Identification

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Name
Gilteritinib
Accession Number
DB12141
Type
Small Molecule
Groups
Approved, Investigational
Description

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.1 It is a pyrazinecarboxamide derivative that showed high selectivity to FLT3 preventing the c-Kit -driven myelosuppression observed in other therapies.5 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.7

Structure
Thumb
Synonyms
  • Gilteritinib
External IDs
ASP-2215 / ASP2215
Product Ingredients
IngredientUNIICASInChI Key
Gilteritinib fumarate5RZZ0Z1GJT1254053-84-3UJOUWHLYTQFUCU-WXXKFALUSA-N
Prescription Products
NameDosageStrengthRouteLabellerMarketing StartMarketing End
XospataTablet40 mg/1OralAstellas Pharma US, Inc.2018-11-29Not applicableUs
Additional Data Available
  • Application Number
    Application Number

    A unique ID assigned by the FDA when a product is submitted for approval by the labeller.

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  • Product Code
    Product Code

    A governmentally-recognized ID which uniquely identifies the product within its regulatory market.

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Categories
UNII
66D92MGC8M
CAS number
1254053-43-4
Weight
Average: 552.724
Monoisotopic: 552.353637309
Chemical Formula
C29H44N8O3
InChI Key
GYQYAJJFPNQOOW-UHFFFAOYSA-N
InChI
InChI=1S/C29H44N8O3/c1-4-23-28(31-20-9-17-40-18-10-20)34-29(26(33-23)27(30)38)32-21-5-6-24(25(19-21)39-3)37-11-7-22(8-12-37)36-15-13-35(2)14-16-36/h5-6,19-20,22H,4,7-18H2,1-3H3,(H2,30,38)(H2,31,32,34)
IUPAC Name
6-ethyl-3-({3-methoxy-4-[4-(4-methylpiperazin-1-yl)piperidin-1-yl]phenyl}amino)-5-[(oxan-4-yl)amino]pyrazine-2-carboxamide
SMILES
CCC1=C(NC2CCOCC2)N=C(NC2=CC=C(N3CCC(CC3)N3CCN(C)CC3)C(OC)=C2)C(=N1)C(N)=O

Pharmacology

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.7

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.8

Associated Conditions
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.5 Another important result in vivo was the localization in high levels in xenografted tumors which indicated high selectivity.6

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.1

In phase III clinical trials, gilteritinib reported a complete remission or complete remission with partial hematologic recovery in 21% of the patients.7

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.2 In the same note, gilteritinib also inhibits AXL and ALK tyrosine kinases.3 FLT3 and AXL are molecules involved in the growth of cancer cells.4 The activity of gilteritinib permits an inhibition of the phosphorylation of FLT3 and its downstream targets such as STAT5, ERK and AKT.6

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.1 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.4

TargetActionsOrganism
AReceptor-type tyrosine-protein kinase FLT3
inhibitor
Humans
NSerotonin Receptors
inhibitor
Humans
ATyrosine-protein kinase receptor UFO
inhibitor
Humans
AALK tyrosine kinase receptor
inhibitor
Humans
Additional Data Available
Adverse Effects

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Additional Data Available
Contraindications

Structured data covering drug contraindications. Each contraindication describes a scenario in which the drug is not to be used. Includes restrictions on co-administration, contraindicated populations, and more.

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Additional Data Available
Blackbox Warnings

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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.6 The steady-state plasma level is reached within 15 days of dosing with an approximate 10-fold bioaccumulation.9

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.10

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.10

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.10

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.11

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.11

Half life

The reported median half-life of gilteritinib was of approximate 45-159 hours.9

Clearance

The estimated clearance of gilteritinib is 14.85 L/h.10

Toxicity

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.Label

Affected organisms
  • Humans
Pathways
Not Available
Pharmacogenomic Effects/ADRs
Not Available

