Drug/Small Molecule:
desipramine

last updated 01/16/2013

CPIC Dosing Guideline for desipramine and CYP2D6

Summary

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

Annotation

Guidelines regarding the use of pharmacogenomic tests in dosing for tricyclic antidepressants have been published in Clinical Pharmacology and Therapeutics by the Clinical Pharmacogenetics Implementation Consortium (CPIC).

Download: article and supplement

Excerpt from the dosing guidelines:

Amitriptyline and nortriptyline are used as model drugs for this guideline because the majority of pharmacogenomic studies have focused on these two drugs. Because the tricyclics have comparable pharmacokinetic properties, it may be reasonable to apply this guideline to other tricyclics including desipramine (Supplementary Table S15), with the acknowledgement that there are fewer data supporting dose adjustments for these drugs than for amitriptyline or nortriptyline.

See nortriptyline for excerpts and a table that summarize CYP2D6-based dosing recommendations for nortriptyline when higher initial starting doses are warranted (article).


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 desipramine and CYP2D6

This label is on the FDA Biomarker List
Actionable PGx

Summary

The FDA-approved drug label for desipramine (NORPRAMIN) notes that CYP2D6 poor metabolizers have higher than expected plasma concentrations of tricyclic antidepressants (TCAs), such as desipramine, when given typical doses. Additionally, certain drugs inhibit the activity of this isozyme and make normal metabolizers resemble poor metabolizers. It is therefore desirable to monitor TCA plasma levels whenever a TCA is going to be co-administered with another drug known to be a CYP2D6 inhibitor.

Annotation

Desipramine (NORPRAMIN) is an antidepressant drug belonging to the tricyclic antidepressants class.The FDA-approved drug label for desipramine highlights information regarding CYP2D6 poor metabolizers, as well as information about usage of drugs that inhibit CYP2D6, one of the enzymes responsible for desipramine metabolism.

Excerpt from the desipramine (NORPRAMIN) label:

The biochemical activity of the drug metabolizing isozyme cytochrome P450 2D6...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). In addition, certain drugs inhibit the activity of this isozyme and make normal metabolizers resemble poor metabolizers...It is desirable to monitor TCA plasma levels whenever a TCA including is going to be co-administered with another drug known to be an inhibitor of P450 2D6.

For the complete drug label text with sections containing pharmacogenetic information highlighted, see the desipramine 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
  • Depressive Disorder
    • Indications & usage section, Warnings section, Adverse reactions section, Precautions section
    • source: PHONT
  • Depressive Disorder, Major
    • Indications & usage section, Warnings section, Adverse reactions section, Precautions section
    • source: PHONT
  • CYP2D6
    • Precautions section, 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.

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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 CYP2D6*1XN , CYP2D6 CYP2D6*2XN , CYP2D6 CYP2D6*4XN , CYP2D6 CYP2D6*10XN , CYP2D6 CYP2D6*17XN , CYP2D6 CYP2D6*35XN , CYP2D6 CYP2D6*41XN , CYP2D6 *35 , CYP2D6 *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 , CYP2D6 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 CYP2D6*XN , CYP2D6 *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 CYP2D6*XN , CYP2D6 *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
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 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 No VIP available VA CYP2D6 *6 N/A N/A N/A
VIP No VIP available VA CYP2D6 *9 N/A N/A N/A
VIP CA VA CYP2D6 *10 N/A N/A N/A
VIP CA 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 CA VA CYP2D6 *41 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 VA
CYP2D6 poor metabolizer 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
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
rs2228478 -2205A>G, 1547225A>G, 3192A>G, 7322A>G, 89986608A>G, 942A>G, Thr314=
A > G
5' Flanking
Thr314Thr
No VIP available CA VA
rs2228479 1546557G>A, 2524G>A, 274G>A, 6654G>A, 89985940G>A, Val92Met
G > A
Missense
Val92Met
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
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
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
Alleles, Functions, and Amino Acid Translations are all sourced from dbSNP 138
2D structure from PubChem
provided by PubChem

