Gilteritinib 40mg tablets
Prescription only
Requires a prescription from a doctor or prescriber
Tablet
40mg
Oral
Cytotoxic drugs
Active ingredients:
Gilteritinib
No active safety alerts
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
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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.
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Suspected adverse reactions reported for Gilteritinib
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Xospata 40mg tablets
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WHO defined daily dose (DDD)
120 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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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
Gilteritinib
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(6)
Gilteritinib for treating relapsed or refractory acute myeloid leukaemia (TA642)
TA642
Technology appraisal
Updated Aug 2020Venetoclax with azacitidine for untreated acute myeloid leukaemia when intensive chemotherapy is unsuitable (TA765)
TA765
Technology appraisal
Updated Feb 2022Venetoclax with low dose cytarabine for untreated acute myeloid leukaemia when intensive chemotherapy is unsuitable (TA787)
TA787
Technology appraisal
Updated Apr 2022Quizartinib for induction, consolidation and maintenance treatment of newly diagnosed FLT3-ITD-positive acute myeloid leukaemia (TA1013)
TA1013
Technology appraisal
Updated Oct 2024Ivosidenib with azacitidine for untreated acute myeloid leukaemia with an IDH1 R132 mutation (TA979)
TA979
Technology appraisal
Updated Jun 2024Belumosudil for treating chronic graft-versus-host disease after 2 or more systemic treatments in people 12 years and over (TA949)
TA949
Technology appraisal
Updated Feb 2024Source: 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
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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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Searching UK clinical trials...
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
45-159 hours
Mechanism
Gilteritinib is a potent selective inhibitor of both of the mutations, internal…
Food interactions
4 warnings
Human targets
3 targets
Data: DrugBank · CC BY-NC 4.0
Pharmacokinetics at a glance
Absorption
2 hours
In preclinical trials, the maximal plasma concentration of gilteritinib was observed 2 hours after oral administration and followed by a maximal intratumor concentration after 4-8 hours.…
Half-life
45-159 hours
The reported median half-life of gilteritinib was of approximate 45-159 hours.
[L4833]
[L4833]
Protein binding
94%
Gilteritinib is reported to be highly bound to plasma proteins, representing 94% of the dose.…
Volume of distribution
1092 L
The estimated apparent central and peripheral volume of distribution is 1092 L and 1100 L respectively.…
Metabolism
Gilteritinib is primarily metabolized in the liver by the activity of CYP3A4.…
Elimination
64.5%
From the administered dose, gilteritinib is mainly excreted in feces which represents 64.5%…
Clearance
14.85 L/h
The estimated clearance of gilteritinib is 14.85 L/h.
[L4834]
[L4834]
Pharmacokinetic data: DrugBank · CC BY-NC 4.0
Status:
Approved
Investigational
Small molecule
About this compound
Gilteritinib, also known as ASP2215, is a small molecule part of the FLT3 tyrosine kinase inhibitors that presented a greater selectivity and potency when compared with other agents from this group.[A40036] It is a pyrazinecarboxamide derivative that showed high selectivity to FLT3 preventing the c-Kit -driven myelosuppression observed in other therapies.[A40044] Gilteritinib was developed by Astellas Pharma and FDA approved on November 28, 2018. This drug was approved after being designed as an orphan drug with a fast track and priority review status.[L4830]
Properties:
solid
Avg. mass: 552.72 Da
DrugBank indication
Gilteritinib is indicated for the treatment of adult patients who have relapsed or refractory acute myeloid leukemia with an FLT3 mutation detected by an FDA-approved test. This indication was expanded for a companion diagnostic to include use with gilteritinib such as the LeukoStrat CDx FLT3 Mutation Assay.
[L4830]
Acute myeloid leukemia is cancer that impacts the blood and bone marrow with a rapid progression. This condition produces low numbers of normal blood cells and the requirement of continuous need for transfusions.
[L4832]
[L4830]
Acute myeloid leukemia is cancer that impacts the blood and bone marrow with a rapid progression. This condition produces low numbers of normal blood cells and the requirement of continuous need for transfusions.
