Dacomitinib 45mg tablets
Prescription only
Requires a prescription from a doctor or prescriber
Tablet
45mg
Oral
Cytotoxic drugs
Active ingredients:
Dacomitinib
1 safety notice
Safety information for pregnancy and breastfeeding
Pregnancy
In animal studies, dacomitinib was shown to induce embryo-fetal toxicity, as demonstrated by an increased incidence of a post-implantation loss and reduced fetal body weight at doses resulting in exposures near the exposure at the 45mg human dose following administration in rats during the period of organogenesis.
Always consult your doctor or midwife before taking any medicine during pregnancy or while breastfeeding. Source: DrugBank (CC BY-NC 4.0).
Official documents, adverse reaction reporting, and safety monitoring
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Official medicine documents
Source: MHRA Products DatabaseOGL 3.0
Updated 3 months ago(16 Jan 2026)Safety monitoring data
Yellow Card reports
MHRA
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 Dacomitinib
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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
EMA
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Suspected adverse reactions reported for Dacomitinib
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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.
1 branded products available
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Vizimpro 45mg tablets
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WHO defined daily dose (DDD)
45 mg
Not a recommended dose. The DDD is the assumed average maintenance dose per day for a drug used for its main indication in adults. It is a statistical measure used for research and comparison purposes only.
Source: WHO Collaborating Centre for Drug Statistics Methodology, distributed via NHS dm+d BNF mapping files. Contains public sector information licensed under the Open Government Licence v3.0.
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Dacomitinib 15mg tablets
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Dacomitinib 30mg tablets
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Same therapeutic group
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
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Clinical guidelines and formulary information
British National Formulary
Dacomitinib
BNF
Drug monograph — bnf.nice.org.ukSource: British National Formulary, NICE. Joint Formulary Committee. Contains public sector information licensed under the Open Government Licence v3.0.
NICE clinical guidance(2)
Dacomitinib for untreated EGFR mutation-positive non-small-cell lung cancer (TA595)
TA595
Technology appraisal
Updated Aug 2019Atezolizumab for treating locally advanced or metastatic non-small-cell lung cancer after chemotherapy (TA520)
TA520
Technology appraisal
Updated May 2018Source: National Institute for Health and Care Excellence (NICE). Contains public sector information licensed under the Open Government Licence v3.0.
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Supply & product information
Official product databases and supply status monitoring
Pharmacy links redirect to the retailer's own search and do not represent real-time stock levels. emc (electronic medicines compendium) is operated by Datapharm Ltd. Shortage information sourced from NHS Specialist Pharmacy Service (SPS), sps.nhs.uk.
Codes for healthcare professionals and prescribing systems
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These codes are used by healthcare IT systems and prescribers to identify this medicine.
NHS UK identifiers
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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
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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
70 hours
Mechanism
Dacomitinib is an irreversible small molecule inhibitor of the activity of the h…
Food interactions
5 warnings
Human targets
3 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
45 mg
Dacomitinib has shown a linear kinetics after single and multiple dose range studies.…
Half-life
70 hours
Dacomitinib is reported to have a very large half-life of 70 hours.T367
Protein binding
98%
Dacomitinib is known to present a protein binding of 98%.T367
Volume of distribution
2415 L
The volume of distribution of dacomitinib was reported to be of 2415 L.
[A40019]
[A40019]
Metabolism
Dacomitinib presents an oxidative and conjugative metabolism marked mainly by the activity of glutathione and cytochrome P450 enzymes.
[A40012]…
[A40012]…
Elimination
79%
From the administered dose, 79% is recovered in feces, from which 20% represents the unmodified form of dacomitinib, and 3% is recovered in urine, from which <1% is represented by the unchanged form.
[A40019]
[A40019]
Clearance
27.06 L/h
The geometric apparent clearance of dacomitinib is 27.06 L/h.
[A40019]
[A40019]
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Status:
Approved
Investigational
Small molecule
About this compound
Dacomitinib, designed as (2E)-N-16-4-(piperidin-1-yl) but-2-enamide, is an oral highly selective quinazalone part of the second-generation tyrosine kinase inhibitors which are characterized by the irreversible binding at the ATP domain of the epidermal growth factor receptor family kinase domains.[A40009]
Dacomitinib was developed by Pfizer Inc and approved by the FDA on September 27, 2018.[L4810] Some evidence in the literature suggests the therapeutic potential of dacomitinib in the epithelial ovarian cancer model[A39624], although further investigations are needed.
Dacomitinib was developed by Pfizer Inc and approved by the FDA on September 27, 2018.[L4810] Some evidence in the literature suggests the therapeutic potential of dacomitinib in the epithelial ovarian cancer model[A39624], although further investigations are needed.
Properties:
View FDA drug labelsolid
Avg. mass: 469.94 Da
DrugBank indication
Dacomitinib is indicated as the first-line treatment of patients with metastatic non-small cell lung cancer (NSCLC) with epidermal growth factor receptor (EGFR) exon 19 deletion or exon 21 L858R substitution mutations as verified by an FDA-approved test.
[L4812]
Lung cancer is the leading cause of cancer death and NSCLC accounts for 85% of lung cancer cases. From the cases of NSCLC, approximately 75% of the patients present a late diagnosis with metastatic and advanced disease which produces a survival rate of 5%. The presence of a mutation in EGFR accounts for more than the 60% of the NSCLC cases and the overexpression of EGFR is associated with frequent lymph node metastasis and poor chemosensitivity.
[A40018][A19201]
[L4812]
Lung cancer is the leading cause of cancer death and NSCLC accounts for 85% of lung cancer cases. From the cases of NSCLC, approximately 75% of the patients present a late diagnosis with metastatic and advanced disease which produces a survival rate of 5%. The presence of a mutation in EGFR accounts for more than the 60% of the NSCLC cases and the overexpression of EGFR is associated with frequent lymph node metastasis and poor chemosensitivity.
