Chemical: Drug
amitriptyline

Available Guidelines

  1. CPIC Guideline for amitriptyline and CYP2C19,CYP2D6
  2. DPWG Guideline for amitriptyline and CYP2D6

last updated 09/15/2016

1. CPIC Guideline for amitriptyline and CYP2C19,CYP2D6

Summary

The CPIC Dosing Guideline for amitriptyline recommends an alternative drug for CYP2D6 or CYP2C19 ultrarapid metabolizers and for CYP2D6 poor metabolizers. Consider a 50% dose reduction for CYP2C19 poor metabolizers and a 25% dose reduction for CYP2D6 intermediate metabolizers.

Annotation

May 2013

Advance online publication January 2013.

  • Guidelines regarding the use of pharmacogenomic tests in dosing of amitriptyline and nortriptyline have been published in Clinical Pharmacology and Therapeutics by the Clinical Pharmacogenetics Implementation Consortium (CPIC).
  • Excerpt from the 2013 dosing guidelines:
    • "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."
    • "At the time of the development of this recommendation, there is a lack of strong evidence available on the possible role of CYP2D6 or CYP2C19 in amitriptyline response in pediatric patient populations; however, there is no reason to suspect that CYP2D6 or CYP2C19 variant alleles would affect amitriptyline metabolism differently in children compared to adults."
  • The guideline includes dosing recommendation for amitriptyline based on:

Please note: "Because there is only sparse clinical evidence for an additive effect of CYP2D6 and CYP2C19 on amitriptyline dosing, the recommendations in the combined table are classified as optional."

Table 1: Dosing recommendations for amitriptyline based on CYP2D6 phenotype:a,b,c

Adapted from Tables 1 and 2 of the 2013 guideline manuscript.

Likely phenotype__Activity scoreGenotypesExamples of diplotypesImplications for TCA metabolismTherapeutic RecommendationsClassification of recommendation for amitriptyline/nortriptyline therapy
Ultrarapid metabolizer (~1-2% of patients)>2.0An individual carrying more than two copies of functional alleles*1/*1xN, *1/*2xNIncreased metabolism of tricyclics to less active compounds when compared to extensive metabolizers. Lower plasma concentrations will increase probability of pharmacotherapy failure.Avoid tricyclic use due to potential lack of efficacy. Consider alternative drug not metabolized by CYP2D6.
If a tricyclic is warranted, consider increasing the starting dose. Utilize therapeutic drug monitoring to guide dose adjustments.
Strong
Extensive metabolizer (~77-92% of patients)1.0-2.0**An individual carrying two alleles encoding full or reduced function or one full function allele together with either one nonfunctional or one reduced-function allele*1/*1, *1/*2, *2/*2, *1/*41, *1/*4, *2/*5, *10/*10Normal metabolism of tricyclics.Initiate therapy with recommended starting dose.Strong
Intermediate metabolizer (~2-11% of patients)0.5An individual carrying one reduced and one nonfunctional allele*4/*10, *5/*41Reduced metabolism of tricyclics to less active compounds when compared to extensive metabolizers. Higher plasma concentrations will increase the probability of side effects.Consider 25% reduction of recommended starting dose. Utilize therapeutic drug monitoring to guide dose adjustments.Moderate
Poor metabolizer (~5-10% of patients)0An individual carrying no functional alleles*4/*4, *4/*5, *5/*5, *4/*6Greatly reduced metabolism of tricyclics to less active compounds when compared to extensive metabolizers. Higher plasma concentrations 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 tricyclic is warranted, consider 50% reduction of recommended starting dose. Utilize therapeutic drug monitoring to guide dose adjustments.
Strong

*CYP2D6 metabolizer status frequencies are based on data from Caucasians and may differ from other ethnicities.

**Patients with an activity score of 1.0 may be classified as intermediate metabolizers by some reference laboratories. See Supplementary Table S4 for additional information about CYP2D6 activity score and its limitations.

a Patients may receive an initial low dose of tricyclics, 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.

b If CYP2C19 genotyping results are also available see Table 2 below.

c Dosing recommendations only apply to higher initial doses of amitriptyline or nortriptyline for treatment of conditions such as depression.

Table 2: Dosing recommendations for amitriptyline based on CYP2C19 phenotype:a,b,c

Adapted from Tables 1 and 3 of the 2013 guideline manuscript.

Phenotype (Genotype)GenotypesExamples of diplotypesImplications for amitriptylineTherapeutic recommendationsClassification of recommendations
CYP2C19 Ultrarapid metabolizer (UM)An individual carrying two gain-of-function alleles or one functional allele and one gain-of-function allele*17/*17, *1/*17Increased metabolism of amitriptyline when compared to extensive metabolizers.Consider alternative drug not metabolized by CYP2C19.
If a tricyclic is warranted, utilize therapeutic drug monitoring to guide dose adjustments.
Optional
CYP2C19 Extensive metabolizer (EM)An individual carrying two functional alleles*1/*1Normal metabolism of amitriptyline.Initiate therapy with recommended starting dose.aStrong
CYP2C19 Intermediate metabolizer (IM)An individual carrying one functional allele and one loss-of-function allele*1/*2, *1/*3Reduced metabolism of amitriptyline when compared to extensive metabolizers.Initiate therapy with recommended starting dose.aStrong
CYP2C19 Poor metabolizer (PM)An individual carrying two loss-of-function alleles*2/*2, *2/*3, *3/*3Greatly reduced metabolism of amitriptyline when compared to extensive metabolizers. Higher plasma concentrations of amitriptyline will increase the probability of side effects.Consider 50% reduction of recommended starting dose.a Utilize therapeutic drug monitoring to guide dose adjustments.Moderate

a Patients may receive an initial low dose of tricyclics, 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.

b If CYP2D6 genotyping results are also available see Table 1 above.

c Dosing recommendations only apply to higher initial doses of amitriptyline for treatment of conditions such as depression.

Table 3: Dosing recommendations for amitriptyline based on both CYP2D6 and CYP2C19 phenotype: 1,2,3,4

Adapted from Supplemental Table S19 of the 2013 guideline supplements.

Because there is only sparse clinical evidence for an additive effect of CYP2D6 and CYP2C19 on amitriptyline dosing, the recommendations in the table below are classified as optional. The optional dosing recommendations provided in the table below were developed by assessment of the supporting data in Supplemental Table S12, and by combining the dosing recommendations for CYP2D6 and CYP2C19. However, further studies are needed to develop moderate or strong dosing recommendations for tricyclics when considering combined CYP2D6/CYP2C19 phenotypes.

PhenotypeCYP2D6 Ultrarapid metabolizerCYP2D6 Extensive metabolizerCYP2D6 Intermediate metabolizerCYP2D6 Poor metabolizer
CYP2C19 Ultrarapid metabolizerAvoid tricyclic use. If a tricyclic is warranted utilize therapeutic drug monitoring to guide dose adjustment.Consider alternative drug not metabolized by CYP2C19. If a tricyclic is warranted, utilize therapeutic drug monitoring to guide dose adjustments.Consider alternative drug not metabolized by CYP2C19. If a tricyclic is warranted, utilize therapeutic drug monitoring to guide dose adjustments.Avoid tricyclic use. If a tricyclic is warranted utilize therapeutic drug monitoring to guide dose adjustment.
CYP2C19 Extensive metabolizerAvoid tricyclic use. If a tricyclic is warranted consider increasing the starting dose. 1 Utilize therapeutic drug monitoring to guide dose adjustments.Initiate therapy with recommended starting dose. 1Consider 25% reduction of recommended starting dose. 1 Utilize therapeutic drug monitoring to guide dose adjustments.Avoid tricyclic use. If a tricyclic is warranted consider 50% reduction of recommended starting dose. 1 Utilize therapeutic drug monitoring to guide dose adjustment.
CYP2C19 Intermediate metabolizerAvoid tricyclic use. If a tricyclic is warranted utilize therapeutic drug monitoring to guide dose adjustments.Initiate therapy with recommended starting dose. 1Consider 25% reduction of recommended starting dose. 1 Utilize therapeutic drug monitoring to guide dose adjustments.Avoid tricyclic use. If a tricyclic is warranted consider 50% reduction of recommended starting dose a Utilize therapeutic drug monitoring to guide dose adjustment.
CYP2C19 Poor metabolizerAvoid tricyclic use. If a tricyclic is warranted utilize therapeutic drug monitoring to guide dose adjustments.Consider 50% reduction of recommended starting dose. 1 Utilize therapeutic drug monitoring to guide dose adjustments.Avoid tricyclic use. If a tricyclic is warranted utilize therapeutic drug monitoring to guide dose adjustments.Avoid tricyclic use. If a tricyclic is warranted utilize therapeutic drug monitoring to guide dose adjustments.

1 Patients may receive an initial low dose of tricyclics, 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.

2 The classification for all of the dosing recommendations in this table is optional.

3 Dosing recommendations only apply to higher initial doses of amitriptyline for treatment of conditions such as depression.

4 The dosing recommendations are based on studies focusing on amitriptyline. Therapeutic drug monitoring of tricyclic antidepressants is well described in the literature. Because certain phenotype combinations are rare (e.g., CYP2C19 ultrarapid metabolizer also having CYP2D6 ultrarapid metabolism) sparse data are available to develop dosing recommendations. Therefore, we strongly recommend utilizing therapeutic drug monitoring if a tricyclic is prescribed to a patient with CYP2D6 ultrarapid, intermediate or poor metabolism in combination with CYP2C19 ultrarapid, intermediate or poor metabolism.


last updated 09/15/2016

2. DPWG Guideline for amitriptyline and CYP2D6

Summary

The Dutch Pharmacogenetics Working Group Guideline for amitriptyline recommends to select an alternative drug or monitor amitriptyline and nortriptyline plasma concentration for patients who are CYP2D6 poor or ultrarapid metabolizers. Reduce the initial dose for patients who are intermediate metabolizers or select an alternative drug.