Overview

Generic Names
  • DMI
  • Demethylimipramine
  • Desimipramine
  • Desimpramine
  • Desipramin
  • Desipramine Hcl
  • Desmethylimipramine
  • Dezipramine
  • Dimethylimipramine
  • Methylaminopropyliminodibenzyl
  • Monodemethylimipramine
  • Norimipramine
  • Norpramine
Trade Names
  • Norpramin
  • Pentofran
  • Pertofran
  • Pertrofane
  • Sertofran
Brand Mixture Names

PharmGKB Accession Id:
PA449233

Description

Desipramine hydrochloride is a dibenzazepine-derivative tricyclic antidepressant (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, desipramine does not affect mood or arousal, but may cause sedation. In depressed individuals, desipramine exerts a positive effect on mood. TCAs are potent inhibitors of serotonin and norepinephrine reuptake. Secondary amine TCAs, such as desipramine and nortriptyline, are more potent inhibitors of norepinephrine reuptake than tertiary amine TCAs, such as amitriptyline and doxepine. 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. See toxicity section below for a complete listing of side effects. Desipramine exerts less anticholinergic and sedative side effects compared to tertiary amine TCAs, such as amitriptyline and clomipramine. Desipramine may be used to treat depression, neuropathic pain (unlabeled use), agitation and insomnia (unlabeled use) and attention-deficit hyperactivity disorder (unlabeled use).

Source: Drug Bank

Indication

For relief of symptoms in various depressive syndromes, especially endogenous depression. It has also been used to manage chronic peripheral neuropathic pain, as a second line agent for the management of anxiety disorders (e.g. panic disorder, generalized anxiety disorder), and as a second or third line agent in the ADHD management.

Source: Drug Bank

Other Vocabularies

Information pulled from DrugBank has not been reviewed by PharmGKB.

Pharmacology, Interactions, and Contraindications

Mechanism of Action

Desipramine is a tricyclic antidepressant (TCA) that selectively blocks reuptake of norepinephrine (noradrenaline) from the neuronal synapse. It also inhibits serotonin reuptake, but to a lesser extent compared to tertiary amine TCAs such as imipramine. Inhibition of neurotransmitter reuptake increases stimulation of the post-synaptic neuron. Chronic use of desipramine also leads to down-regulation of beta-adrenergic receptors in the cerebral cortex and sensitization of serotonergic receptors. An overall increase in serotonergic transmission likely confers desipramine its antidepressant effects. Desipramine also possesses minor anticholinergic activity, through its affinity for muscarinic receptors. TCAs are believed to act by restoring normal levels of neurotransmitters via synaptic reuptake inhibition and by increasing serotonergic neurotransmission via serotonergic receptor sensitization in the central nervous system.

Source: Drug Bank

Pharmacology

Desipramine, a secondary amine tricyclic antidepressant, is structurally related to both the skeletal muscle relaxant cyclobenzaprine and the thioxanthene antipsychotics such as thiothixene. It is the active metabolite of imipramine, a tertiary amine TCA. The acute effects of desipramine include inhibition of noradrenaline re-uptake at noradrenergic nerve endings and inhibition of serotonin (5-hydroxy tryptamine, 5HT) re-uptake at the serotoninergic nerve endings in the central nervous system. Desipramine exhibits greater noradrenergic re-uptake inhibition compared to the tertiary amine TCA imipramine. In addition to inhibiting neurotransmitter re-uptake, desipramine down-regulates beta-adrenergic receptors in the cerebral cortex and sensitizes serotonergic receptors with chronic use. The overall effect is increased serotonergic transmission. Antidepressant effects are typically observed 2 - 4 weeks following the onset of therapy though some patients may require up to 8 weeks of therapy prior to symptom improvement. Patients experiencing more severe depressive episodes may respond quicker than those with mild depressive symptoms.