[L4832]
Also known as(56)
Gilteritinib
2.7.10.1
CD135
Fetal liver kinase-2
FL cytokine receptor
FLK-2
FLK2
FLT-3
Dosage forms(3)
Tablet (Oral) — 40 mg
Tablet (Oral) — 40 mg/1
Tablet, film coated (Oral) — 40 mg
Molecular properties(19)
Drug interactions(1109)
Known interactions with other medications. Always consult a healthcare professional.
Ivabradine
Moderate
Ivabradine may increase the QTc-prolonging activities of Gilteritinib.
Ranolazine
Unknown severity
The serum concentration of Gilteritinib can be increased when it is combined with Ranolazine.
The metabolism of Gilteritinib can be increased when combined with Phenytoin.
Fosphenytoin
Moderate
The metabolism of Gilteritinib can be increased when combined with Fosphenytoin.
Propacetamol
Unknown severity
The serum concentration of Propacetamol can be increased when it is combined with Gilteritinib.
Lumacaftor
Unknown severity
The serum concentration of Gilteritinib can be decreased when it is combined with Lumacaftor.
Anagrelide
Unknown severity
The risk or severity of QTc prolongation can be increased when Gilteritinib is combined with Anagrelide.
Disopyramide
Unknown severity
The risk or severity of QTc prolongation can be increased when Gilteritinib is combined with Disopyramide.
Clemastine
Unknown severity
The risk or severity of QTc prolongation can be increased when Gilteritinib is combined with Clemastine.
The risk or severity of QTc prolongation can be increased when Gilteritinib is combined with Ibutilide.
Valproic acid
Unknown severity
The risk or severity of QTc prolongation can be increased when Gilteritinib is combined with Valproic acid.
Grepafloxacin
Unknown severity
The risk or severity of QTc prolongation can be increased when Gilteritinib is combined with Grepafloxacin.
The risk or severity of QTc prolongation can be increased when Gilteritinib is combined with Quinine.
The risk or severity of QTc prolongation can be increased when Gilteritinib is combined with Sotalol.
The risk or severity of QTc prolongation can be increased when Gilteritinib is combined with Erlotinib.
Toremifene
Unknown severity
The risk or severity of QTc prolongation can be increased when Gilteritinib is combined with Toremifene.
The risk or severity of QTc prolongation can be increased when Gilteritinib is combined with Imatinib.
Trovafloxacin
Unknown severity
The risk or severity of QTc prolongation can be increased when Gilteritinib is combined with Trovafloxacin.
Mifepristone
Unknown severity
The risk or severity of QTc prolongation can be increased when Gilteritinib is combined with Mifepristone.
The risk or severity of methemoglobinemia can be increased when Gilteritinib is combined with Cocaine.
Procainamide
Unknown severity
The risk or severity of QTc prolongation can be increased when Gilteritinib is combined with Procainamide.
Arsenic trioxide
Unknown severity
The risk or severity of QTc prolongation can be increased when Gilteritinib is combined with Arsenic trioxide.
Domperidone
Unknown severity
The risk or severity of QTc prolongation can be increased when Gilteritinib is combined with Domperidone.
Sparfloxacin
Unknown severity
The risk or severity of QTc prolongation can be increased when Gilteritinib is combined with Sparfloxacin.
Halofantrine
Unknown severity
The risk or severity of QTc prolongation can be increased when Gilteritinib is combined with Halofantrine.
The risk or severity of QTc prolongation can be increased when Gilteritinib is combined with Bepridil.
Temafloxacin
Unknown severity
The risk or severity of QTc prolongation can be increased when Gilteritinib is combined with Temafloxacin.
Tetrabenazine
Unknown severity
The risk or severity of QTc prolongation can be increased when Gilteritinib is combined with Tetrabenazine.
Vandetanib
Unknown severity
The risk or severity of QTc prolongation can be increased when Gilteritinib is combined with Vandetanib.
Romidepsin
Unknown severity
The risk or severity of QTc prolongation can be increased when Gilteritinib is combined with Romidepsin.
Artemether
Unknown severity
The risk or severity of QTc prolongation can be increased when Gilteritinib is combined with Artemether.
Lumefantrine
Unknown severity
The risk or severity of QTc prolongation can be increased when Gilteritinib is combined with Lumefantrine.
The risk or severity of QTc prolongation can be increased when Gilteritinib is combined with Glasdegib.
Deutetrabenazine
Unknown severity
The risk or severity of QTc prolongation can be increased when Gilteritinib is combined with Deutetrabenazine.