Annotation

The Royal Dutch Pharmacists Association - Pharmacogenetics Working Group has evaluated therapeutic dose recommendations for amitriptyline based on CYP2D6 genotypes [Article:21412232]. They recommend selecting an alternative drug or reducing the initial dose for patients carrying intermediate metabolizer alleles and selecting alternative drugs or monitor amitypityline and nortriptyline plasma concentration for patients carrying the poor metabolizer or ultrarapid metabolizer alleles.

Phenotype (Genotype)Therapeutic Dose RecommendationLevel of EvidenceClinical Relevance
PM (two inactive (*3-*8, *11-*16, *19-*21, *38, *40, *42) alleles)Insufficient data to allow calculation of dose adjustment. Select alternative drug (e.g., citalopram, sertraline) or monitor amitriptyline and nortriptyline plasma concentration.Published controlled studies of moderate quality* relating to phenotyped and/or genotyped patients or healthy volunteers, and having relevant pharmacokinetic or clinical endpoints.Minor clinical effect (S): QTc prolongation (<450 ms female, <470 ms male); INR increase < 4.5; Kinetic effect (S)
IM (two decreased-activity (*9, *10, *17, *29, *36, *41) alleles or carrying one active (*1, *2, *33, *35) and one inactive (*3-*8, *11-*16, *19-*21, *38, *40, *42) allele, or carrying one decreased-activity (*9, *10, *17, *29, *36, *41) allele and one inactive (*3-*8, *11-*16, *19-*21, *38, *40, *42) allele)Reduce dose by 25% and monitor plasma concentration or select alternative drug (e.g., citalopram, sertraline).Published controlled studies of good quality* relating to phenotyped and/or genotyped patients or healthy volunteers, and having relevant pharmacokinetic or clinical endpoints.Clinical effect (S): long-standing discomfort (48-168 hr) without permanent injury e.g. failure of therapy with tricyclic antidepressants, atypical antipsychotic drugs; extrapyramidal side effects; parkinsonism; ADE resulting from increased bioavailability of tricyclic antidepressants, metoprolol, propafenone (central effects e.g. dizziness); INR 4.5-6.0; neutropenia 1.0-1.5x109/l; leucopenia 2.0-3.0x109/l; thrombocytopenia 50-75x109/l
UM (a gene duplication in absence of inactive (*3-*8, *11-*16, *19-*21, *38, *40, *42) or decreased-activity (*9, *10, *17, *29, *36, *41) alleles)Insufficient data to allow calculation of dose adjustment. Select alternative drug (e.g., citalopram,sertraline) or monitor (E-10-hydroxy)amitriptyline plasma concentration.Published controlled studies of moderate quality* relating to phenotyped and/or genotyped patients or healthy volunteers, and having relevant pharmacokinetic or clinical endpoints.Clinical effect (S): long-standing discomfort (48-168 hr) without permanent injury e.g. failure of therapy with tricyclic antidepressants, atypical antipsychotic drugs; extrapyramidal side effects; parkinsonism; ADE resulting from increased bioavailability of tricyclic antidepressants, metoprolol, propafenone (central effects e.g. dizziness); INR 4.5-6.0; neutropenia 1.0-1.5x109/l; leucopenia 2.0-3.0x109/l; thrombocytopenia 50-75x109/l.
  • *See Methods or [Article:18253145] for definition of "good" and "moderate" quality.
  • S: statistically significant difference.
  • Please see attached PDF for detailed information about the evaluated studies: Amitriptyline CYP2D6


last updated 09/01/2016

1. FDA Label for amitriptyline and CYP2D6

Actionable PGx
Full label available at DailyMed

Genes and/or phenotypes found in this label

  • Depression
    • Indications & usage section, Contraindications section, Warnings section, Adverse reactions section, Precautions section
    • source: PHONT
  • Depression, Postpartum
    • Indications & usage section, Contraindications section, Warnings section, Adverse reactions section, Precautions section
    • source: PHONT
  • Pain
    • Warnings section, Adverse reactions section
    • source: PHONT
  • CYP2D6
    • metabolism/PK, Precautions 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 rs2032583 (ABCB1), amitriptyline, antidepressants, citalopram, fluvoxamine, paroxetine, sertraline, venlafaxine, Depression, Depressive Disorder and Depressive Disorder, Major (level 3 Efficacy)

Level of Evidence
Level 3
Type
Efficacy
Variant
rs2032583
Genes
ABCB1
Phenotypes
Depression, Depressive Disorder, Depressive Disorder, Major
OMB Race
White
Race Notes
One study in mostly German patients, the other unknown race.

