Drug/Small Molecule:
imipramine

Available Guidelines

  1. CPIC Dosing Guideline for imipramine and CYP2C19, CYP2D6
  2. Dutch Pharmacogenetics Working Group Guideline for imipramine and CYP2C19
  3. Dutch Pharmacogenetics Working Group Guideline for imipramine and CYP2D6

last updated 01/16/2013

CPIC Dosing Guideline for imipramine and CYP2C19, CYP2D6

Summary

Tricyclic antidepressants have comparable pharmacokinetic properties, it may be reasonable to apply the CPIC Dosing Guideline for amitriptyline and CYP2C19, CYP2D6 to other tricyclics including imipramine. In the guideline for amitriptyline, an alternative drug is recommended for CYP2D6 or CYP2C19 ultrarapid metabolizers and for CYP2D6 poor metabolizers. Consider a 50% dose reduction for CYP2C19 poor metabolizers and a 25% dose reduction for CYP2D6 intermediate metabolizers.

There's more of this guideline. Read more.


last updated 08/10/2011

Dutch Pharmacogenetics Working Group Guideline for imipramine and CYP2C19

Summary

The Dutch Pharmacogenetics Working Group Guideline for imipramine recommends to reduce the dose by 30% in CYP2C19 poor metabolizers, and monitor the plasma concentration of imipramine and desipramine or select alternative drug. For CYP2C19 intermediate metabolizers, select an alternative drug.

There's more of this guideline. Read more.


last updated 08/10/2011

Dutch Pharmacogenetics Working Group Guideline for imipramine and CYP2D6

Summary

The Dutch Pharmacogenetics Working Group Guideline for imipramine recommends to reduce the dose for CYP2D6 poor and intermediate metabolizer patients, and monitor imipramine and desipramine plasma concentrations. Select an alternative drug for CYP2D6 ultrarapid metabolizers.

There's more of this guideline. Read more.


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 imipramine and CYP2D6

This label is on the FDA Biomarker List
Actionable PGx

Summary

Poor metabolizers have higher than expected plasma concentrations of TCAs when given usual doses. Concomitant use of TCAs with drugs that can inhibit cytochrome P450 2D6 may require lower doses than usually prescribed for either the tricyclic antidepressant or the other drug; monitor TCA plasma levels.

Annotation

PGx information can be found in the Drug Interactions label sections.

Excerpts from the imipramine label:

The biochemical activity of the drug metabolizing isozyme cytochrome P450 2D6 (debrisoquin hydroxylase) is reduced in a subset of the Caucasian population (about 7% to 10% of Caucasians are so-called "poor metabolizers"); reliable estimates of the prevalence of reduced P450 2D6 isozyme activity among Asian, African, and other populations are not yet available. Poor metabolizers have higher than expected plasma concentrations of tricyclic antidepressants (TCAs) when given usual doses. Depending on the fraction of drug metabolized by P450 2D6, the increase in plasma concentration may be small, or quite large (8-fold increase in plasma AUC of the TCA).

Concomitant use of tricyclic antidepressants with drugs that can inhibit cytochrome P450 2D6 may require lower doses than usually prescribed for either the tricyclic antidepressant or the other drug.

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

  • Depression
    • Indications & usage section, Warnings section, Adverse reactions section, Precautions section
    • source: PHONT
  • CYP2D6
    • Drug interactions section, Precautions section, dosage, metabolism/PK
    • source: FDA Label

Clinical Variants that meet the highest level of criteria, manually curated by PharmGKB, are shown below.

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.

? = Mouse-over for quick help

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 , Variant in CYP2C19 , CYP2D6*1XN , CYP2D6*2XN , CYP2D6*4XN , CYP2D6*10XN , CYP2D6*17XN , CYP2D6*35XN , CYP2D6*41XN , *35 , *36
DMET Plus (Affymetrix, Inc) Variant in CYP2C19 , Variant in CYP2D6
VeraCode ADME Core Panel (Illumina, Inc) Variant in CYP2C19 , Variant in CYP2D6
TaqMan Drug Metabolism Genotyping Assay Sets (Applied Biosystems, Inc) Variant in CYP2C19 , Variant in CYP2D6
Laboratory Corporation of America Variant in CYP2C19 , Variant in CYP2D6
Quest Diagnostics, Inc Variant in CYP2D6
iPLEX ADME PGx (Sequenom, Inc) CYP2C19*1, CYP2C19*12, CYP2C19*17, CYP2C19*2, CYP2C19*3, CYP2C19*4, CYP2C19*5A, CYP2C19*5B, CYP2C19*6, CYP2C19*7, CYP2C19*8
AmpliChip CYP450 Test (Roche Molecular Systems, Inc) CYP2C19*2, CYP2C19*3
eSensor 2C19 Genotyping Test (GenMark Diagnostics, Inc) CYP2C19*10, CYP2C19*13, CYP2C19*17, CYP2C19*2, CYP2C19*3, CYP2C19*4, CYP2C19*5, CYP2C19*6, CYP2C19*7, CYP2C19*8, CYP2C19*9
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
Spartan RX CYP2C19 System CYP2C19*17, CYP2C19*2, CYP2C19*3 , rs12248560 , rs4986893 , rs4244285
INFINITI CYP2C19 (AutoGenomics, Inc) CYP2C19*17, CYP2C19*2, CYP2C19*3 , rs12248560 , rs4986893 , rs4244285
INFINITI CYP450 2C19+ (AutoGenomics, Inc) CYP2C19*10, CYP2C19*17, CYP2C19*2, CYP2C19*3, CYP2C19*4, CYP2C19*5, CYP2C19*6, CYP2C19*7, CYP2C19*8, CYP2C19*9 , rs12248560 , rs28399504 , rs41291556 , rs72552267 , rs17884712 , rs4986893 , rs6413438 , rs4244285 , rs72558186 , rs56337013
Cytochrome P450 2D6 (CYP2D6) CYP2D6*2, CYP2D6*5, CYP2D6*8 , rs28371725 , rs5030867 , rs5030656 , rs35742686 , rs3892097 , rs5030865 , rs5030655 , rs61736512 , rs28371706 , rs5030862 , rs1065852
GenoChip CYP2D6 (PharmGenomics, GmbH) CYP2D6*5 , rs59421388 , rs28371725 , rs5030867 , rs5030656 , rs35742686 , rs3892097 , rs5030865 , rs5030655 , rs28371706 , rs5030863 , rs1065852 , *xN (gene duplication)
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 CA VA CYP2C19 *1 N/A N/A N/A
No VIP available CA VA CYP2C19 *2 N/A N/A N/A
VIP No VIP available No VIP available CYP2C19 *2A N/A N/A N/A
No VIP available CA VA CYP2C19 *3 N/A N/A N/A
VIP No VIP available No VIP available CYP2C19 *3A N/A N/A N/A
No VIP available CA VA CYP2C19 *17 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 CA No VIP available 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 No VIP available 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 No VIP available CYP2D6 *10 N/A N/A N/A
VIP No VIP available No VIP available 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 No VIP available CYP2D6 *41 N/A N/A N/A
No VIP available No Clinical Annotations available VA
CYP2C19 poor metabolizers 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
CYP2D6 poor metabolizers N/A N/A N/A
No VIP available No Clinical Annotations available Variant in CYP2D6
Variant in CYP2D6 N/A N/A N/A
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 CA VA
rs11188072 -3402, 1599C>T, 47323525C>T, 96519061C>T, CYP2C19:, CYP2C19: -3402C>T, part of CYP2C19*17
C > T
Not Available
No VIP available CA VA
rs12248560 -806C>A, -806C>T, 4195C>A, 4195C>T, 47326121C>A, 47326121C>T, 96521657C>A, 96521657C>T, CYP2C19*17, CYP2C19*17 CYP2C19: -806C>T, CYP2C19: -806C>T
C > T
C > A
5' Flanking
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
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
rs35742686 -1793delT, -1830delT, -1940delT, 23418678delT, 40+2664delT, 42128242delT, 50569delT, 50583delT, 598delA, 622delA, 6750delA, 775delA, Arg200Glyfs, Arg208Glyfs, Arg259Glyfs
T > -
Not Available
Arg208Gly
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
rs4244285 24154G>A, 24154G>C, 47346080G>A, 47346080G>C, 681G>A, 681G>C, 96541616G>A, 96541616G>C, CYP2C19*2, CYP2C19:681G>A, CYP2C19:G681A, Pro227=
G > C
G > A
Synonymous
Pro227Pro
rs4986893 22948G>A, 47344874G>A, 636G>A, 96540410G>A, CYP2C19*3, CYP2C19:636G>A, CYP2C19:G636A, Trp212Ter
G > A
Stop Codon
Trp212null
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
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
Alleles, Functions, and Amino Acid Translations are all sourced from dbSNP 138
2D structure from PubChem
provided by PubChem

