Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (808 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
A quinazoline and butenamide derivative that acts as a tyrosine kinase inhibitor of epidermal growth factor receptors (erbb receptors) and is used in the treatment of metastatic non-small cell lung cancer.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: (2E)-N-(4-(3-Chloro-4-fluoroanilino)-7-(((3S)-oxolan-3-yl)oxy)quinoxazolin-6-yl)-4-(dimethylamino)but-2-enamide; BIBW 2992; BIBW-2992; BIBW2992; Gilotrif; Afatinib Dimaleate; BIBW-2992-MA2; BIBW 2992 MA2.
Where it fits in the MeSH classification
- Broader topics
- Amides; Quinazolines
Related concepts
- Erbb Receptors
- Non-Small Cell Lung Cancer
Research landscape
PubMed indexes 1,193 records tagged with the MeSH heading “Afatinib” (counts retrieved 2026-10-31). 512 of them (42.9%) were published from 2020 onward, and the busiest period so far is 2010-2019 with 685 records.
Reviews account for 143 records (12.0%) and meta-analyses for 27. Randomized controlled trials number 68 (5.7%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 0 |
| 2000-2009 | 9 |
| 2010-2019 | 685 |
| 2020 onward | 512 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 143 | 12.0% |
| Meta-analyses | 27 | 2.3% |
| Randomized controlled trials | 68 | 5.7% |
Method: PubMed query "Afatinib"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in drugs and chemicals
Studies of a chemical or drug can answer very different questions: what it is and how it behaves in cells and animals, how the body handles it, and whether it changes outcomes in people. Laboratory and animal findings often do not carry over to patients, and observational studies of exposures are confounded by who uses a substance and why. Nothing on this page is a recommendation to use, avoid, start or stop any substance or medicine; talk to a qualified clinician or pharmacist about your own situation. Check the dose, the species, the comparison group and whether a patient-relevant outcome was measured.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
Afatinib and Temozolomide combination inhibits tumorigenesis by targeting EGFRvIII-cMet signaling in glioblastoma cells [1]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundGlioblastoma (GBM) is an aggressive brain tumor with universal recurrence and poor prognosis.
- Closing excerpt
- Our results warrant evaluation of this drug combination in EGFR and EGFRvIII amplified GBM patients.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (273 words)
BackgroundGlioblastoma (GBM) is an aggressive brain tumor with universal recurrence and poor prognosis. The recurrence is largely driven by chemoradiation resistant cancer stem cells (CSCs). Epidermal growth factor receptor (EGFR) and its mutant EGFRvIII are amplified in ~ 60% and ~ 30% of GBM patients, respectively; however, therapies targeting EGFR have failed to improve disease outcome. EGFRvIII-mediated cross-activation of tyrosine kinase receptor, cMET, regulates GBM CSC maintenance and promote tumor recurrence. Here, we evaluated the efficacy of pan-EGFR inhibitor afatinib and Temozolomide (TMZ) combination on GBM in vitro and in vivo.MethodsWe analyzed the effect of afatinib and temozolomide (TMZ) combination on GBM cells U87MG and U251 engineered to express wild type (WT) EGFR, EGFRvIII or EGFRvIII dead kinase, CSCs isolated from U87 and U87EGFRvIII in vitro. The therapeutic utility of the drug combination was investigated on tumor growth and progression using intracranially injected U87EGFRvIII GBM xenografts.ResultsAfatinib and TMZ combination synergistically inhibited the proliferation, clonogenic survival, motility, invasion and induced senescence of GBM cells compared to monotherapy. Mechanistically, afatinib decreased U87EGFRvIII GBM cell proliferation and motility/invasion by inhibiting EGFRvIII/AKT, EGFRvIII/JAK2/STAT3, and focal adhesion kinase (FAK) signaling pathways respectively. Interestingly, afatinib specifically inhibited EGFRvIII-cMET crosstalk in CSCs, resulting in decreased expression of Nanog and Oct3/4, and in combination with TMZ significantly decreased their self-renewal property in vitro. More interestingly, afatinib and TMZ combination significantly decreased the xenograft growth and progression compared to single drug alone.ConclusionOur study demonstrated significant inhibition of GBM tumorigenicity, CSC maintenance in vitro, and delayed tumor growth and progression in vivo by combination of afatinib and TMZ. Our results warrant evaluation of this drug combination in EGFR and EGFRvIII amplified GBM patients.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 31215502 · DOI · PMC6582495
Anti-inflammatory effect of afatinib (an EGFR-TKI) on OGD-induced neuroinflammation [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Activated epidermal growth factor receptor (EGFR) has been proposed in the pathophysiology of neurodegenerative diseases.
- Closing excerpt
- Furthermore, EGFR-TKIs may be promising in inhibiting neuroinflammation in the CNS neurodegenerative diseases.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (198 words)
Activated epidermal growth factor receptor (EGFR) has been proposed in the pathophysiology of neurodegenerative diseases. In the present study, the anti-inflammatory effect of afatinib, an EGFR-tyrosine kinase inhibitor (EGFR-TKIs) was investigated using CTX-TNA2 cells and primary cultured astrocytes subjected to oxygen/glucose deprivation (OGD). We found that OGD induced EGFR phosphorylation and activated subsequent signaling pathways, including phosphorylation of AKT and extracellular signal-regulated kinases (ERK). Afatinib blocked OGD-induced phosphorylation of EGFR, AKT and ERK. At the same time, afatinib attenuated OGD-induced elevations in glial fibrillary acidic protein (a biomarker of activated astrocytes) and proliferating cell nuclear antigen expression (a cell proliferating biomarker) as well as hypoxia-induced migratory ability. Furthermore, afatinib decreased OGD-induced increases in cyclooxygenase-II and inducible nitric oxide synthase expression of the treated astrocytes as well as NO content in the culture medium. Moreover, afatinib attenuated OGD-induced caspase 1 activation (a biomarker of inflammasome activation) and interleukin-1β levels (a pro-inflammatory cytokine). Collectively, afatinib could block OGD-induced EGFR activation and its downstream signaling pathways in astrocytes. Moreover, afatinib attenuated OGD-induced astrocyte activation, proliferation and inflammasome activation. These data support the involvement of EGFR activation in neuroinflammation. Furthermore, EGFR-TKIs may be promising in inhibiting neuroinflammation in the CNS neurodegenerative diseases.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 30792526 · DOI · PMC6385176
Safety Profile of Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitors: A Disproportionality Analysis of FDA Adverse Event Reporting System [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Adverse event reports submitted to the US Food and Drug Administration (FDA) were analyzed to map the safety profile of epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs).
- Closing excerpt
- The results of this study are consistent with clinical observation, suggesting the usefulness of pharmacovigilance research should be corroborated with the real-world FAERS data.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (175 words)
Adverse event reports submitted to the US Food and Drug Administration (FDA) were analyzed to map the safety profile of epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs). We conducted a disproportionality analysis of the adverse events (AEs) of EGFR-TKIs (gefitinib, erlotinib, afatinib, osimertinib) by data mining using the FDA adverse event reporting system (AERS) database, and by calculating the reporting odds ratios (ROR) with 95% confidence intervals. The FDA AERS database contained 27,123 EGFR-TKI-associated AERs within the reporting period from January 1, 2004 to March 31, 2018. Thirty-three preferred terms (PTs) were selected for analysis, and significant RORs were most commonly observed in the skin, nail, gastrointestinal tract, hepatic, eyes, and lungs. Unexpected adverse drug reactions were found in the "intestinal obstruction" and "hypokalaemia" in gefitinib and erlotinib, "hyponatraemia" in gefitinib, erlotinib and afatinib, "alopecia"in erlotinib, "hair growth abnormal" in afatinib, but not in "nausea" and "vomiting" listed on drug labels. The results of this study are consistent with clinical observation, suggesting the usefulness of pharmacovigilance research should be corroborated with the real-world FAERS data.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 32179761 · DOI · PMC7075865
Acquired Resistance to Afatinib Mediated by EGFR T790M in Lung Adenocarcinoma Patients Harboring EGFR-KDD: A Case Report and Literature Review [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Epidermal growth factor receptor (EGFR)-kinase domain duplication (KDD) represents an atypical mutation distinct from classical EGFR mutations in lung adenocarcinoma (LUAD).
