Crizotinib 200mg capsules
Requires a prescription from a doctor or prescriber
Cytotoxic drugs
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Official medicine documents
Safety monitoring data
Yellow Card reports
The MHRA Yellow Card scheme collects reports of suspected side effects from healthcare professionals and patients. View the Drug Analysis Profile (iDAP) for real-world adverse reaction data.
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Suspected adverse reactions reported for Crizotinib
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Data from the MHRA Yellow Card scheme. A reported reaction does not necessarily mean the medicine caused it. Contains public sector information licensed under the Open Government Licence v3.0.
EudraVigilance
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Suspected adverse reactions reported for Crizotinib
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EudraVigilance data is published by the European Medicines Agency (EMA). A suspected adverse reaction is not necessarily caused by the medicine.
2 branded products available
MHRA licensed products
View all licensed products for Crizotinib on the MHRA register
Xalkori 200mg capsules
Therapeutically similar medicines
Similarity based on WHO Anatomical Therapeutic Chemical (ATC) classification and NHS BNF section grouping. Source data: NHS dm+d via TRUD (OGL v3.0), WHO ATC/DDD Index.
NHS prescribing volume and spending trends
Clinical guidelines and formulary information
British National Formulary
Crizotinib
Source: British National Formulary, NICE. Joint Formulary Committee. Contains public sector information licensed under the Open Government Licence v3.0.
NICE clinical guidance(13)
Crizotinib for treating ROS1-positive advanced non-small-cell lung cancer (TA1021)
Crizotinib for untreated anaplastic lymphoma kinase-positive advanced non-small-cell lung cancer (TA406)
Crizotinib for previously treated anaplastic lymphoma kinase-positive advanced non-small-cell lung cancer (TA422)
Brigatinib for treating ALK-positive advanced non-small-cell lung cancer after crizotinib (TA571)
Ceritinib for untreated ALK-positive non-small-cell lung cancer (TA500)
Alectinib for untreated ALK-positive advanced non-small-cell lung cancer (TA536)
Brigatinib for ALK-positive advanced non-small-cell lung cancer that has not been previously treated with an ALK inhibitor (TA670)
Entrectinib for treating ROS1-positive advanced non-small-cell lung cancer (TA643)
Lorlatinib for ALK-positive advanced non-small-cell lung cancer that has not been treated with an ALK inhibitor (TA1103)
Ceritinib for previously treated anaplastic lymphoma kinase positive non-small-cell lung cancer (TA395)
Lorlatinib for previously treated ALK-positive advanced non-small-cell lung cancer (TA628)
Alectinib for previously treated anaplastic lymphoma kinase-positive advanced non-small-cell lung cancer (terminated appraisal) (TA438)
Ramucirumab for previously treated locally advanced or metastatic non-small-cell lung cancer (TA403)
Source: National Institute for Health and Care Excellence (NICE). Contains public sector information licensed under the Open Government Licence v3.0.
Check stock at pharmacies and supply information
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Supply & product information
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Codes for healthcare professionals and prescribing systems
These codes are used by healthcare IT systems and prescribers to identify this medicine.
NHS UK identifiers
Browse tools
SNOMED CT and dm+d codes from NHS TRUD (Technology Reference data Update Distribution), licensed under the Open Government Licence v3.0. BNF codes from NHS Business Services Authority (NHSBSA). ATC codes from the WHO Collaborating Centre for Drug Statistics Methodology (whocc.no).
Active and completed clinical studies from ClinicalTrials.gov
Source: ClinicalTrials.gov, a database of the U.S. National Library of Medicine (NLM), National Institutes of Health (NIH). Data accessed via ClinicalTrials.gov API v2. Trial information is provided for research purposes and does not constitute medical advice.