[A40018][A19201]
Also known as(90)
Dacomitinib
Dacomitinib anhydrous
Dacomitinibum
2.7.10.1
ERBB
ERBB1
HER1
Proto-oncogene c-ErbB-1
Dosage forms(13)
Tablet, film coated (Oral) — 15.576 MG
Tablet, film coated (Oral) — 31.153 MG
Tablet, film coated (Oral) — 46.729 MG
Tablet (Oral) — 15 mg
Tablet (Oral) — 30 mg
Tablet (Oral) — 45 mg
Tablet, film coated (Oral) — 15 mg/1
Tablet, film coated (Oral) — 30 mg/1
Molecular properties(19)
Drug interactions(1107)
Known interactions with other medications. Always consult a healthcare professional.
The serum concentration of Afatinib can be increased when it is combined with Dacomitinib.
Armodafinil
Moderate
The metabolism of Dacomitinib can be increased when combined with Armodafinil.
The metabolism of Dacomitinib can be increased when combined with Modafinil.
The serum concentration of Bosutinib can be increased when it is combined with Dacomitinib.
Brentuximab vedotin
Unknown severity
The serum concentration of Brentuximab vedotin can be increased when it is combined with Dacomitinib.
Colchicine
Unknown severity
The serum concentration of Colchicine can be increased when it is combined with Dacomitinib.
The serum concentration of Edoxaban can be increased when it is combined with Dacomitinib.
Ledipasvir
Unknown severity
The serum concentration of Ledipasvir can be increased when it is combined with Dacomitinib.
The serum concentration of Naloxegol can be increased when it is combined with Dacomitinib.
The serum concentration of Pazopanib can be increased when it is combined with Dacomitinib.
Prucalopride
Unknown severity
The serum concentration of Prucalopride can be increased when it is combined with Dacomitinib.
Ranolazine
Unknown severity
The serum concentration of Ranolazine can be increased when it is combined with Dacomitinib.
The excretion of Silodosin can be decreased when combined with Dacomitinib.
The serum concentration of Topotecan can be increased when it is combined with Dacomitinib.
The metabolism of Dacomitinib can be increased when combined with Phenytoin.
Fosphenytoin
Moderate
The metabolism of Dacomitinib can be increased when combined with Fosphenytoin.
Everolimus
Unknown severity
The serum concentration of Everolimus can be increased when it is combined with Dacomitinib.
The serum concentration of Rifaximin can be increased when it is combined with Dacomitinib.
Irinotecan
Unknown severity
The risk or severity of neutropenia can be increased when Dacomitinib is combined with Irinotecan.
Metreleptin
Moderate
The metabolism of Dacomitinib can be increased when combined with Metreleptin.
Atomoxetine
Moderate
The metabolism of Atomoxetine can be decreased when combined with Dacomitinib.
Brexpiprazole
Moderate
The metabolism of Brexpiprazole can be decreased when combined with Dacomitinib.
Vortioxetine
Moderate
The metabolism of Vortioxetine can be decreased when combined with Dacomitinib.
Eliglustat
Moderate
The metabolism of Dacomitinib can be decreased when combined with Eliglustat.
Iloperidone
Moderate
The metabolism of Iloperidone can be decreased when combined with Dacomitinib.
Tetrabenazine
Moderate
The metabolism of Tetrabenazine can be decreased when combined with Dacomitinib.
Crizotinib
Moderate
The metabolism of Dacomitinib can be decreased when combined with Crizotinib.
Mirabegron
Unknown severity
The serum concentration of Dacomitinib can be increased when it is combined with Mirabegron.
Vincristine
Unknown severity
The excretion of Vincristine can be decreased when combined with Dacomitinib.
Doxorubicin
Unknown severity
The serum concentration of Doxorubicin can be increased when it is combined with Dacomitinib.
Lumacaftor
Unknown severity
The serum concentration of Dacomitinib can be decreased when it is combined with Lumacaftor.
Cyclosporine
Moderate
The metabolism of Dacomitinib can be decreased when combined with Cyclosporine.
Rolapitant
Moderate
The metabolism of Dacomitinib can be decreased when combined with Rolapitant.
Primaquine
Moderate
The metabolism of Dacomitinib can be decreased when combined with Primaquine.
The serum concentration of Dacomitinib can be increased when it is combined with Clobazam.
Cimetidine
Moderate
The metabolism of Dacomitinib can be decreased when combined with Cimetidine.
Panobinostat
Moderate
The metabolism of Dacomitinib can be decreased when combined with Panobinostat.
Abiraterone
Moderate
The metabolism of Dacomitinib can be decreased when combined with Abiraterone.
Nicardipine
Moderate
The metabolism of Dacomitinib can be decreased when combined with Nicardipine.
Sulfaphenazole
Moderate
The metabolism of Dacomitinib can be decreased when combined with Sulfaphenazole.
Tranylcypromine
Moderate
The metabolism of Dacomitinib can be decreased when combined with Tranylcypromine.
Manidipine
Moderate
The metabolism of Dacomitinib can be decreased when combined with Manidipine.
Cholecalciferol
Moderate
The metabolism of Dacomitinib can be decreased when combined with Cholecalciferol.
Phenylbutyric acid
Moderate
The metabolism of Dacomitinib can be decreased when combined with Phenylbutyric acid.
Ritanserin
Moderate
The metabolism of Dacomitinib can be decreased when combined with Ritanserin.
The metabolism of Dacomitinib can be decreased when combined with Rhein.
Fluvoxamine
Moderate
The metabolism of Dacomitinib can be decreased when combined with Fluvoxamine.
Metoprolol
Moderate
The metabolism of Dacomitinib can be decreased when combined with Metoprolol.
Venlafaxine
Moderate
The metabolism of Dacomitinib can be decreased when combined with Venlafaxine.
The serum concentration of Clozapine can be increased when it is combined with Dacomitinib.
Showing 50 of 1107 interactions
Food & lifestyle interactions
Avoid Grapefruit
Avoid grapefruit products. Grapefruit inhibits CYP3A4 metabolism, which may increase the serum concentration of dacomitinib.
Advice
Exercise caution with St. John's Wort. This herb induces CYP3A4 metabolism, which may reduce serum levels of dacomitinib.
Advice
Take at the same time every day.