Macimorelin
Unknown severity
The risk or severity of QTc prolongation can be increased when Gilteritinib is combined with Macimorelin.
Terodiline
Unknown severity
The risk or severity of QTc prolongation can be increased when Gilteritinib is combined with Terodiline.
Dofetilide
Unknown severity
The risk or severity of QTc prolongation can be increased when Gilteritinib is combined with Dofetilide.
Astemizole
Unknown severity
The risk or severity of QTc prolongation can be increased when Gilteritinib is combined with Astemizole.
The risk or severity of QTc prolongation can be increased when Gilteritinib is combined with Quinidine.
The risk or severity of QTc prolongation can be increased when Gilteritinib is combined with Pimozide.
Dronedarone
Unknown severity
The risk or severity of QTc prolongation can be increased when Gilteritinib is combined with Dronedarone.
Eliglustat
Unknown severity
The serum concentration of Gilteritinib can be increased when it is combined with Eliglustat.
Leuprolide
Unknown severity
The risk or severity of QTc prolongation can be increased when Leuprolide is combined with Gilteritinib.
The risk or severity of QTc prolongation can be increased when Goserelin is combined with Gilteritinib.
Moxifloxacin
Unknown severity
The risk or severity of QTc prolongation can be increased when Moxifloxacin is combined with Gilteritinib.
Sulfisoxazole
Unknown severity
The risk or severity of QTc prolongation can be increased when Sulfisoxazole is combined with Gilteritinib.
The risk or severity of QTc prolongation can be increased when Sulpiride is combined with Gilteritinib.
Prochlorperazine
Unknown severity
The risk or severity of QTc prolongation can be increased when Prochlorperazine is combined with Gilteritinib.
Droperidol
Unknown severity
The risk or severity of QTc prolongation can be increased when Droperidol is combined with Gilteritinib.
Perflutren
Unknown severity
The risk or severity of QTc prolongation can be increased when Perflutren is combined with Gilteritinib.
Showing 50 of 1109 interactions
Food & lifestyle interactions
Avoid Grapefruit
Avoid grapefruit products. Grapefruit inhibits CYP3A metabolism, which may increase the serum concentration of gilteritinib.
Advice
Avoid St. John's Wort. This herb induces CYP3A4 and p-glycoprotein, which may reduce the serum concentration of gilteritinib.
Advice
Take at the same time every day.
Advice
Take with or without food.
Toxicity & overdose
Gilteritinib is not reported to be mutagenic in bacterial mutagenesis assays nor clastogenic in aberration test assays in Chinese hamster lung cells. However, it resulted positive for the induction of micronuclei in mouse bone marrow and for the degeneration and necrosis of germ cells and spermatid giant cell formation in testis as well as single cell necrosis of the epididymal duct epithelia.[FDA label]
How it works
Mechanism of action
Gilteritinib is a potent selective inhibitor of both of the mutations, internal tandem duplication (ITD) and tyrosine kinase domain (TKD), of the FLT3 receptor.[A40039] In the same note, gilteritinib also inhibits AXL and ALK tyrosine kinases.[A40040] FLT3 and AXL are molecules involved in the growth of cancer cells.[A40043] The activity of gilteritinib permits an inhibition of the phosphorylation of FLT3 and its downstream targets such as STAT5, ERK and AKT.[A40048]
The interest in FLT3 transmembrane tyrosine kinases was raised when studies reported that approximately 30% of the patients with acute myeloid leukemia presented a mutationally activated isoform.[A40036] As well, the mutation ITD is associated with poor patient outcomes while the mutation TKD produces a resistance mechanism to FLT3 tyrosine kinase inhibitors and the AXL tyrosine kinase tends to produce a resistance mechanism to chemotherapies.[A40043]
The interest in FLT3 transmembrane tyrosine kinases was raised when studies reported that approximately 30% of the patients with acute myeloid leukemia presented a mutationally activated isoform.[A40036] As well, the mutation ITD is associated with poor patient outcomes while the mutation TKD produces a resistance mechanism to FLT3 tyrosine kinase inhibitors and the AXL tyrosine kinase tends to produce a resistance mechanism to chemotherapies.[A40043]
