Afatinib (original) (raw)

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Description

An anticancer medication used to treat certain types of cancers in the lungs.

Description

An anticancer medication used to treat certain types of cancers in the lungs.

DrugBank ID

DB08916

Type

Small Molecule

US Approved

YES

Other Approved

YES

Therapeutic Categories

• Kinase Inhibitor

Summary

Afatinib is an antineoplastic agent used for the treatment of locally advanced or metastatic non-small cell lung cancer (NSCLC) with non-resistant EGFR mutations or resistance to platinum-based chemotherapy.

Brand Names

Gilotrif, Giotrif

Generic Name

Afatinib

DrugBank Accession Number

DB08916

Background

Afatinib is a 4-anilinoquinazoline tyrosine kinase inhibitor in the form of a dimaleate salt available as Boehringer Ingelheim's brand name Gilotrif Label. For oral use, afatinib tablets are a first-line (initial) treatment for patients with metastatic non-small cell lung cancer (NSCLC) with common epidermal growth factor receptor (EGFR) mutations as detected by an FDA-approved test 4. Gilotrif (afatinib) is the first FDA-approved oncology product from Boehringer Ingelheim 4.

Type

Small Molecule

Groups

Approved

Structure

Weight

Average: 485.938
Monoisotopic: 485.162995603

Chemical Formula

C24H25ClFN5O3

Synonyms

• Afatinib
• Afatinibum

External IDs

• BIBW 2992
• BIBW-2992
• BIBW2992

Indication

Afatinib is a kinase inhibitor indicated as monotherapy 3 for the first-line Label treatment of (a) Epidermal Growth Factor Receptor (EGFR) TKI (tyrosine kinase inhibitor)-naive adult patients with locally advanced or metastatic non-small cell lung cancer (NSCLC) whose tumours have non-resistant EGFR mutations as detected by an FDA-approved test Label, and (b) adult patients with locally advanced or metastatic NSCLC of squamous histology progressing on or after platinum-based chemotherapy Label,3.

Recently, as of January 2018, the US FDA approved a supplemental New Drug Application for Boehringer Ingelheim's Gilotrif (afatinib) for the first line treatment of patients with metastatic non-small cell lung cancer (NSCLC) whose tumors have non-resistant epidermal growth factor receptor (EGFR) mutations as detected by an FDA-approved test 4. The new label includes data on three additional EGFR mutations: L861Q, G719X and S768I 4.

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Associated Conditions

Contraindications & Blackbox Warnings

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Pharmacodynamics

Aberrant ErbB signaling triggered by receptor mutations, and/or amplification, and/or receptor ligand overexpression contributes to the malignant phenotype 3. Mutation in EGFR defines a distinct molecular subtype of lung cancer 3.

In non-clinical disease models with ErbB pathway deregulation, afatinib as a single agent effectively blocks ErbB receptor signaling resulting in tumor growth inhibition or tumor regression 3. NSCLC tumors with common activating EGFR mutations (Del 19, L858R) and several less common EGFR mutations in exon 18 (G719X) and exon 21 (L861Q) are particularly sensitive to afatinib treatment in non-clinical and clinical settings 3. Limited non-clinical and/or clinical activity was observed in NSCLC tumors with insertion mutations in exon 20 3.

The acquisition of a secondary T790M mutation is a major mechanism of acquired resistance to afatinib and gene dosage of the T790M-containing allele correlates with the degree of resistance in vitro 3. The T790M mutation is found in approximately 50% of patients' tumors upon disease progression on afatinib, for which T790M targeted EGFR TKIs may be considered as a next line treatment option 3. Other potential mechanisms of resistance to afatinib have been suggested preclinically and MET gene amplification has been observed clinically 3.

At the same time, the effect of multiple doses of afatinib (50 mg once daily) on cardiac electrophysiology and the QTc interval was evaluated in an open-label, single-arm study in patients with relapsed or refractory solid tumors Label. Ultimately, no large changes in the mean QTc interval (i.e., >20 ms) were detected in the study Label.

