Chemical: Drug
clomipramine

Available Prescribing Info

Dosing Guidelines
  1. Annotation of CPIC Guideline for clomipramine and CYP2C19,CYP2D6
  2. Annotation of DPWG Guideline for clomipramine and CYP2D6
last updated 03/15/2017

1. Annotation of CPIC Guideline for clomipramine 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 clomipramine. 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:
  • 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 phenotypeActivity scoreGenotypesExamples of diplotypesImplicationsTherapeutic Recommendationsa, bClassification of recommendation for other TCAs c
CYP2D6 Ultrarapid metabolizer (~1-20% of patients)d>2.0An individual carrying more than two copies of functional alleles*1/*1xN, *1/*2xNIncreased 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)d1.0-2.0fAn 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/*5Normal metabolism of TCAs.Initiate therapy with recommended starting dose.gStrong
CYP2D6 Intermediate metabolizer (~1-13% of patients)d0.5An individual carrying one decreased and one no function allele*4/*41, *5/*9, *4/*10Reduced 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.eOptional
CYP2D6 Poor metabolizer (~1-10% of patients)d0An individual carrying only no function alleles*4/*4, *4/*4xN, *3/*4, *5/*5, *5/*6Greatly 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 phenotypeGenotypesExamples of diplotypesImplicationsTherapeutic recommendationsa,bClassification of recommendations for amitriptylinec
CYP2C19 Ultrarapid metabolizer (~2-5% of patients)dAn individual carrying two increased function alleles*17/*17Increased 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)dAn individual carrying one normal and one increased function allele*1/*17Increased 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)dAn individual carrying two normal function alleles*1/*1Normal metabolism of tertiary amines.Initiate therapy with recommended starting dose.fStrong
CYP2C19 Intermediate metabolizer (~18-45% of patients)dAn individual carrying one normal and one no function allele or one no and one increased function allele*1/*2, *1/*3, *2/*17gReduced metabolism of tertiary amines compared to normal metabolizers.Initiate therapy with recommended starting dose.fOptional
CYP2C19 Poor metabolizer (~2-15% of patients)dAn individual carrying two no function alleles*2/*2, *2/*3, *3/*3Greatly 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.

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 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).

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 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 S14), 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).

last updated 08/10/2011

2. Annotation of DPWG Guideline for clomipramine and CYP2D6

Summary

The Dutch Pharmacogenetics Working Group Guideline for clomipramine recommends to reduce the dose by 50% for CYP2D6 poor metabolizers, and select an alternative drug for ultrarapid metabolizers. Monitor (desmethyl)clomipramine plasma concentration.

Annotation

The Royal Dutch Pharmacists Association - Pharmacogenetics Working Group has evaluated therapeutic dose recommendations for clomipramine based on CYP2D6 genotypes [Article:21412232]. They recommend lower dose for patients carrying the poor metabolizer (PM) alleles and alternative drug for patients carrying the ultrarapid metabolizer (UM) allleles.

Phenotype (Genotype)Therapeutic Dose RecommendationLevel of EvidenceClinical Relevance
PM (two inactive (*3-*8, *11-*16, *19-*21, *38, *40, *42) alleles)Reduce dose by 50% and monitor (desmethyl) clomipramine plasma concentration.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.
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)Insufficient data to allow calculation of dose adjustment. Monitor (desmethyl)clomipramine plasma concentrationPublished 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)Select alternative drug (e.g., citalopram, sertralin) or monitor (desmethyl)clomipramine plasma concentration.Published case reports, well documented, and having relevant pharmacokinetic or clinical endpoints. Well documented case series.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 quality."
  • S: statistically significant difference.
  • Please see attached PDF for detailed information about the evaluated studies: Clomipramine CYP2D6
last updated 10/25/2013

1. Annotation of FDA Label for clomipramine and CYP2D6

On FDA Biomarker List
Actionable PGx

Summary

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

Annotation

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

Excerpt from the clomipramine (Anafranil) label:

The biochemical activity of the drug metabolizing isozyme cytochrome P450 2D6...is reduced in a subset of the Caucasian population (about 7% to 10% of Caucasians are so-called "poor metabolizers"); reliable estimates of the prevalence of reduced P450 2D6 isozyme activity among Asian, African and other populations are not yet available. Poor metabolizers have higher than expected plasma concentrations of tricyclic antidepressants (TCAs) when given usual doses. Depending on the fraction of drug metabolized by P450 2D6, the increase in plasma concentration may be small, or quite large (8 fold increase in plasma AUC of the TCA). In addition, certain drugs inhibit the activity of this isozyme and make normal metabolizers resemble poor metabolizers...It is desirable to monitor TCA plasma levels whenever an agent of the tricyclic antidepressant class including Anafranil is going to be co-administered with another drug known to be an inhibitor of P450 2D6...

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

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

Full label available at DailyMed

Genes and/or phenotypes found in this label

  • Depression
    • Warnings section, Adverse reactions section, Precautions section
    • source: PHONT
  • Depression, Postpartum
    • Warnings section, Adverse reactions section, Precautions section
    • source: PHONT
  • Inflammation
    • Adverse reactions section
    • source: PHONT
  • Neoplasms
    • Adverse reactions section, Precautions section
    • source: PHONT
  • Schizophrenia
    • Precautions section
    • source: PHONT
  • CYP1A2
    • metabolism/PK, Precautions section
    • source: U.S. Food and Drug Administration
  • 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.