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

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 amitriptyline

Gene ? Variant?
(147)
Alternate Names ? Chemicals ? Alleles ?
(+ chr strand)
Function ? Amino Acid?
Translation
No VIP available CA VA CYP2C19 *1 N/A N/A N/A
No VIP available No VIP available VA CYP2C19 *1A N/A N/A N/A
No VIP available CA VA CYP2C19 *2 N/A N/A N/A
VIP No VIP available VA CYP2C19 *2A N/A N/A N/A
No VIP available CA VA CYP2C19 *3 N/A N/A N/A
VIP No VIP available No VIP available CYP2C19 *3A N/A N/A N/A
No VIP available CA VA CYP2C19 *17 N/A N/A N/A
VIP CA VA CYP2D6 *1 N/A N/A N/A
No VIP available CA VA CYP2D6 *1xN N/A N/A N/A
VIP CA VA CYP2D6 *2 N/A N/A N/A
No VIP available CA VA CYP2D6 *2xN N/A N/A N/A
VIP CA VA CYP2D6 *3 N/A N/A N/A
VIP CA VA CYP2D6 *4 N/A N/A N/A
No VIP available CA VA CYP2D6 *5 N/A N/A N/A
VIP CA VA CYP2D6 *6 N/A N/A N/A
VIP No VIP available VA CYP2D6 *9 N/A N/A N/A
VIP CA VA CYP2D6 *10 N/A N/A N/A
VIP No VIP available No VIP available CYP2D6 *17 N/A N/A N/A
VIP No VIP available No VIP available CYP2D6 *29 N/A N/A N/A
VIP CA VA CYP2D6 *41 N/A N/A N/A
No VIP available No VIP available VA CYP2D6 *87 N/A N/A N/A
No VIP available No VIP available VA CYP2D6 *88 N/A N/A N/A
No VIP available No VIP available VA CYP2D6 *89 N/A N/A N/A
No VIP available No VIP available VA CYP2D6 *90 N/A N/A N/A
No VIP available No VIP available VA CYP2D6 *91 N/A N/A N/A
No VIP available No VIP available VA CYP2D6 *93 N/A N/A N/A
No VIP available No VIP available VA CYP2D6 *94 N/A N/A N/A
No VIP available No VIP available VA CYP2D6 *95 N/A N/A N/A
No VIP available No VIP available VA CYP2D6 *97 N/A N/A N/A
No VIP available No VIP available VA CYP2D6 *98 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 CA VA
rs10248420 NC_000007.13:g.87164986A>G, NC_000007.14:g.87535670A>G, NG_011513.1:g.182579T>C, NM_000927.4:c.2481+788T>C, rs56939197
A > G
SNP
No VIP available CA VA
rs10280101 NC_000007.13:g.87153585A>C, NC_000007.14:g.87524269A>C, NG_011513.1:g.193980T>G, NM_000927.4:c.2686-3393T>G, rs56546728, rs57009801
A > C
SNP
VIP No Clinical Annotations available No Variant Annotations available
rs1065852 NC_000022.10:g.42526694G=, NC_000022.10:g.42526694G>A, NC_000022.11:g.42130692G=, NC_000022.11:g.42130692G>A, NG_008376.3:g.4300C=, NG_008376.3:g.4300C>T, NM_000106.5:c.100C=, NM_000106.5:c.100C>T, NM_001025161.2:c.100C=, NM_001025161.2:c.100C>T, NP_000097.3:p.Pro34=, NP_000097.3:p.Pro34Ser, NP_001020332.2:p.Pro34=, NP_001020332.2:p.Pro34Ser, NT_187682.1:g.53033G=, NT_187682.1:g.53033G>A, NW_004504305.1:g.53019A=, NW_004504305.1:g.53019A>G, NW_009646208.1:g.16258A=, NW_009646208.1:g.16258A>G, XM_005278353.1:c.100T=, XM_005278353.1:c.100T>C, XM_005278354.1:c.-1454C>T, XM_005278354.1:c.-1454T>C, XM_005278354.3:c.-1454C>T, XM_005278354.3:c.-1454T>C, XM_011529966.1:c.100C=, XM_011529966.1:c.100C>T, XM_011529967.1:c.100C=, XM_011529967.1:c.100C>T, XM_011529968.1:c.100C=, XM_011529968.1:c.100C>T, XM_011529969.1:c.37+605C>T, XM_011529969.1:c.37+605T>C, XM_011529970.1:c.100C=, XM_011529970.1:c.100C>T, XM_011529971.1:c.37+605C>T, XM_011529971.1:c.37+605T>C, XM_011529972.1:c.100C=, XM_011529972.1:c.100C>T, XM_011547541.1:c.-1454C>T, XM_011547541.1:c.-1454T>C, XM_011547750.1:c.37+605C>T, XM_011547750.1:c.37+605T>C, XM_011547751.1:c.-1114C>T, XM_011547751.1:c.-1114T>C, XM_011547756.1:c.42+469A>G, XM_011547756.1:c.42+469G>A, XM_011548819.1:c.-1454C>T, XM_011548819.1:c.-1454T>C, XP_005278410.1:p.Ser34=, XP_005278410.1:p.Ser34Pro, XP_011528268.1:p.Pro34=, XP_011528268.1:p.Pro34Ser, XP_011528269.1:p.Pro34=, XP_011528269.1:p.Pro34Ser, XP_011528270.1:p.Pro34=, XP_011528270.1:p.Pro34Ser, XP_011528272.1:p.Pro34=, XP_011528272.1:p.Pro34Ser, XP_011528274.1:p.Pro34=, XP_011528274.1:p.Pro34Ser, XR_430455.2:n.328+4A>G, XR_430455.2:n.328+4G>A, XR_952536.1:n.-1751A>G, XR_952536.1:n.-1751G>A, XR_952537.1:n.-1751A>G, XR_952537.1:n.-1751G>A, XR_952538.1:n.-1751A>G, XR_952538.1:n.-1751G>A, XR_952539.1:n.-1462A>G, XR_952539.1:n.-1462G>A, XR_952745.1:n.1257C=, XR_952745.1:n.1257C>T, rs117813846, rs58862176
G > A
SNP
P34S
No VIP available CA VA
rs11983225 NC_000007.13:g.87161520T>C, NC_000007.14:g.87532204T>C, NG_011513.1:g.186045A>G, NM_000927.4:c.2482-707A>G
T > C
SNP
No VIP available CA VA
rs12248560 NC_000010.10:g.96521657C>T, NC_000010.11:g.94761900C>T, NG_008384.2:g.4195C>T, NM_000769.2:c.-806C>T, rs117093607, rs17442305, rs17879736
C > A
C > T
SNP
No VIP available CA VA
rs12720067 NC_000007.13:g.87169356C>T, NC_000007.14:g.87540040C>T, NG_011513.1:g.178209G>A, NM_000927.4:c.2320-695G>A, rs17276510, rs60504551
C > T
SNP
VIP No Clinical Annotations available No Variant Annotations available
rs16947 NC_000022.10:g.42523943A=, NC_000022.10:g.42523943A>G, NC_000022.11:g.42127941G=, NC_000022.11:g.42127941G>A, NG_008376.3:g.7051C=, NG_008376.3:g.7051C>T, NM_000106.5:c.886C=, NM_000106.5:c.886C>T, NM_001025161.2:c.733C=, NM_001025161.2:c.733C>T, NP_000097.3:p.Arg296=, NP_000097.3:p.Arg296Cys, NP_001020332.2:p.Arg245=, NP_001020332.2:p.Arg245Cys, NT_187682.1:g.50282A=, NT_187682.1:g.50282A>G, NW_004504305.1:g.50268G=, NW_004504305.1:g.50268G>A, NW_009646208.1:g.13507G=, NW_009646208.1:g.13507G>A, XM_005278353.1:c.742C=, XM_005278353.1:c.742C>T, XM_005278354.1:c.586C=, XM_005278354.1:c.586C>T, XM_005278354.3:c.586C=, XM_005278354.3:c.586C>T, XM_011529966.1:c.886C=, XM_011529966.1:c.886C>T, XM_011529967.1:c.886C=, XM_011529967.1:c.886C>T, XM_011529968.1:c.886C=, XM_011529968.1:c.886C>T, XM_011529969.1:c.742C=, XM_011529969.1:c.742C>T, XM_011529970.1:c.733C=, XM_011529970.1:c.733C>T, XM_011529971.1:c.742C=, XM_011529971.1:c.742C>T, XM_011529972.1:c.843+233C>T, XM_011529972.1:c.843+233T>C, XM_011547541.1:c.586C=, XM_011547541.1:c.586C>T, XM_011547750.1:c.742T=, XM_011547750.1:c.742T>C, XM_011547751.1:c.670T=, XM_011547751.1:c.670T>C, XM_011547756.1:c.-2094A>G, XM_011547756.1:c.-2094G>A, XM_011548819.1:c.586C=, XM_011548819.1:c.586C>T, XP_005278410.1:p.Arg248=, XP_005278410.1:p.Arg248Cys, XP_005278411.1:p.Arg196=, XP_005278411.1:p.Arg196Cys, XP_011528268.1:p.Arg296=, XP_011528268.1:p.Arg296Cys, XP_011528269.1:p.Arg296=, XP_011528269.1:p.Arg296Cys, XP_011528270.1:p.Arg296=, XP_011528270.1:p.Arg296Cys, XP_011528271.1:p.Arg248=, XP_011528271.1:p.Arg248Cys, XP_011528272.1:p.Arg245=, XP_011528272.1:p.Arg245Cys, XP_011528273.1:p.Arg248=, XP_011528273.1:p.Arg248Cys, XP_011545843.1:p.Arg196=, XP_011545843.1:p.Arg196Cys, XP_011546052.1:p.Cys248=, XP_011546052.1:p.Cys248Arg, XP_011546053.1:p.Cys224=, XP_011546053.1:p.Cys224Arg, XP_011547121.1:p.Arg196=, XP_011547121.1:p.Arg196Cys, XR_430455.2:n.-1930A>G, XR_430455.2:n.-1930G>A, XR_952745.1:n.2000+233C>T, XR_952745.1:n.2000+233T>C, rs117039205, rs57836231
A > G
SNP
R296C
No VIP available No Clinical Annotations available VA
rs2032582 NC_000007.13:g.87160618A>C, NC_000007.13:g.87160618A>T, NC_000007.14:g.87531302A>C, NC_000007.14:g.87531302A>T, NG_011513.1:g.186947T>A, NG_011513.1:g.186947T>G, NM_000927.4:c.2677T>A, NM_000927.4:c.2677T>G, NP_000918.2:p.Ser893Ala, NP_000918.2:p.Ser893Thr, rs10228331, rs2229106, rs386553610, rs57135550, rs9641018
A > C
SNP
S893A
No VIP available CA VA
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
A > G
SNP
No VIP available CA VA
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
C > A
SNP
No VIP available CA VA
rs2235040 NC_000007.13:g.87165750C>T, NC_000007.14:g.87536434C>T, NG_011513.1:g.181815G>A, NM_000927.4:c.2481+24G>A, rs10383656, rs386562018, rs59503449, rs60553448
C > T
SNP
No VIP available CA VA
rs2235067 NC_000007.13:g.87149922C>T, NC_000007.14:g.87520606C>T, NG_011513.1:g.197643G>A, NM_000927.4:c.2786+170G>A, rs10345072, rs17149713, rs386562030, rs57277203
C > T
SNP
VIP No Clinical Annotations available No Variant Annotations available
rs28371706 NC_000022.10:g.42525772G>A, NC_000022.11:g.42129770G>A, NG_008376.3:g.5222C>T, NM_000106.5:c.320C>T, NM_001025161.2:c.320C>T, NP_000097.3:p.Thr107Ile, NP_001020332.2:p.Thr107Ile, NT_187682.1:g.52111G>A, NW_004504305.1:g.52097G>A, NW_009646208.1:g.15336G>A, XM_005278353.1:c.320C>T, XM_005278354.1:c.-532C>T, XM_005278354.3:c.-532C>T, XM_011529966.1:c.320C>T, XM_011529967.1:c.320C>T, XM_011529968.1:c.320C>T, XM_011529969.1:c.177C>T, XM_011529970.1:c.320C>T, XM_011529971.1:c.177C>T, XM_011529972.1:c.320C>T, XM_011547541.1:c.-532C>T, XM_011547750.1:c.177C>T, XM_011547751.1:c.-192C>T, XM_011547756.1:c.-265G>A, XM_011548819.1:c.-532C>T, XP_005278410.1:p.Thr107Ile, XP_011528268.1:p.Thr107Ile, XP_011528269.1:p.Thr107Ile, XP_011528270.1:p.Thr107Ile, XP_011528271.1:p.His59=, XP_011528272.1:p.Thr107Ile, XP_011528273.1:p.His59=, XP_011528274.1:p.Thr107Ile, XP_011546052.1:p.His59=, XR_430455.2:n.-101G>A, XR_952745.1:n.1477C>T, rs587777915, rs59604033