Overview

Generic Names
Trade Names
  • Antideprin
  • Berkomine
  • Censtim
  • Censtin
  • DPID
  • Declomipramine
  • Dimipressin
  • Dyna-Zina
  • Dynaprin
  • Estraldine
  • Eupramin
  • IM
  • Imavate
  • Imidobenzyle
  • Imipramina
  • Imipramine Hcl
  • Imiprin
  • Imizin
  • Imizine
  • Imizinum
  • Impramine
  • Intalpram
  • Iramil
  • Irmin
  • Janimine
  • Melipramin
  • Melipramine
  • Nelipramin
  • Norfranil
  • Pramine
  • Prazepine
  • Presamine
  • Promiben
  • Psychoforin
  • Sk-Pramine
  • Surplix
  • Timolet
  • Tipramine
  • Tofranil, Base
  • Tofranil-PM (imipramine pamoate)
  • Tofranil-Pm
  • Tofraniln A
  • Trimipramine Maleate
Brand Mixture Names

PharmGKB Accession Id:
PA449969

Description

Imipramine, the prototypical tricyclic antidepressant (TCA), is a dibenzazepine-derivative TCA. TCAs are structurally similar to phenothiazines. They contain a tricyclic ring system with an alkyl amine substituent on the central ring. In non-depressed individuals, imipramine does not affect mood or arousal, but may cause sedation. In depressed individuals, imipramine exerts a positive effect on mood. TCAs are potent inhibitors of serotonin and norepinephrine reuptake. Tertiary amine TCAs, such as imipramine and amitriptyline, are more potent inhibitors of serotonin reuptake than secondary amine TCAs, such as nortriptyline and desipramine. TCAs also down-regulate cerebral cortical beta-adrenergic receptors and sensitize post-synaptic serotonergic receptors with chronic use. The antidepressant effects of TCAs are thought to be due to an overall increase in serotonergic neurotransmission. TCAs also block histamine H 1 receptors, alpha 1-adrenergic receptors and muscarinic receptors, which accounts for their sedative, hypotensive and anticholinergic effects (e.g. blurred vision, dry mouth, constipation, urinary retention), respectively. Imipramine has less sedative and anticholinergic effects than the tertiary amine TCAs, amitriptyline and clomipramine. See toxicity section below for a complete listing of side effects. Imipramine may be used to treat depression and nocturnal enuresis in children. Unlabeled indications include chronic and neuropathic pain (including diabetic neuropathy), panic disorder, attention-deficit/hyperactivity disorder (ADHD), and post-traumatic stress disorder (PTSD).

Source: Drug Bank

Indication

For the relief of symptoms of depression and as temporary adjunctive therapy in reducing enuresis in children aged 6 years and older. May also be used to manage panic disorders, with or without agoraphobia, as a second line agent in ADHD, management of eating disorders, for short-term management of acute depressive episodes in bipolar disorder and schizophrenia, and for symptomatic treatment of postherpetic neuralgia.

Source: Drug Bank

Other Vocabularies

Information pulled from DrugBank has not been reviewed by PharmGKB.

Pharmacology, Interactions, and Contraindications

Mechanism of Action

Imipramine works by inhibiting the neuronal reuptake of the neurotransmitters norepinephrine and serotonin. It binds the sodium-dependent serotonin transporter and sodium-dependent norepinephrine transporter preventing or reducing the reuptake of norepinephrine and serotonin by nerve cells. Depression has been linked to a lack of stimulation of the post-synaptic neuron by norepinephrine and serotonin. Slowing the reuptake of these neurotransmitters increases their concentration in the synaptic cleft, which is thought to contribute to relieving symptoms of depression. In addition to acutely inhibiting neurotransmitter re-uptake, imipramine causes down-regulation of cerebral cortical beta-adrenergic receptors and sensitization of post-synaptic serotonergic receptors with chronic use. This leads to enhanced serotonergic transmission.

