Drug/Small Molecule:
imatinib

PharmGKB contains no dosing guidelines for this drug/small molecule. To report known genotype-based dosing guidelines, or if you are interested in developing guidelines, click here.

PharmGKB gathers information regarding PGx on FDA drug labels from the FDA's "Table of Pharmacogenomic Biomarkers in Drug Labels", and from FDA-approved FDA and EMA-approved (European Medicines Agency) EMA labels brought to our attention. Excerpts from the label and downloadable highlighted label PDFs are manually curated by PharmGKB.

Please note that some drugs may have been removed from or added to the FDA's "Table of Pharmacogenomic Biomarkers in Drug Labels" without our knowledge. We periodically check the table for additions to this table and update PharmGKB accordingly.

There is currently no such list for European drug labels - we are working with the EMA to establish a list of European Public Assessment Reports (EPAR)s that contain PGx information. We are constructing this list by initially searching for drugs for which we have PGx-containing FDA drug labels - of these 44 EMA EPARs were identified and are being curated for pgx information.

We welcome any information regarding drug labels containing PGx information approved by the FDA, EMA or other Medicine Agencies around the world - please contact feedback.


last updated 10/25/2013

FDA Label for imatinib and ABL1, BCR, KIT

This label is on the FDA Biomarker List
Genetic testing required

Summary

The decision of whether to treat patients with imatinib is based on the presence of genetic biomarkers, including BCR-ABL (the Philadelphia chromosome), KIT, and PDGFR gene rearrangements.

Annotation

The decision of whether to treat patients with imatinib is based on the presence of genetic biomarkers, including BCR-ABL (the Philadelphia chromosome), KIT, and PDGFR gene rearrangements.

Excerpt from the imatinib drug label:

Gleevec is a kinase inhibitor indicated for the treatment of:
Newly diagnosed adult patients with Philadelphia chromosome positive chronic myeloid leukemia (Ph+ CML) in chronic phase.
. . .
Adult patients with myelodysplastic/myeloproliferative diseases (MDS/MPD) associated with PDGFR (platelet-derived growth factor receptor) gene re-arrangements (1.5)
Adult patients with aggressive systemic mastocytosis (ASM) without the D816V c-Kit mutation or with c-Kit mutational status unknown (1.6)
. . .
Patients with Kit (CD117) positive unresectable and/or metastatic malignant gastrointestinal stromal tumors (GIST). (1.9)
Adjuvant treatment of adult patients following resection of Kit (CD117) positive GIST (1.10)

If patients must be administered a strong CYP3A4 inducer, based on pharmacokinetic studies, the dosage of Gleevec should be increased by at least 50%, and clinical response should be carefully monitored.

Imatinib is an inhibitor of the BCR-ABL tyrosine kinase that is created by the Philadelphia chromosome rearrangement in chronic myeloid leukemia. Imatinib also inhibits the kinases encoded by the PDGFRB and KIT genes. The KIT:D816V mutation, found in many patients with aggressive systemic mastocytosis, is a gain-of-function mutation that is resistant to treatment with imatinib.

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

  • Gastrointestinal Stromal Tumors
    • Indications & usage section, Warnings section, Adverse reactions section
    • source: PHONT
  • Glioma
    • Indications & usage section, Warnings section, Adverse reactions section
    • source: PHONT
  • Heart Failure
    • Warnings section, Adverse reactions section
    • source: PHONT
  • Leukemia
    • Warnings section, Adverse reactions section
    • source: PHONT
  • Leukemia, Myelogenous, Chronic, BCR-ABL Positive
    • Indications & usage section, Warnings section, Adverse reactions section
    • source: PHONT
  • Leukemia, Myeloid
    • Indications & usage section, Warnings section, Adverse reactions section
    • source: PHONT
  • Leukemia, Myeloid, Acute
    • Indications & usage section, Warnings section
    • source: PHONT
  • Neoplasms
    • Indications & usage section, Warnings section, Adverse reactions section
    • source: PHONT
  • Philadelphia Chromosome
    • Indications & usage section, Dosage & administration section, dosage, efficacy
    • source: FDA Label
  • CYP2D6
    • Drug interactions section, Clinical pharmacology section, metabolism/PK
    • source: FDA Label
  • CYP3A4
    • Dosage & administration section, Drug interactions section, Clinical pharmacology section, dosage, metabolism/PK
    • source: FDA Label
  • KIT
    • Indications & usage section, Dosage & administration section, Clinical pharmacology section, Clinical studies section, dosage, efficacy
    • source: FDA Label

European Medicines Agency (EMA) Label for imatinib and ABL1, BCR, FIP1L1, KIT, PDGFRB

Genetic testing required

Summary

The EMA European Public Assessment Report (EPAR) for imatinib (Glivec) contains pharmacogenetic information regarding the indication of the drug in patients with tumors positive for biomarkers including KIT (CD117), BCR-ABL (Philadelphia chromosome), PDGFR and FIP1L1-PDGFRalpha rearrangements.

Annotation

Excerpt from the imatinib (Glivec) EPAR:

Glivec is indicated for the treatment of

  • adult and paediatric patients with newly diagnosed Philadelphia chromosome (bcr-abl) positive (Ph+) chronic myeloid leukaemia (CML) for whom bone marrow transplantation is not considered as the first line of treatment.
  • adult and paediatric patients with Ph+ CML in chronic phase after failure of interferon-alpha therapy, or in accelerated phase or blast crisis.
  • adult patients with newly diagnosed Philadelphia chromosome positive acute lymphoblastic leukaemia (Ph+ ALL) integrated with chemotherapy.
  • adult patients with relapsed or refractory Ph+ ALL as monotherapy.
  • adult patients with myelodysplastic/myeloproliferative diseases (MDS/MPD) associated with platelet-derived growth factor receptor (PDGFR) gene re-arrangements.
  • adult patients with advanced hypereosinophilic syndrome (HES) and/or chronic eosinophilic leukaemia (CEL) with FIP1L1-PDGFR rearrangement.

Glivec is indicated for

  • the treatment of adult patients with Kit (CD 117) positive unresectable and/or metastatic malignant gastrointestinal stromal tumours (GIST).
  • the adjuvant treatment of adult patients who are at significant risk of relapse following resection of Kit (CD117)-positive GIST. Patients who have a low or very low risk of recurrence should not receive adjuvant treatment.

