (source: Drug Bank)
fluoxetine Possible ergotism and severe ischemia with this combination (source: Drug Bank)
fluoxetine Possible ergotism and severe ischemia with this combination (source: Drug Bank)
fluoxetine Possible serotoninergic syndrome with this combination (source: Drug Bank)
fluoxetine Possible serotoninergic syndrome with this combination (source: Drug Bank)
fluoxetine Risk of serotoninergic syndrome (source: Drug Bank)
fluoxetine Risk of serotoninergic syndrome (source: Drug Bank)
acenocoumarol The SSRI increases the effect of anticoagulant (source: Drug Bank)
acenocoumarol The SSRI, fluoxetine, increases the effect of anticoagulant, acenocoumarol. (source: Drug Bank)
almotriptan Increased risk of CNS adverse effects (source: Drug Bank)
almotriptan Increased risk of CNS adverse effects (source: Drug Bank)
amitriptyline Fluoxetine increases the effect and toxicity of tricyclics (source: Drug Bank)
amitriptyline The SSRI, fluoxetine, may increase the serum concentration of the tricyclic antidepressant, amitriptyline, by decreasing its metabolism. Additive modulation of serotonin activity also increases the risk of serotonin syndrome. Monitor for development of serotonin syndrome during concomitant therapy. Monitor for changes in the therapeutic and adverse effects of amitriptyline if fluoxetine is initiated, discontinued or dose changed. (source: Drug Bank)
amoxapine Fluoxetine increases the effect and toxicity of tricyclics (source: Drug Bank)
amoxapine The SSRI, fluoxetine, may increase the serum concentration of the tricyclic antidepressant, amoxapine, by decreasing its metabolism. Additive modulation of serotonin activity also increases the risk of serotonin syndrome. Monitor for development of serotonin syndrome during concomitant therapy. Monitor for changes in the therapeutic and adverse effects of amoxapine if fluoxetine is initiated, discontinued or dose changed. (source: Drug Bank)
amphetamine Risk of serotoninergic syndrome (source: Drug Bank)
amphetamine Risk of serotoninergic syndrome (source: Drug Bank)
anisindione The SSRI increases the effect of anticoagulant (source: Drug Bank)
anisindione The SSRI, fluoxetine, increases the effect of anticoagulant, anisindione. (source: Drug Bank)
astemizole Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank)
astemizole Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank)
atomoxetine The CYP2D6 inhibitor could increase the effect and toxicity of atomoxetine (source: Drug Bank)
atomoxetine The CYP2D6 inhibitor could increase the effect and toxicity of atomoxetine (source: Drug Bank)
benzphetamine Risk of serotoninergic syndrome (source: Drug Bank)
benzphetamine Risk of serotoninergic syndrome (source: Drug Bank)
carbamazepine Increases the effect of carbamazepine (source: Drug Bank)
carbamazepine Increases the effect of carbamazepine (source: Drug Bank)
carvedilol The SSRI increases the effect of the beta-blocker (source: Drug Bank)
carvedilol The SSRI, fluoxetine, may increase the bradycardic effect of the beta-blocker, carvedilol. (source: Drug Bank)
cilostazol Increases the effect of cilostazol (source: Drug Bank)
cilostazol Increases the effect of cilostazol (source: Drug Bank)
clarithromycin Possible serotoninergic syndrome with this combination (source: Drug Bank)
clarithromycin Possible serotoninergic syndrome with this combination (source: Drug Bank)
clomipramine Fluoxetine increases the effect and toxicity of tricyclics (source: Drug Bank)
clomipramine The SSRI, fluoxetine, may increase the serum concentration of the tricyclic antidepressant, clomipramine, by decreasing its metabolism. Additive modulation of serotonin activity also increases the risk of serotonin syndrome. Monitor for development of serotonin syndrome during concomitant therapy. Monitor for changes in the therapeutic and adverse effects of clomipramine if fluoxetine is initiated, discontinued or dose changed. (source: Drug Bank)
clozapine The antidepressant increases the effect of clozapine (source: Drug Bank)
clozapine The antidepressant increases the effect of clozapine (source: Drug Bank)
cyclosporine The antidepressant increases the effect and toxicity of cyclosporine (source: Drug Bank)
cyclosporine The antidepressant increases the effect and toxicity of cyclosporine (source: Drug Bank)
cyproheptadine Possible antagonism of action (source: Drug Bank)
cyproheptadine Possible antagonism of action (source: Drug Bank)
desipramine Fluoxetine increases the effect and toxicity of tricyclics (source: Drug Bank)
desipramine The SSRI, fluoxetine, may increase the serum concentration of the tricyclic antidepressant, desipramine, by decreasing its metabolism. Additive modulation of serotonin activity also increases the risk of serotonin syndrome. Monitor for development of serotonin syndrome during concomitant therapy. Monitor for changes in the therapeutic and adverse effects of desipramine if fluoxetine is initiated, discontinued or dose changed. (source: Drug Bank)
dexfenfluramine Risk of serotoninergic syndrome (source: Drug Bank)
dexfenfluramine Risk of serotoninergic syndrome (source: Drug Bank)
dextroamphetamine Risk of serotoninergic syndrome (source: Drug Bank)
dextroamphetamine Risk of serotoninergic syndrome (source: Drug Bank)
dextromethorphan Combination associated with possible serotoninergic syndrome (source: Drug Bank)
dextromethorphan Combination associated with possible serotoninergic syndrome (source: Drug Bank)
dicumarol The SSRI increases the effect of anticoagulant (source: Drug Bank)
dicumarol The SSRI, fluoxetine, increases the effect of anticoagulant, dicumarol. (source: Drug Bank)
diethylpropion Risk of serotoninergic syndrome (source: Drug Bank)
diethylpropion Risk of serotoninergic syndrome (source: Drug Bank)
dihydroergotamine Possible ergotism and severe ischemia with this combination (source: Drug Bank)
dihydroergotamine Possible ergotism and severe ischemia with this combination (source: Drug Bank)
doxepin Fluoxetine increases the effect and toxicity of tricyclics (source: Drug Bank)
doxepin The SSRI, fluoxetine, may increase the serum concentration of the tricyclic antidepressant, doxepin, by decreasing its metabolism. Additive modulation of serotonin activity also increases the risk of serotonin syndrome. Monitor for development of serotonin syndrome during concomitant therapy. Monitor for changes in the therapeutic and adverse effects of doxepin if fluoxetine is initiated, discontinued or dose changed. (source: Drug Bank)
eletriptan Increased risk of CNS adverse effects (source: Drug Bank)
eletriptan Increased risk of CNS adverse effects (source: Drug Bank)
ergotamine Possible ergotism and severe ischemia with this combination (source: Drug Bank)
ergotamine Possible ergotism and severe ischemia with this combination (source: Drug Bank)
erythromycin Possible serotoninergic syndrome with this combination (source: Drug Bank)
erythromycin Possible serotoninergic syndrome with this combination (source: Drug Bank)
ethotoin Fluoxetine increases the effect of phenytoin (source: Drug Bank)
