Chemical: Drug
trimipramine

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Prescribing Info (1) Drug Labels (1) Clinical Annotations (4)

last updated 03/15/2017

1. Annotation of CPIC Guideline for trimipramine 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 trimipramine. The CPIC Dosing Guideline update for amitriptyline recommends an alternative drug for CYP2D6 ultrarapid or poor metabolizers and CYP2C19 ultrarapid, rapid or poor metabolizers. If amitriptyline is warranted, consider a 50% dose reduction in CYP2D6 or CYP2C19 poor metabolizers. For CYP2D6 intermediate metabolizers, a 25% dose reduction should be considered.

Annotation

This annotation is based on the CPIC® guideline for tricyclic antidepressants and CYP2D6 and CYP2C19.

December 2016 Update

Advance online publication December 2016.

The 2016 update of CPIC guidelines regarding the use of pharmacogenomic tests in dosing of tricyclic antidepressants (TCAs) have been published in Clinical Pharmacology and Therapeutics by the Clinical Pharmacogenetics Implementation Consortium (CPIC). Literature up to July 2016 was reviewed, recommendations and supplemental information were updated.
Excerpt from the 2016 dosing guideline update:
- "Both amitriptyline and nortriptyline are used as representative TCAs for this guideline because the majority of pharmacogenomic studies have focused on these two drugs. However, the results of these studies may apply to other TCAs because these drugs have comparable pharmacokinetic properties."
- "There is substantial evidence linking CYP2D6 and CYP2C19 genotypes to phenotypic variability in tricyclic side-effect and pharmacokinetic profiles. Modifying pharmacotherapy for patients who have CYP2D6 or CYP2C19 genomic variants that affect drug efficacy and safety could potentially improve clinical outcomes and reduce the failure rate of initial treatment."
- " There are scarce studies focusing solely on CYP2D6 or CYP2C19 genotype and association with pharmacokinetic parameters or treatment outcomes of TCAs in pediatric patients. CYP2D6 activity is fully mature by early childhood, but CYP2C19 activity may be increased in children relative to adults. Although further genomic ontogeny studies are needed, there is a lack of evidence suggesting that this guideline cannot be extrapolated to pediatric patients."
The guideline includes dosing recommendation for TCAs based on:
- CYP2D6 phenotype (Table 1 below)
- CYP2C19 phenotype (Table 2 below)
Download and read:

Table 1: Dosing recommendations for TCAs based on CYP2D6 phenotype:

Adapted from Tables 1 and 2 of the 2016 guideline update.

Likely phenotype	Activity score	Genotypes	Examples of diplotypes	Implications	Therapeutic Recommendations^{a, b}	Classification of recommendation for other TCAs ^c
CYP2D6 Ultrarapid metabolizer (~1-20% of patients)^d	>2.0	An individual carrying more than two copies of functional alleles	1/1xN, 1/2xN	Increased metabolism of TCAs to less active compounds compared to normal metabolizers. Lower plasma concentrations of active drug will increase probability of pharmacotherapy failure.	Avoid tricyclic use due to potential lack of efficacy. Consider alternative drug not metabolized by CYP2D6. If a TCA is warranted, consider titrating to a higher target dose (compared to normal metabolizers). Utilize therapeutic drug monitoring to guide dose adjustments.^e	Optional
CYP2D6 Normal metabolizer (~72-88% of patients)^d	1.0-2.0^f	An individual carrying two normal function alleles or two decreased function alleles or one normal and no function allele or one normal and decreased function allele or combinations of duplicated alleles that result in an activity score of 1.0-2.0	1/1, 1/2, 2/2, 1/9, 1/41, 41/41, 1/4, 1/5	Normal metabolism of TCAs.	Initiate therapy with recommended starting dose.^g	Strong
CYP2D6 Intermediate metabolizer (~1-13% of patients)^d	0.5	An individual carrying one decreased and one no function allele	4/41, 5/9, 4/10	Reduced metabolism of TCAs to less active compounds when compared to normal metabolizers. Higher plasma concentrations of active drug will increase the probability of side effects.	Consider 25% reduction of recommended starting dose.^g Utilize therapeutic drug monitoring to guide dose adjustments.^e	Optional
CYP2D6 Poor metabolizer (~1-10% of patients)^d	0	An individual carrying only no function alleles	4/4, 4/4xN, 3/4, 5/5, 5/6	Greatly reduced metabolism of TCAs to less active compounds compared to normal metabolizers. Higher plasma concentrations of active drug will increase the probability of side effects.	Avoid tricyclic use due to potential for side effects. Consider alternative drug not metabolized by CYP2D6. If a TCA is warranted, consider 50% reduction of recommended starting dose.^g Utilize therapeutic drug monitoring to guide dose adjustments.^e	Optional

^a For tertiary amines (e.g., amitriptyline), if CYP2C19 genotype results are also available, see Table 2 for CYP2C19-based dosing recommendations and Table 3 below for CYP2D6/CYP2C19-based dosing recommendations.

^b Dosing recommendations only apply to higher initial doses of TCAs for treatment of conditions such as depression. See other considerations in the guideline for dosing recommendations for conditions where lower initial doses are used, such as neuropathic pain.

^c The rating scheme for the recommendation of classification is described in the Supplement. It may be reasonable to apply amitriptyline recommendation to other TCAs also metabolized by CYP2D6 including clomipramine, desipramine, doxepin, imipramine, and trimipramine. There are fewer clinical and pharmacokinetic data supporting genotype-guided dose adjustments for these drugs when compared to amitriptyline or nortriptyline (Supplemental Tables S8-S16).

^d CYP2D6 and CYP2C19 metabolizer status frequencies are based on average multi-ethnic frequencies. See the CYP2C19 and CYP2D6 Frequency Tables for population-specific allele and phenotype frequencies.

^e Titrate dose to observed clinical response with symptom improvement and minimal (if any) side effects.

^f Patients with an activity score of 1.0 may be classified as intermediate metabolizers by some reference laboratories.

^g Patients may receive an initial low dose of a tricyclic, which is then increased over several days to the recommended steady-state dose. The starting dose in this guideline refers to the recommended steady-state dose.

Table 2: Dosing recommendations for TCAs based on CYP2C19 phenotype:

Adapted from Tables 1 and 3 of the 2016 guideline update.

Likely phenotype	Genotypes	Examples of diplotypes	Implications	Therapeutic recommendations^a,b	Classification of recommendations for amitriptyline^c
CYP2C19 Ultrarapid metabolizer (~2-5% of patients)^d	An individual carrying two increased function alleles	17/17	Increased metabolism of tertiary amines compared to normal metabolizers. Greater conversion of tertiary amines to secondary amines may affect response or side effects.	Avoid tertiary amine use due to potential for sub-optimal response. Consider alternative drug not metabolized by CYP2C19. TCAs without major CYP2C19 metabolism include the secondary amines nortriptyline and desipramine. If a tertiary amine is warranted, utilize therapeutic drug monitoring to guide dose adjustments.^e	Optional
CYP2C19 Rapid metabolizer (~2-30% of patients)^d	An individual carrying one normal and one increased function allele	1/17	Increased metabolism of tertiary amines compared to normal metabolizers. Greater conversion of tertiary amines to secondary amines may affect response or side effects.	Avoid tertiary amine use due to potential for sub-optimal response. Consider alternative drug not metabolized by CYP2C19. TCAs without major CYP2C19 metabolism include the secondary amines nortriptyline and desipramine. If a tertiary amine is warranted, utilize therapeutic drug monitoring to guide dose adjustments.^e	Optional
CYP2C19 Normal metabolizer (~35-50% of patients)^d	An individual carrying two normal function alleles	1/1	Normal metabolism of tertiary amines.	Initiate therapy with recommended starting dose.^f	Strong
CYP2C19 Intermediate metabolizer (~18-45% of patients)^d	An individual carrying one normal and one no function allele or one no and one increased function allele	1/2, 1/3, 2/17^g	Reduced metabolism of tertiary amines compared to normal metabolizers.	Initiate therapy with recommended starting dose.^f	Optional
CYP2C19 Poor metabolizer (~2-15% of patients)^d	An individual carrying two no function alleles	2/2, 2/3, 3/3	Greatly reduced metabolism of tertiary amines compared to normal metabolizers. Decreased conversion of tertiary amines to secondary amines may affect response or side effects.	Avoid tertiary amine use due to potential for sub-optimal response. Consider alternative drug not metabolized by CYP2C19. TCAs without major CYP2C19 metabolism include the secondary amines nortriptyline and desipramine. For tertiary amines, consider a 50% reduction of the recommended starting dose.^f Utilize therapeutic drug monitoring to guide dose adjustments.^e	Optional

^a For tertiary amines (e.g., amitriptyline), if CYP2D6 genotype results are also available, see Table 1 for CYP2D6-based dosing recommendations above and Table 3 below for CYP2D6/CYP2C19-based dosing recommendations.