Advice
Take separate from antacids. Take dacomitinib at least 6 hours before or 10 hours after administering antacids.
Advice
Take with or without food.
Toxicity & overdose
The maximum asymptomatic dose in rats was 50 mg/kg MSDS. In animal studies, dacomitinib was shown to induce embryo-fetal toxicity, as demonstrated by an increased incidence of a post-implantation loss and reduced fetal body weight at doses resulting in exposures near the exposure at the 45mg human dose following administration in rats during the period of organogenesis. On the other hand, dacomitinib was showed to lack a mutagenic potential in a bacterial reverse mutation assay, in human lymphocyte chromosome aberration assay and in clastogenic or aneugenic in vivo rat bone marrow micronucleus assay.[FDA Label]
The dose-limiting and overdose toxicities include stomatitis, rash, palmar-plantar erythrodysesthesia syndrome, dehydration, paronychia, and diarrhea.
From these findings, the maximum tolerated dose (defined by the dose in which the dose-limiting toxicities did not exceed 33%) is 45 mg.
[A40012]
The dose-limiting and overdose toxicities include stomatitis, rash, palmar-plantar erythrodysesthesia syndrome, dehydration, paronychia, and diarrhea.
From these findings, the maximum tolerated dose (defined by the dose in which the dose-limiting toxicities did not exceed 33%) is 45 mg.
[A40012]
How it works
Mechanism of action
Dacomitinib is an irreversible small molecule inhibitor of the activity of the human epidermal growth factor receptor (EGFR) family (EGFR/HER1, HER2, and HER4) tyrosine kinases. It achieves irreversible inhibition via covalent bonding to the cysteine residues in the catalytic domains of the HER receptors.[A40011] The affinity of dacomitinib has been shown to have an IC50 of 6 nmol/L.[A40009]
The ErbB or epidermal growth factor (EGF) family plays a role in tumor growth, metastasis, and treatment resistance by activating downstream signal transduction pathways such as such as Ras-Raf-MAPK, PLCgamma-PKC-NFkB and PI3K/AKT through the tyrosine kinase-driven phosphorylation at the carboxy-terminus.[A39624] Around 40% of cases show amplification of EGFR gene and 50% of the cases present the EGFRvIII mutation which represents a deletion that produces a continuous activation of the tyrosine kinase domain of the receptor.[A40016]
The ErbB or epidermal growth factor (EGF) family plays a role in tumor growth, metastasis, and treatment resistance by activating downstream signal transduction pathways such as such as Ras-Raf-MAPK, PLCgamma-PKC-NFkB and PI3K/AKT through the tyrosine kinase-driven phosphorylation at the carboxy-terminus.[A39624] Around 40% of cases show amplification of EGFR gene and 50% of the cases present the EGFRvIII mutation which represents a deletion that produces a continuous activation of the tyrosine kinase domain of the receptor.[A40016]
Pharmacodynamics
Preclinical data suggested that dacomitinib increases the inhibition of the epidermal growth factor receptor kinase domain as well as the activity in cell lines harboring resistance mutations such as T790M. This activity further produced a significant reduction of EGFR phosphorylation and cell viability. In these studies, non-small cell lymphoma cancer cell lines with L858R/T790M mutations where used and an IC50 of about 280 nmol/L was observed.[A40010]
In clinical trials with patients with advanced non-small cell lung carcinoma who progressed after chemotherapy, there was an objective response rate of 5% with a progression-free survival of 2.8 months and an overall survival of 9.5 months. As well, phase I/II studies showed positive dacomitinib activity despite prior failure with tyrosine kinase inhibitors.[A40009]
Phase III clinical trials (ARCHER 1050), done in patients suffering from advanced or metastatic non-small cell lung carcinoma with EGFR-activating mutations, reported a significant improvement in progression-free survival when compared with gefitinib.[A40015]
In clinical trials with patients with advanced non-small cell lung carcinoma who progressed after chemotherapy, there was an objective response rate of 5% with a progression-free survival of 2.8 months and an overall survival of 9.5 months. As well, phase I/II studies showed positive dacomitinib activity despite prior failure with tyrosine kinase inhibitors.[A40009]
Phase III clinical trials (ARCHER 1050), done in patients suffering from advanced or metastatic non-small cell lung carcinoma with EGFR-activating mutations, reported a significant improvement in progression-free survival when compared with gefitinib.[A40015]
Pharmacokinetics
How the body processes this drug — absorption, distribution, metabolism, and elimination
Absorption
Dacomitinib has shown a linear kinetics after single and multiple dose range studies. The absorption and distribution do not seem to be affected by food or the consumption of antacids. The peak plasma concentration after a dosage of 45 mg for 4 days is of 104 ng/ml.
[A40012]
The reported AUC0-24h and tmax are of 2213 ng.h/mL and 6 hours, respectively.
As well, following oral administration, the absolute oral bioavailability is 80% [FDA Label].
[A40012]
The reported AUC0-24h and tmax are of 2213 ng.h/mL and 6 hours, respectively.
As well, following oral administration, the absolute oral bioavailability is 80% [FDA Label].
Half-life
Dacomitinib is reported to have a very large half-life of 70 hours.T367
Protein binding
Dacomitinib is known to present a protein binding of 98%.T367
Volume of distribution
The volume of distribution of dacomitinib was reported to be of 2415 L.
[A40019]
[A40019]
Metabolism
Dacomitinib presents an oxidative and conjugative metabolism marked mainly by the activity of glutathione and cytochrome P450 enzymes.
[A40012]
After metabolism, its major circulating metabolite is an O-desmethyl dacomitinib form named PF-05199265.
[A40014]
This metabolite has been shown to be formed by an oxidative step by CYP2D6 and to a smaller extent by CYP2C9. The following steps of the metabolism are mainly mediated by CYP3A4 for the formation of smaller metabolites.
[A40019]
From these metabolic studies, it was shown that dacomitinib inhibited strongly the activities of CYP2D6.
[A40013]
[A40012]
After metabolism, its major circulating metabolite is an O-desmethyl dacomitinib form named PF-05199265.