Interactions

Drug Interactions
DrugInteraction
(R)-warfarinThe metabolism of Gilteritinib can be decreased when combined with (R)-warfarin.
(S)-WarfarinThe metabolism of (S)-Warfarin can be decreased when combined with Gilteritinib.
2,5-Dimethoxy-4-ethylthioamphetamineThe therapeutic efficacy of 2,5-Dimethoxy-4-ethylthioamphetamine can be decreased when used in combination with Gilteritinib.
3,5-diiodothyropropionic acidThe therapeutic efficacy of 3,5-diiodothyropropionic acid can be decreased when used in combination with Gilteritinib.
3,5-DiiodotyrosineThe therapeutic efficacy of 3,5-Diiodotyrosine can be decreased when used in combination with Gilteritinib.
4-Bromo-2,5-dimethoxyamphetamineThe therapeutic efficacy of 4-Bromo-2,5-dimethoxyamphetamine can be decreased when used in combination with Gilteritinib.
4-Bromo-2,5-dimethoxyphenethylamineThe therapeutic efficacy of 4-Bromo-2,5-dimethoxyphenethylamine can be decreased when used in combination with Gilteritinib.
4-hydroxycoumarinThe metabolism of 4-hydroxycoumarin can be decreased when combined with Gilteritinib.
5-androstenedioneThe metabolism of Gilteritinib can be decreased when combined with 5-androstenedione.
5-methoxy-N,N-dimethyltryptamineThe therapeutic efficacy of 5-methoxy-N,N-dimethyltryptamine can be decreased when used in combination with Gilteritinib.
Additional Data Available
  • Extended Description
    Extended Description

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  • Severity
    Severity

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  • Evidence Level
    Evidence Level

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  • Action
    Action

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Food Interactions
Not Available

References

General References
  1. Stone RM: 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. [PubMed:30466756]
  2. Fathi AT, Chen YB: The role of FLT3 inhibitors in the treatment of FLT3-mutated acute myeloid leukemia. Eur J Haematol. 2017 Apr;98(4):330-336. doi: 10.1111/ejh.12841. Epub 2017 Jan 19. [PubMed:28000291]
  3. Antar A, Otrock ZK, El-Cheikh J, Kharfan-Dabaja MA, Battipaglia G, Mahfouz R, Mohty M, Bazarbachi A: Inhibition of FLT3 in AML: a focus on sorafenib. Bone Marrow Transplant. 2017 Mar;52(3):344-351. doi: 10.1038/bmt.2016.251. Epub 2016 Oct 24. [PubMed:27775694]
  4. Thom C: Preliminary data on ASP2215: tolerability and efficacy in acute myeloid leukemia patients. Future Oncol. 2015 Sep;11(18):2499-501. doi: 10.2217/fon.15.188. Epub 2015 Aug 17. [PubMed:26279055]
  5. Lee LY, Hernandez D, Rajkhowa T, Smith SC, Raman JR, Nguyen B, Small D, Levis M: Preclinical studies of gilteritinib, a next-generation FLT3 inhibitor. Blood. 2017 Jan 12;129(2):257-260. doi: 10.1182/blood-2016-10-745133. Epub 2016 Dec 1. [PubMed:27908881]
  6. 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 Oct;35(5):556-565. doi: 10.1007/s10637-017-0470-z. Epub 2017 May 17. [PubMed:28516360]
  7. FDA news [Link]
  8. NIH [Link]
  9. American Society of Clinical Oncology [Link]
  10. Clinical trials [Link]
  11. Clinical trials [Link]
External Links
PubChem Compound
49803313
PubChem Substance
347828438
ChemSpider
32055842
BindingDB
144315
ChEMBL
CHEMBL3301622
Wikipedia
AXL_receptor_tyrosine_kinase