ethotoin Fluoxetine increases the effect of phenytoin (source: Drug Bank)
fenfluramine Risk of serotoninergic syndrome (source: Drug Bank)
fenfluramine Risk of serotoninergic syndrome (source: Drug Bank)
fosphenytoin Fluoxetine increases the effect of phenytoin (source: Drug Bank)
fosphenytoin Fluoxetine increases the effect of phenytoin (source: Drug Bank)
frovatriptan Increased risk of CNS adverse effects (source: Drug Bank)
frovatriptan Increased risk of CNS adverse effects (source: Drug Bank)
imipramine Fluoxetine increases the effect and toxicity of tricyclics (source: Drug Bank)
imipramine The SSRI, fluoxetine, may increase the serum concentration of the tricyclic antidepressant, imipramine, by decreasing its metabolism. Additive modulation of serotonin activity also increases the risk of serotonin syndrome. Monitor for development of serotonin syndrome during concomitant therapy. Monitor for changes in the therapeutic and adverse effects of imipramine if fluoxetine is initiated, discontinued or dose changed. (source: Drug Bank)
isocarboxazid Possible severe adverse reaction with this combination (source: Drug Bank)
isocarboxazid Possible severe adverse reaction with this combination (source: Drug Bank)
josamycin Possible serotoninergic syndrome with this combination (source: Drug Bank)
josamycin Possible serotoninergic syndrome with this combination (source: Drug Bank)
linezolid Combination associated with possible serotoninergic syndrome (source: Drug Bank)
linezolid Combination associated with possible serotoninergic syndrome (source: Drug Bank)
lithium The SSRI increases serum levels of lithium (source: Drug Bank)
lithium The SSRI, fluoxetine, increases serum levels of lithium. (source: Drug Bank)
mazindol Risk of serotoninergic syndrome (source: Drug Bank)
mazindol Risk of serotoninergic syndrome (source: Drug Bank)
mephenytoin Fluoxetine increases the effect of phenytoin (source: Drug Bank)
mephenytoin Fluoxetine increases the effect of phenytoin (source: Drug Bank)
mesoridazine Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank)
mesoridazine Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank)
methamphetamine Risk of serotoninergic syndrome (source: Drug Bank)
methamphetamine Risk of serotoninergic syndrome (source: Drug Bank)
metoprolol The SSRI increases the effect of the beta-blocker (source: Drug Bank)
metoprolol The SSRI, fluoxetine, may increase the bradycardic effect of the beta-blocker, metoprolol. (source: Drug Bank)
moclobemide Risk of serotoninergic syndrome (source: Drug Bank)
moclobemide Risk of serotoninergic syndrome (source: Drug Bank)
naratriptan Increased risk of CNS adverse effects (source: Drug Bank)
naratriptan Increased risk of CNS adverse effects (source: Drug Bank)
nortriptyline Fluoxetine increases the effect and toxicity of tricyclics (source: Drug Bank)
nortriptyline The SSRI, fluoxetine, may increase the serum concentration of the tricyclic antidepressant, nortriptyline, by decreasing its metabolism. Additive modulation of serotonin activity also increases the risk of serotonin syndrome. Monitor for development of serotonin syndrome during concomitant therapy. Monitor for changes in the therapeutic and adverse effects of nortriptyline if fluoxetine is initiated, discontinued or dose changed. (source: Drug Bank)
oxycodone Increased risk of serotonin syndrome (source: Drug Bank)
oxycodone Increased risk of serotonin syndrome (source: Drug Bank)
phendimetrazine Risk of serotoninergic syndrome (source: Drug Bank)
phendimetrazine Risk of serotoninergic syndrome (source: Drug Bank)
phenelzine Possible severe adverse reaction with this combination (source: Drug Bank)
phenelzine Possible severe adverse reaction with this combination (source: Drug Bank)
phentermine Risk of serotoninergic syndrome (source: Drug Bank)
phentermine Risk of serotoninergic syndrome (source: Drug Bank)
phenylpropanolamine Risk of serotoninergic syndrome (source: Drug Bank)
phenylpropanolamine Risk of serotoninergic syndrome (source: Drug Bank)
phenytoin Fluoxetine increases the effect of phenytoin (source: Drug Bank)
phenytoin Fluoxetine increases the effect of phenytoin (source: Drug Bank)
propafenone Increases the effect and toxicity of propafenone (source: Drug Bank)
propafenone Increases the effect and toxicity of propafenone (source: Drug Bank)
propranolol The SSRI increases the effect of the beta-blocker (source: Drug Bank)
propranolol The SSRI, fluoxetine, may increase the bradycardic effect of the beta-blocker, propranolol. (source: Drug Bank)
protriptyline Fluoxetine increases the effect and toxicity of tricyclics (source: Drug Bank)
protriptyline The SSRI, fluoxetine, may increase the serum concentration of the tricyclic antidepressant, protriptyline, by decreasing its metabolism. Additive modulation of serotonin activity also increases the risk of serotonin syndrome. Monitor for development of serotonin syndrome during concomitant therapy. Monitor for changes in the therapeutic and adverse effects of protriptyline if fluoxetine is initiated, discontinued or dose changed. (source: Drug Bank)
rasagiline Possible severe adverse reaction with this combination (source: Drug Bank)
rasagiline Possible severe adverse reaction with this combination (source: Drug Bank)
risperidone The SSRI increases the effect and toxicity of risperidone (source: Drug Bank)
risperidone The SSRI, fluoxetine, increases the effect and toxicity of risperidone. (source: Drug Bank)
ritonavir Increased risk of serotonin syndrome (source: Drug Bank)
ritonavir Increased risk of serotonin syndrome (source: Drug Bank)
rizatriptan Increased risk of CNS adverse effects (source: Drug Bank)
rizatriptan Increased risk of CNS adverse effects (source: Drug Bank)
selegiline Possible severe adverse reaction with this combination (source: Drug Bank)
selegiline Possible severe adverse reaction with this combination (source: Drug Bank)
sibutramine Risk of serotoninergic syndrome (source: Drug Bank)
sibutramine Risk of serotoninergic syndrome (source: Drug Bank)
sumatriptan Increased risk of CNS adverse effects (source: Drug Bank)
sumatriptan Increased risk of CNS adverse effects (source: Drug Bank)
terfenadine Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank)
terfenadine Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank)
thioridazine Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank)
thioridazine Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank)
tramadol Increased risk of serotonin syndrome (source: Drug Bank)
tramadol Increased risk of serotonin syndrome (source: Drug Bank)
tranylcypromine Possible severe adverse reaction with this combination (source: Drug Bank)
tranylcypromine Possible severe adverse reaction with this combination (source: Drug Bank)
trimipramine Fluoxetine increases the effect and toxicity of tricyclics (source: Drug Bank)