G > A
SNP
T107I
VIP No Clinical Annotations available No Variant Annotations available
rs28371725 NC_000022.10:g.42523805C>T, NC_000022.11:g.42127803C>T, NG_008376.3:g.7189G>A, NM_000106.5:c.985+39G>A, NM_001025161.2:c.832+39G>A, NT_187682.1:g.50144C>T, NW_004504305.1:g.50130C>T, NW_009646208.1:g.13369C>T, XM_005278353.1:c.841+39G>A, XM_005278354.1:c.685+39G>A, XM_005278354.3:c.685+39G>A, XM_011529966.1:c.985+39G>A, XM_011529967.1:c.985+39G>A, XM_011529968.1:c.985+39G>A, XM_011529969.1:c.841+39G>A, XM_011529970.1:c.832+39G>A, XM_011529971.1:c.841+39G>A, XM_011529972.1:c.844-169G>A, XM_011547541.1:c.724G>A, XM_011547750.1:c.841+39G>A, XM_011547751.1:c.769+39G>A, XM_011548819.1:c.724G>A, XP_011545843.1:p.Glu242Lys, XP_011547121.1:p.Glu242Lys, XR_952745.1:n.2001-169G>A, rs57124011, rs587777916
C > T
SNP
VIP No Clinical Annotations available No Variant Annotations available
rs35742686 NC_000022.10:g.42524244delT, NC_000022.11:g.42128242delT, NG_008376.3:g.6750delA, NM_000106.5:c.775delA, NM_001025161.2:c.622delA, NP_000097.3:p.Arg259Glyfs, NP_001020332.2:p.Arg208Glyfs, NT_187682.1:g.50583delT, NW_004504305.1:g.50569delT, NW_009646208.1:g.13808delT, XM_005278353.1:c.631delA, XM_005278354.1:c.475delA, XM_005278354.3:c.475delA, XM_011529966.1:c.775delA, XM_011529967.1:c.775delA, XM_011529968.1:c.775delA, XM_011529969.1:c.631delA, XM_011529970.1:c.622delA, XM_011529971.1:c.631delA, XM_011529972.1:c.775delA, XM_011547541.1:c.475delA, XM_011547750.1:c.631delA, XM_011547751.1:c.559delA, XM_011547756.1:c.-1793delT, XM_011548819.1:c.475delA, XP_005278410.1:p.Arg211Glyfs, XP_005278411.1:p.Arg159Glyfs, XP_011528268.1:p.Arg259Glyfs, XP_011528269.1:p.Arg259Glyfs, XP_011528270.1:p.Arg259Glyfs, XP_011528271.1:p.Arg211Glyfs, XP_011528272.1:p.Arg208Glyfs, XP_011528273.1:p.Arg211Glyfs, XP_011528274.1:p.Arg259Glyfs, XP_011545843.1:p.Arg159Glyfs, XP_011546052.1:p.Arg211Glyfs, XP_011546053.1:p.Arg187Glyfs, XP_011547121.1:p.Arg159Glyfs, XR_430455.2:n.-1629delT, XR_952745.1:n.1932delA, rs45593132, rs60790764
T > -
T > T
indel
R259G
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
C > T
SNP
No VIP available CA VA
rs4148739 NC_000007.13:g.87161049T>C, NC_000007.14:g.87531733T>C, NG_011513.1:g.186516A>G, NM_000927.4:c.2482-236A>G, rs10381901, rs117890992
T > C
SNP
No VIP available CA VA
rs4148740 NC_000007.13:g.87152103A>G, NC_000007.14:g.87522787A>G, NG_011513.1:g.195462T>C, NM_000927.4:c.2686-1911T>C, rs10380430
A > G
SNP
rs4244285 NC_000010.10:g.96541616G>A, NC_000010.11:g.94781859G>A, NG_008384.2:g.24154G>A, NM_000769.1:c.681G>A, NM_000769.2:c.681G>A, NP_000760.1:p.Pro227=, rs116940633, rs17879456, rs60361278
G > A
SNP
P227P
VIP No Clinical Annotations available No Variant Annotations available
rs4986893 NC_000010.10:g.96540410G>A, NC_000010.11:g.94780653G>A, NG_008384.2:g.22948G>A, NM_000769.2:c.636G>A, NP_000760.1:p.Trp212Ter, rs52827375, rs57081121
G > A
SNP
W212*
VIP No Clinical Annotations available No Variant Annotations available
rs5030655 NC_000022.10:g.42525086delA, NC_000022.11:g.42129084delA, NG_008376.3:g.5908delT, NM_000106.5:c.454delT, NM_001025161.2:c.353-140delT, NP_000097.3:p.Trp152Glyfs, NT_187682.1:g.51425delA, NW_004504305.1:g.51411delA, NW_009646208.1:g.14650delA, XM_005278353.1:c.363-141delT, XM_005278354.1:c.155delT, XM_005278354.3:c.155delT, XM_011529966.1:c.454delT, XM_011529967.1:c.454delT, XM_011529968.1:c.454delT, XM_011529969.1:c.311delT, XM_011529970.1:c.353-140delT, XM_011529971.1:c.311delT, XM_011529972.1:c.454delT, XM_011547541.1:c.155delT, XM_011547750.1:c.311delT, XM_011547751.1:c.238delT, XM_011547756.1:c.-951delA, XM_011548819.1:c.155delT, XP_005278411.1:p.Val52Glyfs, XP_011528268.1:p.Trp152Glyfs, XP_011528269.1:p.Trp152Glyfs, XP_011528270.1:p.Trp152Glyfs, XP_011528271.1:p.Val104Glyfs, XP_011528273.1:p.Val104Glyfs, XP_011528274.1:p.Trp152Glyfs, XP_011545843.1:p.Val52Glyfs, XP_011546052.1:p.Val104Glyfs, XP_011546053.1:p.Trp80Glyfs, XP_011547121.1:p.Val52Glyfs, XR_430455.2:n.-787delA, XR_952745.1:n.1611delT, rs11568727, rs28371709
A > -
A > A
indel
W152G
VIP No Clinical Annotations available No Variant Annotations available
rs5030656 NC_000022.10:g.42524176_42524178delCTT, NC_000022.11:g.42128174_42128176delCTT, NG_008376.3:g.6816_6818delAAG, NM_000106.5:c.841_843delAAG, NM_001025161.2:c.688_690delAAG, NP_000097.3:p.Lys281del, NP_001020332.2:p.Lys230del, NT_187682.1:g.50515_50517delCTT, NW_004504305.1:g.50501_50503delCTT, NW_009646208.1:g.13740_13742delCTT, XM_005278353.1:c.697_699delAAG, XM_005278354.1:c.541_543delAAG, XM_005278354.3:c.541_543delAAG, XM_011529966.1:c.841_843delAAG, XM_011529967.1:c.841_843delAAG, XM_011529968.1:c.841_843delAAG, XM_011529969.1:c.697_699delAAG, XM_011529970.1:c.688_690delAAG, XM_011529971.1:c.697_699delAAG, XM_011529972.1:c.841_843delAAG, XM_011547541.1:c.541_543delAAG, XM_011547750.1:c.697_699delAAG, XM_011547751.1:c.625_627delAAG, XM_011547756.1:c.-1861_-1859del, XM_011548819.1:c.541_543delAAG, XP_005278410.1:p.Lys233del, XP_005278411.1:p.Lys181del, XP_011528268.1:p.Lys281del, XP_011528269.1:p.Lys281del, XP_011528270.1:p.Lys281del, XP_011528271.1:p.Lys233del, XP_011528272.1:p.Lys230del, XP_011528273.1:p.Lys233del, XP_011528274.1:p.Lys281del, XP_011545843.1:p.Lys181del, XP_011546052.1:p.Lys233del, XP_011546053.1:p.Lys209del, XP_011547121.1:p.Lys181del, XR_430455.2:n.-1697_-1695del, XR_952745.1:n.1998_2000delAAG, rs587777919
CTT > -
CTT > CTT
indel
VIP No Clinical Annotations available No Variant Annotations available
rs59421388 NC_000022.10:g.42523610C>T, NC_000022.11:g.42127608C>T, NG_008376.3:g.7384G>A, NM_000106.5:c.1012G>A, NM_001025161.2:c.859G>A, NP_000097.3:p.Val338Met, NP_001020332.2:p.Val287Met, NT_187682.1:g.49949C>T, NW_004504305.1:g.49935C>T, NW_009646208.1:g.13174C>T, XM_005278353.1:c.868G>A, XM_005278354.1:c.712G>A, XM_005278354.3:c.712G>A, XM_011529966.1:c.1012G>A, XM_011529967.1:c.1012G>A, XM_011529968.1:c.1012G>A, XM_011529969.1:c.868G>A, XM_011529970.1:c.859G>A, XM_011529971.1:c.868G>A, XM_011529972.1:c.870G>A, XM_011547541.1:c.*118G>A, XM_011547750.1:c.868G>A, XM_011547751.1:c.796G>A, XM_011548819.1:c.*118G>A, XP_005278410.1:p.Val290Met, XP_005278411.1:p.Val238Met, XP_011528268.1:p.Val338Met, XP_011528269.1:p.Val338Met, XP_011528270.1:p.Val338Met, XP_011528271.1:p.Val290Met, XP_011528272.1:p.Val287Met, XP_011528273.1:p.Val290Met, XP_011528274.1:p.Thr290=, XP_011546052.1:p.Val290Met, XP_011546053.1:p.Val266Met, XR_952745.1:n.2027G>A
C > T
SNP
V338M
VIP No Clinical Annotations available No Variant Annotations available
rs61736512 NC_000022.10:g.42525134C>T, NC_000022.11:g.42129132C>T, NG_008376.3:g.5860G>A, NM_000106.5:c.406G>A, NM_001025161.2:c.353-188G>A, NP_000097.3:p.Val136Met, NT_187682.1:g.51473C>T, NW_004504305.1:g.51459C>T, NW_009646208.1:g.14698C>T, XM_005278353.1:c.363-189G>A, XM_005278354.1:c.107G>A, XM_005278354.3:c.107G>A, XM_011529966.1:c.406G>A, XM_011529967.1:c.406G>A, XM_011529968.1:c.406G>A, XM_011529969.1:c.263G>A, XM_011529970.1:c.353-188G>A, XM_011529971.1:c.263G>A, XM_011529972.1:c.406G>A, XM_011547541.1:c.107G>A, XM_011547750.1:c.263G>A, XM_011547751.1:c.190G>A, XM_011547756.1:c.-903C>T, XM_011548819.1:c.107G>A, XP_005278411.1:p.Arg36His, XP_011528268.1:p.Val136Met, XP_011528269.1:p.Val136Met, XP_011528270.1:p.Val136Met, XP_011528271.1:p.Arg88His, XP_011528273.1:p.Arg88His, XP_011528274.1:p.Val136Met, XP_011545843.1:p.Arg36His, XP_011546052.1:p.Arg88His, XP_011546053.1:p.Val64Ile, XP_011547121.1:p.Arg36His, XR_430455.2:n.-739C>T, XR_952745.1:n.1563G>A
C > T
SNP
V136M
No VIP available CA VA
rs7787082 NC_000007.13:g.87157051G>A, NC_000007.14:g.87527735G>A, NG_011513.1:g.190514C>T, NM_000927.4:c.2685+3559C>T, rs10352064, rs17333784, rs56434207, rs56854239
G > A
SNP
Alleles, Functions, and Amino Acid Translations are all sourced from dbSNP 147