Clinical Trials

Clinical Trials
PhaseStatusPurposeConditionsCount
1Active Not RecruitingTreatmentHealthy Volunteers1
1Active Not RecruitingTreatmentLeukemia Acute Myeloid Leukemia (AML)1
1CompletedBasic ScienceHealthy Volunteers / Hepatic Impairment1
1CompletedTreatmentAdvanced Solid Tumors / Pharmacokinetics of 14C-labeled Gilteritinib1
1CompletedTreatmentLeukemia Acute Myeloid Leukemia (AML)1
1RecruitingTreatmentLeukemia Acute Myeloid Leukemia (AML)2
1, 2CompletedTreatmentLeukemia Acute Myeloid Leukemia (AML)1
1, 2Enrolling by InvitationTreatmentAdvanced Solid Tumors / Leukemia Acute Myeloid Leukemia (AML)1
1, 2RecruitingTreatmentAcute Myeloid Leukemia With FMS-like Tyrosine Kinase (FLT3) Mutation / Leukemia Acute Myeloid Leukemia (AML)1
1, 2RecruitingTreatmentPreviously Untreated Acute Myeloid Leukemia1
1, 2TerminatedTreatmentLung Cancer Non-Small Cell Cancer (NSCLC)1
2Active Not RecruitingTreatmentAcute Myeloid Leukemia With FMS-like Tyrosine Kinase (FLT3) / Internal Tandem Duplication (ITD) Mutation / Leukemia Acute Myeloid Leukemia (AML)1
2Not Yet RecruitingTreatmentLeukemia Acute Myeloid Leukemia (AML)1
2, 3RecruitingTreatmentAcute Myeloid Leukemia With FMS-like Tyrosine Kinase (FLT3) Mutation / Leukemia Acute Myeloid Leukemia (AML)1
3Active Not RecruitingTreatmentLeukemia Acute Myeloid Leukemia (AML)1
3RecruitingTreatmentAcute Myeloid Leukemia With FMS-like Tyrosine Kinase (FLT3) Mutation1
3RecruitingTreatmentLeukemia Acute Myeloid Leukemia (AML)1
Not AvailableAvailableNot AvailableFMS-like Tyrosine Kinase-3 (FLT3) Mutations / Leukemia Acute Myeloid Leukemia (AML)1
Not AvailableNo Longer AvailableNot AvailableFMS-like Tyrosine Kinase-3 (FLT3) Mutations / Leukemia Acute Myeloid Leukemia (AML)1
Not AvailableNo Longer AvailableNot AvailableLeukemia Acute Myeloid Leukemia (AML)1

Pharmacoeconomics

Manufacturers
Not Available
Packagers
Not Available
Dosage forms
FormRouteStrength
TabletOral40 mg/1
Prices
Not Available
Patents
Patent NumberPediatric ExtensionApprovedExpires (estimated)
US9487491No2016-11-082030-07-28Us
US8969336No2015-03-032031-01-27Us
Additional Data Available
  • Filed On
    Filed On

    The date on which a patent was filed with the relevant government.

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Properties

State
Solid
Experimental Properties
PropertyValueSource
boiling point (°C)696 ºC at 760 mm Hg'MSDS'
water solubility<1 mg/mL 'MSDS'
logP99'MSDS'
Predicted Properties
PropertyValueSource
Water Solubility0.0223 mg/mLALOGPS
logP3.51ALOGPS
logP2.79ChemAxon
logS-4.4ALOGPS
pKa (Strongest Acidic)14.21ChemAxon
pKa (Strongest Basic)8.47ChemAxon
Physiological Charge1ChemAxon
Hydrogen Acceptor Count10ChemAxon
Hydrogen Donor Count3ChemAxon
Polar Surface Area121.11 Å2ChemAxon
Rotatable Bond Count9ChemAxon
Refractivity159.84 m3·mol-1ChemAxon
Polarizability62.92 Å3ChemAxon
Number of Rings5ChemAxon
Bioavailability1ChemAxon
Rule of FiveNoChemAxon
Ghose FilterNoChemAxon
Veber's RuleNoChemAxon
MDDR-like RuleYesChemAxon
Predicted ADMET features
Not Available

Spectra

Mass Spec (NIST)
Not Available
Spectra
SpectrumSpectrum TypeSplash Key
Predicted MS/MS Spectrum - 10V, Positive (Annotated)Predicted LC-MS/MSNot Available
Predicted MS/MS Spectrum - 20V, Positive (Annotated)Predicted LC-MS/MSNot Available
Predicted MS/MS Spectrum - 40V, Positive (Annotated)Predicted LC-MS/MSNot Available
Predicted MS/MS Spectrum - 10V, Negative (Annotated)Predicted LC-MS/MSNot Available
Predicted MS/MS Spectrum - 20V, Negative (Annotated)Predicted LC-MS/MSNot Available
Predicted MS/MS Spectrum - 40V, Negative (Annotated)Predicted LC-MS/MSNot Available