This information is highlighted in the following sections:
Therapeutic indications, posology and method of administration, pharmacodynamic properties, package leaflet: information for the user.

The label also states that caution be taken when imatinib is taken concomittantly with CYP3A4 inhibitors and CYP3A4 inducers should be avoided.

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

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


PharmGKB contains no Clinical Variants that meet the highest level of criteria.

To see more Clinical Variants with lower levels of criteria, click the button at the bottom of the page.

Disclaimer: The PharmGKB's clinical annotations reflect expert consensus based on clinical evidence and peer-reviewed literature available at the time they are written and are intended only to assist clinicians in decision-making and to identify questions for further research. New evidence may have emerged since the time an annotation was submitted to the PharmGKB. The annotations are limited in scope and are not applicable to interventions or diseases that are not specifically identified.

The annotations do not account for individual variations among patients, and cannot be considered inclusive of all proper methods of care or exclusive of other treatments. It remains the responsibility of the health-care provider to determine the best course of treatment for a patient. Adherence to any guideline is voluntary, with the ultimate determination regarding its application to be made solely by the clinician and the patient. PharmGKB assumes no responsibility for any injury or damage to persons or property arising out of or related to any use of the PharmGKB clinical annotations, or for any errors or omissions.

? = Mouse-over for quick help

This is a non-comprehensive list of genetic tests with pharmacogenetics relevance, typically submitted by the manufacturer and manually curated by PharmGKB. The information listed is provided for educational purposes only and does not constitute an endorsement of any listed test or manufacturer.

A more complete listing of genetic tests is found at the Genetic Testing Registry (GTR).

PGx Test Variants Assayed Gene?
BCR-ABL Quantitation; ABL Kinase Domain Sequencing BCR-ABL (reciprocal translocation involving chromosomes 9 and 22, t(9,22)(q34, q11))

The table below contains information about pharmacogenomic variants on PharmGKB. Please follow the link in the "Variant" column for more information about a particular variant. Each link in the "Variant" column leads to the corresponding PharmGKB Variant Page. The Variant Page contains summary data, including PharmGKB manually curated information about variant-drug pairs based on individual PubMed publications. The PMIDs for these PubMed publications can be found on the Variant Page.

The tags in the first column of the table indicate what type of information can be found on the corresponding Variant Page.

Links in the "Gene" column lead to PharmGKB Gene Pages.

Gene ? Variant?
(138)
Alternate Names / Tag SNPs ? Drugs ? Alleles ?
(+ chr strand)
Function ? Amino Acid?
Translation
No VIP available No Clinical Annotations available VA
rs1045642 208920T>A, 208920T>C, 25171488A>G, 25171488A>T, 3435T>A, 3435T>C, 87138645A>G, 87138645A>T, ABCB1*6, ABCB1: 3435C>T, ABCB1: C3435T, ABCB1: c.3435C>T, ABCB1:3435C>T, Ile1145=, Ile1145Ile, MDR1 3435C>T, MDR1 C3435T, PGP C3435T, c.3435C>T, mRNA 3853C>T
A > T
A > G
Synonymous
Ile1145Ile
No VIP available CA VA
rs1050152 131676320C>T, 1507C>T, 39990192C>T, 51176C>T, 560-5701G>A, SLC22A4: L305F, SLC22A4: L503F
C > T
Intronic
Leu503Phe
No VIP available No Clinical Annotations available VA
rs1061018 13590574A>G, 42159T>C, 623T>C, 89042853A>G, Phe208Ser
A > G
Missense
Phe208Ser
No VIP available No Clinical Annotations available VA
rs1128503 1236T>C, 167964T>C, 25212444A>G, 87179601A>G, ABCB1 1236C>T, ABCB1*8, ABCB1: c.1236T>C, ABCB1:1236C>T, ABCB1:1236T>C, Gly412=, Gly412Gly, mRNA 1654T>C, p.Gly412Gly
A > G
Synonymous
Gly412Gly
No VIP available No Clinical Annotations available VA
rs2032582 186947T>A, 186947T>G, 25193461A>C, 25193461A>T, 2677A, 2677G, 2677T, 2677T>A, 2677T>G, 3095G>T/A, 87160618A>C, 87160618A>T, 893 Ala, 893 Ser, 893 Thr, ABCB1*7, ABCB1: 2677G>T/A, ABCB1: 2677T/A>G, ABCB1: A893S, ABCB1: G2677T/A, ABCB1: c.2677G>T/A, ABCB1:2677G>A/T, ABCB1:2677G>T/A, ABCB1:A893T, Ala893Ser/Thr, MDR1, MDR1 G2677T/A, Ser893Ala, Ser893Thr, mRNA 3095G>T/A, p.Ala893Ser/Thr
A > C
A > T
Missense
Ser893Ala
Ser893Thr
No VIP available No Clinical Annotations available VA
rs2231137 13608835C>T, 23898G>A, 34G>A, 89061114C>T, ABCG2:V12M, Val12Met
C > T
Missense
Val12Met
No VIP available No Clinical Annotations available VA
rs2231142 13600044G>T, 32689C>A, 421C>A, 89052323G>T, ABCG2: Q141K, ABCG2:421C>A, ABCG2:Q141K, ABCG2:c.421C>A, Gln141Lys, rs2231142
G > T
Missense
Gln141Lys
No VIP available No Clinical Annotations available VA
rs2290573 1403-9C>T, 45920151G>A, 75129594G>A
G > A
Intronic
No VIP available No Clinical Annotations available VA
rs2631367 -207C>G, 131705458C>G, 40019330C>G, 5058C>G, 73+78G>C, SLC22A5: ¿207G>C
C > G
Intronic
No VIP available CA VA
rs2631372 -2087G>C, 131703578G>C, 3178G>C, 40017450G>C, 74-1105C>G
G > C
Intronic
No VIP available No Clinical Annotations available VA
rs3764043 -423G>A, -62-361G>A, 14248128C>T, 21488004C>T
C > T
5' Flanking
No VIP available No Clinical Annotations available VA
rs41282401 13583887C>G, 48846G>C, 886G>C, 89036166C>G, Asp296His
C > G
Missense
Asp296His
No VIP available No Clinical Annotations available VA
rs4148977 -1167G>A, -62-1105G>A, 14248872C>T, 21488748C>T
C > T
5' Flanking
No VIP available No Clinical Annotations available VA
rs4148978 -1094G>A, -62-1032G>A, 14248799C>T, 21488675C>T
C > T
5' Flanking
No VIP available No Clinical Annotations available VA
rs45605536 13566391C>T, 1582G>A, 66342G>A, 89018670C>T, Ala528Thr
C > T
Missense
Ala528Thr
No VIP available No Clinical Annotations available VA
rs58818712 13566399A>C, 1574T>G, 66334T>G, 89018678A>C, Leu525Arg
A > C
Missense
Leu525Arg
No VIP available No Clinical Annotations available VA
rs628031 1222A>G, 160560845A>G, 64730302A>G, Met408Val
A > G
Missense
Met408Val
VIP No Clinical Annotations available No Variant Annotations available
rs72552763 1260_1262delGAT, 160560883_160560885delGAT, 64730340_64730342delGAT, Met420_Ile421delinsIle
GAT > -
Non-synonymous
VIP No Clinical Annotations available No Variant Annotations available
rs776746 12083G>A, 219-237G>A, 321-1G>A, 37303382C>T, 581-237G>A, 689-1G>A, 99270539C>T, CYP3A5*1, CYP3A5*3, CYP3A5*3C, CYP3A5:6986A>G, g.6986A>G, intron 3 splicing defect, rs776746 A>G
C > T
Acceptor
No VIP available CA VA
rs9561765 3870+3616C>T, 8772919G>A, 95683243G>A
G > A
Intronic
Alleles, Functions, and Amino Acid Translations are all sourced from dbSNP 138
2D structure from PubChem
provided by PubChem