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 clomipramine

Gene ? Variant?
(147) 		Alternate Names ? Chemicals ? Alleles ?
(+ chr strand) 		Function ? Amino Acid?
Translation
No VIP available No VIP available VA CYP1A2 *1A N/A N/A N/A
No VIP available No VIP available VA CYP1A2 *1F N/A N/A N/A
No VIP available CA VA CYP2C19 *1 N/A N/A N/A
No VIP available CA VA CYP2C19 *2 N/A N/A N/A
VIP No VIP available No VIP available CYP2C19 *2A N/A N/A N/A
No VIP available CA VA CYP2C19 *3 N/A N/A N/A
VIP No VIP available No VIP available CYP2C19 *3A N/A N/A N/A
No VIP available CA VA CYP2C19 *17 N/A N/A N/A
VIP CA VA CYP2D6 *1 N/A N/A N/A
No VIP available CA VA CYP2D6 *1xN N/A N/A N/A
VIP CA VA CYP2D6 *2 N/A N/A N/A
No VIP available CA No VIP available CYP2D6 *2xN N/A N/A N/A
VIP CA VA CYP2D6 *3 N/A N/A N/A
VIP CA VA CYP2D6 *4 N/A N/A N/A
No VIP available CA VA CYP2D6 *5 N/A N/A N/A
VIP CA VA CYP2D6 *6 N/A N/A N/A
VIP No VIP available No VIP available CYP2D6 *9 N/A N/A N/A
VIP No VIP available VA CYP2D6 *10 N/A N/A N/A
VIP No VIP available VA CYP2D6 *17 N/A N/A N/A
VIP No VIP available No VIP available CYP2D6 *29 N/A N/A N/A
VIP No VIP available VA CYP2D6 *41 N/A N/A N/A
No VIP available No VIP available VA CYP3A5 *1A N/A N/A N/A
No VIP available No VIP available VA CYP3A5 *3A N/A N/A N/A
No VIP available CA VA SLC6A4 HTTLPR long form (L allele) N/A N/A N/A
No VIP available CA VA SLC6A4 HTTLPR short form (S allele) N/A N/A N/A
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 No Clinical Annotations available VA
rs1080985 NC_000022.10:g.42528382C=, NC_000022.10:g.42528382C>G, NC_000022.11:g.42132375G=, NC_000022.11:g.42132375G>C, NG_008376.3:g.2617C=, NG_008376.3:g.2617C>G, NM_000106.5:c.-1584C>G, NM_000106.5:c.-1584G>C, NM_001025161.2:c.-1584C>G, NM_001025161.2:c.-1584G>C, NT_187682.1:g.54721C=, NT_187682.1:g.54721C>G, NW_004504305.1:g.54705G=, NW_004504305.1:g.54705G>C, NW_009646208.1:g.17943G=, NW_009646208.1:g.17943G>C, XM_005278353.1:c.-1587C>G, XM_005278353.1:c.-1587G>C, XM_011529966.1:c.-1584C>G, XM_011529966.1:c.-1584G>C, XM_011529967.1:c.-1045-539C>G, XM_011529967.1:c.-1045-539G>C, XM_011529968.1:c.-1584C>G, XM_011529968.1:c.-1584G>C, XM_011529969.1:c.-1042C>G, XM_011529969.1:c.-1042G>C, XM_011529970.1:c.-1584C>G, XM_011529970.1:c.-1584G>C, XM_011529971.1:c.-1042C>G, XM_011529971.1:c.-1042G>C, XM_011529972.1:c.-1584C>G, XM_011529972.1:c.-1584G>C, XM_011547750.1:c.-1047C>G, XM_011547750.1:c.-1047G>C, XM_011547756.1:c.42+2157C>G, XM_011547756.1:c.42+2157G>C, XR_430455.2:n.650C>G, XR_430455.2:n.650G>C, XR_952536.1:n.-65C>G, XR_952536.1:n.-65G>C, XR_952537.1:n.-65C>G, XR_952537.1:n.-65G>C, XR_952538.1:n.-65C>G, XR_952538.1:n.-65G>C, XR_952539.1:n.40+185C>G, XR_952539.1:n.40+185G>C, XR_952540.1:n.-1399C>G, XR_952540.1:n.-1399G>C, XR_952745.1:n.-432C>G, XR_952745.1:n.-432G>C, rs61604987
C > G
 SNP
VIP No Clinical Annotations available No Variant Annotations available
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
rs130058 NC_000006.11:g.78173281T>A, NC_000006.12:g.77463564T>A, NM_000863.2:c.-161A>T, XR_942706.1:n.545-10962T>A, XR_942707.1:n.545-10962T>A, XR_942708.1:n.545-10962T>A, XR_942709.1:n.545-10962T>A, rs17273665
T > A
 SNP
No VIP available CA VA
rs1360780 NC_000006.11:g.35607571T>C, NC_000006.12:g.35639794T>C, NG_012645.2:g.93790A>G, NM_001145775.2:c.106-2636A>G, NM_001145776.1:c.106-2636A>G, NM_001145777.1:c.106-2636A>G, NM_004117.3:c.106-2636A>G, XR_926743.1:n.287+5974T>C, rs58091271
T > C
 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 CA 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
A > T
 SNP
S893A
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
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
No VIP available No Clinical Annotations available VA
rs4680 NC_000022.10:g.19951271G>A, NC_000022.11:g.19963748G>A, NG_011526.1:g.27009G>A, NM_000754.3:c.472G>A, NM_001135161.1:c.472G>A, NM_001135162.1:c.472G>A, NM_007310.2:c.322G>A, NP_000745.1:p.Val158Met, NP_001128633.1:p.Val158Met, NP_001128634.1:p.Val158Met, NP_009294.1:p.Val108Met, NR_039918.1:n.-5G>A, XM_005261229.1:c.472G>A, XM_011529885.1:c.586G>A, XM_011529886.1:c.586G>A, XM_011529887.1:c.472G>A, XM_011529888.1:c.472G>A, XM_011529889.1:c.472G>A, XM_011529890.1:c.472G>A, XM_011529891.1:c.472G>A, XP_005261286.1:p.Val158Met, XP_011528187.1:p.Val196Met, XP_011528188.1:p.Val196Met, XP_011528189.1:p.Val158Met, XP_011528190.1:p.Val158Met, XP_011528191.1:p.Val158Met, XP_011528192.1:p.Val158Met, XP_011528193.1:p.Val158Met, rs1131157, rs11544671, rs165688, rs17295216, rs17349704, rs17818178, rs17849308, rs17850006, rs2070104, rs3177905, rs3190784, rs3747070, rs58002978
G > A
 SNP
V158M
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
No VIP available No Clinical Annotations available VA
rs5569 NC_000016.10:g.55697923G>A, NC_000016.9:g.55731835G>A, NG_016969.1:g.47294G>A, NM_001043.3:c.1287G>A, NM_001172501.1:c.1287G>A, NM_001172502.1:c.972G>A, NM_001172504.1:c.1287G>A, NP_001034.1:p.Thr429=, NP_001165972.1:p.Thr429=, NP_001165973.1:p.Thr324=, NP_001165975.1:p.Thr429=, XM_006721263.2:c.1287G>A, XM_011523295.1:c.1287G>A, XM_011523296.1:c.1152G>A, XM_011523297.1:c.1152G>A, XM_011523298.1:c.1174G>A, XM_011523299.1:c.564G>A, XM_011523300.1:c.564G>A, XP_006721326.1:p.Thr429=, XP_011521597.1:p.Thr429=, XP_011521598.1:p.Thr384=, XP_011521599.1:p.Thr384=, XP_011521600.1:p.Gly392Arg, XP_011521601.1:p.Thr188=, XP_011521602.1:p.Thr188=, XR_933403.1:n.1904G>A, rs17308809, rs386599040, rs59357911, rs998425
G > A
 SNP
T429T
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
No VIP available No Clinical Annotations available VA
rs6113 NC_000014.8:g.95053849T>C, NC_000014.9:g.94587512T>C, NG_032908.2:g.31071T>C, NM_000624.5:c.150T>C, NP_000615.3:p.Phe50=, XM_005267722.1:c.150T>C, XM_005267723.1:c.150T>C, XM_005267724.1:c.150T>C, XM_005267725.1:c.53+97T>C, XP_005267779.1:p.Phe50=, XP_005267780.1:p.Phe50=, XP_005267781.1:p.Phe50=, rs59626785, rs933175
T > C
 SNP
F50F
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 No Clinical Annotations available VA
rs6296 NC_000006.11:g.78172260C>G, NC_000006.12:g.77462543C>G, NM_000863.2:c.861G>C, NP_000854.1:p.Val287=, XR_942706.1:n.545-11983C>G, XR_942707.1:n.545-11983C>G, XR_942708.1:n.545-11983C>G, XR_942709.1:n.545-11983C>G, rs3748086, rs61223995
C > G
 SNP
V287V
No VIP available No Clinical Annotations available VA
rs6305 NC_000013.10:g.47466622G>A, NC_000013.11:g.46892487G>A, NG_013011.1:g.9548C>T, NM_000621.4:c.516C>T, NM_001165947.2:c.264C>T, NP_000612.1:p.Asp172=, NP_001159419.1:p.Asp88=
G > A
 SNP
D172D
No VIP available No Clinical Annotations available VA
rs6313 NC_000013.10:g.47469940G>A, NC_000013.11:g.46895805G>A, NG_013011.1:g.6230C>T, NM_000621.4:c.102C>T, NM_001165947.2:c.160+869C>T, NP_000612.1:p.Ser34=, rs17367493, rs3742280, rs386602276, rs57425741
G > A
 SNP
S34S
Alleles, Functions, and Amino Acid Translations are all sourced from dbSNP 147
2D structure from PubChem
provided by PubChem