Pharmacodynamics
In preclinical trials, gilteritinib demonstrate an IC50 for the wild-type receptor of 5 nM, 0.7-1.8 nM for ITD-mutated and comparable inhibition to other therapies in the TKD-mutated. As well, data showed a gilteritinib-driven inhibition of the receptor tyrosine kinase AXL which is known to modulate the activity of FLT3 in acute myeloid leukemia.[A40044] Another important result in vivo was the localization in high levels in xenografted tumors which indicated high selectivity.[A40048]
In phase 1/2 clinical trials, gilteritinib was shown to present a composite complete response of 41%, an overall response rate of 52%, a median duration of response of 20 weeks with a median overall survival of 31 weeks.[A40036]
In phase III clinical trials, gilteritinib reported a complete remission or complete remission with partial hematologic recovery in 21% of the patients.[L4830]
In phase 1/2 clinical trials, gilteritinib was shown to present a composite complete response of 41%, an overall response rate of 52%, a median duration of response of 20 weeks with a median overall survival of 31 weeks.[A40036]
In phase III clinical trials, gilteritinib reported a complete remission or complete remission with partial hematologic recovery in 21% of the patients.[L4830]
Pharmacokinetics
How the body processes this drug — absorption, distribution, metabolism, and elimination
Absorption
In preclinical trials, the maximal plasma concentration of gilteritinib was observed 2 hours after oral administration and followed by a maximal intratumor concentration after 4-8 hours. The maximum concentration, as well as the AUC, were modified correspondingly with the dose and were reported to be 374 ng/ml and 6943 ng.h/ml, respectively.
[A40048]
The steady-state plasma level is reached within 15 days of dosing with an approximate 10-fold bioaccumulation.
[L4833]
In a fasted state in humans, the tmax is reported to be of 4-6 hours. The Cmax and AUC were decreased by 26% and 10% respectively by the co-ingestion of a high-fat meal with a tmax delay of 2 hours.
[L4834]
[A40048]
The steady-state plasma level is reached within 15 days of dosing with an approximate 10-fold bioaccumulation.
[L4833]
In a fasted state in humans, the tmax is reported to be of 4-6 hours. The Cmax and AUC were decreased by 26% and 10% respectively by the co-ingestion of a high-fat meal with a tmax delay of 2 hours.
[L4834]
Half-life
The reported median half-life of gilteritinib was of approximate 45-159 hours.
[L4833]
[L4833]
Protein binding
Gilteritinib is reported to be highly bound to plasma proteins, representing 94% of the dose. From this ratio, the main protein-bound is serum albumin.
[L4834]
[L4834]
Volume of distribution
The estimated apparent central and peripheral volume of distribution is 1092 L and 1100 L respectively. This value indicated an extensive tissue distribution.
[L4834]
[L4834]
Metabolism
Gilteritinib is primarily metabolized in the liver by the activity of CYP3A4. Its metabolism is driven by reactions of N-dealkylation and oxidation which forms the metabolite M17, M16 and M10. From the plasma concentration, the major form is the unchanged drug.
[L4835]
[L4835]
Route of elimination
From the administered dose, gilteritinib is mainly excreted in feces which represents 64.5% of the administered dose while 16.4% is recovered in urine either as the unchanged drug or as its metabolites.
[L4835]
[L4835]
Clearance
The estimated clearance of gilteritinib is 14.85 L/h.
[L4834]
[L4834]
Drug targets(3)
Proteins and enzymes this drug interacts with in the body
Receptor-type tyrosine-protein kinase FLT3
FLT3
inhibitor
Specific functionATP binding
Cellular location
Membrane
General function & pharmacology
Tyrosine-protein kinase that acts as a cell-surface receptor for the cytokine FLT3LG and regulates differentiation, proliferation and survival of hematopoietic progenitor cells and of dendritic cells. Promotes phosphorylation of SHC1 and AKT1, and activation of the downstream effector MTOR. Promotes activation of RAS signaling and phosphorylation of downstream kinases, including MAPK1/ERK2 and/or MAPK3/ERK1.