trimipramine The SSRI, fluoxetine, may increase the serum concentration of the tricyclic antidepressant, trimipramine, by decreasing its metabolism. Additive modulation of serotonin activity also increases the risk of serotonin syndrome. Monitor for development of serotonin syndrome during concomitant therapy. Monitor for changes in the therapeutic and adverse effects of trimipramine if fluoxetine is initiated, discontinued or dose changed. (source: Drug Bank)
troleandomycin Possible serotoninergic syndrome with this combination (source: Drug Bank)
troleandomycin Possible serotoninergic syndrome with this combination (source: Drug Bank)
warfarin The SSRI increases the effect of anticoagulant (source: Drug Bank)
warfarin The SSRI, fluoxetine, increases the effect of anticoagulant, warfarin. (source: Drug Bank)
zolmitriptan Increased risk of CNS adverse effects (source: Drug Bank)
zolmitriptan Increased risk of CNS adverse effects (source: Drug Bank)
fluoxetine Fluoxetine increases the effect of phenytoin (source: Drug Bank)
fluoxetine Increased risk of CNS adverse effects (source: Drug Bank)
fluoxetine Additive anticoagulant/antiplatelet effects may increase bleed risk. Concomitant therapy should be avoided. (source: Drug Bank)
fluoxetine Fluoxetine increases the effect and toxicity of tricyclics (source: Drug Bank)
fluoxetine The SSRI, fluoxetine, may increase the serum concentration of the tricyclic antidepressant, imipramine, by decreasing its metabolism. Additive modulation of serotonin activity also increases the risk of serotonin syndrome. Monitor for development of serotonin syndrome during concomitant therapy. Monitor for changes in the therapeutic and adverse effects of imipramine if fluoxetine is initiated, discontinued or dose changed. (source: Drug Bank)
fluoxetine Possible severe adverse reaction with this combination (source: Drug Bank)
fluoxetine Possible severe adverse reaction with this combination (source: Drug Bank)
fluoxetine Concomitant therapy may result in additive antiplatelet effects and increase the risk of bleeding. Monitor for increased risk of bleeding during concomitant therapy. (source: Drug Bank)
fluoxetine Possible increase of arterial pressure (source: Drug Bank)
fluoxetine Possible increase of arterial pressure (source: Drug Bank)
fluoxetine The SSRI increases serum levels of lithium (source: Drug Bank)
fluoxetine The SSRI, fluoxetine, increases serum levels of lithium. (source: Drug Bank)
fluoxetine Risk of serotoninergic syndrome (source: Drug Bank)
fluoxetine Risk of serotoninergic syndrome (source: Drug Bank)
fluoxetine Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank)
fluoxetine Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank)
fluoxetine The SSRI increases the effect of the beta-blocker (source: Drug Bank)
fluoxetine The SSRI increases the effect of the beta-blocker (source: Drug Bank)
fluoxetine Risk of serotoninergic syndrome (source: Drug Bank)
fluoxetine Risk of serotoninergic syndrome (source: Drug Bank)
fluoxetine Increased risk of CNS adverse effects (source: Drug Bank)
fluoxetine Increased risk of CNS adverse effects (source: Drug Bank)
fluoxetine Fluoxetine increases the effect and toxicity of tricyclics (source: Drug Bank)
fluoxetine The SSRI, fluoxetine, may increase the serum concentration of the tricyclic antidepressant, nortriptyline, by decreasing its metabolism. Additive modulation of serotonin activity also increases the risk of serotonin syndrome. Monitor for development of serotonin syndrome during concomitant therapy. Monitor for changes in the therapeutic and adverse effects of nortriptyline if fluoxetine is initiated, discontinued or dose changed. (source: Drug Bank)
fluoxetine Increased risk of serotonin syndrome (source: Drug Bank)
fluoxetine Increased risk of serotonin syndrome (source: Drug Bank)
fluoxetine Possible severe adverse reaction with this combination (source: Drug Bank)
fluoxetine Possible severe adverse reaction with this combination (source: Drug Bank)
fluoxetine Risk of serotoninergic syndrome (source: Drug Bank)
fluoxetine Risk of serotoninergic syndrome (source: Drug Bank)
fluoxetine Fluoxetine increases the effect of phenytoin (source: Drug Bank)
fluoxetine Fluoxetine increases the effect of phenytoin (source: Drug Bank)
fluoxetine Fluoxetine increases the effect and toxicity of propafenone (source: Drug Bank)
fluoxetine Fluoxetine increases the effect and toxicity of propafenone (source: Drug Bank)
fluoxetine The SSRI increases the effect of the beta-blocker (source: Drug Bank)
fluoxetine The SSRI, fluoxetine, may increase the bradycardic effect of the beta-blocker, propranolol. (source: Drug Bank)
fluoxetine Possible severe adverse reaction with this combination (source: Drug Bank)
fluoxetine The metabolism of Tacrine, a CYP1A2 substrate, may be reduced by Fluoxetine, a CYP1A2 inhibitors. Monitor the efficacy and toxicity of Tacrine if Fluoxetine is initiated, discontinued or if the dose is changed. (source: Drug Bank)
fluoxetine Additive QTc-prolongation may occur increasing the risk of serious ventricular arrhythmias. Concomitant therapy should be used with caution. (source: Drug Bank)
fluoxetine Fluoxetine may decrease the therapeutic effect of Tamoxifen by decreasing the production of active metabolites. Concomitant therapy should be avoided. (source: Drug Bank)
fluoxetine Fluoxetine may decrease the therapeutic effect of Tamoxifen by decreasing the production of active metabolites. Concomitant therapy should be avoided. (source: Drug Bank)
fluoxetine Fluoxetine, a CYP2D6 inhibitor, may decrease the metabolism and clearance of Tamsulosin, a CYP2D6 substrate. Monitor for changes in therapeutic/adverse effects of Tamsulosin if Fluoxetine is initiated, discontinued, or dose changed. (source: Drug Bank)
fluoxetine Fluoxetine, a CYP2D6 inhibitor, may decrease the metabolism and clearance of Tamsulosin, a CYP2D6 substrate. Monitor for changes in therapeutic/adverse effects of Tamsulosin if Fluoxetine is initiated, discontinued, or dose changed. (source: Drug Bank)
fluoxetine Terbinafine may reduce the metabolism and clearance of Fluoxetine. Consider alternate therapy or monitor for therapeutic/adverse effects of Fluoxetine if Terbinafine is initiated, discontinued or dose changed. (source: Drug Bank)
fluoxetine Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank)
fluoxetine Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank)
fluoxetine Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank)
fluoxetine Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank)
fluoxetine May cause additive QTc-prolonging effects. Increased risk of ventricular arrhythmias. Consider alternate therapy. Thorough risk:benefit assessment is required prior to co-administration. (source: Drug Bank)
fluoxetine May cause additive QTc-prolonging effects. Increased risk of ventricular arrhythmias. Consider alternate therapy. Thorough risk:benefit assessment is required prior to co-administration. (source: Drug Bank)
fluoxetine Additive antiplatelet effects increase the risk of bleeding. Consider alternate therapy or monitor for increased bleeding. (source: Drug Bank)
fluoxetine Tipranavir increases the concentration of Fluoxetine. The Fluoxetine dose may require an adjustment. (source: Drug Bank)
