Afatinib
Identification
- 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
Structure for Afatinib (DB08916)
- Weight
- Average: 485.938
Monoisotopic: 485.162995603 - Chemical Formula
- C24H25ClFN5O3
- Synonyms
- Afatinib
- Afatinibum
- External IDs
- BIBW 2992
- BIBW-2992
- BIBW2992
Pharmacology
- 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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- Contraindications & Blackbox Warnings
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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.
Target Actions Organism AEpidermal growth factor receptor inhibitorHumans AReceptor tyrosine-protein kinase erbB-2 inhibitorHumans AReceptor tyrosine-protein kinase erbB-4 inhibitorHumans - 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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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
Interacting Gene/Enzyme Allele name Genotype(s) Defining Change(s) Type(s) Description Details Epidermal growth factor receptor L861Q (A;A) / (A;T) / (G;G) / (G;T) T > A or G Effect Directly Studied The presence of this polymorphism in EGFR is associated with a higher response rate to afatinib. Details Epidermal growth factor receptor L858R (G;G) / (G;T) T > G Effect Directly Studied The presence of this polymorphism in EGFR is associated with a higher response rate to afatinib. Details Epidermal growth factor receptor G719A/C (T;T) / (G;T) / (A;A) / (A;G) / (C;C) / (C;G) G > A or C or T Effect Directly Studied The presence of this polymorphism in EGFR is associated with a higher response rate to afatinib. Details
Interactions
- 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.
Drug Interaction Integrate drug-drug
interactions in your softwareAbaloparatide The therapeutic efficacy of Abaloparatide can be decreased when used in combination with Afatinib. Abemaciclib The serum concentration of Abemaciclib can be increased when it is combined with Afatinib. Acetaminophen The serum concentration of Acetaminophen can be increased when it is combined with Afatinib. Alectinib Alectinib may decrease the excretion rate of Afatinib which could result in a higher serum level. Allopurinol Afatinib may decrease the excretion rate of Allopurinol which could result in a higher serum level. Alpelisib The serum concentration of Alpelisib can be increased when it is combined with Afatinib. Ambrisentan The serum concentration of Ambrisentan can be increased when it is combined with Afatinib. Amiodarone The serum concentration of Afatinib can be increased when it is combined with Amiodarone. Apalutamide The serum concentration of Afatinib can be decreased when it is combined with Apalutamide. Apixaban Afatinib may decrease the excretion rate of Apixaban which could result in a higher serum level. 
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- Take separate from meals. Take at least one hour before or two hours after a meal.
Products
Drug product information from 10+ global regionsOur datasets provide approved product information including:dosage, form, labeller, route of administration, and marketing period.Access drug product information from over 10 global regions.- Product Ingredients
Ingredient UNII CAS InChI Key Afatinib dimaleate V1T5K7RZ0B 850140-73-7 USNRYVNRPYXCSP-JUGPPOIOSA-N - Brand Name Prescription Products
Name Dosage Strength Route Labeller Marketing Start Marketing End Region Image Gilotrif Tablet, film coated 30 mg/1 Oral Boehringer Ingelheim Pharmaceuticals, Inc. 2013-07-12 Not applicable US 