Overview

Generic Names
  • 3-Chloroimipramine
  • Chlorimipramine
  • Clomipramina [INN-Spanish]
  • Clomipramine HCL
  • Clomipraminum [INN-Latin]
  • Monochlorimipramine
Trade Names
  • Anafranil
  • Hydiphen
Brand Mixture Names

PharmGKB Accession Id

PA449048

Type(s):

Drug

Description

Clomipramine, the 3-chloro analog of imipramine, is a dibenzazepine-derivative tricyclic antidepressant (TCA). TCAs are structurally similar to phenothiazines. They contain a tricyclic ring system with an alkyl amine substituent on the central ring. In non-depressed individuals, clomipramine does not affect mood or arousal, but may cause sedation. In depressed individuals, clomipramine exerts a positive effect on mood. TCAs are potent inhibitors of serotonin and norepinephrine reuptake. Tertiary amine TCAs, such as clomipramine, are more potent inhibitors of serotonin reuptake than secondary amine TCAs, such as nortriptyline and desipramine. TCAs also down-regulate cerebral cortical beta-adrenergic receptors and sensitize post-synaptic serotonergic receptors with chronic use. The antidepressant effects of TCAs are thought to be due to an overall increase in serotonergic neurotransmission. TCAs also block histamine-H ~1~ receptors, alpha ~1~-adrenergic receptors and muscarinic receptors, which accounts for their sedative, hypotensive and anticholinergic effects (e.g. blurred vision, dry mouth, constipation, urinary retention), respectively. See toxicity section below for a complete listing of side effects. Clomipramine may be used to treat obsessive-compulsive disorder and disorders with an obsessive-compulsive component (e.g. depression, schizophrenia, Tourette's disorder). Unlabeled indications include panic disorder, chronic pain (e.g. central pain, idiopathic pain disorder, tension headache, diabetic peripheral neuropathy, neuropathic pain), cataplexy and associated narcolepsy, autistic disorder, trichotillomania, onchophagia, stuttering, premature ejaculation, and premenstrual syndrome. Clomipramine is rapidly absorbed from the gastrointestinal tract and demethylated in the liver to its primary active metabolite, desmethylclomipramine.

Source: Drug Bank

Indication

May be used to treat obsessive-compulsive disorder and disorders with an obsessive-compulsive component (e.g. depression, schizophrenia, Tourette's disorder). Unlabeled indications include: depression, panic disorder, chronic pain (e.g. central pain, idiopathic pain disorder, tension headache, diabetic peripheral neuropathy, neuropathic pain), cataplexy and associated narcolepsy (limited evidence), autistic disorder (limited evidence), trichotillomania (limited evidence), onchophagia (limited evidence), stuttering (limited evidence), premature ejaculation, and premenstrual syndrome.

Source: Drug Bank

Other Vocabularies

Information pulled from DrugBank has not been reviewed by PharmGKB.

Pharmacology, Interactions, and Contraindications

Mechanism of Action

Clomipramine is a strong, but not completely selective serotonin reuptake inhibitor (SRI), as the active main metabolite desmethyclomipramine acts preferably as an inhibitor of noradrenaline reuptake. alpha ~1~-receptor blockage and beta-down-regulation have been noted and most likely play a role in the short term effects of clomipramine. A blockade of sodium-channels and NDMA-receptors might, as with other tricyclics, account for its effect in chronic pain, in particular the neuropathic type.

Source: Drug Bank

Pharmacology

Clomipramine, a tricyclic antidepressant, is the 3-chloro derivative of Imipramine. It was thought that tricyclic antidepressants work exclusively 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: alpha ~1~ and beta ~1~ receptors are sensitized, alpha ~2~ receptors are desensitized (leading to increased noradrenaline production). Tricyclics are also known as effective analgesics for different types of pain, especially neuropathic or neuralgic pain.

Source: Drug Bank

Food Interaction

Avoid alcohol.|Take with food to reduce irritation.|Grapefruit and grapefruit juice should be avoided throughout treatment, grapefruit can modify serum levels of clomipramine and its metabolite desmethyl-clomipramine.

Source: Drug Bank

Absorption, Distribution, Metabolism, Elimination & Toxicity

Biotransformation

Extensively metabolized in the liver. The main active metabolite is desmethylclomipramine, which is formed by _N_-demethylation of clomipramine via CYP2C19, 3A4 and 1A2. Other metabolites and their glucuronide conjugates are also produced. Other metabolites of clomipramine include 8-hydroxyclomipramine formed via 8-hydroxylation, 2-hydroxyclomipramine formed via 2-hydroxylation, and clomipramine _N_-oxide formed by _N_-oxidation. Desmethylclomipramine is further metabolized to 8-hydroxydesmethylclomipramine and didesmethylclomipramine, which are formed by 8-hydroxylation and _N_-demethylation, respectively. 8-Hydroxyclomipramine and 8-hydroxydesmethylclomipramine are pharmacologically active; however, their clinical contribution remains unknown.