^c The rating scheme for the recommendation of classification is described in the Supplement. It may be reasonable to apply amitriptyline recommendation to other TCAs also metabolized by CYP2C19 including clomipramine, doxepin, imipramine, and trimipramine. There are fewer clinical and pharmacokinetic data supporting dose adjustments for these drugs when compared to amitriptyline or nortriptyline (Supplemental Tables S8-S16).

^e Titrate dose to observed clinical response with symptom improvement and minimal (if any) side effects.

^f Patients may receive an initial low dose of a tricyclic, which is then increased over several days to the recommended steady-state dose. The starting dose in this guideline refers to the recommended steady-state dose.

^g The predicted metabolizer phenotype for the*2/*17 genotype is a provisional classification. The currently available evidence indicates that the CYP2C19*17 increased function allele is unable to completely compensate for the CYP2C19*2 no function allele.

May 2013

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 clomipramine (Supplementary Table S18), with the acknowledgement that there are fewer data supporting dose adjustments for these drugs than for amitriptyline or nortriptyline.

See amitriptyline for excerpts and tables that summarize CYP2D6-based and CYP2C19-based dosing recommendations for amitriptyline when higher initial starting doses are warranted (article).

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last updated 10/25/2013

1. Annotation of FDA Label for trimipramine and CYP2D6

On FDA Biomarker List

Actionable PGx

Summary

Trimipramine (Surmontil) is a tricyclic antidepressant used to treat depression. Like many antidepressants, it has a black box warning for increased risk of suicidal thoughts and behavior. Trimipramine is metabolized by CYP2D6 and poor metabolizers my experience higher plasma concentrations of the drug at typical doses.

Annotation

Excerpt from the Trimipramine (Surmontil) drug label:

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 Trimipramine drug label PDF.

*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
Depression, Postpartum
- Indications & usage section, Warnings section, Adverse reactions section, Precautions section
- source: PHONT
CYP2D6
- metabolism/PK, Drug interactions section
- source: U.S. Food and Drug Administration

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.

Clinical Annotation for rs3892097 (CYP2D6), amitriptyline, antidepressants, clomipramine, desipramine, doxepin, imipramine, nortriptyline, trimipramine and Depression (level 1A Dosage, Toxicity/ADR)

Level of Evidence: Level 1A
Type: Dosage, Toxicity/ADR
Variant: rs3892097
Genes: CYP2D6
Phenotypes: Depression
OMB Race: White

To see the rest of this clinical annotation please register or sign in.

Clinical Annotation for CYP2C191, CYP2C192, trimipramine (level 2A Metabolism/PK)

Level of Evidence: Level 2A
Type: Metabolism/PK
Variant: *1, *2
Genes: CYP2C19
OMB Race: Unknown

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Clinical Annotation for CYP2D61, CYP2D62xN, CYP2D63, CYP2D64, CYP2D65, CYP2D66, trimipramine (level 2A)

Level of Evidence: Level 2A
Type: Other
Variant: *1, *2xN, *3, *4, *5, *6
Genes: CYP2D6
OMB Race: Unknown

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Clinical Annotation for CYP2C91, CYP2C93, trimipramine (level 3)

Level of Evidence: Level 3
Type: Other
Variant: *1, *3
Genes: CYP2C9
OMB Race: Unknown

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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

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.

List of all variant annotations for trimipramine

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	Gene ?	Variant? (147)	Alternate Names ?	Chemicals ?	Alleles ? (+ chr strand)	Function ?	Amino Acid? Translation
CA VA	CYP2C19	*1		trimipramine	N/A	N/A	N/A
CA VA	CYP2C19	*2		trimipramine	N/A	N/A	N/A
CA	CYP2C9	*1		trimipramine	N/A	N/A	N/A
CA VA	CYP2C9	*3		trimipramine	N/A	N/A	N/A
CA VA	CYP2D6	*1		trimipramine	N/A	N/A	N/A
CA VA	CYP2D6	*2xN		trimipramine	N/A	N/A	N/A
CA VA	CYP2D6	*3		trimipramine	N/A	N/A	N/A
CA VA	CYP2D6	*4		trimipramine	N/A	N/A	N/A
CA VA	CYP2D6	*5		trimipramine	N/A	N/A	N/A
CA VA	CYP2D6	*6		trimipramine	N/A	N/A	N/A
VA	ABCB1	rs2032583	NC_000007.13:g.87160561A>G, NC_000007.14:g.87531245A>G, NG_011513.1:g.187004T>C, NM_000927.4:c.2685+49T>C, rs386553611, rs58572471	nortriptyline venlafaxine citalopram Selective serotonin reuptake inhibitors amitriptyline paroxetine trimipramine escitalopram sertraline	A > G	SNP
VA	ABCB1	rs2235015	NC_000007.13:g.87199564C>A, NC_000007.14:g.87570248C>A, NG_011513.1:g.148001G>T, NM_000927.4:c.287-25G>T, rs59310468	nortriptyline venlafaxine citalopram Selective serotonin reuptake inhibitors amitriptyline paroxetine trimipramine escitalopram sertraline	C > A	SNP
CA	CYP2D6	rs3892097	NC_000022.10:g.42524947C=, NC_000022.10:g.42524947C>T, NC_000022.11:g.42128945C=, NC_000022.11:g.42128945C>T, NG_008376.3:g.6047G=, NG_008376.3:g.6047G>A, NM_000106.5:c.506-1A>G, NM_000106.5:c.506-1G>A, NM_001025161.2:c.353-1A>G, NM_001025161.2:c.353-1G>A, NT_187682.1:g.51286C=, NT_187682.1:g.51286C>T, NW_004504305.1:g.51272T=, NW_004504305.1:g.51272T>C, NW_009646208.1:g.14511C=, NW_009646208.1:g.14511C>T, XM_005278353.1:c.363-2A>G, XM_005278353.1:c.363-2G>A, XM_005278354.1:c.207-2A>G, XM_005278354.1:c.207-2G>A, XM_005278354.3:c.207-2A>G, XM_005278354.3:c.207-2G>A, XM_011529966.1:c.506-1A>G, XM_011529966.1:c.506-1G>A, XM_011529967.1:c.506-1A>G, XM_011529967.1:c.506-1G>A, XM_011529968.1:c.506-1A>G, XM_011529968.1:c.506-1G>A, XM_011529969.1:c.363-2A>G, XM_011529969.1:c.363-2G>A, XM_011529970.1:c.353-1A>G, XM_011529970.1:c.353-1G>A, XM_011529971.1:c.363-2A>G, XM_011529971.1:c.363-2G>A, XM_011529972.1:c.506-1A>G, XM_011529972.1:c.506-1G>A, XM_011547541.1:c.207-2A>G, XM_011547541.1:c.207-2G>A, XM_011547750.1:c.363-2A>G, XM_011547750.1:c.363-2G>A, XM_011547751.1:c.290-1A>G, XM_011547751.1:c.290-1G>A, XM_011547756.1:c.-1090C>T, XM_011547756.1:c.-1090T>C, XM_011548819.1:c.207-2A>G, XM_011548819.1:c.207-2G>A, XR_430455.2:n.-926C>T, XR_430455.2:n.-926T>C, XR_952745.1:n.1663-1A>G, XR_952745.1:n.1663-1G>A, rs1800716, rs28371711, rs60082401, rs606231227	clomipramine nortriptyline desipramine amitriptyline trimipramine antidepressants imipramine doxepin	C > T	SNP

Alleles, Functions, and Amino Acid Translations are all sourced from dbSNP 147

[ see larger image ] [ see 3D structure ]

provided by PubChem

Overview

Generic Names

Trimeprimina [Italian]
Trimeprimine
Trimipramina [INN-Spanish]
Trimipraminum [INN-Latin]
beta-Methylimipramine

Trade Names

Sapilent
Surmontil
Surmontyl
Temaril

Brand Mixture Names

PharmGKB Accession Id

PA451791

Type(s):

Drug

Description

Tricyclic antidepressant similar to imipramine, but with more antihistaminic and sedative properties.

Source: Drug Bank

Indication

For the treatment of depression and depression accompanied by anxiety, agitation or sleep disturbance

Source: Drug Bank

Other Vocabularies

ATC: Non-selective monoamine reuptake inhibitors (N06AA)
UMLS: Trimipramine (C0041056)
RxNorm: Trimipramine (10834)
NDFRT: TRIMIPRAMINE (N0000148047)

Information pulled from DrugBank has not been reviewed by PharmGKB.

