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
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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Associated Conditions
Indication TypeIndicationCombined Product DetailsApproval LevelAge GroupPatient CharacteristicsDose Form
Treatment ofMetastatic non-small cell lung cancer••••••••••••
Treatment ofMetastatic non-small cell lung cancer•••••••••••••••• •••• •• ••••••••
Treatment ofRefractory, metastatic squamous cell non-small cell lung cancer••••••••••••
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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.

TargetActionsOrganism
AEpidermal growth factor receptor
inhibitor
Humans
AReceptor tyrosine-protein kinase erbB-2
inhibitor
Humans
AReceptor tyrosine-protein kinase erbB-4
inhibitor
Humans
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 Browse all" title="About SNP Mediated Effects/ADRs" id="snp-actions-info" class="drug-info-popup" href="javascript:void(0);">
Interacting Gene/EnzymeAllele nameGenotype(s)Defining Change(s)Type(s)DescriptionDetails
Epidermal growth factor receptorL861Q(A;A) / (A;T) / (G;G) / (G;T)T > A or GEffect Directly StudiedThe presence of this polymorphism in EGFR is associated with a higher response rate to afatinib.Details
Epidermal growth factor receptorL858R(G;G) / (G;T)T > GEffect Directly StudiedThe presence of this polymorphism in EGFR is associated with a higher response rate to afatinib.Details
Epidermal growth factor receptorG719A/C(T;T) / (G;T) / (A;A) / (A;G) / (C;C) / (C;G)G > A or C or TEffect Directly StudiedThe presence of this polymorphism in EGFR is associated with a higher response rate to afatinib.Details

Interactions

Drug Interactions Learn More" title="About Drug Interactions" id="structured-interactions-info" class="drug-info-popup" href="javascript:void(0);">
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.
DrugInteraction
AbemaciclibThe serum concentration of Abemaciclib can be increased when it is combined with Afatinib.
AbrocitinibThe serum concentration of Afatinib can be increased when it is combined with Abrocitinib.
AcetaminophenThe serum concentration of Acetaminophen can be increased when it is combined with Afatinib.
AdagrasibThe serum concentration of Afatinib can be increased when it is combined with Adagrasib.
AlectinibAlectinib may decrease the excretion rate of Afatinib which could result in a higher serum level.
Food Interactions
  • Take separate from meals. Take at least one hour before or two hours after a meal.

Products

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Product Ingredients
IngredientUNIICASInChI Key
Afatinib dimaleateV1T5K7RZ0B850140-73-7USNRYVNRPYXCSP-JUGPPOIOSA-N
Brand Name Prescription Products
NameDosageStrengthRouteLabellerMarketing StartMarketing EndRegionImage
GilotrifTablet, film coated30 mg/1OralBoehringer Ingelheim Pharmaceuticals, Inc.2013-07-12Not applicableUS flag
GilotrifTablet, film coated20 mg/1OralBoehringer Ingelheim Pharmaceuticals, Inc.2013-07-12Not applicableUS flag
GilotrifTablet, film coated40 mg/1OralBoehringer Ingelheim Pharmaceuticals, Inc.2013-07-12Not applicableUS flag
GiotrifTablet, film coated30 mgOralBoehringer Ingelheim2020-12-16Not applicableEU flag
GiotrifTablet, film coated20 mgOralBoehringer Ingelheim2020-12-16Not applicableEU flag

Categories

ATC Codes
L01EB03 — Afatinib
Drug Categories
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
  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]
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
Download (427 KB)
MSDS
Download (26.7 KB)

Clinical Trials

Clinical Trials Learn More" title="About Clinical Trials" id="clinical-trials-info" class="drug-info-popup" href="javascript:void(0);">
PhaseStatusPurposeConditionsCount
4Active Not RecruitingTreatmentNon-squamous Non-small-cell Lung Cancer (NSQ NSCLC)1
4CompletedTreatmentErbB Receptors / Non-Small Cell Lung Carcinoma1
4CompletedTreatmentNon-Small Cell Lung Carcinoma1
4Not Yet RecruitingTreatmentNRG1-fused Non-small Cell Lung Cancer1
4TerminatedTreatmentErbB Receptors / Non-Small Cell Lung Carcinoma1

Pharmacoeconomics

Manufacturers
Not Available
Packagers
Not Available
Dosage Forms
FormRouteStrength
Tablet, film coatedOral20 mg/1
Tablet, film coatedOral30 mg/1
Tablet, film coatedOral40 mg/1
TabletOral20 mg
TabletOral29.560 mg
TabletOral30 mg
TabletOral40 mg
Tablet, film coatedOral
Tablet, film coatedOral20 MG
Tablet, film coatedOral30 MG
Tablet, film coatedOral40 MG
Tablet, film coatedOral50 MG
Tablet, film coatedOral20.0000 mg
Tablet, film coatedOral30.0000 mg
Tablet, film coatedOral40.0000 mg
Tablet, film coatedOral50.0000 mg
Tablet, coatedOral40 mg
Tablet, coatedOral50 mg
Tablet, coatedOral20 mg
Tablet, coatedOral30 mg
Prices
Not Available
Patents
Patent NumberPediatric ExtensionApprovedExpires (estimated)Region
US6251912No2001-06-262018-07-29US flag
US8426586Yes2013-04-232030-04-10US flag
USRE43431Yes2012-05-292026-07-13US flag
US8545884Yes2013-10-012030-06-19US flag
US9539258Yes2017-01-102027-05-09US flag
US10004743Yes2018-06-262031-01-05US flag