Source: Drug Bank

Pharmacology

Imipramine is a tricyclic antidepressant with general pharmacological properties similar to those of structurally related tricyclic antidepressant drugs such as amitriptyline and doxepin. A tertiary amine, imipramine inhibits the reuptake of serotonin more so than most secondary amine tricyclics, meaning that it blocks the reuptake of neurotransmitters serotonin and noradrenaline almost equally. With chronic use, imipramine also down-regulates cerebral cortical beta-adrenergic receptors and sensitizes post-synaptic sertonergic receptors, which also contributes to increased serotonergic transmission. It takes approximately 2 - 4 weeks for antidepressants effects to occur. The onset of action may be longer, up to 8 weeks, in some individuals. It is also effective in migraine prophylaxis, but not in abortion of acute migraine attack.

Source: Drug Bank

Food Interaction

Avoid St.John's Wort.|Avoid alcohol.|Avoid excessive quantities of coffee or tea (caffeine).|Do not take fibers at the same time.|Take with food.

Source: Drug Bank

Absorption, Distribution, Metabolism, Elimination & Toxicity

Biotransformation

Exclusively metabolized by the liver. Imipramine is converted in the liver by various CYP isoenzymes (e.g. CYP1A2, CYP2D6, CYP3A4, CYP2C9) to active metabolites desipramine and 2-hydroxydesipramine.

Source: Drug Bank

Protein Binding

60-95%

Source: Drug Bank

Absorption

Rapidly and well absorbed after oral administration. Bioavailability is approximately 43%. Peak plasma concentrations usually attained 1 - 2 hours following oral administration. Absorption is unaffected by food.

Source: Drug Bank

Half-Life

Imipramine - 8-20 hours; Desipramine (active metabolite) - up to 125 hours

Source: Drug Bank

Toxicity

Oral, rat LD 50: 355 to 682 mg/kg. Toxic signs proceed progressively from depression, irregular respiration and ataxia to convulsions and death. Antagonism of the histamine H 1 and alpha 1 receptors can lead to sedation and hypotension. Antimuscarinic and anticholinergic side effects such as blurred vision, dry mouth, constipation and urine retention may occur. Cardiotoxicity may occur with high doses of imipramine. Cardiovascular side effects in postural hypotension, tachycardia, hypertension, ECG changes and congestive heart failure. Psychotoxic effects include impaired memory and delirium. Induction of hypomanic or manic episodes may occur in patients with a history of bipolar disorder. Withdrawal symptoms include GI disturbances (e.g. nausea, vomiting, abdominal pain, diarrhea), anxiety, insomnia, nervousness, headache and malaise.

Source: Drug Bank

Route of Elimination

Approximately 40% of an orally administered dose is eliminated in urine within 24 hours, 70% in 72 hours. Small amounts are eliminated in feces via the biliary elimination.

Source: Drug Bank

Chemical Properties

Chemical Formula

C19H24N2

Source: Drug Bank

Isomeric SMILES

CN(C)CCCN1c2ccccc2CCc3c1cccc3

Source: OpenEye

Canonical SMILES

CN(C)CCCN1C2=CC=CC=C2CCC2=CC=CC=C12

Source: Drug Bank

Average Molecular Weight

280.4073

Source: Drug Bank

Monoisotopic Molecular Weight

280.193948778

Source: Drug Bank

PharmGKB Curated Pathways

Pathways created internally by PharmGKB based primarily on literature evidence.

  1. Imipramine/Desipramine Pathway, Pharmacokinetics
    Representation of the candidate genes involved in the metabolism of the tricyclic antidepressants imipramine and desipramine.

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
ADORA1 (source: Drug Bank)
ADRA1A (source: Drug Bank)
ADRA1D (source: Drug Bank)
CHRM1 (source: Drug Bank)
CHRM2 (source: Drug Bank)
CHRM3 (source: Drug Bank)
CHRM4 (source: Drug Bank)
CHRM5 (source: Drug Bank)
HRH1 (source: Drug Bank)
HTR2A (source: Drug Bank)
KCND2 (source: Drug Bank)
KCND3 (source: Drug Bank)
SLC6A2 (source: Drug Bank)
SLC6A4 (source: Drug Bank)