Source: Drug Bank

Food Interaction

Avoid alcohol.|Take with food to reduce irritation, limit caffeine intake.

Source: Drug Bank

Absorption, Distribution, Metabolism, Elimination & Toxicity

Biotransformation

Desipramine is extensively metabolized in the liver by CYP2D6 (major) and CYP1A2 (minor) to 2-hydroxydesipramine, an active metabolite. 2-hydroxydesipramine is thought to retain some amine reuptake inhibition and may possess cardiac depressant activity. The 2-hydroxylation metabolic pathway of desipramine is under genetic control.

Source: Drug Bank

Protein Binding

73-92% bound to plasma proteins

Source: Drug Bank

Absorption

Desipramine hydrochloride is rapidly and almost completely absorbed from the gastrointestinal tract. It undergoes extensive first-pass metabolism. Peak plasma concentrations are attained 4 - 6 hours following oral administration.

Source: Drug Bank

Half-Life

7-60+ hours; 70% eliminated renally

Source: Drug Bank

Toxicity

Male mice: LD50 = 290 mg/kg, female rats: LD50 = 320 mg/kg. Antagonism of the histamine H 1 and alpha 1 receptors can lead to sedation and hypotension. Antimuscarinic activity confers anticholinergic side effects such as blurred vision, dry mouth, constipation and urine retention may occur. Cardiotoxicity may occur with high doses of desipramine. 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

Desipramine is metabolized in the liver, and approximately 70% is excreted in the urine.

Source: Drug Bank

Chemical Properties

Chemical Formula

C18H22N2

Source: Drug Bank

Isomeric SMILES

CNCCCN1c2ccccc2CCc3c1cccc3

Source: OpenEye

Canonical SMILES

CNCCCN1C2=CC=CC=C2CCC2=CC=CC=C12

Source: Drug Bank

Average Molecular Weight

266.3807

Source: Drug Bank

Monoisotopic Molecular Weight

266.178298714

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.
  1. Sympathetic Nerve Pathway (Neuroeffector Junction)
    Simplified diagram of a sympathetic neuroeffector junction displaying genes which may be involved.

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
ADRA1A (source: Drug Bank)
ADRB1 (source: Drug Bank)
ADRB2 (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)
SLC6A2 (source: Drug Bank)
SLC6A4 (source: Drug Bank)
SMPD1 (source: Drug Bank)