Promotes phosphorylation of FES, FER, PTPN6/SHP, PTPN11/SHP-2, PLCG1, and STAT5A and/or STAT5B. Activation of wild-type FLT3 causes only marginal activation of STAT5A or STAT5B. Mutations that cause constitutive kinase activity promote cell proliferation and resistance to apoptosis via the activation of multiple signaling pathways
Promotes phosphorylation of FES, FER, PTPN6/SHP, PTPN11/SHP-2, PLCG1, and STAT5A and/or STAT5B. Activation of wild-type FLT3 causes only marginal activation of STAT5A or STAT5B. Mutations that cause constitutive kinase activity promote cell proliferation and resistance to apoptosis via the activation of multiple signaling pathways
Tyrosine-protein kinase receptor UFO
AXL
inhibitor
Specific functionATP binding
Cellular location
Cell membrane
General function & pharmacology
Receptor tyrosine kinase that transduces signals from the extracellular matrix into the cytoplasm by binding growth factor GAS6 and which is thus regulating many physiological processes including cell survival, cell proliferation, migration and differentiation. Ligand binding at the cell surface induces dimerization and autophosphorylation of AXL. Following activation by ligand, AXL binds and induces tyrosine phosphorylation of PI3-kinase subunits PIK3R1, PIK3R2 and PIK3R3; but also GRB2, PLCG1, LCK and PTPN11.
Other downstream substrate candidates for AXL are CBL, NCK2, SOCS1 and TNS2. Recruitment of GRB2 and phosphatidylinositol 3 kinase regulatory subunits by AXL leads to the downstream activation of the AKT kinase. GAS6/AXL signaling plays a role in various processes such as endothelial cell survival during acidification by preventing apoptosis, optimal cytokine signaling during human natural killer cell development, hepatic regeneration, gonadotropin-releasing hormone neuron survival and migration, platelet activation, or regulation of thrombotic responses.
Also plays an important role in inhibition of Toll-like receptors (TLRs)-mediated innate immune response
Other downstream substrate candidates for AXL are CBL, NCK2, SOCS1 and TNS2. Recruitment of GRB2 and phosphatidylinositol 3 kinase regulatory subunits by AXL leads to the downstream activation of the AKT kinase. GAS6/AXL signaling plays a role in various processes such as endothelial cell survival during acidification by preventing apoptosis, optimal cytokine signaling during human natural killer cell development, hepatic regeneration, gonadotropin-releasing hormone neuron survival and migration, platelet activation, or regulation of thrombotic responses.
Also plays an important role in inhibition of Toll-like receptors (TLRs)-mediated innate immune response
ALK tyrosine kinase receptor
ALK
inhibitor
Specific functionATP binding
Cellular location
Cell membrane
General function & pharmacology
Neuronal receptor tyrosine kinase that is essentially and transiently expressed in specific regions of the central and peripheral nervous systems and plays an important role in the genesis and differentiation of the nervous system .
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
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
Metabolizing enzymes(1)
Enzymes involved in drug metabolism — important for understanding drug interactions
Enzyme activity key
substrate
inhibitor
inducer
CYP3A4Cytochrome P450 3A4
substrate
Transporters(4)
Proteins that transport this drug across cell membranes
ATP-dependent translocase ABCB1
ABCB1
substrate
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
Multidrug and toxin extrusion protein 1
SLC47A1
inhibitor
Specific functionantiporter activity
Cellular location
Cell membrane
General function & pharmacology
Multidrug efflux pump that functions as a H(+)/organic cation antiporter .
PMID:16330770 PMID:17509534
Plays a physiological role in the excretion of cationic compounds including endogenous metabolites, drugs, toxins through the kidney and liver, into urine and bile respectively .
PMID:16330770 PMID:17495125 PMID:17509534 PMID:17582384 PMID:18305230 PMID:19158817 PMID:21128598 PMID:24961373
Mediates the efflux of endogenous compounds such as creatinine, vitamin B1/thiamine, agmatine and estrone-3-sulfate .
PMID:16330770 PMID:17495125 PMID:17509534 PMID:17582384 PMID:18305230 PMID:19158817 PMID:21128598 PMID:24961373
May also contribute to regulate the transport of cationic compounds in testis across the blood-testis-barrier (Probable)
PMID:16330770 PMID:17509534
Plays a physiological role in the excretion of cationic compounds including endogenous metabolites, drugs, toxins through the kidney and liver, into urine and bile respectively .