Drug Interactions

Drug Description
imipramine Increases the effect and toxicity of tricyclics (source: Drug Bank)
imipramine Atazanavir may increase the effect and toxicity of the tricyclic antidepressant, imipramine, by decreasing its metabolism. Monitor for changes in the therapeutic and adverse effects of imipramine if atazanavir if initiated, discontinued or dose changed. (source: Drug Bank)
imipramine The tricyclic increases the effect of carbamazepine (source: Drug Bank)
imipramine Carbamazepine may decrease the serum concentration of the tricyclic antidepressant, imipramine, by increasing its metabolism. Monitor for changes in the therapeutic and adverse effects of imipramine if carbamazepine is initiated, discontinued or dose changed. (source: Drug Bank)
imipramine Increases the effect of tricyclic agent (source: Drug Bank)
imipramine Cimetidine may increase the effect of tricyclic antidepressant, imipramine, by decreasing its metabolism. Monitor for changes in the therapeutic and adverse effects of imipramine if cimetidine is initiated, discontinued or dose changed. (source: Drug Bank)
imipramine Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank)
imipramine Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank)
imipramine The tricyclic decreases the effect of clonidine (source: Drug Bank)
imipramine The tricyclic antidepressant, imipramine, decreases the effect of clonidine. (source: Drug Bank)
imipramine Possible antagonism of action (source: Drug Bank)
imipramine Possible antagonism of action (source: Drug Bank)
imipramine Possible increase in the levels of this agent when used with duloxetine (source: Drug Bank)
imipramine Possible increase in the levels of this agent when used with duloxetine (source: Drug Bank)
imipramine The tricyclic increases the sympathomimetic effect (source: Drug Bank)
imipramine The tricyclic antidepressant, imipramine, increases the sympathomimetic effect of epinephrine. (source: Drug Bank)
imipramine The tricyclic increases the sympathomimetic effect (source: Drug Bank)
imipramine The tricyclic antidepressant, imipramine, increases the sympathomimetic effect of fenoterol. (source: Drug Bank)
imipramine The imidazole increases the effect and toxicity of the tricyclic (source: Drug Bank)
imipramine Fluconazole may increase the effect and toxicity of the tricyclic antidepressant, imipramine, by decreasing its metabolism. Additive QTc-prolonging effects may also occur. Monitor for changes in the therapeutic and adverse effects of imipramine if fluconazole is initiated, discontinued or dose changed. Monitor for the development of torsades de pointes during concomitant therapy. (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)
imipramine Fluvoxamine increases the effect and toxicity of tricyclics (source: Drug Bank)
imipramine The SSRI, fluvoxamine, 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 fluvoxamine is initiated, discontinued or dose changed. (source: Drug Bank)
imipramine Possible antagonism of action (source: Drug Bank)
imipramine Possible antagonism of action (source: Drug Bank)
imipramine Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank)
imipramine Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank)
imipramine The tricyclic decreases the effect of guanethidine (source: Drug Bank)
imipramine The tricyclic antidepressant, imipramine, decreases the effect of guanethidine. (source: Drug Bank)
altretamine Risk of severe hypotension (source: Drug Bank)
altretamine Risk of severe hypotension (source: Drug Bank)
atazanavir Atazanavir increases the effect and toxicity of tricyclics (source: Drug Bank)
atazanavir Atazanavir may increase the effect and toxicity of the tricyclic antidepressant, imipramine, by decreasing its metabolism. Monitor for changes in the therapeutic and adverse effects of imipramine if atazanavir if initiated, discontinued or dose changed. (source: Drug Bank)
carbamazepine The tricyclic increases the effect of carbamazepine (source: Drug Bank)
carbamazepine Carbamazepine may decrease the serum concentration of the tricyclic antidepressant, imipramine, by increasing its metabolism. Monitor for changes in the therapeutic and adverse effects of imipramine if carbamazepine is initiated, discontinued or dose changed. (source: Drug Bank)
cimetidine Cimetidine increases the effect of tricyclic agent (source: Drug Bank)
cimetidine Cimetidine may increase the effect of the tricyclic antidepressant, imipramine, by decreasing its metabolism. Monitor for changes in the therapeutic and adverse effects of imipramine if cimetidine is initiated, discontinued or dose changed. (source: Drug Bank)
cisapride Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank)
cisapride Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank)
clonidine The tricyclic decreases the effect of clonidine (source: Drug Bank)
clonidine The tricyclic antidepressant, imipramine, decreases the effect of clonidine. (source: Drug Bank)
dobutamine The tricyclic increases the sympathomimetic effect (source: Drug Bank)
dobutamine The tricyclic antidepressant, imipramine, increases the sympathomimetic effect of dobutamine. (source: Drug Bank)
donepezil Possible antagonism of action (source: Drug Bank)
donepezil Possible antagonism of action (source: Drug Bank)
dopamine The tricyclic increases the sympathomimetic effect (source: Drug Bank)
dopamine The tricyclic antidepressant, imipramine, increases the sympathomimetic effect of dopamine. (source: Drug Bank)
duloxetine Possible increase in the levels of this agent when used with duloxetine (source: Drug Bank)
duloxetine Possible increase in the levels of this agent when used with duloxetine (source: Drug Bank)
ephedra The tricyclic increases the sympathomimetic effect (source: Drug Bank)
ephedra The tricyclic antidepressant, imipramine, increases the sympathomimetic effect of ephedra. (source: Drug Bank)
ephedrine The tricyclic increases the sympathomimetic effect (source: Drug Bank)
ephedrine The tricyclic antidepressant, imipramine, increases the sympathomimetic effect of ephedrine. (source: Drug Bank)
epinephrine The tricyclic increases the sympathomimetic effect (source: Drug Bank)
epinephrine The tricyclic antidepressant, imipramine, increases the sympathomimetic effect of epinephrine. (source: Drug Bank)
fenoterol The tricyclic increases the sympathomimetic effect (source: Drug Bank)
fenoterol The tricyclic antidepressant, imipramine, increases the sympathomimetic effect of fenoterol. (source: Drug Bank)
fluconazole The imidazole increases the effect and toxicity of the tricyclic (source: Drug Bank)
fluconazole Fluconazole may increase the effect and toxicity of the tricyclic antidepressant, imipramine, by decreasing its metabolism. Additive QTc-prolonging effects may also occur. Monitor for changes in the therapeutic and adverse effects of imipramine if fluconazole is initiated, discontinued or dose changed. Monitor for the development of torsades de pointes during concomitant therapy. (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)
fluvoxamine Fluvoxamine increases the effect and toxicity of tricyclics (source: Drug Bank)
fluvoxamine The SSRI, fluvoxamine, 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 fluvoxamine is initiated, discontinued or dose changed. (source: Drug Bank)
galantamine Possible antagonism of action (source: Drug Bank)
galantamine Possible antagonism of action (source: Drug Bank)
grepafloxacin Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank)