Pharmacology and chemical data from DrugBank
Key facts
Drug status
Approved
Major interactions
None known
Half-life
42 hours
Mechanism
Crizotinib is a tyrosine kinase receptor inhibitor that targets anaplastic lymph…
Food interactions
3 warnings
Human targets
4 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
100 mg
Half-life
42 hours
[L42460]
Protein binding
91%
[L42460]
Volume of distribution
1772 L
[L42460]
Metabolism
[A7418]…
Elimination
250 mg
Clearance
250 mg
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
[L42460]
Crizotinib is also indicated for the treatment of relapsed or refractory, systemic anaplastic large cell lymphoma (ALCL) that is ALK-positive in pediatric patients 1 year of age and older and young adults. The safety and efficacy of crizotinib have not been established in older adults with relapsed or refractory, systemic ALK-positive ALCL.
[L42460]
Additionally, crizotinib is indicated for the treatment of adult and pediatric patients 1 year of age and older with unresectable, recurrent, or refractory inflammatory myofibroblastic tumor (IMT) that is ALK-positive.
[L42460]
Known interactions with other medications. Always consult a healthcare professional.
Showing 50 of 1098 interactions
There is no antidote for crizotinib.
[L42485]
In vitro and in vivo studies have shown that crizotinib is genotoxic, and the Ames test showed that crizotinib was not mutagenic. Carcinogenicity studies with crizotinib have not been performed.
[L42460]
In female rats, 500 mg/kg/day (approximately 10 times the recommended human dose based on body surface area) of crizotinib for 3 days induced single-cell necrosis of ovarian follicles. In male rats, 50 mg/kg/day of crizotinib (greater than 1.7 times the recommended human dose) for 28 days induced testicular pachytene spermatocyte degeneration.
[L42460]
In vitro assays on tumor cell lines demonstrated that crizotinib inhibits ALK, ROS1, and c-Met phosphorylation in a concentration-dependent manner. In vivo studies in mice with tumor xenografts that expressed EML4- or nucleophosmin (NPM)-ALK fusion proteins or c-Met showed that crizotinib has antitumor activity.[L42460]
The use of crizotinib may lead to hepatotoxicity, interstitial lung disease (ILD), pneumonitis, QT interval prolongation, bradycardia, severe visual loss, embryo-fetal toxicity and gastrointestinal toxicity in pediatric and young adult patients with anaplastic large cell lymphoma (ALCL) or pediatric patients with inflammatory myofibroblastic tumor (IMT).[L42460]
How the body processes this drug — absorption, distribution, metabolism, and elimination
[A7419]
A single crizotinib dose of crizotinib is absorbed with a median tmax 4 to 6 hours.
[L42460]
In patients receiving multiple doses of crizotinib 250 mg twice daily (n=167), the mean AUC was is 2321.00 ng⋅hr/mL, the mean Cmax was 99.60 ng/mL, and the median tmax was 5.0 hours.
[A7418]
The mean absolute bioavailability of crizotinib is 43%, ranging from 32% to 66%. High-fat meals reduce the AUC0-INF and Cmax of crizotinib by approximately 14%.
[L42460]
Age, sex at birth, and ethnicity (Asian vs non-Asian patients) did not have a clinically significant effect on crizotinib pharmacokinetics. In patients less than 18 years old, higher body weight was associated with a lower crizotinib exposure.
[L42460]
[L42460]
[L42460]
[L42460]
[A7418]
Non-metabolic elimination, such as biliary excretion, can not be excluded.
[L42465]
PF-06260182 (with two constituent diastereomers, PF-06270079 and PF-06270080) is the only active metabolite of crizotinib that has been identified. In vitro studies suggest that, compared to crizotinib, PF-06270079 and PF-06270080 are approximately 3- to 8-fold less potent against anaplastic lymphoma kinase (ALK) and 2.5- to 4-fold less potent against Hepatocyte Growth Factor Receptor (HGFR, c-Met).
[L42465]
[L42460]
[L42465]
Proteins and enzymes this drug interacts with in the body
PMID:11121404 PMID:11387242 PMID:16317043 PMID:17274988 PMID:30061385 PMID:34646012 PMID:34819673
Also acts as a key thinness protein involved in the resistance to weight gain: in hypothalamic neurons, controls energy expenditure acting as a negative regulator of white adipose tissue lipolysis and sympathetic tone to fine-tune energy homeostasis (By similarity). Following activation by ALKAL2 ligand at the cell surface, transduces an extracellular signal into an intracellular response .