Source: Drug Bank

Protein Binding

Clomipramine is approximately 97-98% bound to plasma proteins, principally to albumin and possibly to alpha ~1~-acid glycoprotein. Desmethylclomipramine is 97-99% bound to plasma proteins.

Source: Drug Bank

Absorption

Well absorbed from the GI tract following oral administration. Bioavailability is approximately 50% orally due to extensive first-pass metabolism. Bioavailability is not affected by food. Peak plasma concentrations occur 2-6 hours following oral administration of a single 50 mg dose. Large interindividual variations in plasma concentrations occur, partly due to genetic differences in clomipramine metabolism. On average, steady state plasma concentrations are achieved in 1-2 weeks following multiple dose oral administration. Smoking appears to lower the steady-state plasma concentration of clomipramine, but not its active metabolite desmethylclomipramine.

Source: Drug Bank

Half-Life

Following oral administration of a single 150 mg dose of clomipramine, the average elimination half-life of clomipramine was 32 hours (range: 19-37 hours) and of desmethylclomipramine was 69 hours (range: 54-77 hours). Elimination half-life may vary substantially with different doses due to probably saturable kinetics (i.e. metabolism).

Source: Drug Bank

Toxicity

Signs and symptoms vary in severity depending upon factors such as the amount of drug absorbed, the age of the patient, and the time elapsed since drug ingestion. Critical manifestations of overdose include cardiac dysrhythmias, severe hypotension, convulsions, and CNS depression including coma. Changes in the electrocardiogram, particularly in QRS axis or width, are clinically significant indicators of tricyclic toxicity. In U.S. clinical trials, 2 deaths occurred in 12 reported cases of acute overdosage with Anafranil either alone or in combination with other drugs. One death involved a patient suspected of ingesting a dose of 7000 mg. The second death involved a patient suspected of ingesting a dose of 5750 mg. 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

Urine (51-60%) and feces via biliary elimination (24-32%)

Source: Drug Bank

Volume of Distribution

Average ~ 17 L/kg (range: 9-25 L/kg)

Source: Drug Bank

Chemical Properties

Chemical Formula

C19H23ClN2

Source: Drug Bank

Isomeric SMILES

CN(C)CCCN1c2ccccc2CCc3c1cc(cc3)Cl

Source: OpenEye

Canonical SMILES

CN(C)CCCN1C2=CC=CC=C2CCC2=C1C=C(Cl)C=C2

Source: Drug Bank

Average Molecular Weight

314.852

Source: Drug Bank

Monoisotopic Molecular Weight

314.154976453

Source: Drug Bank

SMILES

CN(C)CCCN1C2=CC=CC=C2CCC2=C1C=C(Cl)C=C2

Source: Drug Bank

InChI String

InChI=1S/C19H23ClN2/c1-21(2)12-5-13-22-18-7-4-3-6-15(18)8-9-16-10-11-17(20)14-19(16)22/h3-4,6-7,10-11,14H,5,8-9,12-13H2,1-2H3

Source: Drug Bank

PharmGKB Curated Pathways

Pathways created internally by PharmGKB based primarily on literature evidence.

  1. Clomipramine Pathway, Pharmacokinetics
    Schematic representation of clomipramine metabolism in human liver.

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 ?

EvidenceGene
No Dosing Guideline available No Drug Label available CA VA No VIP available No VIP available
ABCB1
No Dosing Guideline available DL No Clinical Annotation available VA No VIP available PW
CYP1A2
DG No Drug Label available CA VA VIP PW
CYP2C19
DG DL CA VA VIP PW
CYP2D6
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available PW
CYP3A4
No Dosing Guideline available No Drug Label available No Clinical Annotation available VA No VIP available No VIP available
CYP3A5
No Dosing Guideline available No Drug Label available CA VA No VIP available No VIP available
FKBP5
No Dosing Guideline available No Drug Label available CA VA No VIP available No VIP available
HTR1B
No Dosing Guideline available No Drug Label available No Clinical Annotation available VA No VIP available No VIP available
HTR2A
No Dosing Guideline available No Drug Label available CA VA No VIP available No VIP available
SLC6A4

Drug Targets

Gene Description
GSTP1 (source: Drug Bank )
HTR2A (source: Drug Bank )
HTR2B (source: Drug Bank )
HTR2C (source: Drug Bank )
SLC6A2 (source: Drug Bank )
SLC6A4 (source: Drug Bank )