Drug Interactions

Drug Description
desipramine Increases the effect and toxicity of tricyclics (source: Drug Bank)
desipramine Atazanavir may increase the effect and toxicity of the tricyclic antidepressant, desipramine, by decreasing its metabolism. Monitor for changes in the therapeutic and adverse effects of desipramine if atazanavir if initiated, discontinued or dose changed. (source: Drug Bank)
desipramine The tricyclic increases the effect of carbamazepine (source: Drug Bank)
desipramine Carbamazepine may decrease the serum concentration of the tricyclic antidepressant, desipramine, by increasing its metabolism. Monitor for changes in the therapeutic and adverse effects of desipramine if carbamazepine is initiated, discontinued or dose changed. (source: Drug Bank)
desipramine Increases the effect of tricyclic agent (source: Drug Bank)
desipramine Cimetidine may increase the effect of the tricyclic antidepressant, desipramine, by decreasing its metabolism. Monitor for changes in the therapeutic and adverse effects of desipramine if cimetidine is initiated, discontinued or dose changed. (source: Drug Bank)
desipramine Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank)
desipramine Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank)
desipramine The tricyclic decreases the effect of clonidine (source: Drug Bank)
desipramine The tricyclic antidepressant, desipramine, decreases the effect of clonidine. (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, desipramine, by decreasing its metabolism. Monitor for changes in the therapeutic and adverse effects of desipramine 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, desipramine, by increasing its metabolism. Monitor for changes in the therapeutic and adverse effects of desipramine 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, desipramine, by decreasing its metabolism. Monitor for changes in the therapeutic and adverse effects of desipramine 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, desipramine, decreases the effect of clonidine. (source: Drug Bank)
dobutamine The tricyclic increases the sympathomimetic effect (source: Drug Bank)
dobutamine The tricyclic antidepressant, desipramine, 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, desipramine, 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, desipramine, increases the sympathomimetic effect of ephedra. (source: Drug Bank)
ephedrine The tricyclic increases the sympathomimetic effect (source: Drug Bank)
ephedrine The tricyclic antidepressant, desipramine, increases the sympathomimetic effect of ephedrine. (source: Drug Bank)
epinephrine The tricyclic increases the sympathomimetic effect (source: Drug Bank)
epinephrine The tricyclic antidepressant, desipramine, increases the sympathomimetic effect of epinephrine. epinephrine. (source: Drug Bank)
fenoterol The tricyclic increases the sympathomimetic effect (source: Drug Bank)
fenoterol The tricyclic antidepressant, desipramine, increases the sympathomimetic effect of fenoterol. (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)
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, 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 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, desipramine, decreases the 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, desipramine, increases the sympathomimetic effect of isoproterenol. (source: Drug Bank)
mephentermine The tricyclic increases the sympathomimetic effect (source: Drug Bank)
mephentermine The tricyclic antidepressant, desipramine, increases the sympathomimetic effect of mephentermine. (source: Drug Bank)
metaraminol The tricyclic increases the sympathomimetic effect (source: Drug Bank)
metaraminol The tricyclic antidepressant, desipramine, increases the sympathomimetic effect of metaraminol. (source: Drug Bank)
methoxamine The tricyclic increases the sympathomimetic effect (source: Drug Bank)
methoxamine The tricyclic antidepressant, desipramine, 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, desipramine, increases the sympathomimetic effect of norepinephrine. (source: Drug Bank)
orciprenaline The tricyclic increases the sympathomimetic effect (source: Drug Bank)
orciprenaline The tricyclic antidepressant, desipramine, 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, desipramine, increases the sympathomimetic effect of phenylephrine. (source: Drug Bank)
phenylpropanolamine The tricyclic increases the sympathomimetic effect (source: Drug Bank)
phenylpropanolamine The tricyclic antidepressant, desipramine, increases the sympathomimetic effect of phenylpropanolamine. (source: Drug Bank)
pirbuterol The tricyclic increases the sympathomimetic effect (source: Drug Bank)
pirbuterol The tricyclic antidepressant, desipramine, increases the sympathomimetic effect of pirbuterol. (source: Drug Bank)
procaterol The tricyclic increases the sympathomimetic effect (source: Drug Bank)
procaterol The tricyclic antidepressant, desipramine, increases the sympathomimetic effect of procaterol. (source: Drug Bank)
pseudoephedrine The tricyclic increases the sympathomimetic effect (source: Drug Bank)