Overview

Generic Names
  • Amitriprolidine
  • Amitriptylin
  • Amitriptyline HCL
  • Amitriptyline Hydrochloride
  • Amitryptiline
  • Amitryptyline
  • Amytriptiline
Trade Names
  • Adepress
  • Adepril
  • Amitid
  • Amitril
  • Damilan
  • Damilen
  • Elanil
  • Elavil
  • Endep
  • Flavyl
  • Hexathane
  • Horizon
  • Lantron
  • Laroxil
  • Laroxyl
  • Lentizol
  • Proheptadiene
  • Redomex
  • Saroten
  • Sarotex
  • Seroten
  • Sylvemid
  • Triptanol
  • Triptilin
  • Triptisol
  • Tryptanol
  • Tryptizol
  • dAmitriptyline
Brand Mixture Names
  • Apo Peram Tab 2-25 (Amitriptyline Hydrochloride + Perphenazine)
  • Apo Peram Tab 3-15 (Amitriptyline Hydrochloride + Perphenazine)
  • Elavil Plus Tab (Amitriptyline Hydrochloride + Perphenazine)
  • Etrafon 2 10 (Amitriptyline Hydrochloride + Perphenazine)
  • Etrafon D Tab (Amitriptyline Hydrochloride + Perphenazine)
  • Etrafon F Tab (Amitriptyline Hydrochloride + Perphenazine)
  • Etrafon a Tab (Amitriptyline Hydrochloride + Perphenazine)
  • Pms-Levazine 2/25 Tab (Amitriptyline Hydrochloride + Perphenazine)
  • Pms-Levazine 3/15 Tab (Amitriptyline Hydrochloride + Perphenazine)
  • Pms-Levazine 4/25 Tab (Amitriptyline Hydrochloride + Perphenazine)
  • Proavil Tab (Amitriptyline Hydrochloride + Perphenazine)
  • Triavil Tab (Amitriptyline Hydrochloride + Perphenazine)

PharmGKB Accession Id

PA448385

Type(s):

Drug

Description

Amitriptyline hydrochloride is a dibenzocycloheptene-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, amitriptyline does not affect mood or arousal, but may cause sedation. In depressed individuals, amitriptyline exerts a positive effect on mood. TCAs are potent inhibitors of serotonin and norepinephrine reuptake. Tertiary amine TCAs, such as amitriptyline, are more potent inhibitors of serotonin reuptake than secondary amine TCAs, such as nortriptyline. 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. Amitriptyline may be used to treat depression, chronic pain (unlabeled use), irritable bowel syndrome (unlabeled use), diabetic neuropathy (unlabeled use), post-traumatic stress disorder (unlabeled use), and for migraine prophylaxis (unlabeled use).