Pharmacology, Interactions, and Contraindications

Mechanism of Action

Trimipramine's mechanism of action differs from other tricyclic antidepressants. Trimipramine acts by decreasing the reuptake of norepinephrine and serotonin (5-HT).

Source: Drug Bank

Pharmacology

Trimipramine is a tricyclic antidepressant. It was thought that tricyclic antidepressants work by inhibiting the re-uptake of the neurotransmitters norepinephrine and serotonin by nerve cells. However, this response occurs immediately, yet mood does not lift for around two weeks. It is now thought that changes occur in receptor sensitivity in the cerebral cortex and hippocampus. The hippocampus is part of the limbic system, a part of the brain involved in emotions. Presynaptic receptors are affected: a1 and b1 receptors are sensitized, a2 receptors are desensitised (leading to increased noradrenaline production). Tricyclics are also known as effective analgesics for different types of pain, especially neuropathic or neuralgic pain. A precise mechanism for their analgesic action is unknown, but it is thought that they modulate anti-pain opioid systems in the CNS via an indirect serotonergic route. They are also effective in migraine prophylaxis, but not in abortion of acute migraine attack. The mechanism of their anti-migraine action is also thought to be serotonergic.

Source: Drug Bank

Absorption, Distribution, Metabolism, Elimination & Toxicity

Biotransformation

Hepatic

Source: Drug Bank

Protein Binding

93%-96% (to plasma proteins)

Source: Drug Bank

Absorption

Rapid absorption

Source: Drug Bank

Half-Life

11-18 hrs

Source: Drug Bank

Toxicity

Side effects include agitation, coma, confusion, convulsions, dilated pupils, disturbed concentration, drowsiness, hallucinations, high fever, irregular heart rate, low body temperature, muscle rigidity, overactive reflexes, severely low blood pressure, stupor, vomiting

Source: Drug Bank

Chemical Properties

Chemical Formula

C20H26N2

Source: Drug Bank

Average Molecular Weight

294.4338

Source: Drug Bank

Monoisotopic Molecular Weight

294.209598842

Source: Drug Bank

SMILES

CC(CN1C2=CC=CC=C2CCC3=CC=CC=C31)CN(C)C

Source: PubChem

InChI String

InChI=1S/C20H26N2/c1-16(14-21(2)3)15-22-19-10-6-4-8-17(19)12-13-18-9-5-7-11-20(18)22/h4-11,16H,12-15H2,1-3H3

Source: PubChem

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 ?

view legend

Evidence	Gene
VA	ABCB1
DG CA VA	CYP2C19
CA VA	CYP2C9
DG DL CA VA	CYP2D6

Drug Targets

Gene	Description
ADRA1A	(source: Drug Bank )
ADRA1B	(source: Drug Bank )
ADRA2B	(source: Drug Bank )
DRD1	(source: Drug Bank )
DRD2	(source: Drug Bank )
HRH1	(source: Drug Bank )
HTR1A	(source: Drug Bank )
HTR2A	(source: Drug Bank )
SLC6A2	(source: Drug Bank )
SLC6A3	(source: Drug Bank )
SLC6A4	(source: Drug Bank )