pseudoephedrine The tricyclic antidepressant, desipramine, 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, desipramine. (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, desipramine, by increasing its metabolism. Monitor for changes in the therapeutic and adverse effects of desipramine 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, desipramine, by increasing its metabolism. Monitor for changes in the therapeutic and adverse effects of desipramine 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, desipramine, by decreasing its metabolism. Monitor for changes in the therapeutic and adverse effects of desipramine 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, desipramine, 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, desipramine, by decreasing its metabolism. Monitor for changes in the therapeutic and adverse effects of desipramine 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, desipramine, 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)
tranylcypromine Possibility of severe adverse effects (source: Drug Bank)
tranylcypromine Possibility of severe adverse effects (source: Drug Bank)
desipramine Possible antagonism of action (source: Drug Bank)
desipramine Possible antagonism of action (source: Drug Bank)
desipramine Possible increase in the levels of this agent when used with duloxetine (source: Drug Bank)
desipramine Possible increase in the levels of this agent when used with duloxetine (source: Drug Bank)
desipramine The tricyclic increases the sympathomimetic effect (source: Drug Bank)
desipramine The tricyclic antidepressant, desipramine, increases the sympathomimetic effect of epinephrine. (source: Drug Bank)
desipramine The tricyclic increases the sympathomimetic effect (source: Drug Bank)
desipramine The tricyclic antidepressant, desipramine, increases the sympathomimetic effect of fenoterol. (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)
desipramine Fluvoxamine increases the effect and toxicity of tricyclics (source: Drug Bank)
desipramine The SSRI, fluvoxamine, 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 fluvoxamine is initiated, discontinued or dose changed. (source: Drug Bank)
desipramine Possible antagonism of action (source: Drug Bank)
desipramine Possible antagonism of action (source: Drug Bank)
desipramine Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank)
desipramine Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank)
desipramine The tricyclic decreases the effect of guanethidine (source: Drug Bank)
desipramine The tricyclic antidepressant, desipramine, decreases the effect of guanethidine. (source: Drug Bank)
desipramine Possibility of severe adverse effects (source: Drug Bank)
desipramine Possibility of severe adverse effects (source: Drug Bank)
desipramine Possible severe adverse reaction with this combination (source: Drug Bank)
desipramine Possible severe adverse reaction with this combination (source: Drug Bank)
desipramine The tricyclic increases the sympathomimetic effect (source: Drug Bank)
desipramine The tricyclic antidepressant, desipramine, increases the sympathomimetic effect of orciprenaline. (source: Drug Bank)
desipramine Possibility of severe adverse effects (source: Drug Bank)
desipramine Possibility of severe adverse effects (source: Drug Bank)
desipramine The tricyclic increases the sympathomimetic effect (source: Drug Bank)
desipramine The tricyclic antidepressant, desipramine, increases the sympathomimetic effect of phenylephrine. (source: Drug Bank)
desipramine The tricyclic antidepressant, desipramine, increases the sympathomimetic effect of phenylpropanolamine. (source: Drug Bank)
desipramine The tricyclic increases the sympathomimetic effect (source: Drug Bank)
desipramine The tricyclic antidepressant, desipramine, increases the sympathomimetic effect of pseudoephedrine. (source: Drug Bank)
desipramine Quinidine increases the effect of the tricyclic agent (source: Drug Bank)
desipramine Additive QTc-prolonging effects may occur. Quinidine may also increase the serum concentration of the tricyclic antidepressant, desipramine, by decreasing its metabolism. Monitor for changes in the therapeutic and adverse effects of desipramine if quinidine is initiated, discontinued or dose changed. Monitor for the development of torsades de pointes during concomitant therapy. (source: Drug Bank)
desipramine Possibility of severe adverse effects (source: Drug Bank)
desipramine The rifamycin decreases the effect of tricyclics (source: Drug Bank)
desipramine The rifamycin, rifabutin, may decrease the effect of the tricyclic antidepressant, desipramine, by increasing its metabolism. Monitor for changes in the therapeutic and adverse effects of desipramine if rifabutin is initiated, discontinued or dose changed. (source: Drug Bank)
desipramine The rifamycin decreases the effect of tricyclics (source: Drug Bank)
desipramine The rifamycin, rifampin, may decrease the effect of the tricyclic antidepressant, desipramine, by increasing its metabolism. Monitor for changes in the therapeutic and adverse effects of desipramine if rifampin is initiated, discontinued or dose changed. (source: Drug Bank)