grepafloxacin Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank)
guanethidine The tricyclic decreases the effect of guanethidine (source: Drug Bank)
guanethidine The tricyclic antidepressant, imipramine, increases the sympathomimetic effect of guanethidine. (source: Drug Bank)
isocarboxazid Possibility of severe adverse effects (source: Drug Bank)
isocarboxazid Possibility of severe adverse effects (source: Drug Bank)
isoproterenol The tricyclic increases the sympathomimetic effect (source: Drug Bank)
isoproterenol The tricyclic antidepressant, imipramine, increases the sympathomimetic effect of isoproterenol. (source: Drug Bank)
ketoconazole The imidazole increases the effect and toxicity of the tricyclic (source: Drug Bank)
ketoconazole Ketoconazole, a moderate CYP2D6 inhibitor, may increase the serum concentration of imipramine by increasing its metabolism. Monitor for changes in the therapeutic and adverse effects of imipramine if ketoconazole is initiated, discontinued or dose changed. (source: Drug Bank)
mephentermine The tricyclic increases the sympathomimetic effect (source: Drug Bank)
mephentermine The tricyclic antidepressant, imipramine, increases the sympathomimetic effect of mephentermine. (source: Drug Bank)
mesoridazine Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank)
mesoridazine Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank)
metaraminol The tricyclic increases the sympathomimetic effect (source: Drug Bank)
metaraminol The tricyclic antidepressant, imipramine, increases the sympathomimetic effect of metaraminol. (source: Drug Bank)
methoxamine The tricyclic increases the sympathomimetic effect (source: Drug Bank)
methoxamine The tricyclic antidepressant, imipramine, increases the sympathomimetic effect of methoxamine. (source: Drug Bank)
moclobemide Possible severe adverse reaction with this combination (source: Drug Bank)
moclobemide Possible severe adverse reaction with this combination (source: Drug Bank)
norepinephrine The tricyclic increases the sympathomimetic effect (source: Drug Bank)
norepinephrine The tricyclic antidepressant, imipramine, increases the sympathomimetic effect of norepinephrine. (source: Drug Bank)
orciprenaline The tricyclic increases the sympathomimetic effect (source: Drug Bank)
orciprenaline The tricyclic antidepressant, imipramine, increases the sympathomimetic effect of orciprenaline. (source: Drug Bank)
phenelzine Possibility of severe adverse effects (source: Drug Bank)
phenelzine Possibility of severe adverse effects (source: Drug Bank)
phenylephrine The tricyclic increases the sympathomimetic effect (source: Drug Bank)
phenylephrine The tricyclic antidepressant, imipramine, increases the sympathomimetic effect of phenylephrine. (source: Drug Bank)
phenylpropanolamine The tricyclic increases the sympathomimetic effect (source: Drug Bank)
phenylpropanolamine The tricyclic antidepressant, imipramine, increases the sympathomimetic effect of phenylpropanolamine. (source: Drug Bank)
pirbuterol The tricyclic increases the sympathomimetic effect (source: Drug Bank)
pirbuterol The tricyclic antidepressant, imipramine, increases the sympathomimetic effect of pirbuterol. (source: Drug Bank)
procaterol The tricyclic increases the sympathomimetic effect (source: Drug Bank)
procaterol The tricyclic antidepressant, imipramine, increases the sympathomimetic effect of procaterol. (source: Drug Bank)
pseudoephedrine The tricyclic increases the sympathomimetic effect (source: Drug Bank)
pseudoephedrine The tricyclic antidepressant, imipramine, increases the sympathomimetic effect of pseudoephedrine. (source: Drug Bank)
quinidine Quinidine increases the effect of tricyclic agent (source: Drug Bank)
quinidine Quinidine increases the effect of tricyclic agent (source: Drug Bank)
quinidine Quinidine barbiturate increases the effect of tricyclic antidepressant, imipramine. (source: Drug Bank)
rasagiline Possibility of severe adverse effects (source: Drug Bank)
rasagiline Possibility of severe adverse effects (source: Drug Bank)
rifabutin The rifamycin decreases the effect of tricyclics (source: Drug Bank)
rifabutin The rifamycin, rifabutin, may decrease the effect of the tricyclic antidepressant, imipramine, by increasing its metabolism. Monitor for changes in the therapeutic and adverse effects of imipramine if rifabutin is initiated, discontinued or dose changed. (source: Drug Bank)
rifampin The rifamycin decreases the effect of tricyclics (source: Drug Bank)
rifampin The rifamycin, rifampin, may decrease the effect of the tricyclic antidepressant, imipramine, by increasing its metabolism. Monitor for changes in the therapeutic and adverse effects of imipramine if rifampin is initiated, discontinued or dose changed. (source: Drug Bank)
ritonavir Ritonavir increases the effect and toxicity of tricyclics (source: Drug Bank)
ritonavir Ritonavir may increase the effect and toxicity of the tricyclic antidepressant, imipramine, by decreasing its metabolism. Monitor for changes in the therapeutic and adverse effects of imipramine if ritonavir if initiated, discontinued or dose changed. (source: Drug Bank)
rivastigmine Possible antagonism of action (source: Drug Bank)
rivastigmine Possible antagonism of action (source: Drug Bank)
salbutamol The tricyclic increases the sympathomimetic effect (source: Drug Bank)
salbutamol The tricyclic antidepressant, imipramine, increases the sympathomimetic effect of salbutamol. (source: Drug Bank)
sibutramine Increased risk of CNS adverse effects (source: Drug Bank)
sibutramine Increased risk of CNS adverse effects (source: Drug Bank)
sparfloxacin Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank)
sparfloxacin Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank)
terbinafine Terbinafine increases the effect and toxicity of the tricyclic (source: Drug Bank)
terbinafine Terbinafine increases the effect and toxicity of the tricyclic antidepressant, imipramine, by decreasing its metabolism. Monitor for changes in the therapeutic and adverse effects of imipramine if terbinafine is initiated, discontinued or dose changed. (source: Drug Bank)
terbutaline The tricyclic increases the sympathomimetic effect (source: Drug Bank)
terbutaline The tricyclic antidepressant, imipramine, increases the sympathomimetic effect of terbutaline. (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)
tranylcypromine Possibility of severe adverse effects (source: Drug Bank)
tranylcypromine Possibility of severe adverse effects (source: Drug Bank)
imipramine Possibility of severe adverse effects (source: Drug Bank)
imipramine Possibility of severe adverse effects (source: Drug Bank)
imipramine The imidazole increases the effect and toxicity of the tricyclic (source: Drug Bank)
imipramine Ketoconazole, a moderate CYP2D6 inhibitor, may increase the serum concentration of imipramine by increasing its metabolism. Monitor for changes in the therapeutic and adverse effects of imipramine if ketoconazole is initiated, discontinued or dose changed. (source: Drug Bank)
imipramine Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank)
imipramine Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank)
imipramine Possible severe adverse reaction with this combination (source: Drug Bank)
imipramine Possible severe adverse reaction with this combination (source: Drug Bank)
imipramine The tricyclic increases the sympathomimetic effect (source: Drug Bank)
imipramine The tricyclic antidepressant, imipramine, increases the sympathomimetic effect of orciprenaline. (source: Drug Bank)