Gilotrif Tablet, film coated 20 mg/1 Oral Boehringer Ingelheim Pharmaceuticals, Inc. 2013-07-12 Not applicable US Gilotrif Tablet, film coated 40 mg/1 Oral Boehringer Ingelheim Pharmaceuticals, Inc. 2013-07-12 Not applicable US Giotrif Tablet, film coated 30 mg Oral Boehringer Ingelheim 2020-12-16 Not applicable EU 
Giotrif Tablet, film coated 40 mg Oral Boehringer Ingelheim 2020-12-16 Not applicable EU Giotrif Tablet 30 mg Oral Boehringer Ingelheim (Canada) Ltd Ltee 2014-01-17 Not applicable Canada 
Giotrif Tablet, film coated 20 mg Oral Boehringer Ingelheim 2020-12-16 Not applicable EU Giotrif Tablet, film coated 30 mg Oral Boehringer Ingelheim 2020-12-16 Not applicable EU Giotrif Tablet, film coated 50 mg Oral Boehringer Ingelheim 2020-12-16 Not applicable EU Giotrif Tablet, film coated 20 mg Oral Boehringer Ingelheim 2020-12-16 Not applicable EU
Categories
- ATC Codes
- L01XE13 — Afatinib
- Drug Categories
- Amides
- Antineoplastic Agents
- Antineoplastic and Immunomodulating Agents
- BCRP/ABCG2 Inhibitors
- BCRP/ABCG2 Substrates
- Enzyme 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 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 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
Chemical Identifiers
- 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
References
- General References
- 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]
- 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]
- Electronic Medicines Compendium: Giotrif 30 mg film-coated tablets Monograph [Link]
- 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
- 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
- Download (427 KB)
- MSDS
- Download (26.7 KB)
Clinical Trials
- Clinical Trials
Phase Status Purpose Conditions Count 4 Completed Treatment ErbB Receptors / Non-Small Cell Lung Carcinoma (NSCLC) 1 4 Completed Treatment Non-Small Cell Lung Carcinoma (NSCLC) 1 4 Not Yet Recruiting Treatment NRG1-fused Non-small Cell Lung Cancer 1 4 Recruiting Treatment Non-squamous Non-small-cell Lung Cancer (NSQ NSCLC) 1 4 Recruiting Treatment Squamous Cell Lung Carcinoma 1 4 Terminated Treatment ErbB Receptors / Non-Small Cell Lung Carcinoma (NSCLC) 1 3 Active Not Recruiting Treatment Neoplasms, Head and Neck 1 3 Active Not Recruiting Treatment Non-Small Cell Lung Carcinoma (NSCLC) 1 3 Completed Treatment Adenocarcinomas / Non-Small Cell Lung Carcinoma (NSCLC) 2 3 Completed Treatment Neoplasms, Breast 1
Pharmacoeconomics
- Manufacturers
- Not Available
- Packagers
- Not Available
- Dosage Forms
Form Route Strength Tablet, film coated Oral 20 mg/1 Tablet, film coated Oral 30 mg/1 Tablet, film coated Oral 40 mg/1 Tablet Oral 20 mg Tablet Oral 30 mg Tablet Oral 40 mg Tablet, film coated Oral Tablet, film coated Oral 20 MG Tablet, film coated Oral 30 MG Tablet, film coated Oral 40 MG Tablet, film coated Oral 50 MG Tablet, film coated Oral 20.0000 mg Tablet, film coated Oral 30.0000 mg Tablet, film coated Oral 40.0000 mg Tablet, film coated Oral 50.0000 mg Tablet, coated Oral 40 mg Tablet, coated Oral 50 mg Tablet, coated Oral 20 mg Tablet, coated Oral 30 mg - Prices
- Not Available
- Patents
Patent Number Pediatric Extension Approved Expires (estimated) Region US6251912 No 2001-06-26 2018-07-29 US US8426586 No 2013-04-23 2029-10-10 US USRE43431 No 2012-05-29 2022-01-22 US US8545884 No 2013-10-01 2029-12-19 US US9539258 No 2017-01-10 2026-11-09 US US10004743 No 2018-06-26 2030-07-05 US
Properties
- State
- Solid
- Experimental Properties
- Not Available
- Predicted Properties