Overview

Generic Names
  • Imatinib Mesylate
  • Imatinib Methansulfonate
  • sti-571
Trade Names
  • Gleevec
  • Glivec
Brand Mixture Names

PharmGKB Accession Id:
PA10804

Description

Imatinib is a drug used to treat certain types of cancer. It is currently marketed by Novartis as Gleevec (USA) or Glivec (Europe/Australia) as its mesylate salt, imatinib mesilate (INN). It is occasionally referred to as CGP57148B or STI571 (especially in older publications). It is used in treating chronic myelogenous leukemia (CML), gastrointestinal stromal tumors (GISTs) and a number of other malignancies.

It is the first member of a new class of agents that act by inhibiting particular tyrosine kinase enzymes, instead of non-specifically inhibiting rapidly dividing cells.

Source: Drug Bank

Indication

For the treatment Philadelphia chromosome positive chronic myeloid leukemia (CML) and malignant gastrointestinal stromal tumors (GIST).

Source: Drug Bank

Other Vocabularies

Information pulled from DrugBank has not been reviewed by PharmGKB.

Pharmacology, Interactions, and Contraindications

Mechanism of Action

Imatinib mesylate is a protein-tyrosine kinase inhibitor that inhibits the Bcr-Abl tyrosine kinase, the constitutive abnormal tyrosine kinase created by the Philadelphia chromosome abnormality in chronic myeloid leukemia (CML). It inhibits proliferation and induces apoptosis in Bcr-Abl positive cell lines as well as fresh leukemic cells from Philadelphia chromosome positive chronic myeloid leukemia. Imatinib also inhibits the receptor tyrosine kinases for platelet derived growth factor (PDGF) and stem cell factor (SCF) - called c-kit. Imatinib was identified in the late 1990s by Dr Brian J. Druker. Its development is an excellent example of rational drug design. Soon after identification of the bcr-abl target, the search for an inhibitor began. Chemists used a high-throughput screen of chemical libraries to identify the molecule 2-phenylaminopyrimidine. This lead compound was then tested and modified by the introduction of methyl and benzamide groups to give it enhanced binding properties, resulting in imatinib.

Source: Drug Bank

Pharmacology

Imatinib is an antineoplastic agent used to treat chronic myelogenous leukemia. Imatinib is a 2-phenylaminopyrimidine derivative that functions as a specific inhibitor of a number of tyrosine kinase enzymes. In chronic myelogenous leukemia, the Philadelphia chromosome leads to a fusion protein of Abl with Bcr (breakpoint cluster region), termed Bcr-Abl. As this is now a continuously active tyrosine kinase, Imatinib is used to decrease Bcr-Abl activity.

Source: Drug Bank

Food Interaction

Take with food to reduce the incidence of gastric irritation. Follow with a large glass of water. A lipid rich meal will slightly reduce and delay absorption. Avoid grapefruit and grapefruit juice throughout treatment, grapefruit can significantly increase serum levels of this product.

Source: Drug Bank

Absorption, Distribution, Metabolism, Elimination & Toxicity

Biotransformation

Primarily hepatic via CYP3A4. Other cytochrome P450 enzymes, such as CYP1A2, CYP2D6, CYP2C9, and CYP2C19, play a minor role in its metabolism. The main circulating active metabolite in humans is the N-demethylated piperazine derivative, formed predominantly by CYP3A4.

Source: Drug Bank

Protein Binding

Very high (95%)

Source: Drug Bank

Absorption

Imatinib is well absorbed with mean absolute bioavailability is 98% with maximum levels achieved within 2-4 hours of dosing

Source: Drug Bank

Half-Life

18 hours for Imatinib, 40 hours for its major active metabolite, the N-desmethyl derivative

Source: Drug Bank

Toxicity

Side effects include nausea, vomiting, diarrhea, loss of appetite, dry skin, hair loss, swelling (especially in the legs or around the eyes) and muscle cramps

Source: Drug Bank

Route of Elimination

Imatinib elimination is predominately in the feces, mostly as metabolites.

Source: Drug Bank

Chemical Properties

Chemical Formula

C29H31N7O

Source: Drug Bank

Isomeric SMILES

Cc1ccc(cc1Nc2nccc(n2)c3cccnc3)NC(=O)c4ccc(cc4)CN5CCN(CC5)C

Source: OpenEye

Canonical SMILES

CN1CCN(CC2=CC=C(C=C2)C(=O)NC2=CC(NC3=NC=CC(=N3)C3=CN=CC=C3)=C(C)C=C2)CC1

Source: Drug Bank

Average Molecular Weight

493.6027

Source: Drug Bank

Monoisotopic Molecular Weight

493.259008649

Source: Drug Bank

Genes that are associated with this drug in PharmGKB's database based on (1) variant annotations, (2) literature review, (3) pathways or (4) information automatically retrieved from DrugBank, depending on the "evidence" and "source" listed below.