Mechanism of action

Afatinib is a potent and selective, irreversible ErbB family blocker 3. Afatinib covalently binds to and irreversibly blocks signaling from all homo and heterodimers formed by the ErbB family members EGFR (ErbB1), HER2 (ErbB2), ErbB3 and ErbB4 3.

In particular, afatinib covalently binds to the kinase domains of EGFR (ErbB1), HER2 (ErbB2), and HER4 (ErbB4) and irreversibly inhibits tyrosine kinase autophosphorylation, resulting in downregulation of ErbB signaling Label. Certain mutations in EGFR, including non-resistant mutations in its kinase domain, can result in increased autophosphorylation of the receptor, leading to receptor activation, sometimes in the absence of ligand binding, and can support cell proliferation in NSCLC Label. Non-resistant mutations are defined as those occurring in exons constituting the kinase domain of EGFR that lead to increased receptor activation and where efficacy is predicted by 1) clinically meaningful tumor shrinkage with the recommended dose of afatinib and/or 2) inhibition of cellular proliferation or EGFR tyrosine kinase phosphorylation at concentrations of afatinib sustainable at the recommended dosage according to validated methods Label. The most commonly found of these mutations are exon 21 L858R substitutions and exon 19 deletions Label.

Moreover, afatinib demonstrated inhibition of autophosphorylation and/or in vitro proliferation of cell lines expressing wild-type EGFR and in those expressing selected EGFR exon 19 deletion mutations, exon 21 L858R mutations, or other less common non-resistant mutations, at afatinib concentrations achieved in patients Label. In addition, afatinib inhibited in vitro proliferation of cell lines overexpressing HER2 Label.

Absorption

Following oral administration, time to peak plasma concentration (Tmax) is 2 to 5 hours Label. Maximum concentration (Cmax) and area under the concentration-time curve from time zero to infinity (AUC0-∞) values increased slightly more than dose proportional in the range of 20 to 50 mg Label. The geometric mean relative bioavailability of 20 mg tablets was 92% as compared to an oral solution Label.

Additionally, systemic exposure to afatinib is decreased by 50% (Cmax) and 39% (AUC0-∞), when administered with a high-fat meal compared to administration in the fasted state 3. Based on population pharmacokinetic data derived from clinical trials in various tumor types, an average decrease of 26% in AUCss was observed when food was consumed within 3 hours before or 1 hour after taking afatinib 3.

Volume of distribution

The volume of distribution of afatinib recorded in healthy male volunteers is documented as 4500 L 2. Such a high volume of distribution in plasma suggests a potentially high tissue distribution 2.

Protein binding

In vitro binding of afatinib to human plasma proteins is approximately 95% 3. Afatinib binds to proteins both non-covalently (traditional protein binding) and covalently 3.

Metabolism

Enzyme-catalyzed metabolic reactions play a negligible role for afatinib in vivo 3. Covalent adducts to proteins were the major circulating metabolites of afatinib 3.

Route of elimination

In humans, excretion of afatinib is primarily via the feces 3. Following administration of an oral solution of 15 mg afatinib, 85.4% of the dose was recovered in the feces and 4.3% in urine 3. The parent compound afatinib accounted for 88% of the recovered dose 3.

Half-life

Afatinib is eliminated with an effective half-life of approximately 37 hours 3. Thus, steady-state plasma concentrations of afatinib were achieved within 8 days of multiple dosing of afatinib resulting in an accumulation of 2.77-fold (AUC0-∞) and 2.11-fold (Cmax) 3. In patients treated with afatinib for more than 6 months, a terminal half-life of 344 h was estimated 3.

Clearance

The apparent total body clearance of afatinib as recorded in healthy male volunteers is documented as being a high geometric mean of 1530 mL/min 2.

Adverse Effects

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Toxicity

Most common adverse reactions (≥20%) are diarrhea, rash/dermatitis, acneiform, stomatitis, paronychia, dry skin, decreased appetite, pruritus Label.

Conversely, overdose in 2 healthy adolescents involving the ingestion of 360 mg each of afatinib (as part of a mixed drug ingestion) was associated with adverse events of nausea, vomiting, asthenia, dizziness, headache, abdominal pain and elevated amylase (< 1.5 times ULN) 3. Both individuals recovered from these adverse events 3.