[A40014]
This metabolite has been shown to be formed by an oxidative step by CYP2D6 and to a smaller extent by CYP2C9. The following steps of the metabolism are mainly mediated by CYP3A4 for the formation of smaller metabolites.
[A40019]
From these metabolic studies, it was shown that dacomitinib inhibited strongly the activities of CYP2D6.
[A40013]
Route of elimination
From the administered dose, 79% is recovered in feces, from which 20% represents the unmodified form of dacomitinib, and 3% is recovered in urine, from which <1% is represented by the unchanged form.
[A40019]
[A40019]
Clearance
The geometric apparent clearance of dacomitinib is 27.06 L/h.
[A40019]
[A40019]
Drug targets(3)
Proteins and enzymes this drug interacts with in the body
Epidermal growth factor receptor
EGFR
inhibitor
Specific functionactin filament binding
Cellular location
Cell membrane
General function & pharmacology
Receptor tyrosine kinase binding ligands of the EGF family and activating several signaling cascades to convert extracellular cues into appropriate cellular responses .
PMID:10805725 PMID:27153536 PMID:2790960 PMID:35538033
Known ligands include EGF, TGFA/TGF-alpha, AREG, epigen/EPGN, BTC/betacellulin, epiregulin/EREG and HBEGF/heparin-binding EGF .
PMID:12297049 PMID:15611079 PMID:17909029 PMID:20837704 PMID:27153536 PMID:2790960 PMID:7679104 PMID:8144591 PMID:9419975
Ligand binding triggers receptor homo- and/or heterodimerization and autophosphorylation on key cytoplasmic residues. The phosphorylated receptor recruits adapter proteins like GRB2 which in turn activates complex downstream signaling cascades. Activates at least 4 major downstream signaling cascades including the RAS-RAF-MEK-ERK, PI3 kinase-AKT, PLCgamma-PKC and STATs modules .
PMID:27153536
May also activate the NF-kappa-B signaling cascade .
PMID:11116146
Also directly phosphorylates other proteins like RGS16, activating its GTPase activity and probably coupling the EGF receptor signaling to the G protein-coupled receptor signaling .
PMID:11602604
Also phosphorylates MUC1 and increases its interaction with SRC and CTNNB1/beta-catenin .
PMID:11483589
Positively regulates cell migration via interaction with CCDC88A/GIV which retains EGFR at the cell membrane following ligand stimulation, promoting EGFR signaling which triggers cell migration .
PMID:20462955
Plays a role in enhancing learning and memory performance (By similarity).
Plays a role in mammalian pain signaling (long-lasting hypersensitivity) (By similarity)
PMID:10805725 PMID:27153536 PMID:2790960 PMID:35538033
Known ligands include EGF, TGFA/TGF-alpha, AREG, epigen/EPGN, BTC/betacellulin, epiregulin/EREG and HBEGF/heparin-binding EGF .
PMID:12297049 PMID:15611079 PMID:17909029 PMID:20837704 PMID:27153536 PMID:2790960 PMID:7679104 PMID:8144591 PMID:9419975
Ligand binding triggers receptor homo- and/or heterodimerization and autophosphorylation on key cytoplasmic residues. The phosphorylated receptor recruits adapter proteins like GRB2 which in turn activates complex downstream signaling cascades. Activates at least 4 major downstream signaling cascades including the RAS-RAF-MEK-ERK, PI3 kinase-AKT, PLCgamma-PKC and STATs modules .
PMID:27153536
May also activate the NF-kappa-B signaling cascade .
PMID:11116146
Also directly phosphorylates other proteins like RGS16, activating its GTPase activity and probably coupling the EGF receptor signaling to the G protein-coupled receptor signaling .
PMID:11602604
Also phosphorylates MUC1 and increases its interaction with SRC and CTNNB1/beta-catenin .
PMID:11483589
Positively regulates cell migration via interaction with CCDC88A/GIV which retains EGFR at the cell membrane following ligand stimulation, promoting EGFR signaling which triggers cell migration .
PMID:20462955
Plays a role in enhancing learning and memory performance (By similarity).
Plays a role in mammalian pain signaling (long-lasting hypersensitivity) (By similarity)
Receptor tyrosine-protein kinase erbB-2
ERBB2
antagonist
Specific functionATP binding
Cellular location
Cell membrane
General function & pharmacology
Protein tyrosine kinase that is part of several cell surface receptor complexes, but that apparently needs a coreceptor for ligand binding. Essential component of a neuregulin-receptor complex, although neuregulins do not interact with it alone. GP30 is a potential ligand for this receptor.
Regulates outgrowth and stabilization of peripheral microtubules (MTs). Upon ERBB2 activation, the MEMO1-RHOA-DIAPH1 signaling pathway elicits the phosphorylation and thus the inhibition of GSK3B at cell membrane. This prevents the phosphorylation of APC and CLASP2, allowing its association with the cell membrane.
In turn, membrane-bound APC allows the localization of MACF1 to the cell membrane, which is required for microtubule capture and stabilization
Regulates outgrowth and stabilization of peripheral microtubules (MTs). Upon ERBB2 activation, the MEMO1-RHOA-DIAPH1 signaling pathway elicits the phosphorylation and thus the inhibition of GSK3B at cell membrane. This prevents the phosphorylation of APC and CLASP2, allowing its association with the cell membrane.
In turn, membrane-bound APC allows the localization of MACF1 to the cell membrane, which is required for microtubule capture and stabilization
Receptor tyrosine-protein kinase erbB-4
ERBB4
antagonist
Specific functionATP binding
Cellular location
Cell membrane
General function & pharmacology
Tyrosine-protein kinase that plays an essential role as cell surface receptor for neuregulins and EGF family members and regulates development of the heart, the central nervous system and the mammary gland, gene transcription, cell proliferation, differentiation, migration and apoptosis. Required for normal cardiac muscle differentiation during embryonic development, and for postnatal cardiomyocyte proliferation. Required for normal development of the embryonic central nervous system, especially for normal neural crest cell migration and normal axon guidance.