Curated Information ?

Drug Targets

Gene Description
ABCB1 (source: Drug Bank)
ABCG2 (source: Drug Bank)
ABL1 (source: Drug Bank)
CSF1R (source: Drug Bank)
DDR1 (source: Drug Bank)
KIT (source: Drug Bank)
NTRK1 (source: Drug Bank)
PDGFRA (source: Drug Bank)
PDGFRB (source: Drug Bank)
RET (source: Drug Bank)

Drug Interactions

Drug Description
imatinib Increased hepatic toxicity of both agents (source: Drug Bank)
imatinib Increased hepatic toxicity of both agents (source: Drug Bank)
imatinib Aprepitant may change levels of the chemotherapy agent, imatinib. (source: Drug Bank)
imatinib Imatinib increases the effect and toxicity of atorvastatin (source: Drug Bank)
imatinib Imatinib increases the effect and toxicity of atorvastatin (source: Drug Bank)
imatinib Imatinib, a strong CYP3A4 inhibitor, may increase the serum concentration of bromazepam by decreasing its metabolism. Consider alternate therapy or monitor for changes in the therapeutic and adverse effects of bromazepam if imatinib is initiated, discontinued or dose changed. Dosage adjustments may be required. (source: Drug Bank)
imatinib Decreases levels of imatinib (source: Drug Bank)
imatinib Decreases levels of imatinib (source: Drug Bank)
imatinib Imatinib increases the effect and toxicity of statin (source: Drug Bank)
imatinib Imatinib increases the effect and toxicity of statin (source: Drug Bank)
imatinib The macrolide increases levels of imatinib (source: Drug Bank)
imatinib The macrolide, clarithromycin, may increase the serum concentration of imatinib. (source: Drug Bank)
imatinib Imatinib increases the effect and toxicity of cyclosporine (source: Drug Bank)
imatinib Imatinib increases the effect and toxicity of cyclosporine (source: Drug Bank)
imatinib Imatinib may increase the serum concentration of dantrolene by decreasing its metabolism. Consider alternate therapy or monitor for changes in the therapeutic and adverse effects of dantrolene if imatinib is initiated, discontinued or dose changed. (source: Drug Bank)
imatinib Decreases levels of imatinib (source: Drug Bank)
imatinib Decreases levels of imatinib (source: Drug Bank)
imatinib The macrolide increases levels of imatinib (source: Drug Bank)
imatinib The macrolide, erythromycin, may increase the serum concentration of imatinib. (source: Drug Bank)
imatinib The hydantoin decreases the levels of imatinib (source: Drug Bank)
acenocoumarol Imatinib increases the anticoagulant effect (source: Drug Bank)
acenocoumarol Imatinib may increase the anticoagulant effect of acenocoumarol. (source: Drug Bank)
acetaminophen Increased hepatic toxicity of both agents (source: Drug Bank)
acetaminophen Increased hepatic toxicity of both agents (source: Drug Bank)
anisindione Imatinib may increase the anticoagulant effect of anisindione. (source: Drug Bank)
aprepitant Aprepitant may change levels of the chemotherapy agent, imatinib. (source: Drug Bank)
atorvastatin Increases the effect and toxicity of atorvastatin (source: Drug Bank)
atorvastatin Increases the effect and toxicity of atorvastatin (source: Drug Bank)
carbamazepine Carbamazepine decreases levels of imatinib (source: Drug Bank)
carbamazepine Carbamazepine decreases levels of imatinib (source: Drug Bank)
cerivastatin Imatinib increases the effect and toxicity of statin (source: Drug Bank)
cerivastatin Imatinib increases the effect and toxicity of statin (source: Drug Bank)
clarithromycin The macrolide increases levels of imatinib (source: Drug Bank)
clarithromycin The macrolide, clarithromycin, may increase the serum concentration of imatinib. (source: Drug Bank)
cyclosporine Imatinib increases the effect and toxicity of cyclosporine (source: Drug Bank)
cyclosporine Imatinib increases the effect and toxicity of cyclosporine (source: Drug Bank)
dexamethasone Dexamethasone decreases levels of imatinib (source: Drug Bank)
dexamethasone Dexamethasone decreases levels of imatinib (source: Drug Bank)
dicumarol Imatinib increases the anticoagulant effect (source: Drug Bank)
dicumarol Imatinib may increase the anticoagulant effect of dicumarol. (source: Drug Bank)
erythromycin The macrolide increases levels of imatinib (source: Drug Bank)
erythromycin The macrolide, erythromycin, may increase the serum concentration of imatinib. (source: Drug Bank)
ethotoin The hydantoin decreases the levels of imatinib (source: Drug Bank)
fosphenytoin The hydantoin decreases the levels of imatinib (source: Drug Bank)
itraconazole The imidazole increases the levels of imatinib (source: Drug Bank)
itraconazole The imidazole increases the levels of imatinib (source: Drug Bank)
josamycin The macrolide, josamycin, may increase the serum concentration of imatinib. (source: Drug Bank)
ketoconazole The imidazole increases the levels of imatinib (source: Drug Bank)
ketoconazole The imidazole increases the levels of imatinib (source: Drug Bank)
lovastatin Imatinib increases the effect and toxicity of statin (source: Drug Bank)
lovastatin Imatinib increases the effect and toxicity of statin (source: Drug Bank)
mephenytoin The hydantoin decreases the levels of imatinib (source: Drug Bank)
mephenytoin The hydantoin decreases the levels of imatinib (source: Drug Bank)
nifedipine Imatinib increases the effect and toxicity of nifedipine (source: Drug Bank)
nifedipine Imatinib increases the effect and toxicity of nifedipine (source: Drug Bank)
phenobarbital Phenobarbital decreases levels of imatinib (source: Drug Bank)
phenobarbital Phenobarbital decreases levels of imatinib (source: Drug Bank)
phenytoin The hydantoin decreases the levels of imatinib (source: Drug Bank)
phenytoin The hydantoin decreases the levels of imatinib (source: Drug Bank)
pimozide Increases the effect and toxicity of pimozide (source: Drug Bank)
pimozide Increases the effect and toxicity of pimozide (source: Drug Bank)
rifampin Rifampin decreases levels of imatinib (source: Drug Bank)
rifampin Rifampin decreases levels of imatinib (source: Drug Bank)
simvastatin Imatinib increases the effect and toxicity of statin (source: Drug Bank)
simvastatin Imatinib increases the effect and toxicity of statin (source: Drug Bank)
warfarin Imatinib increases the anticoagulant effect (source: Drug Bank)
warfarin Imatinib may increase the anticoagulant effect of warfarin. Imatinib may increase the serum concentration of warfarin by decreasing its metabolism. (source: Drug Bank)
imatinib The imidazole increases the levels of imatinib (source: Drug Bank)
imatinib The imidazole increases the levels of imatinib (source: Drug Bank)
imatinib The imidazole increases the levels of imatinib (source: Drug Bank)
imatinib The imidazole increases the levels of imatinib (source: Drug Bank)
imatinib Imatinib increases the effect and toxicity of statin (source: Drug Bank)
imatinib Imatinib increases the effect and toxicity of statin (source: Drug Bank)
imatinib Imatinib increases the effect and toxicity of nifedipine (source: Drug Bank)
imatinib Imatinib increases the effect and toxicity of nifedipine (source: Drug Bank)
imatinib Phenobarbital decreases levels of imatinib (source: Drug Bank)
imatinib Phenobarbital decreases levels of imatinib (source: Drug Bank)
imatinib The hydantoin decreases the levels of imatinib (source: Drug Bank)
imatinib The hydantoin decreases the levels of imatinib (source: Drug Bank)
imatinib Imatinib increases the effect and toxicity of pimozide (source: Drug Bank)
imatinib Imatinib increases the effect and toxicity of pimozide (source: Drug Bank)
imatinib Rifampin decreases levels of imatinib (source: Drug Bank)