Pathways

Not Available

Pharmacogenomic Effects/ADRs

Drug Interactions

This information should not be interpreted without the help of a healthcare provider. If you believe you are experiencing an interaction, contact a healthcare provider immediately. The absence of an interaction does not necessarily mean no interactions exist.

• Approved
• Vet approved
• Nutraceutical
• Illicit
• Withdrawn
• Investigational
• Experimental
• All Drugs

Food Interactions

• Take separate from meals. Take at least one hour before or two hours after a meal.

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Product Ingredients

Brand Name Prescription Products

Generic Prescription Products

ATC Codes

L01EB03 — Afatinib

• L01EB — Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors
• L01E — PROTEIN KINASE INHIBITORS
• L01 — ANTINEOPLASTIC AGENTS
• L — ANTINEOPLASTIC AND IMMUNOMODULATING AGENTS

Drug Categories

• Amides
• Antineoplastic Agents
• Antineoplastic and Immunomodulating Agents
• BCRP/ABCG2 Inhibitors
• BCRP/ABCG2 Substrates
• Enzyme Inhibitors
• Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors
• Heterocyclic Compounds, Fused-Ring
• Kinase Inhibitor
• P-glycoprotein inhibitors
• P-glycoprotein substrates
• Protein Kinase Inhibitors
• Quinazolines
• Tyrosine Kinase Inhibitors

Chemical TaxonomyProvided by Classyfire

Description

This compound belongs to the class of organic compounds known as quinazolinamines. These are heterocyclic aromatic compounds containing a quianazoline moiety substituted by one or more amine groups.

Kingdom

Organic compounds

Super Class

Organoheterocyclic compounds

Class

Diazanaphthalenes

Sub Class

Benzodiazines

Direct Parent

Quinazolinamines

Alternative Parents

N-arylamides / Aniline and substituted anilines / Chlorobenzenes / Fluorobenzenes / Aminopyrimidines and derivatives / Alkyl aryl ethers / Imidolactams / Aryl chlorides / Aryl fluorides / Tetrahydrofurans / Heteroaromatic compounds / Amino acids and derivatives / Trialkylamines / Secondary carboxylic acid amides / Azacyclic compounds / Dialkyl ethers / Oxacyclic compounds / Secondary amines / Carbonyl compounds / Hydrocarbon derivatives / Organic oxides / Organochlorides / Organofluorides / Organopnictogen compounds show 14 more

Substituents

Alkyl aryl ether / Amine / Amino acid or derivatives / Aminopyrimidine / Aniline or substituted anilines / Aromatic heteropolycyclic compound / Aryl chloride / Aryl fluoride / Aryl halide / Azacycle / Benzenoid / Carbonyl group / Carboxamide group / Carboxylic acid derivative / Chlorobenzene / Dialkyl ether / Ether / Fluorobenzene / Halobenzene / Heteroaromatic compound / Hydrocarbon derivative / Imidolactam / Monocyclic benzene moiety / N-arylamide / Organic nitrogen compound / Organic oxide / Organic oxygen compound / Organochloride / Organofluoride / Organohalogen compound / Organonitrogen compound / Organooxygen compound / Organopnictogen compound / Oxacycle / Pyrimidine / Quinazolinamine / Secondary amine / Secondary carboxylic acid amide / Tertiary aliphatic amine / Tertiary amine / Tetrahydrofuran show 31 more

Molecular Framework

Aromatic heteropolycyclic compounds

External Descriptors

organofluorine compound, tertiary amino compound, aromatic ether, enamide, furans, monochlorobenzenes, quinazolines (CHEBI:61390)

Affected organisms

• Humans and other mammals

UNII

41UD74L59M

CAS number

850140-72-6

InChI Key

ULXXDDBFHOBEHA-CWDCEQMOSA-N

InChI

InChI=1S/C24H25ClFN5O3/c1-31(2)8-3-4-23(32)30-21-11-17-20(12-22(21)34-16-7-9-33-13-16)27-14-28-24(17)29-15-5-6-19(26)18(25)10-15/h3-6,10-12,14,16H,7-9,13H2,1-2H3,(H,30,32)(H,27,28,29)/b4-3+/t16-/m0/s1