Required for mammary gland differentiation, induction of milk proteins and lactation. Acts as cell-surface receptor for the neuregulins NRG1, NRG2, NRG3 and NRG4 and the EGF family members BTC, EREG and HBEGF. Ligand binding triggers receptor dimerization and autophosphorylation at specific tyrosine residues that then serve as binding sites for scaffold proteins and effectors.
Ligand specificity and signaling is modulated by alternative splicing, proteolytic processing, and by the formation of heterodimers with other ERBB family members, thereby creating multiple combinations of intracellular phosphotyrosines that trigger ligand- and context-specific cellular responses. Mediates phosphorylation of SHC1 and activation of the MAP kinases MAPK1/ERK2 and MAPK3/ERK1. Isoform JM-A CYT-1 and isoform JM-B CYT-1 phosphorylate PIK3R1, leading to the activation of phosphatidylinositol 3-kinase and AKT1 and protect cells against apoptosis.
Isoform JM-A CYT-1 and isoform JM-B CYT-1 mediate reorganization of the actin cytoskeleton and promote cell migration in response to NRG1. Isoform JM-A CYT-2 and isoform JM-B CYT-2 lack the phosphotyrosine that mediates interaction with PIK3R1, and hence do not phosphorylate PIK3R1, do not protect cells against apoptosis, and do not promote reorganization of the actin cytoskeleton and cell migration. Proteolytic processing of isoform JM-A CYT-1 and isoform JM-A CYT-2 gives rise to the corresponding soluble intracellular domains (4ICD) that translocate to the nucleus, promote nuclear import of STAT5A, activation of STAT5A, mammary epithelium differentiation, cell proliferation and activation of gene expression.
The ERBB4 soluble intracellular domains (4ICD) colocalize with STAT5A at the CSN2 promoter to regulate transcription of milk proteins during lactation. The ERBB4 soluble intracellular domains can also translocate to mitochondria and promote apoptosis
Required for mammary gland differentiation, induction of milk proteins and lactation. Acts as cell-surface receptor for the neuregulins NRG1, NRG2, NRG3 and NRG4 and the EGF family members BTC, EREG and HBEGF. Ligand binding triggers receptor dimerization and autophosphorylation at specific tyrosine residues that then serve as binding sites for scaffold proteins and effectors.
Ligand specificity and signaling is modulated by alternative splicing, proteolytic processing, and by the formation of heterodimers with other ERBB family members, thereby creating multiple combinations of intracellular phosphotyrosines that trigger ligand- and context-specific cellular responses. Mediates phosphorylation of SHC1 and activation of the MAP kinases MAPK1/ERK2 and MAPK3/ERK1. Isoform JM-A CYT-1 and isoform JM-B CYT-1 phosphorylate PIK3R1, leading to the activation of phosphatidylinositol 3-kinase and AKT1 and protect cells against apoptosis.
Isoform JM-A CYT-1 and isoform JM-B CYT-1 mediate reorganization of the actin cytoskeleton and promote cell migration in response to NRG1. Isoform JM-A CYT-2 and isoform JM-B CYT-2 lack the phosphotyrosine that mediates interaction with PIK3R1, and hence do not phosphorylate PIK3R1, do not protect cells against apoptosis, and do not promote reorganization of the actin cytoskeleton and cell migration. Proteolytic processing of isoform JM-A CYT-1 and isoform JM-A CYT-2 gives rise to the corresponding soluble intracellular domains (4ICD) that translocate to the nucleus, promote nuclear import of STAT5A, activation of STAT5A, mammary epithelium differentiation, cell proliferation and activation of gene expression.
The ERBB4 soluble intracellular domains (4ICD) colocalize with STAT5A at the CSN2 promoter to regulate transcription of milk proteins during lactation. The ERBB4 soluble intracellular domains can also translocate to mitochondria and promote apoptosis
Metabolizing enzymes(4)
Enzymes involved in drug metabolism — important for understanding drug interactions
Enzyme activity key
substrate
inhibitor
inducer
CYP2D6Cytochrome P450 2D6
substrate
inhibitor
CYP3A4Cytochrome P450 3A4
substrate
CYP2C9Cytochrome P450 2C9
substrate
UGT1A1UDP-glucuronosyltransferase 1A1
inhibitor
Transporters(3)
Proteins that transport this drug across cell membranes
ATP-dependent translocase ABCB1
ABCB1
substrate
inhibitor
Specific functionABC-type xenobiotic transporter activity
Cellular location
Cell membrane
General function & pharmacology
Translocates drugs and phospholipids across the membrane .
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
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
Broad substrate specificity ATP-binding cassette transporter ABCG2
ABCG2
substrate
inhibitor
Specific functionABC-type xenobiotic transporter activity
Cellular location
Cell membrane
General function & pharmacology
Broad substrate specificity ATP-dependent transporter of the ATP-binding cassette (ABC) family that actively extrudes a wide variety of physiological compounds, dietary toxins and xenobiotics from cells .
PMID:11306452 PMID:12958161 PMID:19506252 PMID:20705604 PMID:28554189 PMID:30405239 PMID:31003562
Involved in porphyrin homeostasis, mediating the export of protoporphyrin IX (PPIX) from both mitochondria to cytosol and cytosol to extracellular space, it also functions in the cellular export of heme .
PMID:20705604 PMID:23189181
Also mediates the efflux of sphingosine-1-P from cells .
PMID:20110355
Acts as a urate exporter functioning in both renal and extrarenal urate excretion .
PMID:19506252 PMID:20368174 PMID:22132962 PMID:31003562 PMID:36749388
In kidney, it also functions as a physiological exporter of the uremic toxin indoxyl sulfate (By similarity). Also involved in the excretion of steroids like estrone 3-sulfate/E1S, 3beta-sulfooxy-androst-5-en-17-one/DHEAS, and other sulfate conjugates .
PMID:12682043 PMID:28554189 PMID:30405239
Mediates the secretion of the riboflavin and biotin vitamins into milk (By similarity). Extrudes pheophorbide a, a phototoxic porphyrin catabolite of chlorophyll, reducing its bioavailability (By similarity).