Property Value Source Water Solubility 0.0128 mg/mL ALOGPS logP 3.77 ALOGPS logP 3.76 ChemAxon logS -4.6 ALOGPS pKa (Strongest Acidic) 12.49 ChemAxon pKa (Strongest Basic) 8.81 ChemAxon Physiological Charge 1 ChemAxon Hydrogen Acceptor Count 7 ChemAxon Hydrogen Donor Count 2 ChemAxon Polar Surface Area 88.61 Å2 ChemAxon Rotatable Bond Count 8 ChemAxon Refractivity 131.38 m3·mol-1 ChemAxon Polarizability 50.07 Å3 ChemAxon Number of Rings 4 ChemAxon Bioavailability 1 ChemAxon Rule of Five Yes ChemAxon Ghose Filter No ChemAxon Veber's Rule No ChemAxon MDDR-like Rule Yes ChemAxon - Predicted ADMET Features
Property Value Probability Human Intestinal Absorption + 1.0 Blood Brain Barrier + 0.8717 Caco-2 permeable - 0.5342 P-glycoprotein substrate Substrate 0.744 P-glycoprotein inhibitor I Inhibitor 0.6776 P-glycoprotein inhibitor II Inhibitor 0.9036 Renal organic cation transporter Non-inhibitor 0.7154 CYP450 2C9 substrate Non-substrate 0.7919 CYP450 2D6 substrate Non-substrate 0.8034 CYP450 3A4 substrate Substrate 0.7504 CYP450 1A2 substrate Non-inhibitor 0.5236 CYP450 2C9 inhibitor Non-inhibitor 0.7294 CYP450 2D6 inhibitor Non-inhibitor 0.7625 CYP450 2C19 inhibitor Non-inhibitor 0.5877 CYP450 3A4 inhibitor Non-inhibitor 0.6486 CYP450 inhibitory promiscuity High CYP Inhibitory Promiscuity 0.7096 Ames test Non AMES toxic 0.5695 Carcinogenicity Non-carcinogens 0.8692 Biodegradation Not ready biodegradable 1.0 Rat acute toxicity 2.5643 LD50, mol/kg Not applicable hERG inhibition (predictor I) Weak inhibitor 0.8956 hERG inhibition (predictor II) Inhibitor 0.7228
Spectra
- Mass Spec (NIST)
- Not Available
- Spectra
Spectrum Spectrum Type Splash Key Predicted MS/MS Spectrum - 10V, Positive (Annotated) Predicted LC-MS/MS Not Available Predicted MS/MS Spectrum - 20V, Positive (Annotated) Predicted LC-MS/MS Not Available Predicted MS/MS Spectrum - 40V, Positive (Annotated) Predicted LC-MS/MS Not Available Predicted MS/MS Spectrum - 10V, Negative (Annotated) Predicted LC-MS/MS Not Available Predicted MS/MS Spectrum - 20V, Negative (Annotated) Predicted LC-MS/MS Not Available Predicted MS/MS Spectrum - 40V, Negative (Annotated) Predicted LC-MS/MS Not Available
Targets
- Kind
- Protein
- Organism
- Humans
- Pharmacological action
- Yes
- Actions
- Inhibitor
- General Function
- Ubiquitin protein ligase binding
- Specific Function
- Receptor tyrosine kinase binding ligands of the EGF family and activating several signaling cascades to convert extracellular cues into appropriate cellular responses. Known ligands include EGF, TG...
- Gene Name
- EGFR
- Uniprot ID
- P00533
- Uniprot Name
- Epidermal growth factor receptor
- Molecular Weight
- 134276.185 Da
References
- 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]
- 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]
- Kind
- Protein
- Organism
- Humans
- Pharmacological action
- Yes
- Actions
- Inhibitor
- General Function
- Transmembrane signaling receptor activity
- Specific 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, alt...
- Gene Name
- ERBB2
- Uniprot ID
- P04626
- Uniprot Name
- Receptor tyrosine-protein kinase erbB-2
- Molecular Weight
- 137909.27 Da
- Kind
- Protein
- Organism
- Humans
- Pharmacological action
- Yes
- Actions
- Inhibitor
- General Function
- Transmembrane receptor protein tyrosine kinase activity
- Specific 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 mamma...
- Gene Name
- ERBB4
- Uniprot ID
- Q15303
- Uniprot Name
- Receptor tyrosine-protein kinase erbB-4
- Molecular Weight
- 146806.865 Da
Transporters
- Kind
- Protein
- Organism
- Humans
- Pharmacological action
- Unknown
- Actions
- SubstrateInhibitor
- 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
- Unknown
- Actions
- SubstrateInhibitor
- 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
Drug created on July 17, 2013 21:59 / Updated on October 18, 2021 04:55