Taxonomy

Description
This compound belongs to the class of organic compounds known as phenylpiperidines. These are compounds containing a phenylpiperidine skeleton, which consists of a piperidine bound to a phenyl group.
Kingdom
Organic compounds
Super Class
Organoheterocyclic compounds
Class
Piperidines
Sub Class
Phenylpiperidines
Direct Parent
Phenylpiperidines
Alternative Parents
Pyrazinecarboxamides / Aminophenyl ethers / Methoxyanilines / 2-heteroaryl carboxamides / Phenoxy compounds / Anisoles / Methoxybenzenes / Dialkylarylamines / Alkyl aryl ethers / Secondary alkylarylamines
show 15 more
Substituents
Phenylpiperidine / Aminophenyl ether / Pyrazine carboxylic acid or derivatives / Pyrazinecarboxamide / Methoxyaniline / 2-heteroaryl carboxamide / Anisole / Phenoxy compound / Phenol ether / Dialkylarylamine
show 36 more
Molecular Framework
Aromatic heteromonocyclic compounds
External Descriptors
Not Available

Targets

Kind
Protein
Organism
Humans
Pharmacological action
Yes
Actions
Inhibitor
General Function
Vascular endothelial growth factor-activated receptor activity
Specific Function
Tyrosine-protein kinase that acts as cell-surface receptor for the cytokine FLT3LG and regulates differentiation, proliferation and survival of hematopoietic progenitor cells and of dendritic cells...
Gene Name
FLT3
Uniprot ID
P36888
Uniprot Name
Receptor-type tyrosine-protein kinase FLT3
Molecular Weight
112902.51 Da
References
  1. Antar A, Otrock ZK, El-Cheikh J, Kharfan-Dabaja MA, Battipaglia G, Mahfouz R, Mohty M, Bazarbachi A: Inhibition of FLT3 in AML: a focus on sorafenib. Bone Marrow Transplant. 2017 Mar;52(3):344-351. doi: 10.1038/bmt.2016.251. Epub 2016 Oct 24. [PubMed:27775694]
  2. Thom C: Preliminary data on ASP2215: tolerability and efficacy in acute myeloid leukemia patients. Future Oncol. 2015 Sep;11(18):2499-501. doi: 10.2217/fon.15.188. Epub 2015 Aug 17. [PubMed:26279055]
  3. 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 Oct;35(5):556-565. doi: 10.1007/s10637-017-0470-z. Epub 2017 May 17. [PubMed:28516360]
Kind
Protein
Organism
Humans
Pharmacological action
Yes
Actions
Inhibitor
General Function
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, ALX 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. Plays also an important role in inhibition of Toll-like receptors (TLRs)-mediated innate immune response.
Specific Function
Atp binding
Gene Name
AXL
Uniprot ID
P30530
Uniprot Name
Tyrosine-protein kinase receptor UFO
Molecular Weight
98335.965 Da
References
  1. Antar A, Otrock ZK, El-Cheikh J, Kharfan-Dabaja MA, Battipaglia G, Mahfouz R, Mohty M, Bazarbachi A: Inhibition of FLT3 in AML: a focus on sorafenib. Bone Marrow Transplant. 2017 Mar;52(3):344-351. doi: 10.1038/bmt.2016.251. Epub 2016 Oct 24. [PubMed:27775694]
  2. Thom C: Preliminary data on ASP2215: tolerability and efficacy in acute myeloid leukemia patients. Future Oncol. 2015 Sep;11(18):2499-501. doi: 10.2217/fon.15.188. Epub 2015 Aug 17. [PubMed:26279055]
  3. 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 Oct;35(5):556-565. doi: 10.1007/s10637-017-0470-z. Epub 2017 May 17. [PubMed:28516360]
Kind
Protein
Organism
Humans
Pharmacological action
Yes
Actions
Inhibitor
General Function
Transmembrane receptor protein tyrosine kinase activity
Specific Function
Neuronal orphan 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 a...
Gene Name
ALK
Uniprot ID
Q9UM73
Uniprot Name
ALK tyrosine kinase receptor
Molecular Weight
176440.535 Da
References
  1. Antar A, Otrock ZK, El-Cheikh J, Kharfan-Dabaja MA, Battipaglia G, Mahfouz R, Mohty M, Bazarbachi A: Inhibition of FLT3 in AML: a focus on sorafenib. Bone Marrow Transplant. 2017 Mar;52(3):344-351. doi: 10.1038/bmt.2016.251. Epub 2016 Oct 24. [PubMed:27775694]
  2. Thom C: Preliminary data on ASP2215: tolerability and efficacy in acute myeloid leukemia patients. Future Oncol. 2015 Sep;11(18):2499-501. doi: 10.2217/fon.15.188. Epub 2015 Aug 17. [PubMed:26279055]
  3. 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 Oct;35(5):556-565. doi: 10.1007/s10637-017-0470-z. Epub 2017 May 17. [PubMed:28516360]