Drug Interactions

Interaction Description
atazanavir - clomipramine Increases the effect and toxicity of tricyclics (source: Drug Bank )
atazanavir - clomipramine Atazanavir may increase the effect and toxicity of the tricyclic antidepressant, clomipramine, by decreasing its metabolism. Monitor for changes in the therapeutic and adverse effects of clomipramine if atazanavir if initiated, discontinued or dose changed. (source: Drug Bank )
cimetidine - clomipramine Increases the effect of tricyclic agent (source: Drug Bank )
cimetidine - clomipramine Cimetidine may increase the effect of the tricyclic antidepressant, clomipramine, by decreasing its metabolism. Monitor for changes in the therapeutic and adverse effects of clomipramine if cimetidine is initiated, discontinued or dose changed. (source: Drug Bank )
cisapride - clomipramine Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank )
cisapride - clomipramine Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank )
clomipramine - altretamine Risk of severe hypotension (source: Drug Bank )
clomipramine - altretamine Risk of severe hypotension (source: Drug Bank )
clomipramine - atazanavir Atazanavir increases the effect and toxicity of tricyclics (source: Drug Bank )
clomipramine - atazanavir Atazanavir may increase the effect and toxicity of the tricyclic antidepressant, clomipramine, by decreasing its metabolism. Monitor for changes in the therapeutic and adverse effects of clomipramine if atazanavir if initiated, discontinued or dose changed. (source: Drug Bank )
clomipramine - cimetidine Cimetidine increases the effect of tricyclic agent (source: Drug Bank )
clomipramine - cimetidine Cimetidine may increase the effect of the tricyclic antidepressant, clomipramine, by decreasing its metabolism. Monitor for changes in the therapeutic and adverse effects of clomipramine if cimetidine is initiated, discontinued or dose changed. (source: Drug Bank )
clomipramine - cisapride Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank )
clomipramine - cisapride Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank )
clomipramine - clonidine The tricycli decreases the effect of clonidine (source: Drug Bank )
clomipramine - clonidine The tricycli decreases the effect of clonidine (source: Drug Bank )
clomipramine - dobutamine The tricyclic increases the sympathomimetic effect (source: Drug Bank )
clomipramine - dobutamine The tricyclic antidepressant, clomipramine, increases the sympathomimetic effect of dobutamine. (source: Drug Bank )
clomipramine - donepezil Possible antagonism of action (source: Drug Bank )
clomipramine - donepezil Possible antagonism of action (source: Drug Bank )
clomipramine - dopamine The tricyclic increases the sympathomimetic effect (source: Drug Bank )
clomipramine - dopamine The tricyclic antidepressant, clomipramine, increases the sympathomimetic effect of dopamine. (source: Drug Bank )
clomipramine - ephedra The tricyclic increases the sympathomimetic effect (source: Drug Bank )
clomipramine - ephedra The tricyclic antidepressant, clomipramine, increases the sympathomimetic effect of ephedra. (source: Drug Bank )
clomipramine - ephedrine The tricyclic increases the sympathomimetic effect (source: Drug Bank )
clomipramine - ephedrine The tricyclic antidepressant, clomipramine, increases the sympathomimetic effect of ephedrine. (source: Drug Bank )
clomipramine - epinephrine The tricyclic increases the sympathomimetic effect (source: Drug Bank )
clomipramine - epinephrine The tricyclic antidepressant, clomipramine, increases the sympathomimetic effect of epinephrine. (source: Drug Bank )
clomipramine - fenoterol The tricyclic increases the sympathomimetic effect (source: Drug Bank )
clomipramine - fenoterol The tricyclic antidepressant, clomipramine, increases the sympathomimetic effect of fenoterol. (source: Drug Bank )
clomipramine - fluoxetine Fluoxetine increases the effect and toxicity of tricyclics (source: Drug Bank )
clomipramine - fluoxetine The SSRI, fluoxetine, may increase the serum concentration of the tricyclic antidepressant, clomipramine, by decreasing its metabolism. Additive modulation of serotonin activity also increases the risk of serotonin syndrome. Monitor for development of serotonin syndrome during concomitant therapy. Monitor for changes in the therapeutic and adverse effects of clomipramine if fluoxetine is initiated, discontinued or dose changed. (source: Drug Bank )
clomipramine - fluvoxamine Fluvoxamine increases the effect and toxicity of tricyclics (source: Drug Bank )
clomipramine - fluvoxamine The SSRI, fluvoxamine, may increase the serum concentration of the tricyclic antidepressant, clomipramine, by decreasing its metabolism. Additive modulation of serotonin activity also increases the risk of serotonin syndrome. Monitor for development of serotonin syndrome during concomitant therapy. Monitor for changes in the therapeutic and adverse effects of clomipramine if fluvoxamine is initiated, discontinued or dose changed. (source: Drug Bank )
clomipramine - galantamine Possible antagonism of action (source: Drug Bank )
clomipramine - galantamine Possible antagonism of action (source: Drug Bank )
clomipramine - grepafloxacin Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank )
clomipramine - grepafloxacin Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank )
clomipramine - guanethidine The tricyclic decreases the effect of guanethidine (source: Drug Bank )
clomipramine - guanethidine The tricyclic antidepressant, clomipramine, decreases the effect of guanethidine. (source: Drug Bank )
clomipramine - isocarboxazid Possibility of severe adverse effects (source: Drug Bank )
clomipramine - isocarboxazid Possibility of severe adverse effects (source: Drug Bank )
clomipramine - isoproterenol The tricyclic increases the sympathomimetic effect (source: Drug Bank )
clomipramine - isoproterenol The tricyclic antidepressant, clomipramine, increases the sympathomimetic effect of isoproterenol. (source: Drug Bank )
clomipramine - mephentermine The tricyclic increases the sympathomimetic effect (source: Drug Bank )
clomipramine - mephentermine The tricyclic antidepressant, clomipramine, increases the sympathomimetic effect of mephentermine. (source: Drug Bank )
clomipramine - metaraminol The tricyclic increases the sympathomimetic effect (source: Drug Bank )
clomipramine - metaraminol The tricyclic antidepressant, clomipramine, increases the sympathomimetic effect of metaraminol. (source: Drug Bank )
clomipramine - methoxamine The tricyclic increases the sympathomimetic effect (source: Drug Bank )
clomipramine - methoxamine The tricyclic antidepressant, clomipramine, increases the sympathomimetic effect of methoxamine. (source: Drug Bank )
clomipramine - moclobemide Possible severe adverse reaction with this combination (source: Drug Bank )
clomipramine - moclobemide Possible severe adverse reaction with this combination (source: Drug Bank )
clomipramine - norepinephrine The tricyclic increases the sympathomimetic effect (source: Drug Bank )
clomipramine - norepinephrine The tricyclic antidepressant, clomipramine, increases the sympathomimetic effect of norepinephrine. (source: Drug Bank )