imipramine Possibility of severe adverse effects (source: Drug Bank)
imipramine Possibility of severe adverse effects (source: Drug Bank)
imipramine The tricyclic increases the sympathomimetic effect (source: Drug Bank)
imipramine The tricyclic antidepressant, imipramine, increases the sympathomimetic effect of phenylephrine. (source: Drug Bank)
imipramine The tricyclic antidepressant, imipramine, increases the sympathomimetic effect of phenylpropanolamine. (source: Drug Bank)
imipramine The tricyclic increases the sympathomimetic effect (source: Drug Bank)
imipramine The tricyclic antidepressant, imipramine, increases the sympathomimetic effect of pseudoephedrine. (source: Drug Bank)
imipramine Quinidine increases the effect of the tricyclic agent (source: Drug Bank)
imipramine Additive QTc-prolonging effects may occur. Quinidine may also increase the serum concentration of the tricyclic antidepressant, imipramine, by decreasing its metabolism. Monitor for changes in the therapeutic and adverse effects of imipramine if quinidine is initiated, discontinued or dose changed. Monitor for the development of torsades de pointes during concomitant therapy. (source: Drug Bank)
imipramine Possibility of severe adverse effects (source: Drug Bank)
imipramine The rifamycin decreases the effect of tricyclics (source: Drug Bank)
imipramine The rifamycin, rifabutin, may decrease the effect of the tricyclic antidepressant, imipramine, by increasing its metabolism. Monitor for changes in the therapeutic and adverse effects of imipramine if rifabutin is initiated, discontinued or dose changed. (source: Drug Bank)
imipramine The rifamycin decreases the effect of tricyclics (source: Drug Bank)
imipramine The rifamycin, rifampin, may decrease the effect of the tricyclic antidepressant, imipramine, by increasing its metabolism. Monitor for changes in the therapeutic and adverse effects of imipramine if rifampin is initiated, discontinued or dose changed. (source: Drug Bank)
imipramine The therapeutic effects of the central acetylcholinesterase inhibitor, Tacrine, and/or the anticholinergic, Imipramine, may be reduced due to antagonism. The interaction may be beneficial when the anticholinergic action is a side effect. Monitor for decreased efficacy of both agents. (source: Drug Bank)
imipramine The therapeutic effects of the central acetylcholinesterase inhibitor, Tacrine, and/or the anticholinergic, Imipramine, may be reduced due to antagonism. The interaction may be beneficial when the anticholinergic action is a side effect. Monitor for decreased efficacy of both agents. (source: Drug Bank)
imipramine Additive QTc-prolongation may occur increasing the risk of serious ventricular arrhythmias. Concomitant therapy should be used with caution. (source: Drug Bank)
imipramine Imipramine may decrease the therapeutic effect of Tamoxifen by decreasing the production of active metabolites. Consider alternate therapy. (source: Drug Bank)
imipramine Imipramine may decrease the therapeutic effect of Tamoxifen by decreasing the production of active metabolites. Consider alternate therapy. (source: Drug Bank)
imipramine Imipramine, a CYP2D6 inhibitor, may decrease the metabolism and clearance of Tamsulosin, a CYP2D6 substrate. Monitor for changes in therapeutic/adverse effects of Tamsulosin if Imipramine is initiated, discontinued, or dose changed. (source: Drug Bank)
imipramine Imipramine, a CYP2D6 inhibitor, may decrease the metabolism and clearance of Tamsulosin, a CYP2D6 substrate. Monitor for changes in therapeutic/adverse effects of Tamsulosin if Imipramine is initiated, discontinued, or dose changed. (source: Drug Bank)
imipramine Terbinafine increases the effect and toxicity of the tricyclic (source: Drug Bank)
imipramine Terbinafine may reduce the metabolism and clearance of Imipramine. Consider alternate therapy or monitor for therapeutic/adverse effects of Imipramine if Terbinafine is initiated, discontinued or dose changed. (source: Drug Bank)
imipramine The tricyclic increases the sympathomimetic effect (source: Drug Bank)
imipramine The tricyclic antidepressant, imipramine, increases the sympathomimetic effect of terbutaline. (source: Drug Bank)
imipramine Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank)
imipramine Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank)
imipramine Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank)
imipramine Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank)
imipramine 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)
imipramine 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)
imipramine Ticlopidine may decrease the metabolism and clearance of Imipramine. Consider alternate therapy or monitor for adverse/toxic effects of Imipramine if Ticlopidine is initiated, discontinued or dose changed. (source: Drug Bank)
imipramine 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)
imipramine Tramadol increases the risk of serotonin syndrome and seizures. Imipramine may decrease the effect of Tramadol by decreasing active metabolite production. (source: Drug Bank)
imipramine 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)
imipramine Increased risk of serotonin syndrome. The 2D6 inhibitor, Trazodone, may also increase the efficacy of Imipramine by decreasing Imipramine metabolism and clearance. Monitor for symptoms of serotonin syndrome and changes in Imipramine efficacy if Trazodone is initiated, discontinued or dose changed. (source: Drug Bank)
imipramine Increased risk of serotonin syndrome. Monitor for symptoms of serotonin syndrome. (source: Drug Bank)
imipramine Trimethobenzamide and Imipramine, two anticholinergics, may cause additive anticholinergic effects and enhance their adverse/toxic effects. Monitor for enhanced anticholinergic effects. (source: Drug Bank)
imipramine Increased risk of serotonin syndrome. Monitor for symptoms of serotonin syndrome. QTc-prolongation may also occur, increasing the risk of serious ventricular arrhythmias. Concomitant therapy should be used with caution. (source: Drug Bank)
imipramine Triprolidine and Imipramine, two anticholinergics, may cause additive anticholinergic effects and enhance their adverse/toxic effects. Additive CNS depressant effects may also occur. Monitor for enhanced anticholinergic and CNS depressant effects. (source: Drug Bank)
imipramine Triprolidine and Imipramine, two anticholinergics, may cause additive anticholinergic effects and enhance their adverse/toxic effects. Additive CNS depressant effects may also occur. Monitor for enhanced anticholinergic and CNS depressant effects. (source: Drug Bank)
imipramine Trospium and Imipramine, two anticholinergics, may cause additive anticholinergic effects and enhanced adverse/toxic effects. Monitor for enhanced anticholinergic effects. (source: Drug Bank)
imipramine Increased risk of serotonin syndrome. Monitor for symptoms of serotonin syndrome. (source: Drug Bank)
imipramine 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)
imipramine 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)
imipramine Additive QTc-prolonging effects may increase the risk of severe arrhythmias. Concomitant therapy is contraindicated. (source: Drug Bank)
imipramine Use of two serotonin modulators, such as zolmitriptan and imipramine, increases the risk of serotonin syndrome. Consider alternate therapy or monitor for serotonin syndrome during concomitant therapy. (source: Drug Bank)
imipramine 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). (source: Drug Bank)