Source: Drug Bank

Indication

For the treatment of depression, chronic pain, irritable bowel syndrome, sleep disorders, diabetic neuropathy, agitation and insomnia, and migraine prophylaxis.

Source: Drug Bank

Other Vocabularies

Information pulled from DrugBank has not been reviewed by PharmGKB.

Pharmacology, Interactions, and Contraindications

Mechanism of Action

Amitriptyline is metabolized to nortriptyline which inhibits the reuptake of norepinephrine and serotonin almost equally. Amitriptyline inhibits the membrane pump mechanism responsible for uptake of norepinephrine and serotonin in adrenergic and serotonergic neurons. Pharmacologically this action may potentiate or prolong neuronal activity since reuptake of these biogenic amines is important physiologically in terminating transmitting activity. This interference with the reuptake of norepinephrine and/or serotonin is believed by some to underlie the antidepressant activity of amitriptyline.

Source: Drug Bank

Pharmacology

Amitriptyline, a tertiary amine tricyclic antidepressant, is structurally related to both the skeletal muscle relaxant cyclobenzaprine and the thioxanthene antipsychotics such as thiothixene. It is extremely sedating, and thus improvement of sleep patterns can be the first benefit of treatment. Amitriptyline exhibits strong anticholinergic activity, cardiovascular effects including orthostatic hypotension, changes in heart rhythm and conduction, and a lowering of the seizure threshold. As with other antidepressants, several weeks of therapy may be required in order to realize the full clinical benefit of amitriptyline. Although not a labelled indication, amitriptyline is widely used in the management of chronic nonmalignant pain (e.g., post-herpetic neuralgia, fibromyalgia).

Source: Drug Bank

Food Interaction

Avoid St.John's Wort.|Avoid alcohol.|Avoid excessive quantities of coffee or tea (caffeine).|Take with food to reduce irritation.

Source: Drug Bank

Absorption, Distribution, Metabolism, Elimination & Toxicity

Biotransformation

Exclusively hepatic, with first pass effect. Amitriptyline is demethylated in the liver to its primary active metabolite, nortriptyline.

Source: Drug Bank

Protein Binding

Very highly protein bound (90% or more) in plasma and tissues

Source: Drug Bank

Absorption

Rapidly and well absorbed following oral administration (bioavailability is 30-60% due to first pass metabolism). Peak plasma concentrations occur 2-12 hours following oral or intramuscular administration.

Source: Drug Bank

Half-Life

10 to 50 hours, with an average of 15 hours

Source: Drug Bank

Toxicity

LD 50=350 mg/kg (in mice). Symptoms of overdose include abnormally low blood pressure, confusion, convulsions, dilated pupils and other eye problems, disturbed concentration, drowsiness, hallucinations, impaired heart function, rapid or irregular heartbeat, reduced body temperature, stupor, and unresponsiveness or coma.
Side effects include: sedation, hypotension, blurred vision, dry mouth, constipation, urinary retention, postural hypotension, tachycardia, hypertension, ECG changes, heart failure, impaired memory and delirium, and precipitation of hypomanic or manic episodes in bipolar depression.
Withdrawal symptoms include gastrointestinal disturbances, anxiety, and insomnia.

Source: Drug Bank

Route of Elimination

Virtually the entire dose is excreted as glucuronide or sulfate conjugate of metabolites, with little unchanged drug appearing in the urine. 25-50% of a single orally administered dose is excreted in urine as inactive metabolites within 24 hours. Small amounts are excreted in feces via biliary elimination.

Source: Drug Bank

Chemical Properties

Chemical Formula

C20H23N

Source: Drug Bank

Isomeric SMILES

CN(C)CCC=C1c2ccccc2CCc3c1cccc3

Source: OpenEye

Canonical SMILES

CN(C)CCC=C1C2=CC=CC=C2CCC2=CC=CC=C12

Source: Drug Bank

Average Molecular Weight

277.4033

Source: Drug Bank

Monoisotopic Molecular Weight

277.183049741

Source: Drug Bank

SMILES

CN(C)CCC=C1C2=CC=CC=C2CCC2=CC=CC=C12

Source: Drug Bank

InChI String

InChI=1S/C20H23N/c1-21(2)15-7-12-20-18-10-5-3-8-16(18)13-14-17-9-4-6-11-19(17)20/h3-6,8-12H,7,13-15H2,1-2H3

Source: Drug Bank

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 )
ADRA1D (source: Drug Bank )
ADRA2A (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 )
HTR1A (source: Drug Bank )
HTR2A (source: Drug Bank )
KCNA1 (source: Drug Bank )
KCND2 (source: Drug Bank )
KCND3 (source: Drug Bank )
KCNQ2 (source: Drug Bank )
NTRK1 (source: Drug Bank )
NTRK2 (source: Drug Bank )
OPRD1 (source: Drug Bank )
OPRK1 (source: Drug Bank )
SLC6A2 (source: Drug Bank )
SLC6A4 (source: Drug Bank )