imatinib Rifampin decreases levels of imatinib (source: Drug Bank)
imatinib The strong CYP3A4 inhibitor, Imatinib, may decrease the metabolism and clearance of Tacrolimus, a CYP3A4 substrate. Consider alternate therapy or monitor for changes in therapeutic and adverse effects of Tacrolimus if Imatinib is initiated, discontinued or dose changed. (source: Drug Bank)
imatinib Imatinib may reduce the metabolism of Tadalafil. Concomitant therapy should be avoided if possible due to high risk of Tadalafil toxicity. (source: Drug Bank)
imatinib Imatinib may increase the serum concentration of Tamoxifen by decreasing its metabolism and clearance. Imatinib may also decrease the therapeutic effect of Tamoxifen by decreasing active metabolite production. Monitor for changes in the therapeutic/adverse effects of Tamoxifen if Imatinib is initiated, discontinued or dose changed. (source: Drug Bank)
imatinib Imatinib may increase the serum concentration of Tamoxifen by decreasing its metabolism and clearance. Imatinib may also decrease the therapeutic effect of Tamoxifen by decreasing active metabolite production. Monitor for changes in the therapeutic/adverse effects of Tamoxifen if Imatinib is initiated, discontinued or dose changed. (source: Drug Bank)
imatinib Imatinib, a CYP3A4/2D6 inhibitor, may decrease the metabolism and clearance of Tamsulosin, a CYP3A4/2D6 substrate. Monitor for changes in therapeutic/adverse effects of Tamsulosin if Imatinib is initiated, discontinued, or dose changed. (source: Drug Bank)
imatinib Imatinib, a CYP3A4/2D6 inhibitor, may decrease the metabolism and clearance of Tamsulosin, a CYP3A4/2D6 substrate. Monitor for changes in therapeutic/adverse effects of Tamsulosin if Imatinib is initiated, discontinued, or dose changed. (source: Drug Bank)
imatinib Co-administration may result in altered plasma concentrations of Imatinib and/or Telithromycin. Consider alternate therapy or monitor the therapeutic/adverse effects of both agents. (source: Drug Bank)
imatinib Imatinib may inhibit the metabolism and clearance of Temsirolimus. Concomitant therapy should be avoided. (source: Drug Bank)
imatinib The strong CYP3A4 inhibitor, Imatinib, may decrease the metabolism and clearance of Teniposide, a CYP3A4 substrate. Consider alternate therapy or monitor for changes in the therapeutic/adverse effects of Teniposide if Imatinib is initiated, discontinued or dose changed. (source: Drug Bank)
imatinib The strong CYP3A4 inhibitor, Imatinib, may decrease the metabolism and clearance of Tiagabine, a CYP3A4 substrate. Consider alternate therapy or monitor for changes in the therapeutic/adverse effects of Tiagabine if Imatinib is initiated, discontinued or dose changed. (source: Drug Bank)
imatinib Imatinib may decrease the metabolism and clearance of Tolterodine. Adjust Tolterodine dose and monitor for efficacy and toxicity. (source: Drug Bank)
imatinib Imatinib may decrease the metabolism and clearance of Tolterodine. Adjust Tolterodine dose and monitor for efficacy and toxicity. (source: Drug Bank)
imatinib The BCRP/ABCG2 inhibitor, Imatinib, may increase the bioavailability and serum concentration of oral Topotecan. Monitor for change in the therapeutic and adverse effects of Topotecan if Imatinib is initiated, discontinued or dose changed. (source: Drug Bank)
imatinib Imatinib may increase Tramadol toxicity by decreasing Tramadol metabolism and clearance. Imatinib may decrease the effect of Tramadol by decreasing active metabolite production. (source: Drug Bank)
imatinib Trastuzumab may increase the risk of neutropenia and anemia. Monitor closely for signs and symptoms of adverse events. (source: Drug Bank)
imatinib The CYP3A4 inhibitor, Imatinib, may increase Trazodone efficacy/toxicity by decreasing Trazodone metabolism and clearance. Consider alternate therapy or monitor for changes in Trazodone efficacy/toxicity if Imatinib is initiated, discontinued or dose changed. (source: Drug Bank)
imatinib The CYP3A4 inhibitor, Imatinib, may increase Trazodone efficacy/toxicity by decreasing Trazodone metabolism and clearance. Consider alternate therapy or monitor for changes in Trazodone efficacy/toxicity if Imatinib is initiated, discontinued or dose changed. (source: Drug Bank)
imatinib The strong CYP3A4 inhibitor, Imatinib, may decrease the metabolism and clearance of Trimipramine, a CYP3A4 substrate. Consider alternate therapy or monitor for changes in therapeutic and adverse effects of Trimipramine if Imatinib is initiated, discontinued or dose changed. (source: Drug Bank)
imatinib Imatinib, a strong CYP3A4 inhibitor, may reduce the metabolism and clearance of Vardenafil. Consider alternate therapy or monitor for changes in the therapeutic and adverse effects of Vardenafil. (source: Drug Bank)
imatinib Imatinib, a CYP3A4 inhibitor, may decrease the metabolism and clearance of Venlafaxine, a CYP3A4 substrate. Monitor for changes in therapeutic/adverse effects of Venlafaxine if Imatinib is initiated, discontinued, or dose changed. (source: Drug Bank)
imatinib Imatinib, a strong CYP3A4 inhibitor, may increase the serum concentration of Veramapil, a CYP3A4 substrate, by decreasing its metabolism and clearance. Consider alternate therapy or monitor for changes in the therapeutic/adverse effects of Verapamil if Imatinib is initiated, discontinued or dose changed. (source: Drug Bank)
imatinib Imatinib, a strong CYP3A4 inhibitor, may decrease the metabolism of Vinblastine. Consider alternate therapy to avoid Vinblastine toxicity. Monitor for changes in the therapeutic/adverse effects of Vinblastine if Imatinib is initiated, discontinued or dose changed. (source: Drug Bank)
imatinib Imatinib, a strong CYP3A4 inhibitor, may increase the serum concentration of Vincristine by decreasing its metabolism. Consider alternate therapy to avoid Vincristine toxicity. Monitor for changes in the therapeutic and adverse effects of Vincristine if Imatinib is initiated, discontinued or dose changed. (source: Drug Bank)
imatinib Imatinib, a strong CYP3A4 inhibitor, may increase the serum concentration of Vinorelbine by decreasing its metabolism. Consider alternate therapy to avoid Vinorelbine toxicity. Monitor for changes in the therapeutic and adverse effects of Vinorelbine if Imatinib is initiated, discontinued or dose changed. (source: Drug Bank)
imatinib Voriconazole, a strong CYP3A4 inhibitor, may increase the serum concentration of imatinib by decreasing its metabolism. Additive QTc prolongation may also occur. Consider alternate therapy or monitor for changes in the therapeutic and adverse effects of imatinib if voriconazole is initiated, discontinued or dose changed. (source: Drug Bank)
imatinib Imatinib may increase the anticoagulant effect of warfarin increasing the risk of bleeding. Monitor for changes in prothrombin time and therapeutic and adverse effects of warfarin if imatinib is initiated, discontinued or dose changed. (source: Drug Bank)
imatinib Imatinib, a strong CYP3A4 inhibitor, may increase the serum concentration of zonisamide by decreasing its metabolism. Consider alternate therapy or monitor for changes in the therapeutic and adverse effects of zonisamide if imatinib is initiated, discontinued or dose changed. (source: Drug Bank)
imatinib Imatinib, a strong CYP3A4 inhibitor, may increase the serum concentration of zopiclone by decreasing its metabolism. Consider alternate therapy or monitor for changes in the therapeutic and adverse effects of zopiclone if imatinib is initiated, discontinued or dose changed. (source: Drug Bank)