fluoxetine Fluoxetine may decrease the metabolism and clearance of Tizanidine. Consider alternate therapy or use caution during co-administration. (source: Drug Bank)
fluoxetine Tolbutamide, a strong CYP2C9 inhibitor, may decrease the metabolism and clearance of Fluoxetine. Consider alternate therapy or monitor for changes in Fluoxetine therapeutic and adverse effects if Tolbutamide is initiated, discontinued or dose changed. (source: Drug Bank)
fluoxetine Tolbutamide, a strong CYP2C9 inhibitor, may decrease the metabolism and clearance of Fluoxetine. Consider alternate therapy or monitor for changes in Fluoxetine therapeutic and adverse effects if Tolbutamide is initiated, discontinued or dose changed. (source: Drug Bank)
fluoxetine Increased antiplatelet effects may enhance the risk of bleeding. Alternate therapy may be considered or monitor for inreased bleeding during concomitant therapy. (source: Drug Bank)
fluoxetine Fluoxetine may decrease the metabolism and clearance of Tolterodine. Monitor for adverse/toxic effects of Tolterodine. (source: Drug Bank)
fluoxetine Fluoxetine may decrease the metabolism and clearance of Tolterodine. Monitor for adverse/toxic effects of Tolterodine. (source: Drug Bank)
fluoxetine Additive QTc-prolongation may occur, increasing the risk of serious ventricular arrhythmias. Consider alternate therapy. A thorough risk:benefit assessment is required prior to co-administration. (source: Drug Bank)
fluoxetine Tramadol increases the risk of serotonin syndrome and seizures. Fluoxetine may decrease the effect of Tramadol by decreasing active metabolite production. (source: Drug Bank)
fluoxetine Increased risk of serotonin syndrome. Concomitant therapy should be avoided. A significant washout period, dependent on the half-lives of the agents, should be employed between therapies. (source: Drug Bank)
fluoxetine Increased risk of serotonin syndrome. The 2D6 inhibitor, Trazodone, may also increase the efficacy of Fluoxetine by decreasing Fluoxetine metabolism and clearance. Monitor for symptoms of serotonin syndrome and changes in Fluoxetine efficacy if Trazodone is initiated, discontinued or dose changed. (source: Drug Bank)
fluoxetine Increased risk of serotonin syndrome. Monitor for symptoms of serotonin syndrome. (source: Drug Bank)
fluoxetine The prostacyclin analogue, Treprostinil, increases the risk of bleeding when combined with the antiplatelet agent, Fluoxetine. Monitor for increased bleeding during concomitant thearpy. (source: Drug Bank)
fluoxetine The SSRI, Fluoxetine, may decrease the metabolism and clearance of Trimipramine. Increased risk of serotonin syndrome. Monitor for changes in Trimipramine efficacy and toxicity if Fluoxetine is initiated, discontinued or dose changed. Additive QTc-prolongation may also occur, increasing the risk of serious ventricular arrhythmias. Concomitant therapy should be used cautiously. (source: Drug Bank)
fluoxetine The CNS depressants, Triprolidine and Fluoxetine, may increase adverse/toxic effects due to additivity. Monitor for increased CNS depressant effects during concomitant therapy. (source: Drug Bank)
fluoxetine The CNS depressants, Triprolidine and Fluoxetine, may increase adverse/toxic effects due to additivity. Monitor for increased CNS depressant effects during concomitant therapy. (source: Drug Bank)
fluoxetine Increased risk of serotonin syndrome. Monitor for symptoms of serotonin syndrome. (source: Drug Bank)
fluoxetine Additive QTc prolongation may occur. Consider alternate therapy or monitor for QTc prolongation as this can lead to Torsade de Pointes (TdP). (source: Drug Bank)
fluoxetine Additive QTc prolongation may occur. Consider alternate therapy or monitor for QTc prolongation as this can lead to Torsade de Pointes (TdP). (source: Drug Bank)
fluoxetine Additive QTc-prolonging effects may increase the risk of severe arrhythmias. Concomitant therapy is contraindicated. (source: Drug Bank)
fluoxetine Use of two serotonin modulators, such as zolmitriptan and fluoxetine, increases the risk of serotonin syndrome. Consider alternate therapy or monitor for serotonin syndrome during concomitant therapy. (source: Drug Bank)
fluoxetine Additive QTc prolongation may occur. Consider alternate therapy or use caution and monitor for QTc prolongation as this can lead to Torsade de Pointes (TdP). Fluoxetine, a strong CYP2D6 inhibitor, may increase the serum concentration of zuclopenthixol by decreasing its metabolism. Consider alternate therapy or monitor for changes in the therapeutic and adverse effects of zuclopenthixol if fluoxetine is initiated, discontinued or dose changed. (source: Drug Bank)

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Publications related to fluoxetine: 134

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Effect of CYP2D6, CYP2C9 and ABCB1 genotypes on fluoxetine plasma concentrations and clinical improvement in children and adolescent patients. The pharmacogenomics journal. 2014. Gassó P, et al. PubMed
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ABCB6, ABCB1 and ABCG1 genetic polymorphisms and antidepressant response of SSRIs in Chinese depressive patients. Pharmacogenomics. 2013. Huang Xiaoye, et al. PubMed
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Challenges in pharmacogenetics. European journal of clinical pharmacology. 2013. Cascorbi Ingolf, et al. PubMed
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Pharmacogenetics in major depression: a comprehensive meta-analysis. Progress in neuro-psychopharmacology & biological psychiatry. 2013. Niitsu Tomihisa, et al. PubMed
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Influence of CYP2D6 and CYP2C19 gene variants on antidepressant response in obsessive-compulsive disorder. The pharmacogenomics journal. 2013. Brandl E J, et al. PubMed
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CYP2D6 ultrarapid metabolism and early dropout from fluoxetine or amitriptyline monotherapy treatment in major depressive patients. Molecular psychiatry. 2013. Peñas-Lledó E M, et al. PubMed
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Serotonin transporter genotype and function in relation to antidepressant response in Koreans. Psychopharmacology. 2013. Myung Woojae, et al. PubMed
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PDLIM5 gene polymorphisms and short term antidepressant response in Chinese major depressive disorders. International journal of clinical and experimental medicine. 2013. Liu Zhongchun, et al. PubMed
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Cytochrome P450-mediated drug metabolism in the brain. Journal of psychiatry & neuroscience : JPN. 2012. Miksys Sharon, et al. PubMed
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TPH1, MAOA, serotonin receptor 2A and 2C genes in citalopram response: possible effect in melancholic and psychotic depression. Neuropsychobiology. 2013. Arias Bárbara, et al. PubMed