Drug Interactions

Interaction	Description
atazanavir - trimipramine	Increases the effect and toxicity of tricyclics (source: Drug Bank )
atazanavir - trimipramine	Atazanavir may increase the effect and toxicity of the tricyclic antidepressant, trimipramine, by decreasing its metabolism. Monitor for changes in the therapeutic and adverse effects of trimipramine if atazanavir if initiated, discontinued or dose changed. (source: Drug Bank )
cimetidine - trimipramine	Increases the effect of tricyclic agent (source: Drug Bank )
cimetidine - trimipramine	Cimetidine may increase the effect of tricyclic antidepressant, trimipramine, by decreasing its metabolism. Monitor for changes in the therapeutic and adverse effects of trimipramine if cimetidine is initiated, discontinued or dose changed. (source: Drug Bank )
cisapride - trimipramine	Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank )
cisapride - trimipramine	Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank )
clonidine - trimipramine	The tricyclic decreases the effect of clonidine (source: Drug Bank )
clonidine - trimipramine	The tricyclic antidepressant, trimipramine, decreases the effect of clonidine. (source: Drug Bank )
donepezil - trimipramine	Possible antagonism of action (source: Drug Bank )
donepezil - trimipramine	Possible antagonism of action (source: Drug Bank )
epinephrine - trimipramine	The tricyclic increases the sympathomimetic effect (source: Drug Bank )
epinephrine - trimipramine	The tricyclic antidepressant, trimipramine, increases the sympathomimetic effect of epinephrine. (source: Drug Bank )
fenoterol - trimipramine	The tricyclic increases the sympathomimetic effect (source: Drug Bank )
fenoterol - trimipramine	The tricyclic antidepressant, trimipramine, increases the sympathomimetic effect of fenoterol. (source: Drug Bank )
fluoxetine - trimipramine	Fluoxetine increases the effect and toxicity of tricyclics (source: Drug Bank )
fluoxetine - trimipramine	The SSRI, fluoxetine, may increase the serum concentration of the tricyclic antidepressant, trimipramine, by decreasing its metabolism. Additive modulation of serotonin activity also increases the risk of serotonin syndrome. Monitor for development of serotonin syndrome during concomitant therapy. Monitor for changes in the therapeutic and adverse effects of trimipramine if fluoxetine is initiated, discontinued or dose changed. (source: Drug Bank )
galantamine - trimipramine	Possible antagonism of action (source: Drug Bank )
galantamine - trimipramine	Possible antagonism of action (source: Drug Bank )
grepafloxacin - trimipramine	Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank )
grepafloxacin - trimipramine	Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank )
guanethidine - trimipramine	The tricyclic decreases the effect of guanethidine (source: Drug Bank )
guanethidine - trimipramine	The tricyclic antidepressant, trimipramine, decreases the effect of guanethidine. (source: Drug Bank )
isocarboxazid - trimipramine	Possibility of severe adverse effects (source: Drug Bank )
isocarboxazid - trimipramine	Possibility of severe adverse effects (source: Drug Bank )
moclobemide - trimipramine	Possible severe adverse reaction with this combination (source: Drug Bank )
moclobemide - trimipramine	Possible severe adverse reaction with this combination (source: Drug Bank )
orciprenaline - trimipramine	The tricyclic increases the sympathomimetic effect (source: Drug Bank )
orciprenaline - trimipramine	The tricyclic antidepressant, trimipramine, increases the sympathomimetic effect of orciprenaline. (source: Drug Bank )
phenelzine - trimipramine	Possibility of severe adverse effects (source: Drug Bank )
phenelzine - trimipramine	Possibility of severe adverse effects (source: Drug Bank )
phenylephrine - trimipramine	The tricyclic increases the sympathomimetic effect (source: Drug Bank )
phenylephrine - trimipramine	The tricyclic antidepressant, trimipramine, increases the sympathomimetic effect of phenylephrine. (source: Drug Bank )
phenylpropanolamine - trimipramine	The tricyclic antidepressant, trimipramine, increases the sympathomimetic effect of phenylpropanolamine. (source: Drug Bank )
pseudoephedrine - trimipramine	The tricyclic increases the sympathomimetic effect (source: Drug Bank )
pseudoephedrine - trimipramine	The tricyclic antidepressant, trimipramine, increases the sympathomimetic effect of pseudoephedrine. (source: Drug Bank )
quinidine - trimipramine	Quinidine increases the effect of the tricyclic agent (source: Drug Bank )
quinidine - trimipramine	Additive QTc-prolonging effects may occur. Quinidine may also increase the serum concentration of the tricyclic antidepressant, trimipramine, by decreasing its metabolism. Monitor for changes in the therapeutic and adverse effects of trimipramine if quinidine is initiated, discontinued or dose changed. Monitor for the development of torsades de pointes during concomitant therapy. (source: Drug Bank )
rasagiline - trimipramine	Possibility of severe adverse effects (source: Drug Bank )
rifabutin - trimipramine	The rifamycin decreases the effect of tricyclics (source: Drug Bank )
rifabutin - trimipramine	The rifamycin, rifabutin, may decrease the effect of the tricyclic antidepressant, trimipramine, by increasing its metabolism. Monitor for changes in the therapeutic and adverse effects of trimipramine if rifabutin is initiated, discontinued or dose changed. (source: Drug Bank )
rifampin - trimipramine	The rifamycin decreases the effect of tricyclics (source: Drug Bank )
rifampin - trimipramine	The rifamycin, rifampin, may decrease the effect of the tricyclic antidepressant, trimipramine, by increasing its metabolism. Monitor for changes in the therapeutic and adverse effects of trimipramine if rifampin is initiated, discontinued or dose changed. (source: Drug Bank )
tacrine - trimipramine	The therapeutic effects of the central acetylcholinesterase inhibitor, Tacrine, and/or the anticholinergic, Trimipramine, 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 )
tacrine - trimipramine	The therapeutic effects of the central acetylcholinesterase inhibitor, Tacrine, and/or the anticholinergic, Trimipramine, 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 )
telithromycin - trimipramine	Telithromycin may reduce clearance of Trimipramine. Consider alternate therapy or monitor for changes in the therapeutic/adverse effects of Trimipramine if Telithromycin is initiated, discontinued or dose changed. (source: Drug Bank )
terbutaline - trimipramine	The tricyclic increases the sympathomimetic effect (source: Drug Bank )
terbutaline - trimipramine	The tricyclic antidepressant, trimipramine, increases the sympathomimetic effect of terbutaline. (source: Drug Bank )
terfenadine - trimipramine	Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank )
terfenadine - trimipramine	Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank )
thiothixene - trimipramine	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 )
thiothixene - trimipramine	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 )
ticlopidine - trimipramine	Ticlopidine may decrease the metabolism and clearance of Trimipramine. Consider alternate therapy or monitor for adverse/toxic effects of Trimipramine if Ticlopidine is initiated, discontinued or dose changed. (source: Drug Bank )
toremifene - trimipramine	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 )
tramadol - trimipramine	Tramadol increases the risk of serotonin syndrome and seizures. (source: Drug Bank )
tranylcypromine - trimipramine	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 )
trazodone - trimipramine	Increased risk of serotonin syndrome. The 2D6 inhibitor, Trazodone, may also increase the efficacy of Trimipramine by decreasing Trimipramine metabolism and clearance. Monitor for symptoms of serotonin syndrome and changes in Trimipramine efficacy if Trazodone is initiated, discontinued or dose changed. (source: Drug Bank )
trazodone - trimipramine	Increased risk of serotonin syndrome. Monitor for symptoms of serotonin syndrome. (source: Drug Bank )
trimethobenzamide - trimipramine	Trimethobenzamide and Trimipramine, two anticholinergics, may cause additive anticholinergic effects and enhance their adverse/toxic effects. Monitor for enhanced anticholinergic effects. (source: Drug Bank )
trimipramine - abarelix	Additive QTc-prolongation may occur, increasing the risk of serious ventricular arrhythmias. Concomitant therapy should be used with caution. (source: Drug Bank )
trimipramine - almotriptan	Increased risk of serotonin syndrome. Monitor for symptoms of serotonin syndrome. (source: Drug Bank )
trimipramine - amiodarone	Additive QTc-prolongation may occur, increasing the risk of serious ventricular arrhythmias. Concomitant therapy should be used with caution. (source: Drug Bank )
trimipramine - amitriptyline	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 )
trimipramine - amobarbital	The barbiturate, Amobarbital, may increase the metabolism and clearance of Trimipramine. Monitor for changes in the therapeutics and adverse effects of Trimipramine if Amobarbital is initiated, discontinued or dose changed. Dose adjustments of Trimipramine may be required. (source: Drug Bank )
trimipramine - amoxapine	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 )
trimipramine - amprenavir	The strong CYP3A4 inhibitor, Amprenavir, may decrease the metabolism and clearance of Trimipramine, a CYP3A4 substrate. Consider alternate therapy or monitor for changes in therapeutic and adverse effects of Trimipramine if Amprenavir is initiated, discontinued or dose changed. (source: Drug Bank )
trimipramine - atazanavir	The strong CYP3A4 inhibitor, Atazanavir, may decrease the metabolism and clearance of Trimipramine, a CYP3A4 substrate. Consider alternate therapy or monitor for changes in therapeutic and adverse effects of Trimipramine if Atazanavir is initiated, discontinued or dose changed. (source: Drug Bank )
trimipramine - bromocriptine	Increased risk of serotonin syndrome. Monitor for symptoms of serotonin syndrome. (source: Drug Bank )
trimipramine - buspirone	Increased risk of serotonin syndrome. Monitor for symptoms of serotonin syndrome. (source: Drug Bank )
trimipramine - butabarbital	The barbiturate, Butabarbital, may increase the metabolism and clearance of Trimipramine. Monitor for changes in the therapeutics and adverse effects of Trimipramine if Butabarbital is initiated, discontinued or dose changed. Dose adjustments of Trimipramine may be required. (source: Drug Bank )
trimipramine - butalbital	The barbiturate, Butalbital, may increase the metabolism and clearance of Trimipramine. Monitor for changes in the therapeutics and adverse effects of Trimipramine if Butalbital is initiated, discontinued or dose changed. Dose adjustments of Trimipramine may be required. (source: Drug Bank )