PMID:30061385 PMID:33411331 PMID:34646012 PMID:34819673
In contrast, ALKAL1 is not a potent physiological ligand for ALK .
PMID:34646012
Ligand-binding to the extracellular domain induces tyrosine kinase activation, leading to activation of the mitogen-activated protein kinase (MAPK) pathway .
PMID:34819673
Phosphorylates almost exclusively at the first tyrosine of the Y-x-x-x-Y-Y motif .
PMID:15226403 PMID:16878150
Induces tyrosine phosphorylation of CBL, FRS2, IRS1 and SHC1, as well as of the MAP kinases MAPK1/ERK2 and MAPK3/ERK1 .
PMID:15226403 PMID:16878150
ALK activation may also be regulated by pleiotrophin (PTN) and midkine (MDK) .
PMID:11278720 PMID:11809760 PMID:12107166 PMID:12122009
PTN-binding induces MAPK pathway activation, which is important for the anti-apoptotic signaling of PTN and regulation of cell proliferation .
PMID:11278720 PMID:11809760 PMID:12107166
MDK-binding induces phosphorylation of the ALK target insulin receptor substrate (IRS1), activates mitogen-activated protein kinases (MAPKs) and PI3-kinase, resulting also in cell proliferation induction .
PMID:12122009
Drives NF-kappa-B activation, probably through IRS1 and the activation of the AKT serine/threonine kinase .
PMID:15226403 PMID:16878150
Recruitment of IRS1 to activated ALK and the activation of NF-kappa-B are essential for the autocrine growth and survival signaling of MDK PMID:15226403 PMID:16878150
Following activation by ligand, interacts with the PI3-kinase subunit PIK3R1, PLCG1, SRC, GRB2, STAT3 or the adapter GAB1. Recruitment of these downstream effectors by MET leads to the activation of several signaling cascades including the RAS-ERK, PI3 kinase-AKT, or PLCgamma-PKC. The RAS-ERK activation is associated with the morphogenetic effects while PI3K/AKT coordinates prosurvival effects.
During embryonic development, MET signaling plays a role in gastrulation, development and migration of neuronal precursors, angiogenesis and kidney formation. During skeletal muscle development, it is crucial for the migration of muscle progenitor cells and for the proliferation of secondary myoblasts (By similarity). In adults, participates in wound healing as well as organ regeneration and tissue remodeling.
Also promotes differentiation and proliferation of hematopoietic cells. May regulate cortical bone osteogenesis (By similarity)
May activate several downstream signaling pathways related to cell differentiation, proliferation, growth and survival including the PI3 kinase-mTOR signaling pathway. Mediates the phosphorylation of PTPN11, an activator of this pathway. May also phosphorylate and activate the transcription factor STAT3 to control anchorage-independent cell growth.
Mediates the phosphorylation and the activation of VAV3, a guanine nucleotide exchange factor regulating cell morphology. May activate other downstream signaling proteins including AKT1, MAPK1, MAPK3, IRS1 and PLCG2
Following activation by ligand, interacts with the PI3-kinase subunit PIK3R1, PLCG1 or the adapter GAB1. Recruitment of these downstream effectors by RON leads to the activation of several signaling cascades including the RAS-ERK, PI3 kinase-AKT, or PLCgamma-PKC. RON signaling activates the wound healing response by promoting epithelial cell migration, proliferation as well as survival at the wound site.
Also plays a role in the innate immune response by regulating the migration and phagocytic activity of macrophages. Alternatively, RON can also promote signals such as cell migration and proliferation in response to growth factors other than MST1 ligand
Enzymes involved in drug metabolism — important for understanding drug interactions
Proteins that transport this drug across cell membranes
PMID:2897240 PMID:35970996 PMID:8898203 PMID:9038218 PMID:35507548
Catalyzes the flop of phospholipids from the cytoplasmic to the exoplasmic leaflet of the apical membrane. Participates mainly to the flop of phosphatidylcholine, phosphatidylethanolamine, beta-D-glucosylceramides and sphingomyelins .