Curated Information ?

Publications related to imatinib: 86

No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Interaction of the Efflux Transporters ABCB1 and ABCG2 With Imatinib, Nilotinib, and Dasatinib. Clinical pharmacology and therapeutics. 2014. Eadie L N, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available VA No VIP available No VIP available
Single-nucleotide polymorphisms of ABCG2 increase the efficacy of tyrosine kinase inhibitors in the K562 chronic myeloid leukemia cell line. Pharmacogenetics and genomics. 2014. Skoglund Karin, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Gemfibrozil impairs imatinib absorption and inhibits the CYP2C8-mediated formation of its main metabolite. Clinical pharmacology and therapeutics. 2013. Filppula A M, et al. PubMed
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Triptolide, a Chinese herbal extract, enhances drug sensitivity of resistant myeloid leukemia cell lines through downregulation of HIF-1alpha and Nrf2. Pharmacogenomics. 2013. Chen Feili, et al. PubMed
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ABCB1 single nucleotide polymorphisms (1236C>T, 2677G>T, and 3435C>T) do not affect transport activity of human P-glycoprotein. Pharmacogenetics and genomics. 2013. Dickens David, 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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Polymorphisms in OCTN1 and OCTN2 transporters genes are associated with prolonged time to progression in unresectable gastrointestinal stromal tumours treated with imatinib therapy. Pharmacological research : the official journal of the Italian Pharmacological Society. 2013. Angelini Sabrina, et al. PubMed
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The hOCT1 SNPs M420del and M408V alter imatinib uptake and M420del modifies clinical outcome in imatinib-treated chronic myeloid leukemia. Blood. 2013. Giannoudis Athina, et al. PubMed
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Pharmacogenomics as a risk mitigation strategy for chemotherapeutic cardiotoxicity. Pharmacogenomics. 2013. Jensen Brian C, et al. PubMed
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PharmGKB summary: very important pharmacogene information for CYP3A5. Pharmacogenetics and genomics. 2012. Lamba Jatinder, et al. PubMed
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Pharmacogenetics and pharmacogenomics: role of mutational analysis in anti-cancer targeted therapy. The pharmacogenomics journal. 2012. Savonarola A, et al. PubMed
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SLC22A1-ABCB1 haplotype profiles predict imatinib pharmacokinetics in Asian patients with chronic myeloid leukemia. PloS one. 2012. Singh Onkar, et al. PubMed
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Cancer Pharmacogenomics. Clinical pharmacology and therapeutics. 2011. Paugh S W, et al. PubMed
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Pharmacokinetic Impact of SLCO1A2 Polymorphisms on Imatinib Disposition in Patients With Chronic Myeloid Leukemia. Clinical pharmacology and therapeutics. 2011. Yamakawa Y, et al. PubMed
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Profiling of a prescription drug library for potential renal drug-drug interactions mediated by the organic cation transporter 2. Journal of medicinal chemistry. 2011. Kido Yasuto, et al. PubMed
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Environmental and Genetic Factors Affecting Transport of Imatinib by OATP1A2. Clinical pharmacology and therapeutics. 2011. Eechoute K, et al. PubMed
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Very important pharmacogene summary: ABCB1 (MDR1, P-glycoprotein). Pharmacogenetics and genomics. 2011. Hodges Laura M, et al. PubMed
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OCT-1 as a Determinant of Response to Antileukemic Treatment. Clinical pharmacology and therapeutics. 2011. Engler J R, et al. PubMed
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Correlation between imatinib pharmacokinetics and clinical response in Japanese patients with chronic-phase chronic myeloid leukemia. Clinical pharmacology and therapeutics. 2010. Takahashi N, et al. PubMed
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Systematic review of pharmacoeconomic studies of pharmacogenomic tests. Pharmacogenomics. 2010. Beaulieu Mathieu, et al. PubMed
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Targeted cancer therapies in the twenty-first century: lessons from imatinib. Clinical pharmacology and therapeutics. 2010. Stegmeier F, et al. PubMed
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Integrating pharmacogenetics and therapeutic drug monitoring: optimal dosing of imatinib as a case-example. European journal of clinical pharmacology. 2010. Li-Wan-Po Alain, et al. PubMed
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Pharmacogenomics of membrane transporters: past, present and future. Pharmacogenomics. 2010. Yee Sook Wah, et al. PubMed
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Pharmacogenomics in acute myeloid leukemia. Pharmacogenomics. 2009. Roumier Christophe, et al. PubMed
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Clinical relevance of a pharmacogenetic approach using multiple candidate genes to predict response and resistance to imatinib therapy in chronic myeloid leukemia. Clinical cancer research : an official journal of the American Association for Cancer Research. 2009. Kim Dong Hwan Dennis, et al. PubMed
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Histone deacetylase inhibitors induce a very broad, pleiotropic anticancer drug resistance phenotype in acute myeloid leukemia cells by modulation of multiple ABC transporter genes. Clinical cancer research : an official journal of the American Association for Cancer Research. 2009. Hauswald Stefanie, et al. PubMed
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Genetic determinants of response to clopidogrel and cardiovascular events. The New England journal of medicine. 2009. Simon Tabassome, et al. PubMed
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Pharmacogenetics of the organic anion transporting polypeptide 1A2. Pharmacogenomics. 2009. Franke Ryan M, et al. PubMed
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The effect of P-gp (Mdr1a/1b), BCRP (Bcrp1) and P-gp/BCRP inhibitors on the in vivo absorption, distribution, metabolism and excretion of imatinib. Investigational new drugs. 2009. Oostendorp Roos L, et al. PubMed