trimipramine - cabergoline	Increased risk of serotonin syndrome. Monitor for symptoms of serotonin syndrome. (source: Drug Bank )
trimipramine - chlorpromazine	Additive QTc-prolongation may occur, increasing the risk of serious ventricular arrhythmias. Chlorpromazine, a strong CYP2D6 inhibitor, may also decrease the metabolism and clearance of Trimipramine, a CYP2D6 substrate. Caution should be used during concomitant therapy. (source: Drug Bank )
trimipramine - cinacalcet	The strong CYP2D6 inhibitor, Cinacalcet, may decrease the metabolism and clearance of Trimipramine, a CYP2D6 substrate. Consider alternate therapy or monitor for changes in therapeutic and adverse effects of Trimipramine if Cinacalcet is initiated, discontinued or dose changed. (source: Drug Bank )
trimipramine - cisapride	Additive QTc-prolongation may occur, increasing the risk of serious ventricular arrhythmias. Concomitant therapy should be used with caution. (source: Drug Bank )
trimipramine - citalopram	The SSRI, Citalopram, may decrease the metabolism and clearance of Trimipramine. Increased risk of serotonin syndrome. Monitor for changes in Trimipramine efficacy and toxicity if Citalopram is initiated, discontinued or dose changed. (source: Drug Bank )
trimipramine - clarithromycin	Additive QTc-prolongation may occur, increasing the risk of serious ventricular arrhythmias. Clarithromycin, a strong CYP3A4 inhibitor, may also decrease the metabolism and clearance of Trimipramine, a CYP3A4 substrate. Concomitant therapy should be used with caution. (source: Drug Bank )
trimipramine - clomipramine	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 )
trimipramine - clonidine	Trimipramine may reduce the antihypertensive effect of the alpha2-agonist, Clonidine. Trimipramine may also increase the rebound hypertensive effect of Clonidine. Consider alternate therapy or monitor for changes in the therapeutic and adverse effects of Clonidine if Trimipramine is initiated, discontinued or dose changed. Clonidine should be withdrawn very gradually to reduce the risk of hypertensive crisis. (source: Drug Bank )
trimipramine - cocaine	The strong CYP2D6 inhibitor, Cocaine, may decrease the metabolism and clearance of Trimipramine, a CYP2D6 substrate. (source: Drug Bank )
trimipramine - darunavir	The strong CYP3A4 inhibitor, Darunavir, may decrease the metabolism and clearance of Trimipramine, a CYP3A4 substrate. Consider alternate therapy or monitor for changes in therapeutic and adverse effects of Trimipramine if Darunavir is initiated, discontinued or dose changed. (source: Drug Bank )
trimipramine - dasatinib	Additive QTc-prolongation may occur, increasing the risk of serious ventricular arrhythmias. Concomitant therapy should be used with caution. (source: Drug Bank )
trimipramine - delavirdine	The strong CYP3A4/CYP2D6 inhibitor, Delavirdine, may decrease the metabolism and clearance of Trimipramine, a CYP3A4/CYP2D6 substrate. Consider alternate therapy or monitor for changes in therapeutic and adverse effects of Trimipramine if Delavirdine is initiated, discontinued or dose changed. (source: Drug Bank )
trimipramine - 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 )
trimipramine - dexmedetomidine	Trimipramine may reduce the antihypertensive effect of the alpha2-agonist, Dexmedetomidine. Trimipramine may also increase the rebound hypertensive effect of Clonidine. Consider alternate therapy or monitor for changes in the therapeutic and adverse effects of Clonidine if Trimipramine is initiated, discontinued or dose changed. Dexmedetomidine should be withdrawn very gradually to reduce the risk of hypertensive crisis. (source: Drug Bank )
trimipramine - dextromethorphan	Increased risk of serotonin syndrome. Monitor for symptoms of serotonin syndrome. (source: Drug Bank )
trimipramine - dihydroergotamine	Increased risk of serotonin syndrome. Monitor for symptoms of serotonin syndrome. (source: Drug Bank )
trimipramine - disopyramide	Additive QTc-prolongation may occur, increasing the risk of serious ventricular arrhythmias. Concomitant therapy should be used with caution. (source: Drug Bank )
trimipramine - dofetilide	Additive QTc-prolongation may occur, increasing the risk of serious ventricular arrhythmias. Concomitant therapy should be used with caution. (source: Drug Bank )
trimipramine - dolasetron	Additive QTc-prolongation may occur, increasing the risk of serious ventricular arrhythmias. Concomitant therapy should be used with caution. (source: Drug Bank )
trimipramine - domperidone	Additive QTc-prolongation may occur, increasing the risk of serious ventricular arrhythmias. Concomitant therapy should be used with caution. (source: Drug Bank )
trimipramine - doxepin	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 )
trimipramine - droperidol	Additive QTc-prolongation may occur, increasing the risk of serious ventricular arrhythmias. Concomitant therapy should be used with caution. (source: Drug Bank )
trimipramine - duloxetine	Increased risk of serotonin syndrome. Monitor for symptoms of serotonin syndrome. (source: Drug Bank )
trimipramine - eletriptan	Increased risk of serotonin syndrome. Monitor for symptoms of serotonin syndrome. (source: Drug Bank )
trimipramine - epinephrine	Trimipramine may increase the vasopressor effect of the direct-acting alpha-/beta-agonist, Epinephrine. Avoid combination if possible. Monitor sympathetic response to therapy if used concomitantly. (source: Drug Bank )
trimipramine - ergonovine	Increased risk of serotonin syndrome. Monitor for symptoms of serotonin syndrome. (source: Drug Bank )
trimipramine - ergotamine	Increased risk of serotonin syndrome. Monitor for symptoms of serotonin syndrome. (source: Drug Bank )
trimipramine - erythromycin	Additive QTc-prolongation may occur, increasing the risk of serious ventricular arrhythmias. Concomitant therapy should be used with caution. (source: Drug Bank )
trimipramine - escitalopram	The SSRI, Escitalopram, may decrease the metabolism and clearance of Trimipramine. Increased risk of serotonin syndrome. Monitor for changes in Trimipramine efficacy and toxicity if Escitalopram is initiated, discontinued or dose changed. (source: Drug Bank )
trimipramine - flecainide	Additive QTc-prolongation may occur, increasing the risk of serious ventricular arrhythmias. Concomitant therapy should be used with caution. (source: Drug Bank )
trimipramine - fluconazole	Additive QTc-prolongation may occur, increasing the risk of serious ventricular arrhythmias. Fluconazole, a strong CYP2C19 inhibitor, may also decrease the metabolism and clearance of Trimipramine, a CYP2C19 substrate. Concomitant therapy should be used with caution. (source: Drug Bank )
trimipramine - fluoxetine	The SSRI, Fluoxetine, may decrease the metabolism and clearance of Trimipramine. Increased risk of serotonin syndrome. Monitor for changes in Trimipramine efficacy and toxicity if Fluoxetine is initiated, discontinued or dose changed. Additive QTc-prolongation may also occur, increasing the risk of serious ventricular arrhythmias. Concomitant therapy should be used cautiously. (source: Drug Bank )
trimipramine - flupenthixol	Additive QTc-prolongation may occur, increasing the risk of serious ventricular arrhythmias. Concomitant therapy should be used with caution. (source: Drug Bank )
trimipramine - fluvoxamine	The strong CYP2C19 inhibitor, Fluvoxamine, may decrease the metabolism and clearance of Trimipramine, a CYP2C19 substrate. Increased risk of serotonin syndrome. Consider alternate therapy or monitor for changes in therapeutic and adverse effects of Trimipramine if Fluvoxamine is initiated, discontinued or dose changed. (source: Drug Bank )
trimipramine - fosamprenavir	The strong CYP3A4 inhibitor, Fosamprenavir, may decrease the metabolism and clearance of Trimipramine, a CYP3A4 substrate. Consider alternate therapy or monitor for changes in therapeutic and adverse effects of Trimipramine if Fosamprenavir is initiated, discontinued or dose changed. (source: Drug Bank )
trimipramine - foscarnet	Additive QTc-prolongation may occur, increasing the risk of serious ventricular arrhythmias. Concomitant therapy should be used with caution. (source: Drug Bank )
trimipramine - frovatriptan	Increased risk of serotonin syndrome. Monitor for symptoms of serotonin syndrome. (source: Drug Bank )
trimipramine - furazolidone	Increased risk of serotonin syndrome. Ensure adequate washout period between therapies to avoid toxicity. Avoid combination or monitor for symptoms of serotonin syndrome and/or hypertensive crisis. (source: Drug Bank )
trimipramine - gatifloxacin	Additive QTc-prolongation may occur, increasing the risk of serious ventricular arrhythmias. Concomitant therapy should be used with caution. (source: Drug Bank )
trimipramine - gemfibrozil	The strong CYP2C19 inhibitor, Gemfibrozil, may decrease the metabolism and clearance of Trimipramine, a CYP2C19 substrate. Consider alternate therapy or monitor for changes in therapeutic and adverse effects of Trimipramine if Gemfibrozil is initiated, discontinued or dose changed. (source: Drug Bank )
trimipramine - guanabenz	Trimipramine may reduce the antihypertensive effect of the alpha2-agonist, Guanabenz. Trimipramine may also increase the rebound hypertensive effect of Clonidine. Consider alternate therapy or monitor for changes in the therapeutic and adverse effects of Clonidine if Trimipramine is initiated, discontinued or dose changed. Guanabenz should be withdrawn very gradually to reduce the risk of hypertensive crisis. (source: Drug Bank )
trimipramine - guanfacine	Trimipramine may reduce the antihypertensive effect of the alpha2-agonist, Guanfacine. Trimipramine may also increase the rebound hypertensive effect of Clonidine. Consider alternate therapy or monitor for changes in the therapeutic and adverse effects of Clonidine if Trimipramine is initiated, discontinued or dose changed. Guanfacine should be withdrawn very gradually to reduce the risk of hypertensive crisis. (source: Drug Bank )
trimipramine - halofantrine	Additive QTc-prolongation may occur, increasing the risk of serious ventricular arrhythmias. Concomitant therapy should be used with caution. (source: Drug Bank )
trimipramine - haloperidol	Additive QTc-prolongation may occur, increasing the risk of serious ventricular arrhythmias. Concomitant therapy should be used with caution. (source: Drug Bank )
trimipramine - ibutilide	Additive QTc-prolongation may occur, increasing the risk of serious ventricular arrhythmias. Concomitant therapy should be used with caution. (source: Drug Bank )
trimipramine - imatinib	The strong CYP3A4 inhibitor, Imatinib, may decrease the metabolism and clearance of Trimipramine, a CYP3A4 substrate. Consider alternate therapy or monitor for changes in therapeutic and adverse effects of Trimipramine if Imatinib is initiated, discontinued or dose changed. (source: Drug Bank )
trimipramine - 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 )
trimipramine - indapamide	Additive QTc-prolongation may occur, increasing the risk of serious ventricular arrhythmias. Concomitant therapy should be used with caution. (source: Drug Bank )
trimipramine - indinavir	The strong CYP3A4 inhibitor, Indinavir, may decrease the metabolism and clearance of Trimipramine, a CYP3A4 substrate. Consider alternate therapy or monitor for changes in therapeutic and adverse effects of Trimipramine if Indinavir is initiated, discontinued or dose changed. (source: Drug Bank )
trimipramine - isocarboxazid	Increased risk of serotonin syndrome. Ensure adequate washout period between therapies to avoid toxicity. Avoid combination or monitor for symptoms of serotonin syndrome and/or hypertensive crisis. (source: Drug Bank )
trimipramine - isoniazid	The strong CYP3A4/CYP2C19 inhibitor, Isoniazide, may decrease the metabolism and clearance of Trimipramine, a CYP3A4/CYP2C19 substrate. Consider alternate therapy or monitor for changes in therapeutic and adverse effects of Trimipramine if Isoniazid is initiated, discontinued or dose changed. (source: Drug Bank )
trimipramine - isradipine	Additive QTc-prolongation may occur, increasing the risk of serious ventricular arrhythmias. Concomitant therapy should be used with caution. (source: Drug Bank )
trimipramine - itraconazole	The strong CYP3A4 inhibitor, Itraconazole, may decrease the metabolism and clearance of Trimipramine, a CYP3A4 substrate. Consider alternate therapy or monitor for changes in therapeutic and adverse effects of Trimipramine if Itraconazole is initiated, discontinued or dose changed. (source: Drug Bank )
trimipramine - ketoconazole	The strong CYP3A4 inhibitor, Ketoconazole, may decrease the metabolism and clearance of Trimipramine, a CYP3A4 substrate. Consider alternate therapy or monitor for changes in therapeutic and adverse effects of Trimipramine if Ketoconazole is initiated, discontinued or dose changed. (source: Drug Bank )
trimipramine - lapatinib	Additive QTc-prolongation may occur, increasing the risk of serious ventricular arrhythmias. Concomitant therapy should be used with caution. (source: Drug Bank )
trimipramine - levofloxacin	Additive QTc-prolongation may occur, increasing the risk of serious ventricular arrhythmias. Concomitant therapy should be used with caution. (source: Drug Bank )
trimipramine - linezolid	Increased risk of serotonin syndrome. Ensure adequate washout period between therapies to avoid toxicity. Avoid combination or monitor for symptoms of serotonin syndrome and/or hypertensive crisis. (source: Drug Bank )
trimipramine - lithium	Increased risk of serotonin syndrome. Monitor for symptoms of serotonin syndrome. (source: Drug Bank )
trimipramine - lopinavir	The strong CYP3A4/CYP2D6 inhibitor, Lopinavir, may decrease the metabolism and clearance of Trimipramine, a CYP3A4/CYP2D6 substrate. Consider alternate therapy or monitor for changes in therapeutic and adverse effects of Trimipramine if Lopinavir is initiated, discontinued or dose changed. (source: Drug Bank )
trimipramine - loxapine	Additive QTc-prolongation may occur, increasing the risk of serious ventricular arrhythmias. Concomitant therapy should be used with caution. (source: Drug Bank )
trimipramine - maprotiline	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 )
trimipramine - mefloquine	Additive QTc-prolongation may occur, increasing the risk of serious ventricular arrhythmias. Concomitant therapy should be used with caution. (source: Drug Bank )
trimipramine - meperidine	Increased risk of serotonin syndrome. Monitor for symptoms of serotonin syndrome. (source: Drug Bank )
trimipramine - mephentermine	Trimipramine may increase the vasopressor effect of the alpha1-agonist, Mephentermine. Avoid combination if possible. Monitor sympathetic response to therapy if used concomitantly. (source: Drug Bank )
trimipramine - mesoridazine	Additive QTc-prolongation may occur, increasing the risk of serious ventricular arrhythmias. Concomitant therapy should be used with caution. (source: Drug Bank )
trimipramine - methadone	Additive QTc-prolongation may occur, increasing the risk of serious ventricular arrhythmias. Concomitant therapy should be used with caution. (source: Drug Bank )
trimipramine - methohexital	The barbiturate, Methohexital, may increase the metabolism and clearance of Trimipramine. Monitor for changes in the therapeutics and adverse effects of Trimipramine if Methohexital is initiated, discontinued or dose changed. Dose adjustments of Trimipramine may be required. (source: Drug Bank )
trimipramine - methoxamine	Trimipramine may increase the vasopressor effect of the alpha1-agonist, Methoxamine. Avoid combination if possible. Monitor sympathetic response to therapy if used concomitantly. (source: Drug Bank )
trimipramine - methylergonovine	Increased risk of serotonin syndrome. Monitor for symptoms of serotonin syndrome. (source: Drug Bank )
trimipramine - miconazole	The strong CYP3A4/2D6/2C19 inhibitor, Miconazole, may decrease the metabolism and clearance of Trimipramine, a CYP3A4/2D6/2C19 substrate. Consider alternate therapy or monitor for changes in therapeutic and adverse effects of Trimipramine if Miconazole is initiated, discontinued or dose changed. (source: Drug Bank )
trimipramine - midodrine	Trimipramine may increase the vasopressor effect of the alpha1-agonist, Midodrine. Avoid combination if possible. Monitor sympathetic response to therapy if used concomitantly. (source: Drug Bank )
trimipramine - mirtazapine	Increased risk of serotonin syndrome. Monitor for symptoms of serotonin syndrome. (source: Drug Bank )
trimipramine - moclobemide	Increased risk of serotonin syndrome. Ensure adequate washout period between therapies to avoid toxicity. Avoid combination or monitor for symptoms of serotonin syndrome and/or hypertensive crisis. (source: Drug Bank )
trimipramine - modafinil	The strong CYP2C19 inhibitor, Modafinil, may decrease the metabolism and clearance of Trimipramine, a CYP2D6 substrate. Consider alternate therapy or monitor for changes in therapeutic and adverse effects of Trimipramine if Modafinil is initiated, discontinued or dose changed. (source: Drug Bank )
trimipramine - moxifloxacin	Additive QTc-prolongation may occur, increasing the risk of serious ventricular arrhythmias. Concomitant therapy should be used with caution. (source: Drug Bank )
trimipramine - naratriptan	Increased risk of serotonin syndrome. Monitor for symptoms of serotonin syndrome. (source: Drug Bank )
trimipramine - nefazodone	Increased risk of serotonin syndrome. Monitor for symptoms of serotonin syndrome. Nefazodone, a strong CYP3A4 inhibitor, may also decrease the metabolism and clearance of Trimipramine, a CYP3A4 substrate. Consider alternate therapy or monitor for changes in therapeutic and adverse effects of Trimipramine if Nefazodone is initiated, discontinued or dose changed. (source: Drug Bank )
trimipramine - nelfinavir	The strong CYP3A4 inhibitor, Nelfinavir, may decrease the metabolism and clearance of Trimipramine, a CYP3A4 substrate. Consider alternate therapy or monitor for changes in therapeutic and adverse effects of Trimipramine if Nelfinavir is initiated, discontinued or dose changed. (source: Drug Bank )
trimipramine - nicardipine	The strong CYP3A4 inhibitor, Nicardipine, may decrease the metabolism and clearance of Trimipramine, a CYP3A4 substrate. Consider alternate therapy or monitor for changes in therapeutic and adverse effects of Trimipramine if Nicardipine is initiated, discontinued or dose changed. (source: Drug Bank )
trimipramine - nilotinib	May cause additive QTc-prolonging effects. Concomitant therapy is contraindicated. (source: Drug Bank )
trimipramine - norepinephrine	Trimipramine may increase the vasopressor effect of the direct-acting alpha-/beta-agonist, Norepinephrine. Avoid combination if possible. Monitor sympathetic response to therapy if used concomitantly. (source: Drug Bank )
trimipramine - norfloxacin	Additive QTc-prolongation may occur, increasing the risk of serious ventricular arrhythmias. Concomitant therapy should be used with caution. (source: Drug Bank )
trimipramine - nortriptyline	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 )
trimipramine - octreotide	Additive QTc-prolongation may occur, increasing the risk of serious ventricular arrhythmias. Concomitant therapy should be used with caution. (source: Drug Bank )
trimipramine - omeprazole	The strong CYP2C19 inhibitor, Omeprazole, may decrease the metabolism and clearance of Trimipramine, a CYP2C19 substrate. Consider alternate therapy or monitor for changes in therapeutic and adverse effects of Trimipramine if Omeprazole is initiated, discontinued or dose changed. (source: Drug Bank )
trimipramine - paroxetine	The SSRI, Paroxetine, may decrease the metabolism and clearance of Trimipramine. Increased risk of serotonin syndrome. Monitor for changes in Trimipramine efficacy and toxicity if Paroxetine is initiated, discontinued or dose changed. (source: Drug Bank )
trimipramine - pentamidine	Additive QTc-prolongation may occur, increasing the risk of serious ventricular arrhythmias. Concomitant therapy should be used with caution. (source: Drug Bank )
trimipramine - pentobarbital	The barbiturate, Pentobarbital, may increase the metabolism and clearance of Trimipramine. Monitor for changes in the therapeutics and adverse effects of Trimipramine if Pentobarbital is initiated, discontinued or dose changed. Dose adjustments of Trimipramine may be required. (source: Drug Bank )
trimipramine - perflutren	Additive QTc-prolongation may occur, increasing the risk of serious ventricular arrhythmias. Concomitant therapy should be used with caution. (source: Drug Bank )
trimipramine - pergolide	Increased risk of serotonin syndrome. Pergolide, a strong CYP2D6 inhibitor, may also decrease the metabolism and clearance of Trimipramine, a CYP2D6 substrate. Monitor for symptoms of serotonin syndrome and changes in Trimipramine therapeutic and adverse effects if Pergolide is initiated, discontinued or dose changed. (source: Drug Bank )
trimipramine - phenelzine	Increased risk of serotonin syndrome. Ensure adequate washout period between therapies to avoid toxicity. Avoid combination or monitor for symptoms of serotonin syndrome and/or hypertensive crisis. (source: Drug Bank )
trimipramine - phenobarbital	The barbiturate, Phenobarbital, may increase the metabolism and clearance of Trimipramine. Monitor for changes in the therapeutics and adverse effects of Trimipramine if Phenobarbital is initiated, discontinued or dose changed. Dose adjustments of Trimipramine may be required. (source: Drug Bank )
trimipramine - phenylephrine	Trimipramine may increase the vasopressor effect of the alpha1-agonist, Phenylephrine. Avoid combination if possible. Monitor sympathetic response to therapy if used concomitantly. (source: Drug Bank )