PMID:8898203
Energy-dependent efflux pump responsible for decreased drug accumulation in multidrug-resistant cells PMID:2897240 PMID:35970996 PMID:9038218
Proteins that carry this drug through the body
PMID:19021548
Major calcium and magnesium transporter in plasma, binds approximately 45% of circulating calcium and magnesium in plasma (By similarity).
Potentially has more than two calcium-binding sites and might additionally bind calcium in a non-specific manner (By similarity). The shared binding site between zinc and calcium at residue Asp-273 suggests a crosstalk between zinc and calcium transport in the blood (By similarity). The rank order of affinity is zinc > calcium > magnesium (By similarity).
Binds to the bacterial siderophore enterobactin and inhibits enterobactin-mediated iron uptake of E.coli from ferric transferrin, and may thereby limit the utilization of iron and growth of enteric bacteria such as E.coli .
PMID:6234017
Does not prevent iron uptake by the bacterial siderophore aerobactin PMID:6234017
Appears to function in modulating the activity of the immune system during the acute-phase reaction
ATC L01ED01
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
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Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Crizotinib
Additional database identifiers
Drugs Product Database (DPD)
21291
ChemSpider
9801307
BindingDB
50306682
PDB
VGH
ZINC
ZINC000035902489
HUGO Gene Nomenclature Committee (HGNC)
HGNC:427
GenAtlas
ALK
GeneCards
ALK
GenBank Gene Database
U62540
GenBank Protein Database
2454168
Guide to Pharmacology
1839
UniProt Accession
ALK_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:7029
GenAtlas
MET
GeneCards
MET
GenBank Gene Database
J02958
GenBank Protein Database
307196
Guide to Pharmacology
1815
UniProt Accession
MET_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10261
GeneCards
ROS1
Guide to Pharmacology
1840
UniProt Accession
ROS1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:7381
GeneCards
MST1R
Guide to Pharmacology
1816
UniProt Accession
RON_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2637
GenAtlas
CYP3A4
GeneCards
CYP3A4
GenBank Gene Database
M18907
Guide to Pharmacology
1337
UniProt Accession
CP3A4_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2638
GenAtlas
CYP3A5
GeneCards
CYP3A5
GenBank Gene Database
J04813
GenBank Protein Database
181346
Guide to Pharmacology
1338
UniProt Accession
CP3A5_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2615
GeneCards
CYP2B6
GenBank Gene Database
M29874
GenBank Protein Database
181296
Guide to Pharmacology
1324
UniProt Accession
CP2B6_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2637
GenAtlas
CYP3A4
GeneCards
CYP3A4
GenBank Gene Database
M18907
Guide to Pharmacology
1337
UniProt Accession
CP3A4_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:17450
GeneCards
CYP3A43
GenBank Gene Database
AF319634
GenBank Protein Database
12642642
UniProt Accession
CP343_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2638
GenAtlas
CYP3A5
GeneCards
CYP3A5
GenBank Gene Database
J04813
GenBank Protein Database
181346
Guide to Pharmacology
1338
UniProt Accession
CP3A5_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2640
GeneCards
CYP3A7
GenBank Gene Database
D00408
GenBank Protein Database
220149
UniProt Accession
CP3A7_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:399
GenAtlas
ALB
GeneCards
ALB
GenBank Gene Database
V00494
GenBank Protein Database
28590
UniProt Accession
ALBU_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8498
GenAtlas
ORM1
GeneCards
ORM1
GenBank Gene Database
X02544
GenBank Protein Database
757907
UniProt Accession
A1AG1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:8499
GeneCards
ORM2
GenBank Gene Database
BC015964
GenBank Protein Database
16359000
UniProt Accession
A1AG2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:40
GenAtlas
ABCB1
GeneCards
ABCB1
GenBank Gene Database
M14758
GenBank Protein Database
307180
Guide to Pharmacology
768
UniProt Accession
MDR1_HUMAN
Patent information
4 active patents, 5 expired
Source: DrugBank · CC BY-NC 4.0. Patent data sourced from national patent offices. Expiry dates may not reflect extensions, regulatory exclusivity periods, or legal challenges.
DrugBank citations
If you use DrugBank data in your research, please cite the following publications: