Delving into the Latest Updates on Afatinib Dimaleate with Synapse

Overview

Basic Info

Drug Type

Small molecule drug

Synonyms

afatinib, Afatinib dimaleate (USAN), Afatinib Maleate

+ [14]

Target

EGFR L858R x EGFR-Ex19del x HER4

Action

inhibitors, antagonists

Mechanism

EGFR exon 19 deletion inhibitors, EGFR exon 21 L858R mutation inhibitors, HER4 antagonists(Receptor tyrosine-protein kinase erbB-4 antagonists)

Therapeutic Areas

NeoplasmsRespiratory DiseasesUrogenital Diseases+ [2]

Active Indication

metastatic non-small cell lung cancerNon-Small Cell Lung CancerEGFR positive non-small cell lung cancer+ [12]

Inactive Indication

Adenocarcinoma of LungAdvanced breast cancerAdvanced cancer+ [71]

Originator Organization

C.H. Boehringer Sohn AG & Co. KG

Active Organization

Boehringer Ingelheim GmbHBoehringer Ingelheim International GmbHBoehringer Ingelheim Pty Ltd.

+ [3]

Inactive Organization

Boehringer Ingelheim RCV GmbH & Co. KGBoehringer Ingelheim Hellas SABoehringer Ingelheim España SA

+ [8]

License Organization-

Drug Highest PhaseApproved

First Approval Date

United States (12 Jul 2013),

EGFR exon 19 Deletions Mutant Non-small Cell Lung CancerEGFR exon 21 Substitution Mutant Non-small Cell Lung Cancer

RegulationOrphan Drug (United States), Orphan Drug (European Union), Fast Track (United States)

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Structure/Sequence

Molecular FormulaC32H33ClFN5O11

InChIKeyUSNRYVNRPYXCSP-JUGPPOIOSA-N

CAS Registry850140-73-7

This is a pilot Phase I open-label randomized single-dose two-period crossover study (in the EDDIS project) evaluating the bioequivalence, pharmacokinetics (PK), safety, and tolerability of inhaled afatinib dimaleate compared with the reference oral afatinib dimaleate in healthy volunteer smokers.
The study will enroll healthy adult volunteers smoker to assess the systemic exposure and lung deposition of inhaled afatinib dimaleate. Participants will receive both the test inhaled formulation and the reference oral formulation in separate periods with delayed phase between treatments.
Key endpoints include maximum plasma concentration (Cmax), area under the concentration-time curve (AUC), and lung deposition assessed via bronchoalveolar lavage (BAL), frequency of occurrence of side effects and cases of toxicity during the studies

Start Date09 Nov 2025

Sponsor / Collaborator-

NCT06753747

/ RecruitingPhase 1/2IIT

A Phase 1b/2 Trial of Afatinib Plus Palbociclib in Previously Treated Recurrent or Metastatic Esophageal Squamous Cell Carcinoma

The goal of this clinical trial is to learn if Afatinib plus Palbociclib works in previously treated recurrent or metastatic esophageal squamous cell carcinoma. It will also learn about the safety of the combination of Afatinib and Palbociclib. The main questions it aims to answer are:
What is the safe and tolerable dose of Afatinib when combined with 100 mg of Palbociclib (administered orally, three weeks on and one week off)?
Does the combination therapy of Afatinib and Palbociclib induce a tumor response in patients with recurrent or metastatic esophageal squamous cell carcinoma who have received prior treatments?

Start Date10 Sep 2025

Sponsor / Collaborator

West China Hospital

NCT06709859

/ RecruitingPhase 2IIT

A Phase II Trial to Evaluate the Efficacy and Safety of Afatinib Combined With Chemotherapy as Conversion Therapy in Unresectable EGFR Sensitive Mutation-positive Stage III Non-small Cell Lung Cancer

This is a phase II, single-arm study to evaluate the efficacy and safety of Afatinib plus chemotherapy as conversion treatment in patients with unresectable EGFR sensitive mutation-positive stage III non-small cell lung cancer.