trimipramine - pimozide	Additive QTc-prolongation may occur, increasing the risk of serious ventricular arrhythmias. Concomitant therapy should be used with caution. (source: Drug Bank )
trimipramine - posaconazole	The strong CYP3A4 inhibitor, Posaconazole, may decrease the metabolism and clearance of Trimipramine, a CYP3A4 substrate. Consider alternate therapy or monitor for changes in therapeutic and adverse effects of Trimipramine if Posaconazole is initiated, discontinued or dose changed. (source: Drug Bank )
trimipramine - pramlintide	The anticholinergic effects of Trimipramine may be enhanced by Pramlintide. Additive effects of reduced GI motility may occur. Pramlintide slows gastic emptying and should not be used with drugs that alter GI motility (e.g. anticholinergics). Consider alternative treatments or use caution during concomitant therapy. (source: Drug Bank )
trimipramine - probucol	Additive QTc-prolongation may occur, increasing the risk of serious ventricular arrhythmias. Concomitant therapy should be used with caution. (source: Drug Bank )
trimipramine - procainamide	Additive QTc-prolongation may occur, increasing the risk of serious ventricular arrhythmias. Concomitant therapy should be used with caution. (source: Drug Bank )
trimipramine - procarbazine	Increased risk of serotonin syndrome. Ensure adequate washout period between therapies to avoid toxicity. Avoid combination or monitor for symptoms of serotonin syndrome and/or hypertensive crisis. (source: Drug Bank )
trimipramine - promethazine	Increased risk of serotonin syndrome. Monitor for symptoms of serotonin syndrome. (source: Drug Bank )
trimipramine - propafenone	Additive QTc-prolongation may occur, increasing the risk of serious ventricular arrhythmias. Concomitant therapy should be used with caution. (source: Drug Bank )
trimipramine - protriptyline	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 )
trimipramine - quetiapine	Additive QTc-prolongation may occur, increasing the risk of serious ventricular arrhythmias. Concomitant therapy should be used with caution. (source: Drug Bank )
trimipramine - quinidine	Additive QTc-prolonging effects may occur, increasing the risk of serious cardiac arrhythmias. Quinidine, a CYP2D6/CYP3A4 inhibitor, may also inhibit the metabolism of Trimipramine, a CYP2D6/CYP3A4 substrate. Monitor for signs of cardiac arrhythmias and for changes in Trimipramine efficacy and toxicity if Quinidine is initiated, discontinued or dose changed. (source: Drug Bank )
trimipramine - ranolazine	Additive QTc-prolongation may occur, increasing the risk of serious ventricular arrhythmias. Concomitant therapy should be used with caution. (source: Drug Bank )
trimipramine - rasagiline	Increased risk of serotonin syndrome. Ensure adequate washout period between therapies to avoid toxicity. Avoid combination or monitor for symptoms of serotonin syndrome and/or hypertensive crisis. (source: Drug Bank )
trimipramine - risperidone	Additive QTc-prolongation may occur, increasing the risk of serious ventricular arrhythmias. Concomitant therapy should be used with caution. (source: Drug Bank )
trimipramine - ritonavir	The strong CYP3A4/CYP2D6 inhibitor, Ritonavir, may decrease the metabolism and clearance of Trimipramine, a CYP3A4/CYP2D6 substrate. Consider alternate therapy or monitor for changes in therapeutic and adverse effects of Trimipramine if Ritonavir is initiated, discontinued or dose changed. (source: Drug Bank )
trimipramine - rizatriptan	Increased risk of serotonin syndrome. Monitor for symptoms of serotonin syndrome. (source: Drug Bank )
trimipramine - s-adenosylmethionine	Increased risk of serotonin syndrome. Monitor for symptoms of serotonin syndrome. (source: Drug Bank )
trimipramine - saquinavir	The strong CYP3A4 inhibitor, Saquinavir, may decrease the metabolism and clearance of Trimipramine, a CYP3A4 substrate. Consider alternate therapy or monitor for changes in therapeutic and adverse effects of Trimipramine if Saquinavir is initiated, discontinued or dose changed. (source: Drug Bank )
trimipramine - secobarbital	The barbiturate, Secobarbital, may increase the metabolism and clearance of Trimipramine. Monitor for changes in the therapeutics and adverse effects of Trimipramine if Secobarbital is initiated, discontinued or dose changed. Dose adjustments of Trimipramine may be required. (source: Drug Bank )
trimipramine - selegiline	Increased risk of serotonin syndrome. Ensure adequate washout period between therapies to avoid toxicity. Avoid combination or monitor for symptoms of serotonin syndrome and/or hypertensive crisis. (source: Drug Bank )
trimipramine - sertraline	The SSRI, Sertraline, may decrease the metabolism and clearance of Trimipramine. Increased risk of serotonin syndrome. Monitor for changes in Trimipramine efficacy and toxicity if Sertraline is initiated, discontinued or dose changed. (source: Drug Bank )
trimipramine - sibutramine	Increased risk of serotonin syndrome. Concomitant therapy is contraindicated. (source: Drug Bank )
trimipramine - sotalol	Additive QTc-prolongation may occur, increasing the risk of serious ventricular arrhythmias. Concomitant therapy should be used with caution. (source: Drug Bank )
trimipramine - sparfloxacin	Additive QTc-prolongation may occur, increasing the risk of serious ventricular arrhythmias. Concomitant therapy should be used with caution. (source: Drug Bank )
trimipramine - sumatriptan	Increased risk of serotonin syndrome. Monitor for symptoms of serotonin syndrome. (source: Drug Bank )
trimipramine - sunitinib	Additive QTc-prolongation may occur, increasing the risk of serious ventricular arrhythmias. Concomitant therapy should be used with caution. (source: Drug Bank )
trimipramine - telithromycin	Additive QTc-prolongation may occur, increasing the risk of serious ventricular arrhythmias. Telithromycin, a strong CYP3A4 inhibitor, may also decrease the metabolism and clearance of Trimipramine, a CYP3A4 substrate. Concomitant therapy should be used with caution. (source: Drug Bank )
trimipramine - terbinafine	Terbinafine may decrease the metabolism and clearance of Trimipramine. Monitor for changes in Trimipramine efficacy and toxicity if Terbinafine is initiated, discontinued or dose changed. Alteration in Trimipramine dose may be required. (source: Drug Bank )
trimipramine - tetrabenazine	May cause additive QTc-prolonging effects. Concomitant therapy should be avoided. (source: Drug Bank )
trimipramine - thiopental	The barbiturate, Thiopental, may increase the metabolism and clearance of Trimipramine. Monitor for changes in the therapeutics and adverse effects of Trimipramine if Thiopental is initiated, discontinued or dose changed. Dose adjustments of Trimipramine may be required. (source: Drug Bank )
trimipramine - thioridazine	May cause additive QTc-prolonging effects. Concomitant therapy is contraindicated. (source: Drug Bank )
trimipramine - thiothixene	Additive QTc-prolongation may occur, increasing the risk of serious ventricular arrhythmias. Concomitant therapy should be used with caution. (source: Drug Bank )
trimipramine - ticlopidine	The strong CYP2C19 inhibitor, Ticlopidine, may decrease the metabolism and clearance of Trimipramine, a CYP2D6 substrate. Consider alternate therapy or monitor for changes in therapeutic and adverse effects of Trimipramine if Ticlopidine is initiated, discontinued or dose changed. (source: Drug Bank )
trimipramine - tizanidine	Trimipramine may reduce the antihypertensive effect of the alpha2-agonist, Tizandine. Trimipramine may also increase the rebound hypertensive effect of Clonidine. Consider alternate therapy or monitor for changes in the therapeutic and adverse effects of Clonidine if Trimipramine is initiated, discontinued or dose changed. Tizandine should be withdrawn very gradually to reduce the risk of hypertensive crisis. (source: Drug Bank )
trimipramine - tramadol	Increased risk of serotonin syndrome. Monitor for symptoms of serotonin syndrome. (source: Drug Bank )
trimipramine - tranylcypromine	Increased risk of serotonin syndrome. Ensure adequate washout period between therapies to avoid toxicity. Avoid combination or monitor for symptoms of serotonin syndrome and/or hypertensive crisis. (source: Drug Bank )
trimipramine - trazodone	Increased risk of serotonin syndrome. Monitor for symptoms of serotonin syndrome. (source: Drug Bank )
trimipramine - venlafaxine	Increased risk of serotonin syndrome. Monitor for symptoms of serotonin syndrome. (source: Drug Bank )
trimipramine - voriconazole	Additive QTc-prolongation may occur, increasing the risk of serious ventricular arrhythmias. Voriconazole, a strong CYP3A4 inhibitor, may also decrease the metabolism and clearance of Trimipramine, a CYP3A4 substrate. Concomitant therapy should be used with caution. (source: Drug Bank )
trimipramine - vorinostat	Additive QTc-prolongation may occur, increasing the risk of serious ventricular arrhythmias. Concomitant therapy should be used with caution. (source: Drug Bank )
trimipramine - ziprasidone	May cause additive QTc-prolonging effects. Concomitant therapy is contraindicated. (source: Drug Bank )
trimipramine - zolmitriptan	Increased risk of serotonin syndrome. Monitor for symptoms of serotonin syndrome. (source: Drug Bank )
trimipramine - zuclopenthixol	Additive QTc-prolongation may occur, increasing the risk of serious ventricular arrhythmias. Concomitant therapy should be used with caution. (source: Drug Bank )
triprolidine - trimipramine	Triprolidine and Trimipramine, 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 )
triprolidine - trimipramine	Triprolidine and Trimipramine, 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 )
trospium - trimipramine	Trospium and Trimipramine, two anticholinergics, may cause additive anticholinergic effects and enhanced adverse/toxic effects. Monitor for enhanced anticholinergic effects. (source: Drug Bank )
venlafaxine - trimipramine	Increased risk of serotonin syndrome. Monitor for symptoms of serotonin syndrome. (source: Drug Bank )
voriconazole - trimipramine	Voriconazole, a strong CYP3A4 inhibitor, may increase the serum concentration of trimipramine by decreasing its metabolism. Additive QTc prolongation may also occur. Monitor for changes in the therapeutic and adverse effects of trimipramine if voriconazole is initiated, discontinued or dose changed. (source: Drug Bank )
vorinostat - trimipramine	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 )
ziprasidone - trimipramine	Additive QTc-prolonging effects may increase the risk of severe arrhythmias. Concomitant therapy is contraindicated. (source: Drug Bank )
zolmitriptan - trimipramine	Use of two serotonin modulators, such as zolmitriptan and trimipramine, increases the risk of serotonin syndrome. Consider alternate therapy or monitor for serotonin syndrome during concomitant therapy. (source: Drug Bank )
zuclopenthixol - trimipramine	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 )