Plays an important role in the exclusion of xenobiotics from the brain (Probable). It confers to cells a resistance to multiple drugs and other xenobiotics including mitoxantrone, pheophorbide, camptothecin, methotrexate, azidothymidine, and the anthracyclines daunorubicin and doxorubicin, through the control of their efflux .
PMID:11306452 PMID:12477054 PMID:15670731 PMID:18056989 PMID:31254042
In placenta, it limits the penetration of drugs from the maternal plasma into the fetus (By similarity). May play a role in early stem cell self-renewal by blocking differentiation (By similarity).
In inflammatory macrophages, exports itaconate from the cytosol to the extracellular compartment and limits the activation of TFEB-dependent lysosome biogenesis involved in antibacterial innate immune response
PMID:11306452 PMID:12958161 PMID:19506252 PMID:20705604 PMID:28554189 PMID:30405239 PMID:31003562
Involved in porphyrin homeostasis, mediating the export of protoporphyrin IX (PPIX) from both mitochondria to cytosol and cytosol to extracellular space, it also functions in the cellular export of heme .
PMID:20705604 PMID:23189181
Also mediates the efflux of sphingosine-1-P from cells .
PMID:20110355
Acts as a urate exporter functioning in both renal and extrarenal urate excretion .
PMID:19506252 PMID:20368174 PMID:22132962 PMID:31003562 PMID:36749388
In kidney, it also functions as a physiological exporter of the uremic toxin indoxyl sulfate (By similarity). Also involved in the excretion of steroids like estrone 3-sulfate/E1S, 3beta-sulfooxy-androst-5-en-17-one/DHEAS, and other sulfate conjugates .
PMID:12682043 PMID:28554189 PMID:30405239
Mediates the secretion of the riboflavin and biotin vitamins into milk (By similarity). Extrudes pheophorbide a, a phototoxic porphyrin catabolite of chlorophyll, reducing its bioavailability (By similarity).
Plays an important role in the exclusion of xenobiotics from the brain (Probable). It confers to cells a resistance to multiple drugs and other xenobiotics including mitoxantrone, pheophorbide, camptothecin, methotrexate, azidothymidine, and the anthracyclines daunorubicin and doxorubicin, through the control of their efflux .
PMID:11306452 PMID:12477054 PMID:15670731 PMID:18056989 PMID:31254042
In placenta, it limits the penetration of drugs from the maternal plasma into the fetus (By similarity). May play a role in early stem cell self-renewal by blocking differentiation (By similarity).
In inflammatory macrophages, exports itaconate from the cytosol to the extracellular compartment and limits the activation of TFEB-dependent lysosome biogenesis involved in antibacterial innate immune response
Solute carrier family 22 member 1
SLC22A1
inhibitor
Specific function(R)-carnitine transmembrane transporter activity
Cellular location
Basolateral cell membrane
General function & pharmacology
Electrogenic voltage-dependent transporter that mediates the transport of a variety of organic cations such as endogenous bioactive amines, cationic drugs and xenobiotics .
PMID:11388889 PMID:11408531 PMID:12439218 PMID:12719534 PMID:15389554 PMID:16263091 PMID:16272756 PMID:16581093 PMID:19536068 PMID:21128598 PMID:23680637 PMID:24961373 PMID:34040533 PMID:9187257 PMID:9260930 PMID:9655880
Functions as a pH- and Na(+)-independent, bidirectional transporter (By similarity). Cation cellular uptake or release is driven by the electrochemical potential (i.e. membrane potential and concentration gradient) and substrate selectivity (By similarity). Hydrophobicity is a major requirement for recognition in polyvalent substrates and inhibitors (By similarity).
Primarily expressed at the basolateral membrane of hepatocytes and proximal tubules and involved in the uptake and disposition of cationic compounds by hepatic and renal clearance from the blood flow (By similarity). Most likely functions as an uptake carrier in enterocytes contributing to the intestinal elimination of organic cations from the systemic circulation .
PMID:16263091
Transports endogenous monoamines such as N-1-methylnicotinamide (NMN), guanidine, histamine, neurotransmitters dopamine, serotonin and adrenaline .
PMID:12439218 PMID:24961373 PMID:35469921 PMID:9260930
Also transports natural polyamines such as spermidine, agmatine and putrescine at low affinity, but relatively high turnover .
PMID:21128598
Involved in the hepatic uptake of vitamin B1/thiamine, hence regulating hepatic lipid and energy metabolism .
PMID:24961373
Mediates the bidirectional transport of acetylcholine (ACh) at the apical membrane of ciliated cell in airway epithelium, thereby playing a role in luminal release of ACh from bronchial epithelium .
PMID:15817714
Transports dopaminergic neuromodulators cyclo(his-pro) and salsolinol with lower efficency .
PMID:17460754
Also capable of transporting non-amine endogenous compounds such as prostaglandin E2 (PGE2) and prostaglandin F2-alpha (PGF2-alpha) .
PMID:11907186
May contribute to the transport of cationic compounds in testes across the blood-testis-barrier (Probable). Also involved in the uptake of xenobiotics tributylmethylammonium (TBuMA), quinidine, N-methyl-quinine (NMQ), N-methyl-quinidine (NMQD) N-(4,4-azo-n-pentyl)-quinuclidine (APQ), azidoprocainamide methoiodide (AMP), N-(4,4-azo-n-pentyl)-21-deoxyajmalinium (APDA) and 4-(4-(dimethylamino)styryl)-N-methylpyridinium (ASP) PMID:11408531 PMID:15389554 PMID:35469921 PMID:9260930
PMID:11388889 PMID:11408531 PMID:12439218 PMID:12719534 PMID:15389554 PMID:16263091 PMID:16272756 PMID:16581093 PMID:19536068 PMID:21128598 PMID:23680637 PMID:24961373 PMID:34040533 PMID:9187257 PMID:9260930 PMID:9655880
Functions as a pH- and Na(+)-independent, bidirectional transporter (By similarity). Cation cellular uptake or release is driven by the electrochemical potential (i.e. membrane potential and concentration gradient) and substrate selectivity (By similarity). Hydrophobicity is a major requirement for recognition in polyvalent substrates and inhibitors (By similarity).
Primarily expressed at the basolateral membrane of hepatocytes and proximal tubules and involved in the uptake and disposition of cationic compounds by hepatic and renal clearance from the blood flow (By similarity). Most likely functions as an uptake carrier in enterocytes contributing to the intestinal elimination of organic cations from the systemic circulation .
PMID:16263091
Transports endogenous monoamines such as N-1-methylnicotinamide (NMN), guanidine, histamine, neurotransmitters dopamine, serotonin and adrenaline .
PMID:12439218 PMID:24961373 PMID:35469921 PMID:9260930
Also transports natural polyamines such as spermidine, agmatine and putrescine at low affinity, but relatively high turnover .
PMID:21128598
Involved in the hepatic uptake of vitamin B1/thiamine, hence regulating hepatic lipid and energy metabolism .
PMID:24961373
Mediates the bidirectional transport of acetylcholine (ACh) at the apical membrane of ciliated cell in airway epithelium, thereby playing a role in luminal release of ACh from bronchial epithelium .
PMID:15817714
Transports dopaminergic neuromodulators cyclo(his-pro) and salsolinol with lower efficency .
PMID:17460754
Also capable of transporting non-amine endogenous compounds such as prostaglandin E2 (PGE2) and prostaglandin F2-alpha (PGF2-alpha) .
PMID:11907186
May contribute to the transport of cationic compounds in testes across the blood-testis-barrier (Probable). Also involved in the uptake of xenobiotics tributylmethylammonium (TBuMA), quinidine, N-methyl-quinine (NMQ), N-methyl-quinidine (NMQD) N-(4,4-azo-n-pentyl)-quinuclidine (APQ), azidoprocainamide methoiodide (AMP), N-(4,4-azo-n-pentyl)-21-deoxyajmalinium (APDA) and 4-(4-(dimethylamino)styryl)-N-methylpyridinium (ASP) PMID:11408531 PMID:15389554 PMID:35469921 PMID:9260930
Carriers(1)
Proteins that carry this drug through the body
Albumin
ALB
binder
Specific functionantioxidant activity
Cellular location
Secreted
General function & pharmacology
Binds water, Ca(2+), Na(+), K(+), fatty acids, hormones, bilirubin and drugs (Probable). Its main function is the regulation of the colloidal osmotic pressure of blood (Probable). Major zinc transporter in plasma, typically binds about 80% of all plasma zinc .
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
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
Scientific references(12)
Momeny M., Zarrinrad G., Moghaddaskho F., Poursheikhani A., Sankanian G., Zaghal A., Mirshahvaladi S., Esmaeili F., Eyvani H., Barghi F., Sabourinejad Z., Alishahi Z., Yousefi H., Ghasemi R., Dardaei L., Bashash D., Chahardouli B., Dehpour A.R., Tavakkoly-Bazzaz J., Alimoghaddam K., Ghavamzadeh A., Ghaffari S.H.
Dacomitinib, a pan-inhibitor of ErbB receptors, suppresses growth and invasive capacity of chemoresistant ovarian carcinoma cells.
Science Reports
2017 Jun 237(1):4204. doi: 10.1038/s41598-017-04147-0
Brzezniak C., Carter C.A., Giaccone G.
Dacomitinib, a new therapy for the treatment of non-small cell lung cancer.
Expert Opinion on Pharmacotherapy
2013 Feb14(2):247-53. doi: 10.1517/14656566.2013.758714. Epub 2013 Jan 7
Engelman J.A., Zejnullahu K., Gale C.M., Lifshits E., Gonzales A.J., Shimamura T., Zhao F., Vincent P.W., Naumov G.N., Bradner J.E., Althaus I.W., Gandhi L., Shapiro G.I., Nelson J.M., Heymach J.V., Meyerson M., Wong K.K., Janne P.A.
PF00299804, an irreversible pan-ERBB inhibitor, is effective in lung cancer models with EGFR and ERBB2 mutations that are resistant to gefitinib.
Cancer Research
2007 Dec 1567(24):11924-32. doi: 10.1158/0008-5472.CAN-07-1885
Fry D.W., Bridges A.J., Denny W.A., Doherty A., Greis K.D., Hicks J.L., Hook K.E., Keller P.R., Leopold W.R., Loo J.A., McNamara D.J., Nelson J.M., Sherwood V., Smaill J.B., Trumpp-Kallmeyer S., Dobrusin E.M.
Specific, irreversible inactivation of the epidermal growth factor receptor and erbB2, by a new class of tyrosine kinase inhibitor.
Proceedings of the National Academy of Sciences
199895(20):12022-12027. doi: 10.1073/pnas.95.20.12022
Janne P.A., Boss D.S., Camidge D.R., Britten C.D., Engelman J.A., Garon E.B., Guo F., Wong S., Liang J., Letrent S., Millham R., Taylor I., Eckhardt S.G., Schellens J.H.
Phase I dose-escalation study of the pan-HER inhibitor, PF299804, in patients with advanced malignant solid tumors.
Clinical Cancer Research
2011 Mar 117(5):1131-9. doi: 10.1158/1078-0432.CCR-10-1220. Epub 2011 Jan 10
Bello C.L., LaBadie R.R., Ni G., Boutros T., McCormick C., Ndongo M.N.
The effect of dacomitinib (PF-00299804) on CYP2D6 activity in healthy volunteers who are extensive or intermediate metabolizers.
Cancer Chemother Pharmacology
2012 Apr69(4):991-7. doi: 10.1007/s00280-011-1793-7. Epub 2011 Dec 7
Sepulveda J.M., Sanchez-Gomez P., Vaz Salgado M.A., Gargini R., Balana C.
Dacomitinib: an investigational drug for the treatment of glioblastoma.
Expert Opinion Investig Drugs
2018 Oct27(10):823-829. doi: 10.1080/13543784.2018.1528225. Epub 2018 Oct 5
Wu Y.L., Cheng Y., Zhou X., Lee K.H., Nakagawa K., Niho S., Tsuji F., Linke R., Rosell R., Corral J., Migliorino M.R., Pluzanski A., Sbar E.I., Wang T., White J.L., Nadanaciva S., Sandin R., Mok T.S.