Properties

State
Solid
Experimental Properties
Not Available
Predicted Properties
PropertyValueSource
Water Solubility0.0128 mg/mLALOGPS
logP3.77ALOGPS
logP3.76Chemaxon
logS-4.6ALOGPS
pKa (Strongest Acidic)12.49Chemaxon
pKa (Strongest Basic)8.81Chemaxon
Physiological Charge1Chemaxon
Hydrogen Acceptor Count7Chemaxon
Hydrogen Donor Count2Chemaxon
Polar Surface Area88.61 Å2Chemaxon
Rotatable Bond Count8Chemaxon
Refractivity131.38 m3·mol-1Chemaxon
Polarizability50.06 Å3Chemaxon
Number of Rings4Chemaxon
Bioavailability1Chemaxon
Rule of FiveYesChemaxon
Ghose FilterNoChemaxon
Veber's RuleNoChemaxon
MDDR-like RuleYesChemaxon
Predicted ADMET Features
PropertyValueProbability
Human Intestinal Absorption+1.0
Blood Brain Barrier+0.8717
Caco-2 permeable-0.5342
P-glycoprotein substrateSubstrate0.744
P-glycoprotein inhibitor IInhibitor0.6776
P-glycoprotein inhibitor IIInhibitor0.9036
Renal organic cation transporterNon-inhibitor0.7154
CYP450 2C9 substrateNon-substrate0.7919
CYP450 2D6 substrateNon-substrate0.8034
CYP450 3A4 substrateSubstrate0.7504
CYP450 1A2 substrateNon-inhibitor0.5236
CYP450 2C9 inhibitorNon-inhibitor0.7294
CYP450 2D6 inhibitorNon-inhibitor0.7625
CYP450 2C19 inhibitorNon-inhibitor0.5877
CYP450 3A4 inhibitorNon-inhibitor0.6486
CYP450 inhibitory promiscuityHigh CYP Inhibitory Promiscuity0.7096
Ames testNon AMES toxic0.5695
CarcinogenicityNon-carcinogens0.8692
BiodegradationNot ready biodegradable1.0
Rat acute toxicity2.5643 LD50, mol/kg Not applicable
hERG inhibition (predictor I)Weak inhibitor0.8956
hERG inhibition (predictor II)Inhibitor0.7228
ADMET data is predicted using admetSAR, a free tool for evaluating chemical ADMET properties. (23092397)

Spectra

Mass Spec (NIST)
Not Available
Spectra
SpectrumSpectrum TypeSplash Key
Predicted MS/MS Spectrum - 10V, Positive (Annotated)Predicted LC-MS/MSsplash10-000i-0001900000-f5858b02b26b748dee8f
Predicted MS/MS Spectrum - 10V, Negative (Annotated)Predicted LC-MS/MSsplash10-014l-0009600000-01d996a573e7a8183a19
Predicted MS/MS Spectrum - 20V, Positive (Annotated)Predicted LC-MS/MSsplash10-00rl-1003900000-975cdf816f9237551172
Predicted MS/MS Spectrum - 20V, Negative (Annotated)Predicted LC-MS/MSsplash10-0006-2205900000-4d3dd975aa5eb15d9672
Predicted MS/MS Spectrum - 40V, Positive (Annotated)Predicted LC-MS/MSsplash10-0kmi-7009400000-7b91e3b766e3565cc58c
Predicted MS/MS Spectrum - 40V, Negative (Annotated)Predicted LC-MS/MSsplash10-00l6-9003500000-2d2aaddc4790bfacf2df
Predicted 1H NMR Spectrum1D NMRNot Applicable
Predicted 13C NMR Spectrum1D NMRNot Applicable
Chromatographic Properties
Collision Cross Sections (CCS)
AdductCCS Value (Å2)Source typeSource
[M-H]-209.42613
predicted
DeepCCS 1.0 (2019)
[M+H]+211.8217
predicted
DeepCCS 1.0 (2019)
[M+Na]+217.7342
predicted
DeepCCS 1.0 (2019)

Targets

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Use our structured and evidence-based datasets to unlock new
insights and accelerate drug research.
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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
  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]
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
Substrate
Inhibitor
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
Substrate
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

Drug created at July 17, 2013 21:59 / Updated at February 20, 2024 23:54