Enzymes

Kind
Protein
Organism
Humans
Pharmacological action
No
Actions
Substrate
General Function
Vitamin d3 25-hydroxylase activity
Specific Function
Cytochromes P450 are a group of heme-thiolate monooxygenases. In liver microsomes, this enzyme is involved in an NADPH-dependent electron transport pathway. It performs a variety of oxidation react...
Gene Name
CYP3A4
Uniprot ID
P08684
Uniprot Name
Cytochrome P450 3A4
Molecular Weight
57342.67 Da
References
  1. Clinical trials [Link]

Carriers

Kind
Protein
Organism
Humans
Pharmacological action
No
Actions
Binder
General Function
Toxic substance binding
Specific Function
Serum albumin, the main protein of plasma, has a good binding capacity for water, Ca(2+), Na(+), K(+), fatty acids, hormones, bilirubin and drugs. Its main function is the regulation of the colloid...
Gene Name
ALB
Uniprot ID
P02768
Uniprot Name
Serum albumin
Molecular Weight
69365.94 Da
References
  1. Clinical trials [Link]

Transporters

Kind
Protein
Organism
Humans
Pharmacological action
No
Actions
Substrate
General Function
Xenobiotic-transporting atpase activity
Specific Function
Energy-dependent efflux pump responsible for decreased drug accumulation in multidrug-resistant cells.
Gene Name
ABCB1
Uniprot ID
P08183
Uniprot Name
Multidrug resistance protein 1
Molecular Weight
141477.255 Da
Kind
Protein
Organism
Humans
Pharmacological action
No
Actions
Inhibitor
General Function
Monovalent cation:proton antiporter activity
Specific Function
Solute transporter for tetraethylammonium (TEA), 1-methyl-4-phenylpyridinium (MPP), cimetidine, N-methylnicotinamide (NMN), metformin, creatinine, guanidine, procainamide, topotecan, estrone sulfat...
Gene Name
SLC47A1
Uniprot ID
Q96FL8
Uniprot Name
Multidrug and toxin extrusion protein 1
Molecular Weight
61921.585 Da
Kind
Protein
Organism
Humans
Pharmacological action
No
Actions
Inhibitor
General Function
Xenobiotic-transporting atpase activity
Specific Function
High-capacity urate exporter functioning in both renal and extrarenal urate excretion. Plays a role in porphyrin homeostasis as it is able to mediates the export of protoporhyrin IX (PPIX) both fro...
Gene Name
ABCG2
Uniprot ID
Q9UNQ0
Uniprot Name
ATP-binding cassette sub-family G member 2
Molecular Weight
72313.47 Da
Kind
Protein
Organism
Humans
Pharmacological action
No
Actions
Inhibitor
General Function
Secondary active organic cation transmembrane transporter activity
Specific Function
Translocates a broad array of organic cations with various structures and molecular weights including the model compounds 1-methyl-4-phenylpyridinium (MPP), tetraethylammonium (TEA), N-1-methylnico...
Gene Name
SLC22A1
Uniprot ID
O15245
Uniprot Name
Solute carrier family 22 member 1
Molecular Weight
61153.345 Da

Drug created on October 20, 2016 15:26 / Updated on July 13, 2019 00:58