Drug Interactions

Interaction Description
amitriptyline - altretamine Risk of severe hypotension (source: Drug Bank )
amitriptyline - altretamine Risk of severe hypotension (source: Drug Bank )
amitriptyline - atazanavir Atazanavir increases the effect and toxicity of tricyclics (source: Drug Bank )
amitriptyline - atazanavir Atazanavir may increase the effect and toxicity of the tricyclic antidepressant, amitriptyline, by decreasing its metabolism. Monitor for changes in the therapeutic and adverse effects of amitriptyline if atazanavir if initiated, discontinued or dose changed. (source: Drug Bank )
amitriptyline - carbamazepine The tricyclics increases the effect of carbamazepine (source: Drug Bank )
amitriptyline - carbamazepine Carbamazepine may decrease the serum concentration of the tricyclic antidepressant, amitriptyline, by increasing its metabolism. Monitor for changes in the therapeutic and adverse effects of amitriptyline if carbamazepine is initiated, discontinued or dose changed. (source: Drug Bank )
amitriptyline - cimetidine Cimetidine increases the effect of tricyclic agent (source: Drug Bank )
amitriptyline - cimetidine Cimetidine may increase the effect of the tricyclic antidepressant, amitriptyline, by decreasing its metabolism. Monitor for changes in the therapeutic and adverse effects of amitriptyline if cimetidine is initiated, discontinued or dose changed. (source: Drug Bank )
amitriptyline - cisapride Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank )
amitriptyline - cisapride Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank )
amitriptyline - clonidine The tricyclic decreases the effect of clonidine (source: Drug Bank )
amitriptyline - clonidine The tricyclic antidepressant, amitriptyline, decreases the effect of clonidine. (source: Drug Bank )
amitriptyline - dobutamine The tricyclic increases the sympathomimetic effect (source: Drug Bank )
amitriptyline - dobutamine The tricyclic antidepressant, amitriptyline, increases the sympathomimetic effect, dobutamine. (source: Drug Bank )
amitriptyline - donepezil Possible antagonism of action (source: Drug Bank )
amitriptyline - donepezil Possible antagonism of action (source: Drug Bank )
amitriptyline - dopamine The tricyclic increases the sympathomimetic effect (source: Drug Bank )
amitriptyline - dopamine The tricyclic antidepressant, amitriptyline, increases the sympathomimetic effect, dopamine. (source: Drug Bank )
amitriptyline - duloxetine Possible increase in the levels of this agent when used with duloxetine (source: Drug Bank )
amitriptyline - duloxetine Possible increase in the levels of this agent when used with duloxetine (source: Drug Bank )
amitriptyline - ephedra The tricyclic increases the sympathomimetic effect (source: Drug Bank )
amitriptyline - ephedra The tricyclic antidepressant, amitriptyline, increases the sympathomimetic effect of ephedra. (source: Drug Bank )
amitriptyline - ephedrine The tricyclic increases the sympathomimetic effect (source: Drug Bank )
amitriptyline - ephedrine The tricyclic antidepressant, amitriptyline, increases the sympathomimetic effect of ephedrine. (source: Drug Bank )
amitriptyline - epinephrine The tricyclic increases the sympathomimetic effect (source: Drug Bank )
amitriptyline - epinephrine The tricyclic antidepressant, amitriptyline, increases the sympathomimetic effect, epinephrine. (source: Drug Bank )
amitriptyline - fenoterol The tricyclic increases the sympathomimetic effect (source: Drug Bank )
amitriptyline - fenoterol The tricyclic antidepressant, amitriptyline, increases the sympathomimetic effect, fenoterol. (source: Drug Bank )
amitriptyline - fluconazole The imidazole increases the effect and toxicity of the tricyclic (source: Drug Bank )
amitriptyline - fluconazole Fluconazole may increase the effect and toxicity of the tricyclic antidepressant, amitriptyline, by decreasing its metabolism. Additive QTc-prolonging effects may also occur. Monitor for changes in the therapeutic and adverse effects of amitriptyline if fluconazole is initiated, discontinued or dose changed. Monitor for the development of torsades de pointes during concomitant therapy. (source: Drug Bank )
amitriptyline - fluoxetine Fluoxetine increases the effect and toxicity of tricyclics (source: Drug Bank )
amitriptyline - fluoxetine The SSRI, fluoxetine, may increase the serum concentration of the tricyclic antidepressant, amitriptyline, by decreasing its metabolism. Additive modulation of serotonin activity also increases the risk of serotonin syndrome. Monitor for development of serotonin syndrome during concomitant therapy. Monitor for changes in the therapeutic and adverse effects of amitriptyline if fluoxetine is initiated, discontinued or dose changed. (source: Drug Bank )
amitriptyline - fluvoxamine Fluvoxamine increases the effect and toxicity of tricyclics (source: Drug Bank )
amitriptyline - fluvoxamine The SSRI, fluvoxamine, may increase the serum concentration of the tricyclic antidepressant, amitriptyline, by decreasing its metabolism. Additive modulation of serotonin activity also increases the risk of serotonin syndrome. Monitor for development of serotonin syndrome during concomitant therapy. Monitor for changes in the therapeutic and adverse effects of amitriptyline if fluvoxamine is initiated, discontinued or dose changed. (source: Drug Bank )
amitriptyline - galantamine Possible antagonism of action (source: Drug Bank )
amitriptyline - galantamine Possible antagonism of action (source: Drug Bank )
amitriptyline - grepafloxacin Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank )
amitriptyline - grepafloxacin Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank )
amitriptyline - guanethidine The tricyclic decreases the effect of guanethidine (source: Drug Bank )
amitriptyline - guanethidine The tricyclic antidepressant, amitriptyline, decreases the effect of guanethidine. (source: Drug Bank )
amitriptyline - isocarboxazid Possibility of severe adverse effects (source: Drug Bank )
amitriptyline - isocarboxazid Possibility of severe adverse effects (source: Drug Bank )
amitriptyline - isoproterenol The tricyclic increases the sympathomimetic effect (source: Drug Bank )
amitriptyline - isoproterenol The tricyclic antidepressant, amitriptyline, increases the sympathomimetic effect of isoproterenol. (source: Drug Bank )
amitriptyline - ketoconazole The imidazole increases the effect and toxicity of the tricyclic (source: Drug Bank )
amitriptyline - ketoconazole Ketoconazole, a moderate CYP2D6 inhibitor, may increase the serum concentration of amitriptyline by increasing its metabolism. Monitor for changes in the therapeutic and adverse effects of amitriptyline if ketoconazole is initiated, discontinued or dose changed. (source: Drug Bank )
amitriptyline - mephentermine The tricyclic increases the sympathomimetic effect (source: Drug Bank )
amitriptyline - mephentermine The tricyclic antidepressant, amitriptyline, increases the sympathomimetic effect of mephentermine. (source: Drug Bank )
amitriptyline - mesoridazine Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank )
amitriptyline - mesoridazine Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank )
amitriptyline - metaraminol The tricyclic increases the sympathomimetic effect (source: Drug Bank )
amitriptyline - metaraminol The tricyclic antidepressant, amitriptyline, increases the sympathomimetic effect of metaraminol. (source: Drug Bank )
amitriptyline - methoxamine The tricyclic increases the sympathomimetic effect (source: Drug Bank )
amitriptyline - methoxamine The tricyclic antidepressant, amitriptyline, increases the sympathomimetic effect of methoxamine. (source: Drug Bank )
amitriptyline - moclobemide Possible severe adverse reaction with this combination (source: Drug Bank )
amitriptyline - moclobemide Possible severe adverse reaction with this combination (source: Drug Bank )
amitriptyline - norepinephrine The tricyclic increases the sympathomimetic effect (source: Drug Bank )
amitriptyline - norepinephrine The tricyclic antidepressant, amitriptyline, increases the sympathomimetic effect of norepinephrine. (source: Drug Bank )
amitriptyline - orciprenaline The tricyclic increases the sympathomimetic effect (source: Drug Bank )
amitriptyline - orciprenaline The tricyclic antidepressant, amitriptyline, increases the sympathomimetic effect of orciprenaline. (source: Drug Bank )
amitriptyline - phenelzine Possibility of severe adverse effects (source: Drug Bank )
amitriptyline - phenelzine Possibility of severe adverse effects (source: Drug Bank )
amitriptyline - phenylephrine The tricyclic increases the sympathomimetic effect (source: Drug Bank )
amitriptyline - phenylephrine The tricyclic antidepressant, amitriptyline, increases the sympathomimetic effect of phenylephrine. (source: Drug Bank )
amitriptyline - phenylpropanolamine The tricyclic increases the sympathomimetic effect (source: Drug Bank )
amitriptyline - phenylpropanolamine The tricyclic antidepressant, amitriptyline, increases the sympathomimetic effect of phenylpropanolamine. (source: Drug Bank )
amitriptyline - pirbuterol The tricyclic increases the sympathomimetic effect (source: Drug Bank )
amitriptyline - pirbuterol The tricyclic antidepressant, amitriptyline, increases the sympathomimetic effect of pirbuterol. (source: Drug Bank )
amitriptyline - procaterol The tricyclic increases the sympathomimetic effect (source: Drug Bank )
amitriptyline - procaterol The tricyclic antidepressant, amitriptyline, increases the sympathomimetic effect of procaterol. (source: Drug Bank )
amitriptyline - pseudoephedrine The tricyclic increases the sympathomimetic effect (source: Drug Bank )
amitriptyline - pseudoephedrine The tricyclic antidepressant, amitriptyline, increases the sympathomimetic effect of pseudoephedrine. (source: Drug Bank )
amitriptyline - quinidine Quinidine increases the effect of tricyclic agent (source: Drug Bank )
amitriptyline - quinidine Quinidine increases the effect of tricyclic agent (source: Drug Bank )
amitriptyline - quinidine Quinidine barbiturate increases the effect of tricyclic antidepressant, amitriptyline. (source: Drug Bank )
amitriptyline - rasagiline Possibility of severe adverse effects (source: Drug Bank )
amitriptyline - rasagiline Possibility of severe adverse effects (source: Drug Bank )
amitriptyline - rifabutin The rifamycin decreases the effect of tricyclics (source: Drug Bank )
amitriptyline - rifabutin The rifamycin, rifabutin, may decrease the effect of the tricyclic antidepressant, amitriptyline, by increasing its metabolism. Monitor for changes in the therapeutic and adverse effects of amitriptyline if rifabutin is initiated, discontinued or dose changed. (source: Drug Bank )
amitriptyline - rifampin The rifamycin decreases the effect of tricyclics (source: Drug Bank )
amitriptyline - rifampin The rifamycin, rifampin, may decrease the effect of the tricyclic antidepressant, amitriptyline, by increasing its metabolism. Monitor for changes in the therapeutic and adverse effects of amitriptyline if rifampin is initiated, discontinued or dose changed. (source: Drug Bank )
amitriptyline - ritonavir Ritonavir increases the effect and toxicity of tricyclics (source: Drug Bank )
amitriptyline - ritonavir Ritonavir may increase the effect and toxicity of the tricyclic antidepressant, amitriptyline, by decreasing its metabolism. Monitor for changes in the therapeutic and adverse effects of amitriptyline if ritonavir if initiated, discontinued or dose changed. (source: Drug Bank )
amitriptyline - rivastigmine Possible antagonism of action (source: Drug Bank )
amitriptyline - rivastigmine Possible antagonism of action (source: Drug Bank )
amitriptyline - salbutamol The tricyclic increases the sympathomimetic effect (source: Drug Bank )
amitriptyline - salbutamol The tricyclic antidepressant, amitriptyline, increases the sympathomimetic effect of salbutamol. (source: Drug Bank )
amitriptyline - sibutramine Increased risk of CNS adverse effects (source: Drug Bank )
amitriptyline - sibutramine Increased risk of CNS adverse effects (source: Drug Bank )
amitriptyline - sparfloxacin Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank )
amitriptyline - sparfloxacin Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank )
amitriptyline - terbutaline The tricyclic increases the sympathomimetic effect (source: Drug Bank )
amitriptyline - terbutaline The tricyclic antidepressant, amitriptyline, increases the sympathomimetic effect of terbutaline. (source: Drug Bank )
amitriptyline - terfenadine Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank )
amitriptyline - terfenadine Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank )
amitriptyline - thioridazine Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank )
amitriptyline - thioridazine Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank )
amitriptyline - tranylcypromine Possibility of severe adverse effects (source: Drug Bank )
amitriptyline - tranylcypromine Possibility of severe adverse effects (source: Drug Bank )
atazanavir - amitriptyline Increases the effect and toxicity of tricyclics (source: Drug Bank )
atazanavir - amitriptyline Atazanavir may increase the effect and toxicity of the tricyclic antidepressant, amitriptyline, by decreasing its metabolism. Monitor for changes in the therapeutic and adverse effects of amitriptyline if atazanavir if initiated, discontinued or dose changed. (source: Drug Bank )
carbamazepine - amitriptyline The tricyclic increases the effect of carbamazepine (source: Drug Bank )
carbamazepine - amitriptyline Carbamazepine may decrease the serum concentration of the tricyclic antidepressant, amitriptyline, by increasing its metabolism. Monitor for changes in the therapeutic and adverse effects of amitriptyline if carbamazepine is initiated, discontinued or dose changed. (source: Drug Bank )
cimetidine - amitriptyline Increases the effect of tricyclic agent (source: Drug Bank )
cimetidine - amitriptyline Cimetidine may increase the effect of tricyclic antidepressant, amitriptyline, by decreasing its metabolism. Monitor for changes in the therapeutic and adverse effects of amitriptyline if cimetidine is initiated, discontinued or dose changed. (source: Drug Bank )
cisapride - amitriptyline Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank )
cisapride - amitriptyline Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank )
clonidine - amitriptyline The tricyclic decreases the effect of clonidine (source: Drug Bank )
clonidine - amitriptyline The tricyclic antidepressant, amitriptyline, decreases the effect of clonidine. (source: Drug Bank )
donepezil - amitriptyline Possible antagonism of action (source: Drug Bank )
donepezil - amitriptyline Possible antagonism of action (source: Drug Bank )
duloxetine - amitriptyline Possible increase in the levels of this agent when used with duloxetine (source: Drug Bank )
duloxetine - amitriptyline Possible increase in the levels of this agent when used with duloxetine (source: Drug Bank )
epinephrine - amitriptyline The tricyclic increases the sympathomimetic effect (source: Drug Bank )
epinephrine - amitriptyline The tricyclic antidepressant, amitriptyline, increases the sympathomimetic effect of epinephrine. (source: Drug Bank )
fenoterol - amitriptyline The tricyclic increases the sympathomimetic effect (source: Drug Bank )
fenoterol - amitriptyline The tricyclic antidepressant, amitriptyline, increases the sympathomimetic effect of fenoterol. (source: Drug Bank )
fluconazole - amitriptyline The imidazole increases the effect and toxicity of the tricyclic (source: Drug Bank )
fluconazole - amitriptyline Fluconazole may increase the effect and toxicity of the tricyclic antidepressant, amitriptyline, by decreasing its metabolism. Additive QTc-prolonging effects may also occur. Monitor for changes in the therapeutic and adverse effects of amitriptyline if fluconazole is initiated, discontinued or dose changed. Monitor for the development of torsades de pointes during concomitant therapy. (source: Drug Bank )
fluoxetine - amitriptyline Fluoxetine increases the effect and toxicity of tricyclics (source: Drug Bank )
fluoxetine - amitriptyline The SSRI, fluoxetine, may increase the serum concentration of the tricyclic antidepressant, amitriptyline, by decreasing its metabolism. Additive modulation of serotonin activity also increases the risk of serotonin syndrome. Monitor for development of serotonin syndrome during concomitant therapy. Monitor for changes in the therapeutic and adverse effects of amitriptyline if fluoxetine is initiated, discontinued or dose changed. (source: Drug Bank )
galantamine - amitriptyline Possible antagonism of action (source: Drug Bank )
galantamine - amitriptyline Possible antagonism of action (source: Drug Bank )
grepafloxacin - amitriptyline Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank )
grepafloxacin - amitriptyline Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank )
guanethidine - amitriptyline The tricyclic decreases the effect of guanethidine (source: Drug Bank )
guanethidine - amitriptyline The tricyclic antidepressant, amitriptyline, decreases the effect of guanethidine. (source: Drug Bank )
isocarboxazid - amitriptyline Possibility of severe adverse effects (source: Drug Bank )
isocarboxazid - amitriptyline Possibility of severe adverse effects (source: Drug Bank )
ketoconazole - amitriptyline The imidazole increases the effect and toxicity of the tricyclic (source: Drug Bank )
ketoconazole - amitriptyline Ketoconazole, a moderate CYP2D6 inhibitor, may increase the serum concentration of amitriptyline by increasing its metabolism. Monitor for changes in the therapeutic and adverse effects of amitriptyline if ketoconazole is initiated, discontinued or dose changed. (source: Drug Bank )
mesoridazine - amitriptyline Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank )
mesoridazine - amitriptyline Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank )
moclobemide - amitriptyline Possible severe adverse reaction with this combination (source: Drug Bank )
moclobemide - amitriptyline Possible severe adverse reaction with this combination (source: Drug Bank )
orciprenaline - amitriptyline The tricyclic increases the sympathomimetic effect (source: Drug Bank )
orciprenaline - amitriptyline The tricyclic antidepressant, amitriptyline, increases the sympathomimetic effect of orciprenaline. (source: Drug Bank )
phenelzine - amitriptyline Possibility of severe adverse effects (source: Drug Bank )
phenelzine - amitriptyline Possibility of severe adverse effects (source: Drug Bank )
phenylephrine - amitriptyline The tricyclic increases the sympathomimetic effect (source: Drug Bank )
phenylephrine - amitriptyline The tricyclic antidepressant, amitriptyline, increases the sympathomimetic effect of phenylephrine. (source: Drug Bank )
phenylpropanolamine - amitriptyline The tricyclic antidepressant, amitriptyline, increases the sympathomimetic effect of phenylpropanolamine. (source: Drug Bank )
pseudoephedrine - amitriptyline The tricyclic increases the sympathomimetic effect (source: Drug Bank )
pseudoephedrine - amitriptyline The tricyclic antidepressant, amitriptyline, increases the sympathomimetic effect of pseudoephedrine. (source: Drug Bank )
quinidine - amitriptyline Quinidine increases the effect of the tricyclic agent (source: Drug Bank )
quinidine - amitriptyline Additive QTc-prolonging effects may occur. Quinidine may also increase the serum concentration of the tricyclic antidepressant, amitriptyline, by decreasing its metabolism. Monitor for changes in the therapeutic and adverse effects of amitriptyline if quinidine is initiated, discontinued or dose changed. Monitor for the development of torsades de pointes during concomitant therapy. (source: Drug Bank )
rasagiline - amitriptyline Possibility of severe adverse effects (source: Drug Bank )
rifabutin - amitriptyline The rifamycin decreases the effect of tricyclics (source: Drug Bank )
rifabutin - amitriptyline The rifamycin, rifabutin, may decrease the effect of the tricyclic antidepressant, amitriptyline, by increasing its metabolism. Monitor for changes in the therapeutic and adverse effects of amitriptyline if rifabutin is initiated, discontinued or dose changed. (source: Drug Bank )
rifampin - amitriptyline The rifamycin decreases the effect of tricyclics (source: Drug Bank )
rifampin - amitriptyline The rifamycin, rifampin, may decrease the effect of the tricyclic antidepressant, amitriptyline, by increasing its metabolism. Monitor for changes in the therapeutic and adverse effects of amitriptyline if rifampin is initiated, discontinued or dose changed. (source: Drug Bank )
tacrine - amitriptyline The therapeutic effects of the central acetylcholinesterase inhibitor, Tacrine, and/or the anticholinergic, Amitriptyline, 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 - amitriptyline The therapeutic effects of the central acetylcholinesterase inhibitor, Tacrine, and/or the anticholinergic, Amitriptyline, 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 )
terbutaline - amitriptyline The tricyclic increases the sympathomimetic effect (source: Drug Bank )
terbutaline - amitriptyline The tricyclic antidepressant, amitriptyline, increases the sympathomimetic effect of terbutaline. (source: Drug Bank )
terfenadine - amitriptyline Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank )
terfenadine - amitriptyline Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank )
thioridazine - amitriptyline Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank )
thioridazine - amitriptyline Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank )
thiothixene - amitriptyline 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 - amitriptyline 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 )
toremifene - amitriptyline 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 - amitriptyline Tramadol increases the risk of serotonin syndrome and seizures. (source: Drug Bank )
tranylcypromine - amitriptyline 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 - amitriptyline Increased risk of serotonin syndrome. The 2D6 inhibitor, Trazodone, may also increase the efficacy of Amitriptyline by decreasing Amitriptyline metabolism and clearance. Monitor for symptoms of serotonin syndrome and changes in Amitriptyline efficacy if Trazodone is initiated, discontinued or dose changed. (source: Drug Bank )
trazodone - amitriptyline Increased risk of serotonin syndrome. Monitor for symptoms of serotonin syndrome. (source: Drug Bank )
trimethobenzamide - amitriptyline Trimethobenzamide and Amitriptyline, two anticholinergics, may cause additive anticholinergic effects and enhance their adverse/toxic effects. Monitor for enhanced anticholinergic effects. (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 )
triprolidine - amitriptyline Triprolidine and Amitriptyline, 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 - amitriptyline Triprolidine and Amitriptyline, 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 - amitriptyline Trospium and Amitriptyline, two anticholinergics, may cause additive anticholinergic effects and enhanced adverse/toxic effects. Monitor for enhanced anticholinergic effects. (source: Drug Bank )
venlafaxine - amitriptyline Increased risk of serotonin syndrome. Monitor for symptoms of serotonin syndrome. (source: Drug Bank )
voriconazole - amitriptyline 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 )
vorinostat - amitriptyline 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 - amitriptyline Additive QTc-prolonging effects may increase the risk of severe arrhythmias. Concomitant therapy is contraindicated. (source: Drug Bank )
zolmitriptan - amitriptyline Use of two serotonin modulators, such as zolmitriptan and amitriptyline, increases the risk of serotonin syndrome. Consider alternate therapy or monitor for serotonin syndrome during concomitant therapy. (source: Drug Bank )
zuclopenthixol - amitriptyline 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 ?