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Association of APC and REEP5 gene polymorphisms with major depression disorder and treatment response to antidepressants in a Han Chinese population. General hospital psychiatry. 2012. Yang Zhenxing, et al. PubMed
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The AmpliChip® CYP450 test and response to treatment in schizophrenia and obsessive compulsive disorder: a pilot study and focus on cases with abnormal CYP2D6 drug metabolism. Genetic testing and molecular biomarkers. 2012. Müller Daniel J, et al. PubMed
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Improvement of glycemic control using methylphenidate treatment of apathy: a preliminary report. Journal of the American Geriatrics Society. 2012. Padala Prasad R, et al. PubMed
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Pharmacogenetics of glutamate system genes and SSRI-associated sexual dysfunction. Psychiatry research. 2012. Bishop Jeffrey R, et al. PubMed
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PharmGKB summary: very important pharmacogene information for cytochrome P450, family 2, subfamily C, polypeptide 19. Pharmacogenetics and genomics. 2011. Scott Stuart A, et al. PubMed
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Pharmacogenetic testing: time for clinical practice guidelines. Clinical pharmacology and therapeutics. 2011. Amstutz U, et al. PubMed
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A polymorphism of the GTP-cyclohydrolase I feedback regulator gene alters transcriptional activity and may affect response to SSRI antidepressants. The pharmacogenomics journal. 2011. McHugh P C, et al. PubMed
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Receptor targets for antidepressant therapy in bipolar disorder: An overview. Journal of affective disorders. 2011. Fountoulakis Konstantinos N, et al. PubMed
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Pharmacogenetics of drug-induced birth defects: what is known so far?. Pharmacogenomics. 2011. Wilffert Bob, et al. PubMed
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Is 5-HTTLPR linked to the response of selective serotonin reuptake inhibitors in MDD?. European archives of psychiatry and clinical neuroscience. 2011. Illi Ari, et al. PubMed
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Very important pharmacogene summary: ABCB1 (MDR1, P-glycoprotein). Pharmacogenetics and genomics. 2011. Hodges Laura M, et al. PubMed
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The role of clinical variables, neuropsychological performance and SLC6A4 and COMT gene polymorphisms on the prediction of early response to fluoxetine in major depressive disorder. Journal of affective disorders. 2010. Gudayol-Ferré Esteve, et al. PubMed
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KCNH2 pharmacogenomics summary. Pharmacogenetics and genomics. 2010. Oshiro Connie, et al. PubMed
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Identifying genomic and developmental causes of adverse drug reactions in children. Pharmacogenomics. 2010. Becker Mara L, et al. PubMed
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Systematic review of pharmacoeconomic studies of pharmacogenomic tests. Pharmacogenomics. 2010. Beaulieu Mathieu, et al. PubMed
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Meta-analysis of FKBP5 gene polymorphisms association with treatment response in patients with mood disorders. Neuroscience letters. 2010. Zou Yan-Feng, et al. PubMed
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Pharmacogenomic implications of variants of monoaminergic-related genes in geriatric psychiatry. Pharmacogenomics. 2010. Shiroma Paulo R, et al. PubMed
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Coprescription of tamoxifen and medications that inhibit CYP2D6. Journal of clinical oncology : official journal of the American Society of Clinical Oncology. 2010. Sideras Kostandinos, et al. PubMed
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Nationwide drug-dispensing data reveal important differences in adherence to drug label recommendations on CYP2D6-dependent drug interactions. British journal of clinical pharmacology. 2010. Mannheimer Buster, et al. PubMed
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Composite functional genetic and comedication CYP2D6 activity score in predicting tamoxifen drug exposure among breast cancer patients. Journal of clinical pharmacology. 2010. Borges Silvana, et al. PubMed
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Human lymphoblastoid cell line panels: novel tools for assessing shared drug pathways. Pharmacogenomics. 2010. Morag Ayelet, et al. PubMed
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Pharmacogenetic considerations in the treatment of psychiatric disorders. Expert opinion on pharmacotherapy. 2010. Lohoff Falk W, et al. PubMed
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Selective serotonin reuptake inhibitors and breast cancer mortality in women receiving tamoxifen: a population based cohort study. BMJ (Clinical research ed.). 2010. Kelly Catherine M, et al. PubMed
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Association of brain-derived neurotrophic factor genetic Val66Met polymorphism with severity of depression, efficacy of fluoxetine and its side effects in Chinese major depressive patients. Neuropsychobiology. 2010. Zou Yan-Feng, et al. PubMed
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Predicting new molecular targets for known drugs. Nature. 2009. Keiser Michael J, et al. PubMed
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Warfarin interactions with substances listed in drug information compendia and in the FDA-approved label for warfarin sodium. Clinical pharmacology and therapeutics. 2009. Anthony M, et al. PubMed
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Expression and association analyses of promoter variants of the neurogenic gene HES6, a candidate gene for mood disorder susceptibility and antidepressant response. Neuroscience letters. 2009. Glubb Dylan M, et al. PubMed
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Cytochrome P450 2D6. Pharmacogenetics and genomics. 2009. Owen Ryan P, et al. PubMed
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Pharmacogenetics of selective serotonin reuptake inhibitors and associated adverse drug reactions. Pharmacotherapy. 2009. Thomas Kelan L H, et al. PubMed
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Histone deacetylase inhibitors induce a very broad, pleiotropic anticancer drug resistance phenotype in acute myeloid leukemia cells by modulation of multiple ABC transporter genes. Clinical cancer research : an official journal of the American Association for Cancer Research. 2009. Hauswald Stefanie, et al. PubMed
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Novel sequence variations in the brain-derived neurotrophic factor gene and association with major depression and antidepressant treatment response. Archives of general psychiatry. 2009. Licinio Julio, et al. PubMed