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KIT kinase mutants show unique mechanisms of drug resistance to imatinib and sunitinib in gastrointestinal stromal tumor patients. Proceedings of the National Academy of Sciences of the United States of America. 2009. Gajiwala Ketan S, et al. PubMed
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Redox regulation of multidrug resistance in cancer chemotherapy: molecular mechanisms and therapeutic opportunities. Antioxidants & redox signaling. 2009. Kuo Macus Tien. PubMed
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The structure of the leukemia drug imatinib bound to human quinone reductase 2 (NQO2). BMC structural biology. 2009. Winger Jonathan A, et al. PubMed
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Translation of the Philadelphia chromosome into therapy for CML. Blood. 2008. Druker Brian J. PubMed
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Several major antiepileptic drugs are substrates for human P-glycoprotein. Neuropharmacology. 2008. Luna-Tortós Carlos, et al. PubMed
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Population pharmacokinetics and pharmacogenetics of imatinib in children and adults. Clinical cancer research : an official journal of the American Association for Cancer Research. 2008. Petain Aurélie, et al. PubMed
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Primary and secondary kinase genotypes correlate with the biological and clinical activity of sunitinib in imatinib-resistant gastrointestinal stromal tumor. Journal of clinical oncology : official journal of the American Society of Clinical Oncology. 2008. Heinrich Michael C, et al. PubMed
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Multidrug resistance gene (MDR1) polymorphisms are associated with major molecular responses to standard-dose imatinib in chronic myeloid leukemia. Blood. 2008. Dulucq Stéphanie, et al. PubMed
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Platelet-derived growth factor-alpha receptor activation is required for human cytomegalovirus infection. Nature. 2008. Soroceanu Liliana, et al. PubMed
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Structure, function and regulation of P-glycoprotein and its clinical relevance in drug disposition. Xenobiotica; the fate of foreign compounds in biological systems. 2008. Zhou S-F. PubMed
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CYP450 pharmacogenetics for personalizing cancer therapy. Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy. 2008. van Schaik Ron H N. PubMed
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Pharmacologic markers and predictors of responses to imatinib therapy in patients with chronic myeloid leukemia. Leukemia & lymphoma. 2008. Clark Richard E, et al. PubMed
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Expression of the uptake drug transporter hOCT1 is an important clinical determinant of the response to imatinib in chronic myeloid leukemia. Clinical pharmacology and therapeutics. 2008. Wang L, et al. PubMed
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A quantitative analysis of kinase inhibitor selectivity. Nature biotechnology. 2008. Karaman Mazen W, et al. PubMed
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Polymorphisms in the drug transporter gene ABCB1 predict antidepressant treatment response in depression. Neuron. 2008. Uhr Manfred, et al. PubMed
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Citalopram enantiomers in plasma and cerebrospinal fluid of ABCB1 genotyped depressive patients and clinical response: a pilot study. Pharmacological research : the official journal of the Italian Pharmacological Society. 2008. Nikisch Georg, et al. PubMed
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Imatinib disposition and ABCB1 (MDR1, P-glycoprotein) genotype. Clinical pharmacology and therapeutics. 2007. Gurney H, et al. PubMed
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Structural biology contributions to the discovery of drugs to treat chronic myelogenous leukaemia. Acta crystallographica. Section D, Biological crystallography. 2007. Cowan-Jacob Sandra W, et al. PubMed
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Cobalamin potentiates vinblastine cytotoxicity through downregulation of mdr-1 gene expression in HepG2 cells. Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology. 2007. Marguerite Véronique, et al. PubMed
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Imatinib: a review of its use in the management of gastrointestinal stromal tumours. Drugs. 2007. Siddiqui M Asif A, et al. PubMed
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Mechanism of inhibition of P-glycoprotein mediated efflux by vitamin E TPGS: influence on ATPase activity and membrane fluidity. Molecular pharmaceutics. 2007. Collnot Eva-Maria, et al. PubMed
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Cardiotoxicity of the cancer therapeutic agent imatinib mesylate. Nature medicine. 2006. Kerkelä Risto, et al. PubMed
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Cancer and leukemia group B gastrointestinal cancer committee. Clinical cancer research : an official journal of the American Association for Cancer Research. 2006. Goldberg Richard M, et al. PubMed
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Gefitinib modulates the function of multiple ATP-binding cassette transporters in vivo. Cancer research. 2006. Leggas Markos, et al. PubMed
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Impact of P-glycoprotein on clopidogrel absorption. Clinical pharmacology and therapeutics. 2006. Taubert Dirk, et al. PubMed
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Single nucleotide polymorphisms in human P-glycoprotein: its impact on drug delivery and disposition. Expert opinion on drug delivery. 2006. Dey Surajit. PubMed
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Metabolism and disposition of imatinib mesylate in healthy volunteers. Drug metabolism and disposition: the biological fate of chemicals. 2005. Gschwind Hans-Peter, et al. PubMed
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Imatinib and regression of type 2 diabetes. The New England journal of medicine. 2005. Veneri Dino, et al. PubMed
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Clinical pharmacokinetics of imatinib. Clinical pharmacokinetics. 2005. Peng Bin, et al. PubMed