- Closing excerpt
- This case suggests that EGFR T790M mediates acquired resistance to first- and second-generation EGFR-TKIs in EGFR-KDD, mirroring the resistance pattern observed in classical EGFR mutations.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (162 words)
Epidermal growth factor receptor (EGFR)-kinase domain duplication (KDD) represents an atypical mutation distinct from classical EGFR mutations in lung adenocarcinoma (LUAD). Although first- and second-generation EGFR-tyrosine kinase inhibitors (TKIs) have demonstrated clinical activity in EGFR-KDD, the mechanisms of acquired resistance in this setting remain poorly characterized. Herein, we present a LUAD patient with EGFR-KDD who achieved a sustained initial response to afatinib lasting 67 months before developing acquired resistance. Re-biopsy with next-generation sequencing (NGS) uncovered EGFR T790M, accompanied by EGFR amplification and EGFR M766T. The patient was switched to firmonertinib, with subsequent tumor regression. We reviewed published EGFR-KDD cases that had both acquired resistance to first- or second-generation EGFR-TKIs and corresponding repeat biopsy findings. Five of the eleven cases harbored EGFR T790M, yielding a prevalence of 45%, which is similar to that seen in classical EGFR mutations. This case suggests that EGFR T790M mediates acquired resistance to first- and second-generation EGFR-TKIs in EGFR-KDD, mirroring the resistance pattern observed in classical EGFR mutations.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42041733 · DOI · PMC13115370
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Afatinib for the treatment of EGFR mutation-positive NSCLC: A review of clinical findings [5]
- Research article Afatinib and Erlotinib in the treatment of squamous-cell lung cancer [6]
- Research article Afatinib in the first-line treatment of patients with non-small cell lung cancer: clinical evidence and experience [7]
- Research article Successful Treatment of a Patient with Lung Adenocarcinoma Harboring Compound EGFR Gene Mutations, G719X and S768I, with Afatinib [8]
- Research article Irreversible tyrosine kinase inhibition of epidermal growth factor receptor with afatinib in EGFR activating mutation-positive advanced non-small-cell lung cancer [9]
- Research article Afatinib Therapy: Practical Management of Adverse Events With an Oral Agent for Non-Small Cell Lung Cancer Treatment [10]
References
- Vengoji R, Macha MA, Nimmakayala RK, Rachagani S, Siddiqui JA, Mallya K, et al.. Afatinib and Temozolomide combination inhibits tumorigenesis by targeting EGFRvIII-cMet signaling in glioblastoma cells. . 2019. PMID 31215502 · DOI · PMC6582495
- Chen YJ, Hsu CC, Shiao YJ, Wang HT, Lo YL, Lin AMY. Anti-inflammatory effect of afatinib (an EGFR-TKI) on OGD-induced neuroinflammation. . 2019. PMID 30792526 · DOI · PMC6385176
- Huang J, Meng L, Yang B, Sun S, Luo Z, Chen H. Safety Profile of Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitors: A Disproportionality Analysis of FDA Adverse Event Reporting System. . 2020. PMID 32179761 · DOI · PMC7075865
- Liu Q, Lv L, Pang G, Wang P. Acquired Resistance to Afatinib Mediated by EGFR T790M in Lung Adenocarcinoma Patients Harboring EGFR-KDD: A Case Report and Literature Review. . 2026. PMID 42041733 · DOI · PMC13115370
- Harvey RD, Adams VR, Beardslee T, Medina P. Afatinib for the treatment of EGFR mutation-positive NSCLC: A review of clinical findings. J Oncol Pharm Pract. 2020. PMID 32567494 · DOI · PMC7448811
- Tagliamento M, Genova C, Rijavec E, Rossi G, Biello F, Dal Bello MG, et al.. Afatinib and Erlotinib in the treatment of squamous-cell lung cancer. Expert Opin Pharmacother. 2018. PMID 30392436 · DOI
- Ricciuti B, Baglivo S, De Giglio A, Chiari R. Afatinib in the first-line treatment of patients with non-small cell lung cancer: clinical evidence and experience. Ther Adv Respir Dis. 2018. PMID 30355049 · DOI · PMC6204616
- Kutsuzawa N, Takahashi F, Tomomatsu K, Obayashi S, Takeuchi T, Takihara T, et al.. Successful Treatment of a Patient with Lung Adenocarcinoma Harboring Compound EGFR Gene Mutations, G719X and S768I, with Afatinib. Tokai J Exp Clin Med. 2020. PMID 32901897
- Abdallah SM, Hirsh V. Irreversible tyrosine kinase inhibition of epidermal growth factor receptor with afatinib in EGFR activating mutation-positive advanced non-small-cell lung cancer. Curr Oncol. 2018. PMID 29910643 · DOI · PMC6001770
- Edwards RL, Andan C, Lalla RV, Lacouture ME, O'Brien D, Sequist LV. Afatinib Therapy: Practical Management of Adverse Events With an Oral Agent for Non-Small Cell Lung Cancer Treatment. Clin J Oncol Nurs. 2018. PMID 30239509 · DOI · PMC9116182
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-31.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.