desipramine The therapeutic effects of the central acetylcholinesterase inhibitor, Tacrine, and/or the anticholinergic, Desipramine, 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)
desipramine The therapeutic effects of the central acetylcholinesterase inhibitor, Tacrine, and/or the anticholinergic, Desipramine, 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)
desipramine Additive QTc-prolongation may occur increasing the risk of serious ventricular arrhythmias. Concomitant therapy should be used with caution. (source: Drug Bank)
desipramine Desipramine may decrease the therapeutic effect of Tamoxifen by decreasing the production of active metabolites. Consider alternate therapy. (source: Drug Bank)
desipramine Desipramine may decrease the therapeutic effect of Tamoxifen by decreasing the production of active metabolites. Consider alternate therapy. (source: Drug Bank)
desipramine Desipramine, a CYP3A4/2D6 inhibitor, may decrease the metabolism and clearance of Tamsulosin, a CYP3A4/2D6 substrate. Monitor for changes in therapeutic/adverse effects of Tamsulosin if Desipramine is initiated, discontinued, or dose changed. (source: Drug Bank)
desipramine Desipramine, a CYP3A4/2D6 inhibitor, may decrease the metabolism and clearance of Tamsulosin, a CYP3A4/2D6 substrate. Monitor for changes in therapeutic/adverse effects of Tamsulosin if Desipramine is initiated, discontinued, or dose changed. (source: Drug Bank)
desipramine Terbinafine increases the effect and toxicity of the tricyclic (source: Drug Bank)
desipramine Terbinafine may reduce the metabolism and clearance of Desipramine. Consider alternate therapy or monitor for therapeutic/adverse effects of Desipramine if Terbinafine is initiated, discontinued or dose changed. (source: Drug Bank)
desipramine The tricyclic increases the sympathomimetic effect (source: Drug Bank)
desipramine The tricyclic antidepressant, desipramine, increases the sympathomimetic effect of terbutaline. (source: Drug Bank)
desipramine Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank)
desipramine Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank)
desipramine 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)
desipramine 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)
desipramine Tipranavir, co-administered with Ritonavir, may increase the concentration of Desipramine. Monitor Desipramine concentration and efficacy/toxicity and adjust dose as required. (source: Drug Bank)
desipramine Desipramine may decrease the metabolism and clearance of Tolterodine. Adjust Tolterodine dose and monitor for efficacy and toxicity. (source: Drug Bank)
desipramine Desipramine may decrease the metabolism and clearance of Tolterodine. Adjust Tolterodine dose and monitor for efficacy and toxicity. (source: Drug Bank)
desipramine 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)
desipramine Tramadol increases the risk of serotonin syndrome and seizures. Desipramine may increase Tramadol toxicity by decreasing Tramadol metabolism and clearance. Desipramine may decrease the effect of Tramadol by decreasing active metabolite production. (source: Drug Bank)
desipramine 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)
desipramine Increased risk of serotonin syndrome. The CYP3A4 inhibitor, Desipramine, may increase Trazodone efficacy/toxicity by decreasing Trazodone metabolism and clearance. The CYP2D6 inhibitor, Trazodone, may increase the efficacy of Desipramine by decreasing Desipramine metabolism and clearance. Monitor for symptoms of serotonin syndrome and changes in Trazodone and Desipramine efficacy/toxicity if either agent is initiated, discontinued or dose changed. (source: Drug Bank)
desipramine Increased risk of serotonin syndrome. Monitor for symptoms of serotonin syndrome. (source: Drug Bank)
desipramine Increased risk of serotonin syndrome. Monitor for symptoms of serotonin syndrome. Additive QTc-prolongation may also occur, increasing the risk of serious ventricular arrhythmias. Concomitant therapy should be used with caution. (source: Drug Bank)
desipramine Triprolidine and Desipramine, 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)
desipramine Triprolidine and Desipramine, 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)
desipramine Trospium and Desipramine, two anticholinergics, may cause additive anticholinergic effects and enhanced adverse/toxic effects. Monitor for enhanced anticholinergic effects. (source: Drug Bank)
desipramine Increased risk of serotonin syndrome. Monitor for symptoms of serotonin syndrome. (source: Drug Bank)
desipramine 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)
desipramine 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)
desipramine Additive QTc-prolonging effects may increase the risk of severe arrhythmias. Concomitant therapy is contraindicated. (source: Drug Bank)
desipramine Use of two serotonin modulators, such as zolmitriptan and desipramine, increases the risk of serotonin syndrome. Consider alternate therapy or monitor for serotonin syndrome during concomitant therapy. (source: Drug Bank)
desipramine 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 desipramine: 104