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Publications related to imipramine: 75

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Genetic Factors Affecting Gene Transcription and Catalytic Activity of UDP-Glucuronosyltransferases in Human Liver. Human molecular genetics. 2014. Liu Wanqing, 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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Clinical Pharmacogenetics Implementation Consortium Guideline for CYP2D6 and CYP2C19 Genotypes and Dosing of Tricyclic Antidepressants. Clinical pharmacology and therapeutics. 2013. Hicks J K, 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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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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Prolonged toxicity after amitriptyline overdose in a patient deficient in CYP2D6 activity. Journal of medical toxicology : official journal of the American College of Medical Toxicology. 2011. Smith Jennifer Cohen, et al. PubMed
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Profiling of a prescription drug library for potential renal drug-drug interactions mediated by the organic cation transporter 2. Journal of medicinal chemistry. 2011. Kido Yasuto, et al. PubMed
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Pharmacogenetics: From Bench to Byte- An Update of Guidelines. Clinical pharmacology and therapeutics. 2011. Swen J J, et al. PubMed
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Pharmacogenetics and gender association with psychotic episodes on nortriptyline lower doses: patient cases. ISRN pharmaceutics. 2011. Piatkov Irina, 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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Association between CYP2C19*17 and metabolism of amitriptyline, citalopram and clomipramine in Dutch hospitalized patients. The pharmacogenomics journal. 2010. de Vos A, et al. PubMed
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The CYP2C19*17 genotype is associated with lower imipramine plasma concentrations in a large group of depressed patients. The pharmacogenomics journal. 2010. Schenk P W, et al. PubMed
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What is the role of lidocaine or phenytoin in tricyclic antidepressant-induced cardiotoxicity?. Clinical toxicology (Philadelphia, Pa.). 2010. Foianini Anthony, et al. PubMed
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Role of human UGT2B10 in N-glucuronidation of tricyclic antidepressants, amitriptyline, imipramine, clomipramine, and trimipramine. Drug metabolism and disposition: the biological fate of chemicals. 2010. Zhou Diansong, 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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Cytochrome P450 2D6. Pharmacogenetics and genomics. 2009. Owen Ryan P, et al. PubMed
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Deletion of the mouse Fmo1 gene results in enhanced pharmacological behavioural responses to imipramine. Pharmacogenetics and genomics. 2009. Hernandez Diana, et al. PubMed
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Polymorphisms in the SLC6A4 and HTR2A genes influence treatment outcome following antidepressant therapy. The pharmacogenomics journal. 2009. Wilkie M J V, et al. PubMed
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Life-threatening dextromethorphan intoxication associated with interaction with amitriptyline in a poor CYP2D6 metabolizer: a single case re-exposure study. Journal of pain and symptom management. 2008. Forget Patrice, et al. PubMed
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Association of graded allele-specific changes in CYP2D6 function with imipramine dose requirement in a large group of depressed patients. Molecular psychiatry. 2008. Schenk P W, 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 CYP2D6 polymorphism in relation to the metabolism of amitriptyline and nortriptyline in the Faroese population. British journal of clinical pharmacology. 2008. Halling Jónrit, et al. PubMed
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A fatal doxepin poisoning associated with a defective CYP2D6 genotype. The American journal of forensic medicine and pathology. 2007. Koski Anna, 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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A poor metabolizer for cytochromes P450 2D6 and 2C19: a case report on antidepressant treatment. CNS spectrums. 2006. Johnson Maria, et al. PubMed
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CYP2D6 and CYP2C19 genotypes and amitriptyline metabolite ratios in a series of medicolegal autopsies. Forensic science international. 2006. Koski Anna, et al. PubMed
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Adverse drug reactions following nonresponse in a depressed patient with CYP2D6 deficiency and low CYP 3A4/5 activity. Pharmacopsychiatry. 2006. Stephan P L, 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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Pharmacogenetics of tamoxifen biotransformation is associated with clinical outcomes of efficacy and hot flashes. Journal of clinical oncology : official journal of the American Society of Clinical Oncology. 2005. Goetz Matthew P, et al. PubMed
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Amitriptyline or not, that is the question: pharmacogenetic testing of CYP2D6 and CYP2C19 identifies patients with low or high risk for side effects in amitriptyline therapy. Clinical chemistry. 2005. Steimer Werner, et al. PubMed
No Dosing Guideline available No Drug Label available CA No Variant Annotation available No VIP available No VIP available
Allele-specific change of concentration and functional gene dose for the prediction of steady-state serum concentrations of amitriptyline and nortriptyline in CYP2C19 and CYP2D6 extensive and intermediate metabolizers. Clinical chemistry. 2004. Steimer Werner, et al. PubMed
No Dosing Guideline available No Drug Label available CA No Variant Annotation available No VIP available No VIP available
Clomipramine, fluoxetine and CYP2D6 metabolic capacity in depressed patients. Human psychopharmacology. 2004. Vandel P, et al. PubMed
No Dosing Guideline available No Drug Label available CA No Variant Annotation available No VIP available No VIP available
Impact of CYP2D6 intermediate metabolizer alleles on single-dose desipramine pharmacokinetics. Pharmacogenetics. 2004. Furman Katherine D, et al. PubMed
No Dosing Guideline available No Drug Label available CA VA No VIP available No VIP available
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
No Dosing Guideline available No Drug Label available CA No Variant Annotation available No VIP available No VIP available
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
No Dosing Guideline available No Drug Label available CA No Variant Annotation available No VIP available No VIP available
Trimipramine pharmacokinetics after intravenous and oral administration in carriers of CYP2D6 genotypes predicting poor, extensive and ultrahigh activity. Pharmacogenetics. 2003. Kirchheiner Julia, et al. PubMed
No Dosing Guideline available No Drug Label available CA No Variant Annotation available No VIP available No VIP available
Effects of polymorphisms in CYP2D6, CYP2C9, and CYP2C19 on trimipramine pharmacokinetics. Journal of clinical psychopharmacology. 2003. Kirchheiner Julia, 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
Inhibitory effects of tricyclic antidepressants (TCAs) on human cytochrome P450 enzymes in vitro: mechanism of drug interaction between TCAs and phenytoin. Drug metabolism and disposition: the biological fate of chemicals. 2002. Shin Jae-Gook, et al. PubMed
No Dosing Guideline available No Drug Label available CA No Variant Annotation available No VIP available No VIP available
Contributions of CYP2D6, CYP2C9 and CYP2C19 to the biotransformation of E- and Z-doxepin in healthy volunteers. Pharmacogenetics. 2002. Kirchheiner Julia, 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
Med-psych drug-drug interactions update. Psychosomatics. 2002. Armstrong Scott C, et al. PubMed
No Dosing Guideline available No Drug Label available CA No Variant Annotation available No VIP available No VIP available