IUPAC Name

(2E)-N-{4-[(3-chloro-4-fluorophenyl)amino]-7-[(3S)-oxolan-3-yloxy]quinazolin-6-yl}-4-(dimethylamino)but-2-enamide

SMILES

CN(C)C\C=C\C(=O)NC1=C(O[C@H]2CCOC2)C=C2N=CN=C(NC3=CC(Cl)=C(F)C=C3)C2=C1

General References

1. Wind S, Schnell D, Ebner T, Freiwald M, Stopfer P: Clinical Pharmacokinetics and Pharmacodynamics of Afatinib. Clin Pharmacokinet. 2017 Mar;56(3):235-250. doi: 10.1007/s40262-016-0440-1. [Article]
2. Stopfer P, Marzin K, Narjes H, Gansser D, Shahidi M, Uttereuther-Fischer M, Ebner T: Afatinib pharmacokinetics and metabolism after oral administration to healthy male volunteers. Cancer Chemother Pharmacol. 2012 Apr;69(4):1051-61. doi: 10.1007/s00280-011-1803-9. Epub 2011 Dec 27. [Article]
3. Electronic Medicines Compendium: Giotrif 30 mg film-coated tablets Monograph [Link]
4. Boehringer Ingelheim: FDA approves new indication for Gilotrif® in EGFR mutation-positive NSCLC [Link]

External Links

KEGG Drug

D09724

PubChem Compound

10184653

PubChem Substance

175427153

ChemSpider

8360155

BindingDB

50322823

RxNav

1430438

ChEBI

61390

ChEMBL

CHEMBL1173655

ZINC

ZINC000003976838

PharmGKB

PA165981154

PDBe Ligand

0WM

Drugs.com

Drugs.com Drug Page

Wikipedia

Afatinib

PDB Entries

4g5j

FDA label

MSDS

Clinical Trials

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Preview package

Manufacturers

Not Available

Packagers

Not Available

Dosage Forms

Prices

Not Available

Patents

Patent Number	Pediatric Extension	Approved	Expires (estimated)	Region
US6251912	No	2001-06-26	2018-07-29
US8426586	Yes	2013-04-23	2030-04-10
USRE43431	Yes	2012-05-29	2026-07-13
US8545884	Yes	2013-10-01	2030-06-19
US9539258	Yes	2017-01-10	2027-05-09
US10004743	Yes	2018-06-26	2031-01-05

State

Solid

Experimental Properties

Not Available

Predicted Properties

Predicted ADMET Features

ADMET data is predicted using admetSAR, a free tool for evaluating chemical ADMET properties. (23092397)

Mass Spec (NIST)

Not Available

Spectra

Chromatographic Properties

Collision Cross Sections (CCS)

Targets

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Kind

Protein

Organism

Humans

Pharmacological action

Yes

Actions

Inhibitor

General Function

Receptor tyrosine kinase binding ligands of the EGF family and activating several signaling cascades to convert extracellular cues into appropriate cellular responses (PubMed:10805725, PubMed:27153536, PubMed:2790960, PubMed:35538033). Known ligands include EGF, TGFA/TGF-alpha, AREG, epigen/EPGN, BTC/betacellulin, epiregulin/EREG and HBEGF/heparin-binding EGF (PubMed:12297049, PubMed:15611079, PubMed:17909029, PubMed:20837704, PubMed:27153536, PubMed:2790960, PubMed:7679104, PubMed:8144591, PubMed: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 (PubMed:27153536). May also activate the NF-kappa-B signaling cascade (PubMed: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 (PubMed:11602604). Also phosphorylates MUC1 and increases its interaction with SRC and CTNNB1/beta-catenin (PubMed: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 (PubMed:20462955). Plays a role in enhancing learning and memory performance (By similarity). Plays a role in mammalian pain signaling (long-lasting hypersensitivity) (By similarity)