Dacomitinib versus gefitinib as first-line treatment for patients with EGFR-mutation-positive non-small-cell lung cancer (ARCHER 1050): a randomised, open-label, phase 3 trial.
The Lancet Oncology
2017 Nov18(11):1454-1466. doi: 10.1016/S1470-2045(17)30608-3. Epub 2017 Sep 25
Mellinghoff I.K., Wang M.Y., Vivanco I., Haas-Kogan D.A., Zhu S., Dia E.Q., Lu K.V., Yoshimoto K., Huang J.H., Chute D.J., Riggs B.L., Horvath S., Liau L.M., Cavenee W.K., Rao P.N., Beroukhim R., Peck T.C., Lee J.C., Sellers W.R., Stokoe D., Prados M., Cloughesy T.F., Sawyers C.L., Mischel P.S.
Molecular determinants of the response of glioblastomas to EGFR kinase inhibitors.
New England Journal of Medicine
2005 Nov 10353(19):2012-24. doi: 10.1056/NEJMoa051918
da Cunha Santos G., Shepherd F.A., Tsao M.S.
EGFR mutations and lung cancer.
Annual Review Pathology
20116:49-69. doi: 10.1146/annurev-pathol-011110-130206
Bethune G., Bethune D., Ridgway N., Xu Z.
The role of osimertinib in epidermal growth factor receptor (EGFR)-mutant non-small cell lung cancer.
Journal of Thoracic Disease
201911(S3):S448-S452. doi: 10.21037/jtd.2018.11.45
Chen X., Jiang J., Giri N., Hu P.
Phase 1 study to investigate the pharmacokinetic properties of dacomitinib in healthy adult Chinese subjects genotyped for CYP2D6.
Xenobiotica
2018 May48(5):459-466. doi: 10.1080/00498254.2017.1342881. Epub 2017 Aug 18
ATC classification(1 code)
ATC L01EB07
Affected organisms(1)
Humans and other mammals
Salt forms(1)
Dacomitinib monohydrate(DBSALT002510)
Experimental properties(4)
Commercial products(10)
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Show
Chemical identifiers
CAS, UNII, InChI Key and database cross-references
Linked compound data from DrugBank Open Data (CC BY-NC 4.0)
Dacomitinib
Additional database identifiers
Drugs Product Database (DPD)
23131
ChemSpider
9685914
BindingDB
112499
PDB
1C9
ZINC
ZINC000072266312
HUGO Gene Nomenclature Committee (HGNC)
HGNC:3236
GenAtlas
EGFR
GeneCards
EGFR
GenBank Gene Database
X00588
GenBank Protein Database
757924
Guide to Pharmacology
1797
UniProt Accession
EGFR_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:3430
GenAtlas
ERBB2
GeneCards
ERBB2
GenBank Gene Database
M11767
GenBank Protein Database
553282
Guide to Pharmacology
2019
UniProt Accession
ERBB2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:3432
GeneCards
ERBB4
Guide to Pharmacology
1799
UniProt Accession
ERBB4_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:2625
GenAtlas
CYP2D6
GeneCards
CYP2D6
GenBank Gene Database
M20403
GenBank Protein Database
181350
Guide to Pharmacology
1329
UniProt Accession
CP2D6_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:2623
GenAtlas
CYP2C9
GeneCards
CYP2C9
GenBank Gene Database
AY341248
Guide to Pharmacology
1326
UniProt Accession
CP2C9_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:12530
GeneCards
UGT1A1
GenBank Gene Database
M57899
GenBank Protein Database
184473
Guide to Pharmacology
2990
UniProt Accession
UD11_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:40
GenAtlas
ABCB1
GeneCards
ABCB1
GenBank Gene Database
M14758
GenBank Protein Database
307180
Guide to Pharmacology
768
UniProt Accession
MDR1_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:74
GenAtlas
ABCG2
GeneCards
ABCG2
GenBank Gene Database
AF103796
GenBank Protein Database
4185796
Guide to Pharmacology
792
UniProt Accession
ABCG2_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:10963
GeneCards
SLC22A1
GenBank Gene Database
X98332
GenBank Protein Database
2511670
Guide to Pharmacology
1019
UniProt Accession
S22A1_HUMAN
Patent information
1 active patent, 3 expired
7772243
United States
Approved 10 Aug 2010 · Expires 26 Aug 2028
2y 4m
10603314
United States
Approved 31 Mar 2020 · Expires 2 Feb 2026
Expired
10596162
United States
Approved 24 Mar 2020 · Expires 2 Feb 2026
Expired
8623883
United States
Approved 7 Jan 2014 · Expires 5 May 2025
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:
Knox C., Wilson M., Klinger C.M., et al
DrugBank 6.
0: the DrugBank Knowledgebase for 2024
Nucleic Acids Res. 2024 Jan 552(D1):D1265-D1275
Wishart D.S., Feunang Y.D., Guo A.C., et al
DrugBank 5.
0: a major update to the DrugBank database for 2018
Nucleic Acids Res. 2017 Nov 846(D1):D1074-D1082
Show earlier publications
Law V., Knox C., Djoumbou Y., et al
DrugBank 4.
0: shedding new light on drug metabolism
Nucleic Acids Res. 2014 Jan 142(1):D1091-7
Knox C., Law V., Jewison T., et al
DrugBank 3.
0: a comprehensive resource for 'omics' research on drugs
Nucleic Acids Res. 2011 Jan39(Database issue):D1035-41
Wishart D.S., Knox C., Guo A.C., et al
DrugBank: a knowledgebase for drugs, drug actions and drug targets.
Nucleic Acids Research
2008 Jan36(Database issue):D901-6
Wishart D.S., Knox C., Guo A.C., et al
DrugBank: a comprehensive resource for in silico drug discovery and exploration.
Nucleic Acids Research
2006 Jan 134(Database issue):D668-72
Source: go.drugbank.comCC BY-NC 4.0
Updated 27 days ago(8 Mar 2026)