clomipramine - orciprenaline The tricyclic increases the sympathomimetic effect (source: Drug Bank )
clomipramine - orciprenaline The tricyclic antidepressant, clomipramine, increases the sympathomimetic effect of orciprenaline. (source: Drug Bank )
clomipramine - phenelzine Possibility of severe adverse effects (source: Drug Bank )
clomipramine - phenelzine Possibility of severe adverse effects (source: Drug Bank )
clomipramine - phenylephrine The tricyclic increases the sympathomimetic effect (source: Drug Bank )
clomipramine - phenylephrine The tricyclic antidepressant, clomipramine, increases the sympathomimetic effect of phenylephrine. (source: Drug Bank )
clomipramine - phenylpropanolamine The tricyclic increases the sympathomimetic effect (source: Drug Bank )
clomipramine - phenylpropanolamine The tricyclic antidepressant, clomipramine, increases the sympathomimetic effect of phenylpropanolamine. (source: Drug Bank )
clomipramine - pirbuterol The tricyclic increases the sympathomimetic effect (source: Drug Bank )
clomipramine - pirbuterol The tricyclic antidepressant, clomipramine, increases the sympathomimetic effect of pirbuterol. (source: Drug Bank )
clomipramine - procaterol The tricyclic increases the sympathomimetic effect (source: Drug Bank )
clomipramine - procaterol The tricyclic antidepressant, clomipramine, increases the sympathomimetic effect of procaterol. (source: Drug Bank )
clomipramine - pseudoephedrine The tricyclic increases the sympathomimetic effect (source: Drug Bank )
clomipramine - pseudoephedrine The tricyclic antidepressant, clomipramine, increases the sympathomimetic effect of pseudoephedrine. (source: Drug Bank )
clomipramine - quinidine Quinidine increases the effect of tricyclic agent (source: Drug Bank )
clomipramine - quinidine Quinidine increases the effect of tricyclic agent (source: Drug Bank )
clomipramine - quinidine Quinidine barbiturate increases the effect of tricyclic antidepressant, clomipramine. (source: Drug Bank )
clomipramine - rasagiline Possibility of severe adverse effects (source: Drug Bank )
clomipramine - rasagiline Possibility of severe adverse effects (source: Drug Bank )
clomipramine - rifabutin The rifamycin decreases the effect of tricyclics (source: Drug Bank )
clomipramine - rifabutin The rifamycin, rifabutin, may decrease the effect of the tricyclic antidepressant, clomipramine, by increasing its metabolism. Monitor for changes in the therapeutic and adverse effects of clomipramine if rifabutin is initiated, discontinued or dose changed. (source: Drug Bank )
clomipramine - rifampin The rifamycin decreases the effect of tricyclics (source: Drug Bank )
clomipramine - rifampin The rifamycin, rifampin, may decrease the effect of the tricyclic antidepressant, clomipramine, by increasing its metabolism. Monitor for changes in the therapeutic and adverse effects of clomipramine if rifampin is initiated, discontinued or dose changed. (source: Drug Bank )
clomipramine - ritonavir Ritonavir increases the effect and toxicity of tricyclics (source: Drug Bank )
clomipramine - ritonavir Ritonavir may increase the effect and toxicity of the tricyclic antidepressant, clomipramine, by decreasing its metabolism. Monitor for changes in the therapeutic and adverse effects of clomipramine if ritonavir if initiated, discontinued or dose changed. (source: Drug Bank )
clomipramine - rivastigmine Possible antagonism of action (source: Drug Bank )
clomipramine - rivastigmine Possible antagonism of action (source: Drug Bank )
clomipramine - salbutamol The tricyclic increases the sympathomimetic effect (source: Drug Bank )
clomipramine - salbutamol The tricyclic antidepressant, clomipramine, increases the sympathomimetic effect of salbutamol. (source: Drug Bank )
clomipramine - sibutramine Increased risk of CNS adverse effects (source: Drug Bank )
clomipramine - sibutramine Increased risk of CNS adverse effects (source: Drug Bank )
clomipramine - sparfloxacin Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank )
clomipramine - sparfloxacin Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank )
clomipramine - terbutaline The tricyclic increases the sympathomimetic effect (source: Drug Bank )
clomipramine - terbutaline The tricyclic antidepressant, clomipramine, increases the sympathomimetic effect of terbutaline. (source: Drug Bank )
clomipramine - terfenadine Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank )
clomipramine - terfenadine Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank )
clomipramine - tranylcypromine Possibility of severe adverse effects (source: Drug Bank )
clomipramine - tranylcypromine Possibility of severe adverse effects (source: Drug Bank )
clonidine - clomipramine The tricyclic decreases the effect of clonidine (source: Drug Bank )
clonidine - clomipramine The tricyclic antidepressant, clomipramine, decreases the effect of clonidine. (source: Drug Bank )
donepezil - clomipramine Possible antagonism of action (source: Drug Bank )
donepezil - clomipramine Possible antagonism of action (source: Drug Bank )
epinephrine - clomipramine The tricyclic increases the sympathomimetic effect (source: Drug Bank )
epinephrine - clomipramine The tricyclic antidepressant, clomipramine, increases the sympathomimetic effect of epinephrine. (source: Drug Bank )
fenoterol - clomipramine The tricyclic increases the sympathomimetic effect (source: Drug Bank )
fenoterol - clomipramine The tricyclic antidepressant, clomipramine, increases the sympathomimetic effect of fenoterol. (source: Drug Bank )
fluoxetine - clomipramine Fluoxetine increases the effect and toxicity of tricyclics (source: Drug Bank )
fluoxetine - clomipramine The SSRI, fluoxetine, may increase the serum concentration of the tricyclic antidepressant, clomipramine, by decreasing its metabolism. Additive modulation of serotonin activity also increases the risk of serotonin syndrome. Monitor for development of serotonin syndrome during concomitant therapy. Monitor for changes in the therapeutic and adverse effects of clomipramine if fluoxetine is initiated, discontinued or dose changed. (source: Drug Bank )
galantamine - clomipramine Possible antagonism of action (source: Drug Bank )
galantamine - clomipramine Possible antagonism of action (source: Drug Bank )
grepafloxacin - clomipramine Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank )
grepafloxacin - clomipramine Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank )
guanethidine - clomipramine The tricyclic decreases the effect of guanethidine (source: Drug Bank )
guanethidine - clomipramine The tricyclic antidepressant, clomipramine, decreases the effect of guanethidine. (source: Drug Bank )
isocarboxazid - clomipramine Possibility of severe adverse effects (source: Drug Bank )
isocarboxazid - clomipramine Possibility of severe adverse effects (source: Drug Bank )
moclobemide - clomipramine Possible severe adverse reaction with this combination (source: Drug Bank )
moclobemide - clomipramine Possible severe adverse reaction with this combination (source: Drug Bank )
orciprenaline - clomipramine The tricyclic increases the sympathomimetic effect (source: Drug Bank )
orciprenaline - clomipramine The tricyclic antidepressant, clomipramine, increases the sympathomimetic effect of orciprenaline. (source: Drug Bank )
phenelzine - clomipramine Possibility of severe adverse effects (source: Drug Bank )
phenelzine - clomipramine Possibility of severe adverse effects (source: Drug Bank )
phenylephrine - clomipramine The tricyclic increases the sympathomimetic effect (source: Drug Bank )
phenylephrine - clomipramine The tricyclic antidepressant, clomipramine, increases the sympathomimetic effect of phenylephrine. (source: Drug Bank )
phenylpropanolamine - clomipramine The tricyclic antidepressant, clomipramine, increases the sympathomimetic effect of phenylpropanolamine. (source: Drug Bank )
pseudoephedrine - clomipramine The tricyclic increases the sympathomimetic effect (source: Drug Bank )
pseudoephedrine - clomipramine The tricyclic antidepressant, clomipramine, increases the sympathomimetic effect of pseudoephedrine. (source: Drug Bank )
quinidine - clomipramine Quinidine increases the effect of the tricyclic agent (source: Drug Bank )
quinidine - clomipramine Additive QTc-prolonging effects may occur. Quinidine may also increase the serum concentration of the tricyclic antidepressant, clomipramine, by decreasing its metabolism. Monitor for changes in the therapeutic and adverse effects of clomipramine if quinidine is initiated, discontinued or dose changed. Monitor for the development of torsades de pointes during concomitant therapy. (source: Drug Bank )
rasagiline - clomipramine Possibility of severe adverse effects (source: Drug Bank )
rifabutin - clomipramine The rifamycin decreases the effect of tricyclics (source: Drug Bank )
rifabutin - clomipramine The rifamycin, rifabutin, may decrease the effect of the tricyclic antidepressant, clomipramine, by increasing its metabolism. Monitor for changes in the therapeutic and adverse effects of clomipramine if rifabutin is initiated, discontinued or dose changed. (source: Drug Bank )
rifampin - clomipramine The rifamycin decreases the effect of tricyclics (source: Drug Bank )
rifampin - clomipramine The rifamycin, rifampin, may decrease the effect of the tricyclic antidepressant, clomipramine, by increasing its metabolism. Monitor for changes in the therapeutic and adverse effects of clomipramine if rifampin is initiated, discontinued or dose changed. (source: Drug Bank )
tacrine - clomipramine The therapeutic effects of the central acetylcholinesterase inhibitor, Tacrine, and/or the anticholinergic, Clomipramine, 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 - clomipramine The therapeutic effects of the central acetylcholinesterase inhibitor, Tacrine, and/or the anticholinergic, Clomipramine, 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 )
tamoxifen - clomipramine Clomipramine may decrease the therapeutic effect of Tamoxifen by decreasing the production of active metabolites. Consider alternate therapy. (source: Drug Bank )
tamoxifen - clomipramine Clomipramine may decrease the therapeutic effect of Tamoxifen by decreasing the production of active metabolites. Consider alternate therapy. (source: Drug Bank )
tamsulosin - clomipramine Clomipramine, a CYP2D6 inhibitor, may decrease the metabolism and clearance of Tamsulosin, a CYP2D6 substrate. Monitor for changes in therapeutic/adverse effects of Tamsulosin if Clomipramine is initiated, discontinued, or dose changed. (source: Drug Bank )
tamsulosin - clomipramine Clomipramine, a CYP2D6 inhibitor, may decrease the metabolism and clearance of Tamsulosin, a CYP2D6 substrate. Monitor for changes in therapeutic/adverse effects of Tamsulosin if Clomipramine is initiated, discontinued, or dose changed. (source: Drug Bank )
terbutaline - clomipramine The tricyclic increases the sympathomimetic effect (source: Drug Bank )
terbutaline - clomipramine The tricyclic antidepressant, clomipramine, increases the sympathomimetic effect of terbutaline. (source: Drug Bank )
terfenadine - clomipramine Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank )
terfenadine - clomipramine Increased risk of cardiotoxicity and arrhythmias (source: Drug Bank )
thiabendazole - clomipramine The strong CYP1A2 inhibitor, Thiabendazole, may increase the effects and toxicity of Clomipramine by decreasing Clomipramine metabolism and clearance. Monitor for changes in the therapeutic and adverse effects of Clomipramine if Thiabendazole is initiated, discontinued or dose changed. (source: Drug Bank )
thiothixene - clomipramine 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 - clomipramine 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 - clomipramine Ticlopidine may decrease the metabolism and clearance of Clomipramine. Consider alternate therapy or monitor for adverse/toxic effects of Clomipramine if Ticlopidine is initiated, discontinued or dose changed. (source: Drug Bank )
toremifene - clomipramine 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 - clomipramine Tramadol increases the risk of serotonin syndrome and seizures. Clomipramine may decrease the effect of Tramadol by decreasing active metabolite production. (source: Drug Bank )
tranylcypromine - clomipramine 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 - clomipramine Increased risk of serotonin syndrome. The 2D6 inhibitor, Trazodone, may also increase the efficacy of Clomipramine by decreasing Clomipramine metabolism and clearance. Monitor for symptoms of serotonin syndrome and changes in Clomipramine efficacy if Trazodone is initiated, discontinued or dose changed. (source: Drug Bank )
trazodone - clomipramine Increased risk of serotonin syndrome. Monitor for symptoms of serotonin syndrome. (source: Drug Bank )
trimethobenzamide - clomipramine Trimethobenzamide and Clomipramine, two anticholinergics, may cause additive anticholinergic effects and enhance their adverse/toxic effects. Monitor for enhanced anticholinergic effects. (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 )
triprolidine - clomipramine Triprolidine and Clomipramine, 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 - clomipramine Triprolidine and Clomipramine, 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 - clomipramine Trospium and Clomipramine, two anticholinergics, may cause additive anticholinergic effects and enhanced adverse/toxic effects. Monitor for enhanced anticholinergic effects. (source: Drug Bank )
venlafaxine - clomipramine Increased risk of serotonin syndrome. Monitor for symptoms of serotonin syndrome. (source: Drug Bank )
voriconazole - clomipramine 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 - clomipramine 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 - clomipramine Additive QTc-prolonging effects may increase the risk of severe arrhythmias. Concomitant therapy is contraindicated. (source: Drug Bank )
zolmitriptan - clomipramine Use of two serotonin modulators, such as zolmitriptan and clomipramine, increases the risk of serotonin syndrome. Consider alternate therapy or monitor for serotonin syndrome during concomitant therapy. (source: Drug Bank )
zuclopenthixol - clomipramine 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 ?