PMID:16330770 PMID:17495125 PMID:17509534 PMID:17582384 PMID:18305230 PMID:19158817 PMID:21128598 PMID:24961373
Mediates the efflux of endogenous compounds such as creatinine, vitamin B1/thiamine, agmatine and estrone-3-sulfate .
PMID:16330770 PMID:17495125 PMID:17509534 PMID:17582384 PMID:18305230 PMID:19158817 PMID:21128598 PMID:24961373
May also contribute to regulate the transport of cationic compounds in testis across the blood-testis-barrier (Probable)
Broad substrate specificity ATP-binding cassette transporter ABCG2
ABCG2
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(6)
Stone R.M.
What FLT3 inhibitor holds the greatest promise? Best Pract Res Clin Haematol. 2018 Dec;31(4):401-404. doi: 10.1016/j.beha.2018.09.
008
Epub 2018 Sep 20
Fathi A.T., Chen Y.B.
The role of FLT3 inhibitors in the treatment of FLT3-mutated acute myeloid leukemia.
European Journal Haematol
2017 Apr98(4):330-336. doi: 10.1111/ejh.12841. Epub 2017 Jan 19
Antar A., Otrock Z.K., El-Cheikh J., Kharfan-Dabaja M.A., Battipaglia G., Mahfouz R., Mohty M., Bazarbachi A.
Inhibition of FLT3 in AML: a focus on sorafenib.
Bone Marrow Transplant
2017 Mar52(3):344-351. doi: 10.1038/bmt.2016.251. Epub 2016 Oct 24
Thom C.
Preliminary data on ASP2215: tolerability and efficacy in acute myeloid leukemia patients.
Future Oncology
2015 Sep11(18):2499-501. doi: 10.2217/fon.15.188. Epub 2015 Aug 17
Lee L.Y., Hernandez D., Rajkhowa T., Smith S.C., Raman J.R., Nguyen B., Small D., Levis M.
Preclinical studies of gilteritinib, a next-generation FLT3 inhibitor.
Blood
2017 Jan 12129(2):257-260. doi: 10.1182/blood-2016-10-745133. Epub 2016 Dec 1
Mori M., Kaneko N., Ueno Y., Yamada M., Tanaka R., Saito R., Shimada I., Mori K., Kuromitsu S.
Gilteritinib, a FLT3/AXL inhibitor, shows antileukemic activity in mouse models of FLT3 mutated acute myeloid leukemia.
Invest New Drugs
2017 Oct35(5):556-565. doi: 10.1007/s10637-017-0470-z. Epub 2017 May 17
ATC classification(1 code)
ATC L01EX13
Affected organisms(1)
Humans
Salt forms(1)
Gilteritinib fumarate(DBSALT002819)
Experimental properties(3)
Commercial products(3)
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)
Gilteritinib
Additional database identifiers
Drugs Product Database (DPD)
23399
ChemSpider
32055842
BindingDB
144315
PDB
C6F
ZINC
ZINC000113476229
HUGO Gene Nomenclature Committee (HGNC)
HGNC:3765
GenAtlas
FLT3
GeneCards
FLT3
GenBank Gene Database
U02687
GenBank Protein Database
409573
Guide to Pharmacology
1807
UniProt Accession
FLT3_HUMAN
HUGO Gene Nomenclature Committee (HGNC)
HGNC:905
GeneCards
AXL
Guide to Pharmacology
1835
UniProt Accession
UFO_HUMAN
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:2637
GenAtlas
CYP3A4
GeneCards
CYP3A4
GenBank Gene Database
M18907
Guide to Pharmacology
1337
UniProt Accession
CP3A4_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:25588
GeneCards
SLC47A1
GenBank Gene Database
AK001709
GenBank Protein Database
7023138
Guide to Pharmacology
1216
UniProt Accession
S47A1_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
8 active patents
10786500
United States
Approved 29 Sept 2020 · Expires 1 Jul 2036
10y 3m
11938133
United States
Approved 26 Mar 2024 · Expires 1 Jul 2036
10y 3m
11944620
United States
Approved 2 Apr 2024 · Expires 1 Jul 2036
10y 3m
11938130
United States
Approved 26 Mar 2024 · Expires 1 Jul 2036
10y 3m
11938131
United States
Approved 26 Mar 2024 · Expires 1 Jul 2036
10y 3m
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 about 1 month ago(4 Mar 2026)