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MAO-A and COMT genotypes as possible regulators of perinatal serotonergic symptoms after in utero exposure to SSRIs. European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology. 2009. Hilli Johanna, et al. PubMed
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ADME pharmacogenetics: current practices and future outlook. Expert opinion on drug metabolism & toxicology. 2009. Grossman Iris. PubMed
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5-HTR1A, 5-HTR2A, 5-HTR6, TPH1 and TPH2 polymorphisms and major depression. Neuroreport. 2009. Illi Ari, et al. PubMed
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Resequencing of serotonin-related genes and association of tagging SNPs to citalopram response. Pharmacogenetics and genomics. 2009. Peters Eric J, et al. PubMed
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Tryptophan hydroxylase 2 gene is associated with major depression and antidepressant treatment response. Progress in neuro-psychopharmacology & biological psychiatry. 2009. Tsai Shih-Jen, et al. PubMed
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Genetic determinants of response to clopidogrel and cardiovascular events. The New England journal of medicine. 2009. Simon Tabassome, et al. PubMed
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Association of a functional polymorphism in the adrenomedullin gene (ADM) with response to paroxetine. The pharmacogenomics journal. 2009. Glubb D M, et al. PubMed
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Differential time- and NADPH-dependent inhibition of CYP2C19 by enantiomers of fluoxetine. Drug metabolism and disposition: the biological fate of chemicals. 2009. Stresser David M, et al. PubMed
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Redox regulation of multidrug resistance in cancer chemotherapy: molecular mechanisms and therapeutic opportunities. Antioxidants & redox signaling. 2009. Kuo Macus Tien. PubMed
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Several major antiepileptic drugs are substrates for human P-glycoprotein. Neuropharmacology. 2008. Luna-Tortós Carlos, et al. PubMed
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Association of PDE11A global haplotype with major depression and antidepressant drug response. Neuropsychiatric disease and treatment. 2009. Luo Huai-Rong, et al. PubMed
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Functional pharmacogenetics/genomics of human cytochromes P450 involved in drug biotransformation. Analytical and bioanalytical chemistry. 2008. Zanger Ulrich M, et al. PubMed
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Drug target identification using side-effect similarity. Science (New York, N.Y.). 2008. Campillos Monica, et al. PubMed
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Structure, function and regulation of P-glycoprotein and its clinical relevance in drug disposition. Xenobiotica; the fate of foreign compounds in biological systems. 2008. Zhou S-F. PubMed
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The FKBP5-gene in depression and treatment response--an association study in the Sequenced Treatment Alternatives to Relieve Depression (STAR*D) Cohort. Biological psychiatry. 2008. Lekman Magnus, et al. PubMed
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CYP2C19 inhibition: the impact of substrate probe selection on in vitro inhibition profiles. Drug metabolism and disposition: the biological fate of chemicals. 2008. Foti Robert S, et al. PubMed
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Semi-quantitative CYP2D6 gene doses in relation to metabolic ratios of psychotropics. European journal of clinical pharmacology. 2008. Hinrichs John W J, et al. PubMed
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Plasminogen activator inhibitor-1 gene is associated with major depression and antidepressant treatment response. Pharmacogenetics and genomics. 2008. Tsai Shih-Jen, et al. PubMed
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Genetic variants in FKBP5 affecting response to antidepressant drug treatment. Pharmacogenomics. 2008. Kirchheiner Julia, et al. PubMed
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Glycogen synthase kinase-3beta gene is associated with antidepressant treatment response in Chinese major depressive disorder. The pharmacogenomics journal. 2008. Tsai S-J, et al. PubMed
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Influence of the CYP2D6*4 polymorphism on dose, switching and discontinuation of antidepressants. British journal of clinical pharmacology. 2008. Bijl Monique J, et al. PubMed
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The antidepressant fluoxetine restores plasticity in the adult visual cortex. Science (New York, N.Y.). 2008. Maya Vetencourt José Fernando, et al. PubMed
Polymorphisms in the drug transporter gene ABCB1 predict antidepressant treatment response in depression. Neuron. 2008. Uhr Manfred, et al. PubMed
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Citalopram enantiomers in plasma and cerebrospinal fluid of ABCB1 genotyped depressive patients and clinical response: a pilot study. Pharmacological research : the official journal of the Italian Pharmacological Society. 2008. Nikisch Georg, et al. PubMed
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Strategy for a genetic assessment of antipsychotic and antidepressant-related proarrhythmia. Current medicinal chemistry. 2008. Drago Antonio, et al. PubMed
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Comparative metabolic capabilities and inhibitory profiles of CYP2D6.1, CYP2D6.10, and CYP2D6.17. Drug metabolism and disposition: the biological fate of chemicals. 2007. Shen Hongwu, et al. PubMed
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Clinical response and risk for reported suicidal ideation and suicide attempts in pediatric antidepressant treatment: a meta-analysis of randomized controlled trials. JAMA : the journal of the American Medical Association. 2007. Bridge Jeffrey A, et al. PubMed
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Association study of corticotropin-releasing hormone receptor1 gene polymorphisms and antidepressant response in major depressive disorders. Neuroscience letters. 2007. Liu Zhongchun, et al. PubMed
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Cobalamin potentiates vinblastine cytotoxicity through downregulation of mdr-1 gene expression in HepG2 cells. Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology. 2007. Marguerite Véronique, et al. PubMed
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Mechanism of inhibition of P-glycoprotein mediated efflux by vitamin E TPGS: influence on ATPase activity and membrane fluidity. Molecular pharmaceutics. 2007. Collnot Eva-Maria, et al. PubMed
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Phosphodiesterase genes are associated with susceptibility to major depression and antidepressant treatment response. Proceedings of the National Academy of Sciences of the United States of America. 2006. Wong Ma-Li, et al. PubMed