Curated Information ?

view legend

Evidence	Disease
VA	Bipolar Disorder
DL CA	Depression
DL	Depression, Postpartum
VA	Mental Disorders
VA	Schizophrenia
VA	sedation

Relationships from National Drug File - Reference Terminology (NDF-RT)

May Treat

trimipramine may treat Depressive Disorder

Contraindicated With

trimipramine contraindicated with Drug Hypersensitivity
trimipramine contraindicated with Myocardial Infarction

Publications related to trimipramine: 39

view legend

	Clinical Pharmacogenetics Implementation Consortium Guideline (CPIC®) for CYP2D6 and CYP2C19 Genotypes and Dosing of Tricyclic Antidepressants: 2016 Update. Clinical pharmacology and therapeutics. 2016. Kevin Hicks J, et al.
VA	Association of ABCB1 gene variants, plasma antidepressant concentration, and treatment response: Results from a randomized clinical study. Journal of psychiatric research. 2016. Breitenstein Barbara, et al.
	Integrated Patient and Tumor Genetic Testing for Individualized Cancer Therapy. Clinical pharmacology and therapeutics. 2015. Hertz Daniel L, et al.
	Challenges in pharmacogenetics. European journal of clinical pharmacology. 2013. Cascorbi Ingolf, et al.
	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.
CA	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.
CA	Pharmacogenetics and gender association with psychotic episodes on nortriptyline lower doses: patient cases. ISRN pharmaceutics. 2011. Piatkov Irina, et al.
CA	Association between CYP2C1917 and metabolism of amitriptyline, citalopram and clomipramine in Dutch hospitalized patients. The pharmacogenomics journal.* 2010. de Vos A, et al.
	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.
	Polymorphisms in GRIK4, HTR2A, and FKBP5 show interactive effects in predicting remission to antidepressant treatment. Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology. 2010. Horstmann Sonja, et al.
CA	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.
CA	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.
CA	Influence of the CYP2D64 polymorphism on dose, switching and discontinuation of antidepressants. British journal of clinical pharmacology.* 2008. Bijl Monique J, et al.
CA	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.
CA	A fatal doxepin poisoning associated with a defective CYP2D6 genotype. The American journal of forensic medicine and pathology. 2007. Koski Anna, et al.
CA	A poor metabolizer for cytochromes P450 2D6 and 2C19: a case report on antidepressant treatment. CNS spectrums. 2006. Johnson Maria, et al.
CA	CYP2D6 and CYP2C19 genotypes and amitriptyline metabolite ratios in a series of medicolegal autopsies. Forensic science international. 2006. Koski Anna, et al.
	Serotonin transporter polymorphisms and side effects in antidepressant therapy--a pilot study. Pharmacogenomics. 2006. Popp Johannes, et al.
CA	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.
CA	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.
CA	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.
CA	Clomipramine, fluoxetine and CYP2D6 metabolic capacity in depressed patients. Human psychopharmacology. 2004. Vandel P, et al.
CA	Impact of CYP2D6 intermediate metabolizer alleles on single-dose desipramine pharmacokinetics. Pharmacogenetics. 2004. Furman Katherine D, et al.
CA	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.
CA VA	Trimipramine pharmacokinetics after intravenous and oral administration in carriers of CYP2D6 genotypes predicting poor, extensive and ultrahigh activity. Pharmacogenetics. 2003. Kirchheiner Julia, et al.
CA VA	Effects of polymorphisms in CYP2D6, CYP2C9, and CYP2C19 on trimipramine pharmacokinetics. Journal of clinical psychopharmacology. 2003. Kirchheiner Julia, et al.
CA	Contributions of CYP2D6, CYP2C9 and CYP2C19 to the biotransformation of E- and Z-doxepin in healthy volunteers. Pharmacogenetics. 2002. Kirchheiner Julia, et al.
CA	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.
	Seizures associated with therapeutic doses of venlafaxine and trimipramine. The Annals of pharmacotherapy. 2000. Schlienger R G, et al.
CA VA	Steady state plasma levels of the enantiomers of trimipramine and of its metabolites in CYP2D6-, CYP2C19- and CYP3A4/5-phenotyped patients. Therapeutic drug monitoring. 2000. Eap C B, et al.
CA	Clomipramine dose-effect study in patients with depression: clinical end points and pharmacokinetics. Danish University Antidepressant Group (DUAG). Clinical pharmacology and therapeutics. 1999.
CA	CYP2D6 phenotype-genotype relationships in African-Americans and Caucasians in Los Angeles. Pharmacogenetics. 1998. Leathart J B, et al.
CA	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.
CA	Steady-state plasma levels of nortriptyline and its 10-hydroxy metabolite: relationship to the CYP2D6 genotype. Psychopharmacology. 1996. Dahl M L, et al.
CA	Single-dose kinetics of clomipramine: relationship to the sparteine and S-mephenytoin oxidation polymorphisms. Clinical pharmacology and therapeutics. 1994. Nielsen K K, et al.
	Metabolism of trimipramine in vitro by human CYP2D6 isozyme. Research communications in chemical pathology and pharmacology. 1993. Bolaji O O, et al.
CA VA	Debrisoquine hydroxylation phenotypes of patients with high versus low to normal serum antidepressant concentrations. Journal of clinical psychopharmacology. 1992. Tacke U, et al.
CA	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.
	Influence of quinidine on the pharmacokinetics of trimipramine and on its effect on the waking EEG of healthy volunteers. A pilot study on two subjects. Neuropsychobiology. 1992. Eap C B, et al.

LinkOuts

Web Resource:: Wikipedia
DrugBank:: DB00726
ChEBI:: 9738

KEGG Drug:: D00394
PubChem Compound:: 5584
PubChem Substance:: 156272; 46507121

Drugs Product Database (DPD):: 761737
ChemSpider:: 5382
Therapeutic Targets Database:: DAP001153

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Chemical: Drug trimipramine

Summary

Annotation

December 2016 Update

Table 1: Dosing recommendations for TCAs based on CYP2D6 phenotype:

Table 2: Dosing recommendations for TCAs based on CYP2C19 phenotype:

May 2013

Excerpt from the dosing guidelines:

Summary

Annotation

Genes and/or phenotypes found in this label

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Description

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Pharmacology, Interactions, and Contraindications

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Pharmacology

Absorption, Distribution, Metabolism, Elimination & Toxicity

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Curated Information ?

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Curated Information ?

May Treat

Contraindicated With

Publications related to trimipramine: 39

LinkOuts

Chemical: Drug
trimipramine