CYP2D6 genotyping with oligonucleotide microarrays and nortriptyline concentrations in geriatric depression. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology. 2001. Murphy G 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
CYP2D6 and CYP2C19 genotype-based dose recommendations for antidepressants: a first step towards subpopulation-specific dosages. Acta psychiatrica Scandinavica. 2001. Kirchheiner J, 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
Pharmacogenomics: translating functional genomics into rational therapeutics. Science (New York, N.Y.). 1999. Evans W E, 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
Identification of a novel splice variant of heat shock cognate protein 70 after chronic antidepressant treatment in rat frontal cortex. Biochemical and biophysical research communications. 1999. Yamada M, et al. PubMed
No Dosing Guideline available No Drug Label available CA No Variant Annotation available No VIP available No VIP available
Clomipramine dose-effect study in patients with depression: clinical end points and pharmacokinetics. Danish University Antidepressant Group (DUAG). Clinical pharmacology and therapeutics. 1999. PubMed
No Dosing Guideline available No Drug Label available CA No Variant Annotation available No VIP available No VIP available
CYP2D6 phenotype-genotype relationships in African-Americans and Caucasians in Los Angeles. Pharmacogenetics. 1998. Leathart J B, et al. PubMed
No Dosing Guideline available No Drug Label available CA No Variant Annotation available No VIP available No VIP available
10-Hydroxylation of nortriptyline in white persons with 0, 1, 2, 3, and 13 functional CYP2D6 genes. Clinical pharmacology and therapeutics. 1998. Dalén P, 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
Inhibition of human hepatic cytochrome P4502E1 by azole antifungals, CNS-active drugs and non-steroidal anti-inflammatory agents. Xenobiotica; the fate of foreign compounds in biological systems. 1998. Tassaneeyakul W, 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
The genetic variant A of human alpha 1-acid glycoprotein limits the blood to brain transfer of drugs it binds. Life sciences. 1998. Jolliet-Riant P, et al. PubMed
No Dosing Guideline available No Drug Label available CA VA No VIP available No VIP available
Effects of genetic defects in the CYP2C19 gene on the N-demethylation of imipramine, and clinical outcome of imipramine therapy. Psychiatry and clinical neurosciences. 1997. Morinobu 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
Reappraisal of human CYP isoforms involved in imipramine N-demethylation and 2-hydroxylation: a study using microsomes obtained from putative extensive and poor metabolizers of S-mephenytoin and eleven recombinant human CYPs. The Journal of pharmacology and experimental therapeutics. 1997. Koyama E, 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
Imipramine demethylation in vivo: impact of CYP1A2, CYP2C19, and CYP3A4. Clinical pharmacology and therapeutics. 1997. Madsen 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
Imipramine metabolism in relation to the sparteine oxidation polymorphism--a family study. Pharmacogenetics. 1996. Madsen H, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available VA No VIP available No VIP available
Steady-state plasma concentrations of imipramine and desipramine in relation to S-mephenytoin 4'-hydroxylation status in Japanese depressive patients. Journal of clinical psychopharmacology. 1996. Koyama E, et al. PubMed
No Dosing Guideline available No Drug Label available CA No Variant Annotation available No VIP available No VIP available
Steady-state plasma levels of nortriptyline and its 10-hydroxy metabolite: relationship to the CYP2D6 genotype. Psychopharmacology. 1996. Dahl M L, et al. PubMed
No Dosing Guideline available No Drug Label available CA VA No VIP available No VIP available
Imipramine metabolism in relation to the sparteine and mephenytoin oxidation polymorphisms--a population study. British journal of clinical pharmacology. 1995. Madsen H, et al. PubMed
No Dosing Guideline available No Drug Label available CA VA No VIP available No VIP available
Metabolic disposition of imipramine in oriental subjects: relation to metoprolol alpha-hydroxylation and S-mephenytoin 4'-hydroxylation phenotypes. The Journal of pharmacology and experimental therapeutics. 1994. Koyama E, et al. PubMed
No Dosing Guideline available No Drug Label available CA No Variant Annotation available No VIP available No VIP available
Single-dose kinetics of clomipramine: relationship to the sparteine and S-mephenytoin oxidation polymorphisms. Clinical pharmacology and therapeutics. 1994. Nielsen K 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
The N-demethylation of imipramine correlates with the oxidation of S-mephenytoin (S/R-ratio). A population study. British journal of clinical pharmacology. 1993. Skjelbo E, et al. PubMed
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Debrisoquine hydroxylation phenotypes of patients with high versus low to normal serum antidepressant concentrations. Journal of clinical psychopharmacology. 1992. Tacke U, et al. PubMed
No Dosing Guideline available No Drug Label available CA No Variant Annotation available No VIP available No VIP available
Analysis of the CYP2D6 gene in relation to debrisoquin and desipramine hydroxylation in a Swedish population. Clinical pharmacology and therapeutics. 1992. Dahl M L, 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
Role of P450IID6, the target of the sparteine-debrisoquin oxidation polymorphism, in the metabolism of imipramine. Clinical pharmacology and therapeutics. 1991. Brøsen K, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available VA No VIP available No VIP available
The mephenytoin oxidation polymorphism is partially responsible for the N-demethylation of imipramine. Clinical pharmacology and therapeutics. 1991. Skjelbo E, et al. PubMed
No Dosing Guideline available No Drug Label available CA VA No VIP available No VIP available
Nonlinear kinetics of imipramine in low and medium plasma level ranges. Therapeutic drug monitoring. 1990. Sindrup 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
Elevated antidepressant plasma levels after addition of fluoxetine. The American journal of psychiatry. 1989. Aranow A B, et al. PubMed
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High blood concentrations of imipramine or clomipramine and therapeutic failure: a case report study using drug monitoring data. Therapeutic drug monitoring. 1989. Balant-Gorgia A E, et al. PubMed
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First-pass metabolism of imipramine and desipramine: impact of the sparteine oxidation phenotype. Clinical pharmacology and therapeutics. 1988. Brøsen K, et al. PubMed
No Dosing Guideline available No Drug Label available CA VA No VIP available No VIP available
Imipramine demethylation and hydroxylation: impact of the sparteine oxidation phenotype. Clinical pharmacology and therapeutics. 1986. Brøsen K, et al. PubMed
Steady-state concentrations of imipramine and its metabolites in relation to the sparteine/debrisoquine polymorphism. European journal of clinical pharmacology. 1986. 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
The clinical application of tricyclic antidepressant pharmacokinetics and plasma levels. The American journal of psychiatry. 1980. Amsterdam J, 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
Single-dose kinetics predict steady-state concentrations on imipramine and desipramine. Archives of general psychiatry. 1980. Potter W Z, et al. PubMed
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Plasma levels of monomethylated tricyclic antidepressants during treatment with imipramine-like compounds. Life sciences. 1967. Hammer W, et al. PubMed

LinkOuts

Web Resource:
Wikipedia
National Drug Code Directory:
53489-330-07
DrugBank:
DB00458
PDB:
IXX
ChEBI:
5881
KEGG Compound:
C07049
PubChem Compound:
3696
PubChem Substance:
46507351
9261
IUPHAR Ligand:
357
Drugs Product Database (DPD):
726397
ChemSpider:
3568
HET:
IXX
Therapeutic Targets Database:
DAP001154
FDA Drug Label at DailyMed:
a6fe8e00-a1ee-4dbb-bac7-46ac2af9aee9

Clinical Trials

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

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