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The genetics of pro-arrhythmic adverse drug reactions. British journal of clinical pharmacology. 2014. Petropoulou Evmorfia, 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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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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Very important pharmacogene summary: ABCB1 (MDR1, P-glycoprotein). Pharmacogenetics and genomics. 2011. Hodges Laura M, et al. PubMed
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Sequence polymorphisms of MC1R gene and their association with depression and antidepressant response. Psychiatric genetics. 2011. Wu Gui-Sheng, 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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Cytochrome P450 2D6. Pharmacogenetics and genomics. 2009. Owen Ryan P, 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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Beta2-adrenoceptors are essential for desipramine, venlafaxine or reboxetine action in neuropathic pain. Neurobiology of disease. 2009. Yalcin Ipek, 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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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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Norepinephrine transporter regulation mediates the long-term behavioral effects of the antidepressant desipramine. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology. 2008. Zhao Zaorui, et al. PubMed
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An in vitro mechanistic study to elucidate the desipramine/bupropion clinical drug-drug interaction. Drug metabolism and disposition: the biological fate of chemicals. 2008. Reese Melinda J, 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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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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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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Prediction of pharmacokinetic drug-drug interactions using human hepatocyte suspension in plasma and cytochrome P450 phenotypic data. II. In vitro-in vivo correlation with ketoconazole. Drug metabolism and disposition: the biological fate of chemicals. 2008. Lu Chuang, 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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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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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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Molecules that mediate mood. The New England journal of medicine. 2007. Thase Michael E. PubMed
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LeuT-desipramine structure reveals how antidepressants block neurotransmitter reuptake. Science (New York, N.Y.). 2007. Zhou Zheng, 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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Tricyclic antidepressant pharmacology and therapeutic drug interactions updated. British journal of pharmacology. 2007. Gillman P K. 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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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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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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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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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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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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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
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Association of a corticotropin-releasing hormone receptor 1 haplotype and antidepressant treatment response in Mexican-Americans. Molecular psychiatry. 2004. Licinio J, et al. PubMed
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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
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Clomipramine, fluoxetine and CYP2D6 metabolic capacity in depressed patients. Human psychopharmacology. 2004. Vandel P, et al. PubMed
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Clinical implications of genetic polymorphism of CYP2D6 in Mexican Americans. Annals of internal medicine. 2004. Flores Deborah L, 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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Impact of CYP2D6 intermediate metabolizer alleles on single-dose desipramine pharmacokinetics. Pharmacogenetics. 2004. Furman Katherine D, et al. PubMed
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Inducible cAMP early repressor regulates corticosterone suppression after tricyclic antidepressant treatment. The Journal of neuroscience : the official journal of the Society for Neuroscience. 2004. Conti Alana C, 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
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 No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Some aspects of genetic polymorphism in the biotransformation of antidepressants. Thérapie. 2004. Brøsen Kim. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Haplotype architecture of the norepinephrine transporter gene SLC6A2 in four populations. Journal of human genetics. 2004. Belfer Inna, 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
Association between norepinephrine transporter gene polymorphism and major depression. Neuropsychobiology. 2004. Ryu Seung-Ho, 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 VIP No VIP available
Genetic polymorphisms of the human MDR1 drug transporter. Annual review of pharmacology and toxicology. 2003. Schwab Matthias, 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