EvidenceDisease
No Dosing Guideline available No Drug Label available No Clinical Annotation available VA No VIP available No VIP available
Agoraphobia
No Dosing Guideline available DL CA VA No VIP available No VIP available
Depression
No Dosing Guideline available DL No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Depression, Postpartum
No Dosing Guideline available No Drug Label available CA VA No VIP available No VIP available
Depressive Disorder, Major
No Dosing Guideline available No Drug Label available No Clinical Annotation available VA No VIP available No VIP available
Drug Toxicity
No Dosing Guideline available DL No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Inflammation
No Dosing Guideline available No Drug Label available No Clinical Annotation available VA No VIP available No VIP available
Mental Disorders
No Dosing Guideline available DL No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Neoplasms
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Obsessive-Compulsive Disorder
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Overdose
No Dosing Guideline available DL No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Schizophrenia
No Dosing Guideline available No Drug Label available No Clinical Annotation available VA No VIP available No VIP available
Serotonin Syndrome

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

May Treat
Contraindicated With

Publications related to clomipramine: 70

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Serum clomipramine and desmethylclomipramine levels in a CYP2C19 and CYP2D6 intermediate metabolizer. Pharmacogenomics. 2017. Brown Jacob T, et al. PubMed
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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. PubMed
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The combination of pharmacogenetic and pharmacokinetic analyses to optimize clomipramine dosing in major depression: a case report. Journal of clinical pharmacy and therapeutics. 2016. Antoniazzi Stefania, 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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Serotonin toxicity from antidepressant overdose and its association with the T102C polymorphism of the 5-HT2A receptor. The pharmacogenomics journal. 2014. Cooper J M, et al. PubMed
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Challenges in pharmacogenetics. European journal of clinical pharmacology. 2013. Cascorbi Ingolf, et al. PubMed
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Pharmacogenetics in major depression: a comprehensive meta-analysis. Progress in neuro-psychopharmacology & biological psychiatry. 2013. Niitsu Tomihisa, et al. PubMed
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Influence of CYP2D6 and CYP2C19 gene variants on antidepressant response in obsessive-compulsive disorder. The pharmacogenomics journal. 2013. Brandl E J, et al. PubMed
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Clinical Pharmacogenetics Implementation Consortium Guideline for CYP2D6 and CYP2C19 Genotypes and Dosing of Tricyclic Antidepressants. Clinical pharmacology and therapeutics. 2013. Hicks J K, et al. PubMed
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Cytochrome P450-mediated drug metabolism in the brain. Journal of psychiatry & neuroscience : JPN. 2012. Miksys Sharon, et al. PubMed
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The AmpliChip® CYP450 test and response to treatment in schizophrenia and obsessive compulsive disorder: a pilot study and focus on cases with abnormal CYP2D6 drug metabolism. Genetic testing and molecular biomarkers. 2012. Müller Daniel J, et al. PubMed
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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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Clinical and genetic correlates of suicidal ideation during antidepressant treatment in a depressed outpatient sample. Pharmacogenomics. 2011. Perroud Nader, et al. PubMed
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Association study between genetic monoaminergic polymorphisms and OCD response to clomipramine treatment. Arquivos de neuro-psiquiatria. 2011. Miguita Karen, et al. PubMed
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Pharmacogenetics and gender association with psychotic episodes on nortriptyline lower doses: patient cases. ISRN pharmaceutics. 2011. Piatkov Irina, et al. PubMed
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Meta-analysis of FKBP5 gene polymorphisms association with treatment response in patients with mood disorders. Neuroscience letters. 2010. Zou Yan-Feng, et al. PubMed
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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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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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FKBP5 polymorphisms and antidepressant response in geriatric depression. American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics. 2010. Sarginson Jane E, et al. PubMed
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Cytochrome P450 2D6. Pharmacogenetics and genomics. 2009. Owen Ryan P, et al. PubMed
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Life-threatening dextromethorphan intoxication associated with interaction with amitriptyline in a poor CYP2D6 metabolizer: a single case re-exposure study. Journal of pain and symptom management. 2008. Forget Patrice, et al. PubMed
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Association of graded allele-specific changes in CYP2D6 function with imipramine dose requirement in a large group of depressed patients. Molecular psychiatry. 2008. Schenk P W, et al. PubMed
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Genetic variants in FKBP5 affecting response to antidepressant drug treatment. Pharmacogenomics. 2008. Kirchheiner Julia, et al. PubMed
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Influence of the CYP2D6*4 polymorphism on dose, switching and discontinuation of antidepressants. British journal of clinical pharmacology. 2008. Bijl Monique J, et al. PubMed
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The CYP2D6 polymorphism in relation to the metabolism of amitriptyline and nortriptyline in the Faroese population. British journal of clinical pharmacology. 2008. Halling Jónrit, et al. PubMed
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Influence of cytochrome P450 polymorphisms on drug therapies: pharmacogenetic, pharmacoepigenetic and clinical aspects. Pharmacology & therapeutics. 2007. Ingelman-Sundberg Magnus, et al. PubMed
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A fatal doxepin poisoning associated with a defective CYP2D6 genotype. The American journal of forensic medicine and pathology. 2007. Koski Anna, et al. PubMed
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Tricyclic antidepressant pharmacology and therapeutic drug interactions updated. British journal of pharmacology. 2007. Gillman P K. PubMed
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Genetic variability at HPA axis in major depression and clinical response to antidepressant treatment. Journal of affective disorders. 2007. Papiol Sergi, et al. PubMed
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A poor metabolizer for cytochromes P450 2D6 and 2C19: a case report on antidepressant treatment. CNS spectrums. 2006. Johnson Maria, et al. PubMed
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CYP2D6 and CYP2C19 genotypes and amitriptyline metabolite ratios in a series of medicolegal autopsies. Forensic science international. 2006. Koski Anna, et al. PubMed
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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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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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Hippocampal upregulation of the cyclooxygenase-2 gene following neonatal clomipramine treatment (a model of depression). The pharmacogenomics journal. 2006. Cassano P, et al. PubMed
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Polymorphisms in FKBP5 are associated with increased recurrence of depressive episodes and rapid response to antidepressant treatment. Nature genetics. 2004. Binder Elisabeth B, et al. PubMed
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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 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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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 effect of CYP2C19 and CYP2D6 genotypes on the metabolism of clomipramine in Japanese psychiatric patients. Journal of clinical psychopharmacology. 2001. Yokono A, 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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Serotonin transporter (5-HTT) promoter genotype may influence the prolactin response to clomipramine. Psychopharmacology. 2000. Whale R, et al. 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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Pronounced differences in the dispositon of clomipramine between Japanese and Swedish patients. Journal of clinical psychopharmacology. 1999. Shimoda K, 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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Ultrarapid metabolism of clomipramine in a therapy-resistant depressive patient, as confirmed by CYP2 D6 genotyping. Pharmacopsychiatry. 1998. Baumann P, et al. PubMed
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Pharmacogenetics of antidepressants: clinical aspects. Acta psychiatrica Scandinavica. Supplementum. 1997. Bertilsson L, 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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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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Molecular basis for rational megaprescribing in ultrarapid hydroxylators of debrisoquine. Lancet. 1993. Bertilsson L, 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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Steady-state plasma levels of clomipramine and its metabolites: impact of the sparteine/debrisoquine oxidation polymorphism. Danish University Antidepressant Group. European journal of clinical pharmacology. 1992. Nielsen K K, et al. PubMed
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High blood concentrations of imipramine or clomipramine and therapeutic failure: a case report study using drug monitoring data. Therapeutic drug monitoring. 1989. Balant-Gorgia A E, et al. PubMed
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High plasma concentrations of desmethylclomipramine after chronic administration of clomipramine to a poor metabolizer. European journal of clinical pharmacology. 1987. 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
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Plasma levels of chlorimipramine and its demethyl metabolite during treatment of depression. Clinical pharmacology and therapeutics. 1979. Träskman L, et al. PubMed

LinkOuts

Web Resource:
Wikipedia
National Drug Code Directory:
0781-2027-31
DrugBank:
DB01242
PDB:
CXX
ChEBI:
47780
KEGG Compound:
C06918
PubChem Compound:
2801
PubChem Substance:
152550
46505157
IUPHAR Ligand:
2398
Drugs Product Database (DPD):
2244818
BindingDB:
50021927
ChemSpider:
2699
HET:
CXX
Therapeutic Targets Database:
DAP000742
FDA Drug Label at DailyMed:
3823106e-6be3-4154-a607-caa3a69dc75c

Clinical Trials

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