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Genetic variant BDNF (Val66Met) polymorphism alters anxiety-related behavior. Science (New York, N.Y.). 2006. Chen Zhe-Yu, et al. PubMed
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Gefitinib modulates the function of multiple ATP-binding cassette transporters in vivo. Cancer research. 2006. Leggas Markos, et al. PubMed
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Impact of P-glycoprotein on clopidogrel absorption. Clinical pharmacology and therapeutics. 2006. Taubert Dirk, et al. PubMed
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Serotonin transporter polymorphisms and side effects in antidepressant therapy--a pilot study. Pharmacogenomics. 2006. Popp Johannes, et al. PubMed
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The complexity of active metabolites in therapeutic drug monitoring of psychotropic drugs. Pharmacopsychiatry. 2006. Hendset M, et al. PubMed
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Essential role of BDNF in the mesolimbic dopamine pathway in social defeat stress. Science (New York, N.Y.). 2006. Berton Olivier, et al. PubMed
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Single nucleotide polymorphisms in human P-glycoprotein: its impact on drug delivery and disposition. Expert opinion on drug delivery. 2006. Dey Surajit. PubMed
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Response to fluoxetine and serotonin 1A receptor (C-1019G) polymorphism in Taiwan Chinese major depressive disorder. The pharmacogenomics journal. 2006. Hong C-J, et al. PubMed
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Influence of CYP2C9, 2C19 and 2D6 genetic polymorphisms on the steady-state plasma concentrations of the enantiomers of fluoxetine and norfluoxetine. Basic & clinical pharmacology & toxicology. 2005. Scordo Maria G, et al. PubMed
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Sequence analysis of the serotonin transporter and associations with antidepressant response. Biological psychiatry. 2005. Kraft Jeffrey B, et al. PubMed
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Polymorphisms in FKBP5 are associated with increased recurrence of depressive episodes and rapid response to antidepressant treatment. Nature genetics. 2004. Binder Elisabeth B, et al. PubMed
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Early-life blockade of the 5-HT transporter alters emotional behavior in adult mice. Science (New York, N.Y.). 2004. Ansorge Mark S, et al. PubMed
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Influence of lipid lowering fibrates on P-glycoprotein activity in vitro. Biochemical pharmacology. 2004. Ehrhardt Manuela, et al. PubMed
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Interactions of human P-glycoprotein with simvastatin, simvastatin acid, and atorvastatin. Pharmaceutical research. 2004. Hochman Jerome H, et al. PubMed
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Breastfeeding during maternal antidepressant treatment with serotonin reuptake inhibitors: infant exposure, clinical symptoms, and cytochrome p450 genotypes. The Journal of clinical psychiatry. 2004. Berle Jan Øystein, et al. PubMed
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Effect of CYP2D6 and CYP2C9 genotypes on fluoxetine and norfluoxetine plasma concentrations during steady-state conditions. European journal of clinical pharmacology. 2004. LLerena Adrián, et al. PubMed
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Polymorphisms in human MDR1 (P-glycoprotein): recent advances and clinical relevance. Clinical pharmacology and therapeutics. 2004. Marzolini Catia, et al. PubMed
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Increased incidence of CYP2D6 gene duplication in patients with persistent mood disorders: ultrarapid metabolism of antidepressants as a cause of nonresponse. A pilot study. European journal of clinical pharmacology. 2004. Kawanishi Chiaki, et al. PubMed
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No evidence of increased adverse drug reactions in cytochrome P450 CYP2D6 poor metabolizers treated with fluoxetine or nortriptyline. Human psychopharmacology. 2004. Roberts Rebecca L, et al. PubMed
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Some aspects of genetic polymorphism in the biotransformation of antidepressants. Thérapie. 2004. Brøsen Kim. PubMed
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Polymorphisms in the CYP 2D6 gene: association with plasma concentrations of fluoxetine and paroxetine. Therapeutic drug monitoring. 2003. Charlier Corinne, et al. PubMed
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Serotonin transporter polymorphisms and adverse effects with fluoxetine treatment. Biological psychiatry. 2003. Perlis Roy H, et al. PubMed
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Regeneration of serotonin from 5-methoxytryptamine by polymorphic human CYP2D6. Pharmacogenetics. 2003. Yu Ai-Ming, et al. PubMed
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Pharmacokinetics of fluoxetine and norfluoxetine in pregnancy and lactation. Clinical pharmacology and therapeutics. 2003. Heikkinen Tuija, et al. PubMed
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Genetic polymorphisms of the human MDR1 drug transporter. Annual review of pharmacology and toxicology. 2003. Schwab Matthias, et al. PubMed
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Expression, purification, biochemical characterization, and comparative function of human cytochrome P450 2D6.1, 2D6.2, 2D6.10, and 2D6.17 allelic isoforms. The Journal of pharmacology and experimental therapeutics. 2002. Yu Aiming, et al. PubMed
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CYP2D6 inhibition by selective serotonin reuptake inhibitors: analysis of achievable steady-state plasma concentrations and the effect of ultrarapid metabolism at CYP2D6. Pharmacotherapy. 2002. Lam Y W Francis, et al. PubMed
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Cytochrome P450 2D6 genotype does not predict SSRI (fluoxetine or paroxetine) induced hyponatraemia. Human psychopharmacology. 2002. Stedman Catherine A M, et al. PubMed
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The antidepressant drug fluoxetine is an inhibitor of human ether-a-go-go-related gene (HERG) potassium channels. The Journal of pharmacology and experimental therapeutics. 2002. Thomas Dierk, et al. PubMed
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Association study of the serotonin transporter promoter polymorphism and symptomatology and antidepressant response in major depressive disorders. Molecular psychiatry. 2002. Yu Y W-Y, et al. PubMed
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Med-psych drug-drug interactions update. Psychosomatics. 2002. Armstrong Scott C, et al. PubMed
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Concentrations of the enantiomers of fluoxetine and norfluoxetine after multiple doses of fluoxetine in cytochrome P4502D6 poor and extensive metabolizers. Journal of clinical psychopharmacology. 2001. Eap C B, et al. PubMed