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

May Treat
Contraindicated With

Publications related to amitriptyline: 84

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Effect of 24 cytochrome P450 2D6 variants found in the Chinese population on the N-demethylation of amitriptyline in vitro. Pharmaceutical biology. 2016. Weng Qinghua, et al. PubMed
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Pharmacogenomically actionable medications in a safety net health care system. SAGE open medicine. 2016. Carpenter Janet S, et al. PubMed
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Integrated Patient and Tumor Genetic Testing for Individualized Cancer Therapy. Clinical pharmacology and therapeutics. 2015. Hertz Daniel L, et al. PubMed
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Drugs with anticholinergic effects and cognitive impairment, falls and all-cause mortality in older adults: a systematic review and meta-analysis. British journal of clinical pharmacology. 2015. Ruxton Kimberley, et al. PubMed
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Clinical applications of CYP genotyping in psychiatry. Journal of neural transmission (Vienna, Austria : 1996). 2015. Spina Edoardo, et al. PubMed
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The genetics of pro-arrhythmic adverse drug reactions. British journal of clinical pharmacology. 2014. Petropoulou Evmorfia, et al. PubMed
No Dosing Guideline available No Drug Label available CA No Variant Annotation available No VIP available No VIP available
ABCB6, ABCB1 and ABCG1 genetic polymorphisms and antidepressant response of SSRIs in Chinese depressive patients. Pharmacogenomics. 2013. Huang Xiaoye, et al. PubMed
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Challenges in pharmacogenetics. European journal of clinical pharmacology. 2013. Cascorbi Ingolf, et al. PubMed
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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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CYP2D6 ultrarapid metabolism and early dropout from fluoxetine or amitriptyline monotherapy treatment in major depressive patients. Molecular psychiatry. 2013. Peñas-Lledó E M, et al. PubMed
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Cytochrome P450-mediated drug metabolism in the brain. Journal of psychiatry & neuroscience : JPN. 2012. Miksys Sharon, et al. PubMed
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ABCB1 gene variants influence tolerance to selective serotonin reuptake inhibitors in a large sample of Dutch cases with major depressive disorder. The pharmacogenomics journal. 2012. de Klerk O L, et al. PubMed
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PharmGKB summary: very important pharmacogene information for cytochrome P450, family 2, subfamily C, polypeptide 19. Pharmacogenetics and genomics. 2011. Scott Stuart A, et al. PubMed
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Prolonged toxicity after amitriptyline overdose in a patient deficient in CYP2D6 activity. Journal of medical toxicology : official journal of the American College of Medical Toxicology. 2011. Smith Jennifer Cohen, et al. PubMed
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Pharmacogenetics: From Bench to Byte- An Update of Guidelines. Clinical pharmacology and therapeutics. 2011. Swen J J, 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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Methylxanthines and pain. Handbook of experimental pharmacology. 2011. Sawynok Jana. 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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Extrapyramidal symptoms with concomitant use of amitriptyline and amiodarone in an elderly patient. The American journal of geriatric pharmacotherapy. 2010. Pawar Pritish S, 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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Genotype-dependent effects of inhibitors of the organic cation transporter, OCT1: predictions of metformin interactions. The pharmacogenomics journal. 2010. Ahlin G, et al. PubMed
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What is the role of lidocaine or phenytoin in tricyclic antidepressant-induced cardiotoxicity?. Clinical toxicology (Philadelphia, Pa.). 2010. Foianini Anthony, et al. PubMed
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Role of human UGT2B10 in N-glucuronidation of tricyclic antidepressants, amitriptyline, imipramine, clomipramine, and trimipramine. Drug metabolism and disposition: the biological fate of chemicals. 2010. Zhou Diansong, et al. PubMed
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Human lymphoblastoid cell line panels: novel tools for assessing shared drug pathways. Pharmacogenomics. 2010. Morag Ayelet, et al. PubMed
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Cytochrome P450 2D6. Pharmacogenetics and genomics. 2009. Owen Ryan P, et al. PubMed
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Pharmacokinetics and efficacy of fluvoxamine and amitriptyline in depression. Journal of pharmacological sciences. 2009. Vezmar Sandra, et al. PubMed
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Functional pharmacogenetics/genomics of human cytochromes P450 involved in drug biotransformation. Analytical and bioanalytical chemistry. 2008. Zanger Ulrich M, et al. PubMed
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Caffeine reverses antinociception by amitriptyline in wild type mice but not in those lacking adenosine A1 receptors. Neuroscience letters. 2008. Sawynok Jana, 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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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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Correlation of inter-individual variations of amitriptyline metabolism examined in hairs with CYP2C19 and CYP2D6 polymorphisms. International journal of legal medicine. 2008. Thieme Detlef, 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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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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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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ABCB1 (P-glycoprotein/MDR1) gene G2677T/a sequence variation (polymorphism): lack of association with side effects and therapeutic response in depressed inpatients treated with amitriptyline. Clinical chemistry. 2006. Laika Barbara, 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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Serotonin transporter polymorphisms and side effects in antidepressant therapy--a pilot study. Pharmacogenomics. 2006. Popp Johannes, et al. PubMed
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Adverse drug reactions following nonresponse in a depressed patient with CYP2D6 deficiency and low CYP 3A4/5 activity. Pharmacopsychiatry. 2006. Stephan P L, et al. PubMed
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The complexity of active metabolites in therapeutic drug monitoring of psychotropic drugs. Pharmacopsychiatry. 2006. Hendset M, et al. PubMed
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Rates of in vivo methylation of desipramine and nortriptyline. Pharmacotherapy. 2006. Kurpius Molly P, et al. PubMed
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Pharmacogenetics of tamoxifen biotransformation is associated with clinical outcomes of efficacy and hot flashes. Journal of clinical oncology : official journal of the American Society of Clinical Oncology. 2005. Goetz Matthew P, et al. PubMed
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Prolonged pharmacokinetic drug interaction between terbinafine and amitriptyline. Therapeutic drug monitoring. 2005. Castberg Ingrid, et al. PubMed
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Metabolic ratios of psychotropics as indication of cytochrome P450 2D6/2C19 genotype. Therapeutic drug monitoring. 2005. van der Weide Jan, 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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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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Impact of polymorphisms of cytochrome-P450 isoenzymes 2C9, 2C19 and 2D6 on plasma concentrations and clinical effects of antidepressants in a naturalistic clinical setting. European journal of clinical pharmacology. 2004. Grasmäder Katja, 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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Increased incidence of CYP2D6 gene duplication in patients with persistent mood disorders: ultrarapid metabolism of antidepressants as a cause of nonresponse. A pilot study. European journal of clinical pharmacology. 2004. Kawanishi Chiaki, et al. PubMed
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No evidence of increased adverse drug reactions in cytochrome P450 CYP2D6 poor metabolizers treated with fluoxetine or nortriptyline. Human psychopharmacology. 2004. Roberts Rebecca L, et al. PubMed
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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
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Effects of polymorphisms in CYP2D6, CYP2C9, and CYP2C19 on trimipramine pharmacokinetics. Journal of clinical psychopharmacology. 2003. Kirchheiner Julia, et al. PubMed
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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
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Contributions of CYP2D6, CYP2C9 and CYP2C19 to the biotransformation of E- and Z-doxepin in healthy volunteers. Pharmacogenetics. 2002. Kirchheiner Julia, et al. PubMed
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The impact of CYP2C19 and CYP2D6 genotypes on metabolism of amitriptyline in Japanese psychiatric patients. Journal of clinical psychopharmacology. 2002. Shimoda Kazutaka, et al. PubMed
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The role of CYP2C19 in amitriptyline N-demethylation in Chinese subjects. European journal of clinical pharmacology. 2002. Jiang Zhi-Ping, et al. PubMed
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Comprehensive survey of the relationship between serum concentration and therapeutic effect of amitriptyline in depression. Clinical pharmacokinetics. 2002. Ulrich Sven, et al. PubMed
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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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CYP2D6 and CYP2C19 genotype-based dose recommendations for antidepressants: a first step towards subpopulation-specific dosages. Acta psychiatrica Scandinavica. 2001. Kirchheiner J, et al. PubMed
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The treatment of neuropathic pain: antidepressants and opioids. The Clinical journal of pain. 2000. Watson C P. PubMed
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Science, medicine, and the future: Pharmacogenetics. BMJ (Clinical research ed.). 2000. Wolf C R, et al. PubMed
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Clomipramine dose-effect study in patients with depression: clinical end points and pharmacokinetics. Danish University Antidepressant Group (DUAG). Clinical pharmacology and therapeutics. 1999. PubMed
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CYP2D6 phenotype-genotype relationships in African-Americans and Caucasians in Los Angeles. Pharmacogenetics. 1998. Leathart J B, et al. PubMed
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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
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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
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Five distinct human cytochromes mediate amitriptyline N-demethylation in vitro: dominance of CYP 2C19 and 3A4. Journal of clinical pharmacology. 1998. Venkatakrishnan K, et al. PubMed
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Fatality associated with combined fluoxetine-amitriptyline therapy. JAMA : the journal of the American Medical Association. 1997. Preskorn S H, et al. PubMed
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Significance of monitoring plasma levels of amitriptyline, and its hydroxylated and desmethylated metabolites in prediction of the clinical outcome of depressive state. Psychiatry and clinical neurosciences. 1997. Shimoda K, et al. PubMed
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The cytochrome P450 2D6 (CYP2D6) enzyme polymorphism: screening costs and influence on clinical outcomes in psychiatry. Clinical pharmacology and therapeutics. 1996. Chen S, et al. PubMed
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Steady-state plasma levels of nortriptyline and its 10-hydroxy metabolite: relationship to the CYP2D6 genotype. Psychopharmacology. 1996. Dahl M L, et al. PubMed
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Steady-state kinetics of fluoxetine and amitriptyline in patients treated with a combination of these drugs as compared with those treated with amitriptyline alone. Journal of clinical pharmacology. 1995. el-Yazigi A, et al. PubMed
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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
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Enantioselective amitriptyline metabolism in patients phenotyped for two cytochrome P450 isozymes. Clinical pharmacology and therapeutics. 1992. Breyer-Pfaff U, et al. PubMed
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Debrisoquine hydroxylation phenotypes of patients with high versus low to normal serum antidepressant concentrations. Journal of clinical psychopharmacology. 1992. Tacke U, et al. PubMed
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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
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Amitriptyline metabolism: association with debrisoquin hydroxylation in nonsmokers. Clinical pharmacology and therapeutics. 1986. Mellström B, et al. PubMed
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Amitriptyline pharmacokinetics and clinical response: II. Metabolic polymorphism assessed by hydroxylation of debrisoquine and mephenytoin. International clinical psychopharmacology. 1986. Baumann P, et al. PubMed
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The nonlinear kinetics of desipramine and 2-hydroxydesipramine in plasma. Clinical pharmacology and therapeutics. 1984. Cooke R G, et al. PubMed
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Role of oxidation polymorphism on blood and urine concentrations of amitriptyline and its metabolites in man. Archiv für Psychiatrie und Nervenkrankheiten. 1982. Balant-Gorgia A E, 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

LinkOuts

Web Resource:
Wikipedia
National Drug Code Directory:
53489-104-07
DrugBank:
DB00321
ChEBI:
2666
KEGG Compound:
C06824
PubChem Compound:
2160
PubChem Substance:
46508798
9042
IUPHAR Ligand:
200
Drugs Product Database (DPD):
654515
ChemSpider:
2075
Therapeutic Targets Database:
DNC001466
FDA Drug Label at DailyMed:
9f85491f-71ec-4772-8307-8ff2e9257546

Clinical Trials

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

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