The role of noradrenaline and selective noradrenaline reuptake inhibition in depression. European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology. 2002. Brunello N, 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
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Duplication of CYP2D6 predicts high clearance of desipramine but high clearance does not predict duplication of CYP2D6. European journal of clinical pharmacology. 2001. Bergmann T K, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available VIP No VIP available
Interaction of omeprazole, lansoprazole and pantoprazole with P-glycoprotein. Naunyn-Schmiedeberg's archives of pharmacology. 2001. Pauli-Magnus C, et al. PubMed
No Dosing Guideline available No Drug Label available CA VA No VIP available No VIP available
Metabolism of desipramine in Japanese psychiatric patients: the impact of CYP2D6 genotype on the hydroxylation of desipramine. Pharmacology & toxicology. 2000. Shimoda 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
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 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 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 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 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 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 CA VA No VIP available No VIP available
Relationship between plasma desipramine levels, CYP2D6 phenotype and clinical response to desipramine: a prospective study. European journal of clinical pharmacology. 1997. Spina 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 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 No Variant Annotation available 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 No Clinical Annotation available No Variant Annotation available 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 No Clinical Annotation available No Variant Annotation available 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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Genetically determined drug-metabolizing activity and desipramine-associated cardiotoxicity: a case report. Clinical pharmacology and therapeutics. 1993. Bluhm R E, et al. PubMed
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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
Polymorphic 2-hydroxylation of desipramine. A population and family study. European journal of clinical pharmacology. 1993. 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
Effect of fluoxetine on plasma desipramine and 2-hydroxydesipramine. Biological psychiatry. 1992. Suckow R F, et al. PubMed
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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 No Variant Annotation available No VIP available No VIP available
2-Hydroxydesipramine and desipramine plasma levels and electrocardiographic effects in depressed younger adults. Journal of clinical psychopharmacology. 1991. Stern S 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
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 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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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 No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Differences in the inhibitory effect of cimetidine on desipramine metabolism between rapid and slow debrisoquin hydroxylators. Clinical pharmacology and therapeutics. 1987. Steiner 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
Hydroxylation of desmethylimipramine: dependence on the debrisoquin hydroxylation phenotype. Clinical pharmacology and therapeutics. 1987. Spina E, et al. PubMed
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Imipramine demethylation and hydroxylation: impact of the sparteine oxidation phenotype. Clinical pharmacology and therapeutics. 1986. Brøsen K, et al. PubMed
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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
Desipramine and 2-hydroxydesipramine plasma levels in endogenous depressed patients. Lack of correlation with therapeutic response. Archives of general psychiatry. 1985. Amsterdam J D, et al. PubMed
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Phenotypic consistency in hydroxylation of desmethylimipramine and debrisoquine in healthy subjects and in human liver microsomes. Clinical pharmacology and therapeutics. 1984. Spina 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
The nonlinear kinetics of desipramine and 2-hydroxydesipramine in plasma. Clinical pharmacology and therapeutics. 1984. Cooke R G, 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 debrisoquine hydroxylation test predicts steady-state plasma levels of desipramine. British journal of clinical pharmacology. 1983. Bertilsson L, et al. PubMed
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Desipramine plasma concentration and antidepressant response. Archives of general psychiatry. 1982. Nelson J C, et al. PubMed
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The clinical application of tricyclic antidepressant pharmacokinetics and plasma levels. The American journal of psychiatry. 1980. Amsterdam J, et al. PubMed
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Single-dose kinetics predict steady-state concentrations on imipramine and desipramine. Archives of general psychiatry. 1980. Potter W Z, et al. PubMed

LinkOuts

Web Resource:
Wikipedia
National Drug Code Directory:
0781-1971-01
DrugBank:
DB01151
PDB:
DSM
ChEBI:
47781
KEGG Compound:
C06943
PubChem Compound:
2995
PubChem Substance:
148551
46504624
IUPHAR Ligand:
2399
Drugs Product Database (DPD):
2216272
BindingDB:
35229
ChemSpider:
2888
HET:
DSM
Therapeutic Targets Database:
DAP001151
FDA Drug Label at DailyMed:
7ec5f73f-32b6-48c3-b16e-891d06edf6eb

Clinical Trials

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

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