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Role of cytochrome P450 activity in the fate of anticancer agents and in drug resistance: focus on tamoxifen, paclitaxel and imatinib metabolism. Clinical pharmacokinetics. 2005. Rochat Bertrand. PubMed
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A novel mode of Gleevec binding is revealed by the structure of spleen tyrosine kinase. The Journal of biological chemistry. 2004. Atwell Shane, et al. PubMed
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Structural basis for the autoinhibition and STI-571 inhibition of c-Kit tyrosine kinase. The Journal of biological chemistry. 2004. Mol Clifford D, et al. PubMed
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Influence of lipid lowering fibrates on P-glycoprotein activity in vitro. Biochemical pharmacology. 2004. Ehrhardt Manuela, et al. PubMed
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Interactions of human P-glycoprotein with simvastatin, simvastatin acid, and atorvastatin. Pharmaceutical research. 2004. Hochman Jerome H, et al. PubMed
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Correlation of major cytogenetic response with a pharmacogenetic marker in chronic myeloid leukemia patients treated with imatinib (STI571). Clinical cancer research : an official journal of the American Association for Cancer Research. 2004. Dressman Marlene A, et al. PubMed
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P-glycoprotein-mediated drug efflux is a resistance mechanism of chronic myelogenous leukemia cells to treatment with imatinib mesylate. Leukemia : official journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 2004. Illmer T, et al. PubMed
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Polymorphisms in human MDR1 (P-glycoprotein): recent advances and clinical relevance. Clinical pharmacology and therapeutics. 2004. Marzolini Catia, et al. PubMed
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Two different point mutations in ABL gene ATP-binding domain conferring Primary Imatinib resistance in a Chronic Myeloid Leukemia (CML) patient: A case report. Biological procedures online. 2004. Iqbal Zafar, et al. PubMed
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STI-571: an anticancer protein-tyrosine kinase inhibitor. Biochemical and biophysical research communications. 2003. Roskoski Robert. PubMed
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Several Bcr-Abl kinase domain mutants associated with imatinib mesylate resistance remain sensitive to imatinib. Blood. 2003. Corbin Amie S, et al. PubMed
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Philadelphia chromosome-positive leukemias: from basic mechanisms to molecular therapeutics. Annals of internal medicine. 2003. Kurzrock Razelle, et al. PubMed
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Genetic polymorphisms of the human MDR1 drug transporter. Annual review of pharmacology and toxicology. 2003. Schwab Matthias, et al. PubMed
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Imatinib mesylate--a new oral targeted therapy. The New England journal of medicine. 2002. Savage David G, et al. PubMed
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Roots of clinical resistance to STI-571 cancer therapy. Science (New York, N.Y.). 2001. Barthe C, et al. PubMed
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Clinical resistance to STI-571 cancer therapy caused by BCR-ABL gene mutation or amplification. Science (New York, N.Y.). 2001. Gorre M E, et al. PubMed
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Interaction of omeprazole, lansoprazole and pantoprazole with P-glycoprotein. Naunyn-Schmiedeberg's archives of pharmacology. 2001. Pauli-Magnus C, et al. PubMed
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Efficacy and safety of a specific inhibitor of the BCR-ABL tyrosine kinase in chronic myeloid leukemia. The New England journal of medicine. 2001. Druker B J, et al. PubMed
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The molecular biology of chronic myeloid leukemia. Blood. 2000. Deininger M W, et al. PubMed
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Selection and characterization of BCR-ABL positive cell lines with differential sensitivity to the tyrosine kinase inhibitor STI571: diverse mechanisms of resistance. Blood. 2000. Mahon F X, et al. PubMed
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Induction of resistance to the Abelson inhibitor STI571 in human leukemic cells through gene amplification. Blood. 2000. le Coutre P, et al. PubMed
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The role of intestinal P-glycoprotein in the interaction of digoxin and rifampin. The Journal of clinical investigation. 1999. Greiner B, et al. PubMed
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Biochemical, cellular, and pharmacological aspects of the multidrug transporter. Annual review of pharmacology and toxicology. 1999. Ambudkar S V, et al. PubMed
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Gain-of-function mutations of c-kit in human gastrointestinal stromal tumors. Science (New York, N.Y.). 1998. Hirota S, et al. PubMed
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Competitive, non-competitive and cooperative interactions between substrates of P-glycoprotein as measured by its ATPase activity. Biochimica et biophysica acta. 1997. Litman T, et al. PubMed
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P-glycoprotein structure and evolutionary homologies. Cytotechnology. 1993. Croop J M. PubMed
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Kinetics and mechanisms of reduction of Cu(II) and Fe(III) complexes by soybean leghemoglobin alpha. Biochimica et biophysica acta. 1991. Bakan D A, et al. PubMed
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http://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?id=9107. [URL:http://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?id=9107]

LinkOuts

Web Resource:
Wikipedia
National Drug Code Directory:
0078-0401-34
DrugBank:
DB00619
PDB:
STI
ChEBI:
45783
KEGG Drug:
D01441
PubChem Compound:
5291
PubChem Substance:
46505055
841977
Drugs Product Database (DPD):
2253283
BindingDB:
13530
ChemSpider:
5101
HET:
STI
Therapeutic Targets Database:
DNC001383
FDA Drug Label at DailyMed:
211ef2da-2868-4a77-8055-1cb2cd78e24b

Clinical Trials

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

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