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Interaction of omeprazole, lansoprazole and pantoprazole with P-glycoprotein. Naunyn-Schmiedeberg's archives of pharmacology. 2001. Pauli-Magnus C, et al. PubMed
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Fluoxetine (Prozac) as a cause of QT prolongation. Archives of internal medicine. 2001. Varriale P. PubMed
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Effects of CYP2C19 genotype and CYP2C9 on fluoxetine N-demethylation in human liver microsomes. Acta pharmacologica Sinica. 2001. Liu Z Q, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
CYP2B6 mediates the in vitro hydroxylation of bupropion: potential drug interactions with other antidepressants. Drug metabolism and disposition: the biological fate of chemicals. 2000. Hesse L M, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Drug metabolism genotypes and their association with adverse drug reactions in selected populations: a pilot study of methodology. Pharmacoepidemiology and drug safety. 2000. Clark D, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Pharmacokinetics of selective serotonin reuptake inhibitors. Pharmacology & therapeutics. 2000. Hiemke C, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Science, medicine, and the future: Pharmacogenetics. BMJ (Clinical research ed.). 2000. Wolf C R, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Penetration of amitriptyline, but not of fluoxetine, into brain is enhanced in mice with blood-brain barrier deficiency due to mdr1a P-glycoprotein gene disruption. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology. 2000. Uhr M, et al. PubMed
No Dosing Guideline available No Drug Label available CA VA No VIP available No VIP available
Serotonin transporter gene polymorphism and antidepressant response. Neuroreport. 2000. Kim D K, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available VA No VIP available No VIP available
Fluoxetine-related death in a child with cytochrome P-450 2D6 genetic deficiency. Journal of child and adolescent psychopharmacology. 2000. Sallee F R, et al. PubMed
No Dosing Guideline available No Drug Label available CA VA No VIP available No VIP available
Fluoxetine inhibits the metabolism of tolterodine-pharmacokinetic implications and proposed clinical relevance. British journal of clinical pharmacology. 1999. Brynne N, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available VIP No VIP available
The role of intestinal P-glycoprotein in the interaction of digoxin and rifampin. The Journal of clinical investigation. 1999. Greiner B, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Metabolic interactions of central nervous system medications and selective serotonin reuptake inhibitors. International clinical psychopharmacology. 1999. Naranjo C A, et al. PubMed
No Dosing Guideline available No Drug Label available CA VA No VIP available No VIP available
The stereoselective metabolism of fluoxetine in poor and extensive metabolizers of sparteine. Pharmacogenetics. 1999. Fjordside L, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available VIP No VIP available
Biochemical, cellular, and pharmacological aspects of the multidrug transporter. Annual review of pharmacology and toxicology. 1999. Ambudkar S V, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Cytochrome P4502C9: an enzyme of major importance in human drug metabolism. British journal of clinical pharmacology. 1998. Miners J O, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Metabolism of the newer antidepressants. An overview of the pharmacological and pharmacokinetic implications. Clinical pharmacokinetics. 1998. Caccia S. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Differences in interactions of SSRIs. International clinical psychopharmacology. 1998. Brøsen K. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available VIP No VIP available
Competitive, non-competitive and cooperative interactions between substrates of P-glycoprotein as measured by its ATPase activity. Biochimica et biophysica acta. 1997. Litman T, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Fatality associated with combined fluoxetine-amitriptyline therapy. JAMA : the journal of the American Medical Association. 1997. Preskorn S H, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Selective serotonin reuptake inhibitors and CNS drug interactions. A critical review of the evidence. Clinical pharmacokinetics. 1997. Sproule B A, et al. PubMed
The disposition of fluoxetine but not sertraline is altered in poor metabolizers of debrisoquin. Clinical pharmacology and therapeutics. 1996. Hamelin B A, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Pharmacokinetic-pharmacodynamic relationship of the selective serotonin reuptake inhibitors. Clinical pharmacokinetics. 1996. Baumann P. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Fluvoxamine and fluoxetine: interaction studies with amitriptyline, clomipramine and neuroleptics in phenotyped patients. Pharmacological research : the official journal of the Italian Pharmacological Society. 1995. Vandel S, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Steady-state kinetics of fluoxetine and amitriptyline in patients treated with a combination of these drugs as compared with those treated with amitriptyline alone. Journal of clinical pharmacology. 1995. el-Yazigi A, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Cytochrome P450 monooxygenases and interactions of psychotropic drugs: a five-year update. International journal of psychiatry in medicine. 1995. Shen W W. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available VIP No VIP available
P-glycoprotein structure and evolutionary homologies. Cytotechnology. 1993. Croop J M. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Effect of fluoxetine on plasma desipramine and 2-hydroxydesipramine. Biological psychiatry. 1992. Suckow R F, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Fluoxetine and norfluoxetine are potent inhibitors of P450IID6--the source of the sparteine/debrisoquine oxidation polymorphism. British journal of clinical pharmacology. 1991. Brøsen K, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Elevated antidepressant plasma levels after addition of fluoxetine. The American journal of psychiatry. 1989. Aranow A B, et al. PubMed

LinkOuts

Web Resource:
Wikipedia
National Drug Code Directory:
63304-632-30
DrugBank:
DB00472
ChEBI:
5118
KEGG Drug:
D00823
PubChem Compound:
3386
PubChem Substance:
181999
46507902
IUPHAR Ligand:
203
Drugs Product Database (DPD):
2242124
BindingDB:
30130
ChemSpider:
3269
Therapeutic Targets Database:
DAP000186
FDA Drug Label at DailyMed:
bfd18a45-06cc-4281-b181-40eb5d192a9b

Clinical Trials

These are trials that mention fluoxetine and are related to either pharmacogenetics or pharmacogenomics.

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Sources for PharmGKB drug information: DrugBank, Open Eye Scientific Software.