Specific Function

actin filament binding

Gene Name

EGFR

Uniprot ID

P00533

Uniprot Name

Epidermal growth factor receptor

Molecular Weight

134276.185 Da

References

1. Masood A, Kancha RK, Subramanian J: Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors in non-small cell lung cancer harboring uncommon EGFR mutations: Focus on afatinib. Semin Oncol. 2019 Jun;46(3):271-283. doi: 10.1053/j.seminoncol.2019.08.004. Epub 2019 Sep 11. [Article]
2. Vasconcelos PENS, Gergis C, Viray H, Varkaris A, Fujii M, Rangachari D, VanderLaan PA, Kobayashi IS, Kobayashi SS, Costa DB: EGFR-A763_Y764insFQEA Is a Unique Exon 20 Insertion Mutation That Displays Sensitivity to Approved and In-Development Lung Cancer EGFR Tyrosine Kinase Inhibitors. JTO Clin Res Rep. 2020 Sep;1(3). doi: 10.1016/j.jtocrr.2020.100051. Epub 2020 May 13. [Article]
3. Zhou Y, Zhang Y, Zhao D, Yu X, Shen X, Zhou Y, Wang S, Qiu Y, Chen Y, Zhu F: TTD: Therapeutic Target Database describing target druggability information. Nucleic Acids Res. 2024 Jan 5;52(D1):D1465-D1477. doi: 10.1093/nar/gkad751. [Article]

Kind

Protein

Organism

Humans

Pharmacological action

Yes

Actions

Inhibitor

General Function

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

Specific Function

ATP binding

Gene Name

ERBB2

Uniprot ID

P04626

Uniprot Name

Receptor tyrosine-protein kinase erbB-2

Molecular Weight

137909.27 Da

References

1. Zhou Y, Zhang Y, Zhao D, Yu X, Shen X, Zhou Y, Wang S, Qiu Y, Chen Y, Zhu F: TTD: Therapeutic Target Database describing target druggability information. Nucleic Acids Res. 2024 Jan 5;52(D1):D1465-D1477. doi: 10.1093/nar/gkad751. [Article]

Kind

Protein

Organism

Humans

Pharmacological action

Yes

Actions

Inhibitor

General Function

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

Specific Function

ATP binding

Gene Name

ERBB4

Uniprot ID

Q15303

Uniprot Name

Receptor tyrosine-protein kinase erbB-4

Molecular Weight

146806.865 Da

References

1. FDA Approved Drug Products: GILOTRIF™ (afatinib) tablets, for oral use [Link]

Transporters

Kind

Protein

Organism

Humans

Pharmacological action

Unknown

Actions

Substrate

Inhibitor

General Function

Translocates drugs and phospholipids across the membrane (PubMed:2897240, PubMed:35970996, PubMed:8898203, PubMed:9038218). 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 (PubMed:8898203). Energy-dependent efflux pump responsible for decreased drug accumulation in multidrug-resistant cells (PubMed:2897240, PubMed:35970996, PubMed:9038218)

Specific Function

ABC-type xenobiotic transporter activity

Gene Name

ABCB1

Uniprot ID

P08183

Uniprot Name

ATP-dependent translocase ABCB1

Molecular Weight

141477.255 Da

Kind

Protein

Organism

Humans

Pharmacological action

Unknown

Actions

Substrate

Inhibitor

General Function

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 (PubMed:11306452, PubMed:12958161, PubMed:19506252, PubMed:20705604, PubMed:28554189, PubMed:30405239, PubMed: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 (PubMed:20705604, PubMed:23189181). Also mediates the efflux of sphingosine-1-P from cells (PubMed:20110355). Acts as a urate exporter functioning in both renal and extrarenal urate excretion (PubMed:19506252, PubMed:20368174, PubMed:22132962, PubMed:31003562, PubMed: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 (PubMed:12682043, PubMed:28554189, PubMed: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 (PubMed:11306452, PubMed:12477054, PubMed:15670731, PubMed:18056989, PubMed: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)

Specific Function

ABC-type xenobiotic transporter activity

Gene Name

ABCG2

Uniprot ID

Q9UNQ0

Uniprot Name

Broad substrate specificity ATP-binding cassette transporter ABCG2

Molecular Weight

72313.47 Da

Drug created at July 17, 2013 21:59 / Updated at November 11, 2024 11:15