Start Date01 May 2025

Sponsor / Collaborator

Shanghai Public Health Clinical Center

100 Clinical Results associated with Afatinib Dimaleate

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100 Translational Medicine associated with Afatinib Dimaleate

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100 Patents (Medical) associated with Afatinib Dimaleate

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3,268

Literatures (Medical) associated with Afatinib Dimaleate

31 Dec 2026·RENAL FAILURE

A tri-scale in silico framework integrating pharmacovigilance and mechanistic modeling suggests tepotinib-associated acute kidney injury risk

Article

Author: Bai, Zhixun ; Wang, Qin ; Zheng, Rubin ; Han, Jinfen ; Lyu, Jiayi ; Lu, Jing ; Deng, Miao ; Chen, Jiaxi

Proactive safety evaluation of molecularly targeted therapies requires generalizable frameworks that integrate real-world evidence with mechanistic insights. As a case in point, tepotinib, a mesenchymal-epithelial transition (MET) inhibitor for non-small cell lung cancer, has a known pulmonary toxicity profile, but its link to acute kidney injury (AKI) and underlying mechanism remain unclear. We devised a tri-scale in silico strategy encompassing population-scale pharmacovigilance signal extraction from the FDA Adverse Event Reporting System (FAERS) (2020-2025) via disproportionality analysis (Reporting Odds Ratio, ROR, and Proportional Reporting Ratio, PRR), network toxicology-based multi-target exploration for shared target and hub gene identification, and mechanistic docking-based molecular plausibility assessment using the Cavity-detection guided Blind Docking (CB-Dock2) platform. Pharmacovigilance analysis identified a significant renal impairment signal (ROR = 20.60). Network toxicology suggested potential nephrotoxicity and revealed 173 shared targets and prioritizing six hub genes (HSP90AA1, AKT1, EGFR, CASP3, TNF, SRC). These genes were shown to be critically involved in PI3K-Akt and MAPK pathways. Molecular docking revealed high-affinity binding between tepotiniband all six hub targets (Vina scores: -8.0 to -10.6 kcal/mol), providing a structural basis for the postulated mechanistic link to AKI. These findings not only highlight the necessity for enhanced renal monitoring in tepotinib-treated patients but, more broadly, establish the FAERS-NetDock Pipeline as a reusable, generalizable and hypothesis-generating framework for evaluating tyrosine kinase inhibitors (TKIs)-induced nephrotoxicity; this framework is immediately applicable to profiling the safety of other TKIs (e.g. crizotinib, capmatinib, savolitinib, afatinib and osimertinib) and is readily adaptable for de-risking a wider spectrum of targeted therapies.

01 Dec 2026·MOLECULAR BIOLOGY REPORTS

Combined treatment of TKIs with Cilengitide overcomes afatinib-resistance in EGFR-mutated NSCLC cells

Article

Author: Kim, Yeonsoo ; Seo, Yujin ; Kang, Hye Eun ; Kim, Jiyeon

BACKGROUND:

Tyrosine kinase inhibitors (TKIs) are widely used to treat non-small cell lung cancer (NSCLC) harboring epidermal growth factor receptor (EGFR) mutations. However, long-term use frequently leads to drug resistance. These resistant cells often exhibit distinct phenotypes from their parental counterparts and may influence cancer progression, including proliferation, migration, and invasion.

METHODS AND RESULTS:

We investigated the effects of afatinib resistance, a second-generation EGFR-targeting TKI, on cell growth, mesenchymal marker expression, and TGF-β1-induced migration and invasion in the NSCLC cell line HCC827. Additionally, we examined the therapeutic potential of cilengitide, a cyclic Arg-Gly-Asp (RGD) peptide, in afatinib-resistant HCC827AR cells and organoids. Unlike parental cells, which were not significantly affected by TGF-β1, HCC827AR cells showed pronounced mesenchymal features such as upregulated N-cadherin and vimentin and increased expression of matrix metalloproteinases (MMPs). Cilengitide exhibited mild growth inhibition but significantly suppressed invasion. Furthermore, co-treatment with afatinib or dovitinib synergistically enhanced the inhibitory effects on proliferation, migration, and invasion. These findings were associated with downregulation of FAK phosphorylation and suppression of migration/invasion-related genes including fibronectin, vitronectin, and MMPs.

CONCLUSION:

Our findings demonstrate that cilengitide, a cyclic RGD peptide, effectively suppresses invasion and migration in afatinib-resistant NSCLC cells through inhibition of the integrin-FAK signaling axis. Although cilengitide showed limited growth inhibition as a monotherapy, its combination with TKIs such as afatinib or dovitinib significantly enhanced anti-proliferative and anti-invasive effects. These synergistic outcomes were associated with reduced expression of integrin-mediated proteins and MMPs, suggesting that cilengitide may potentiate TKI efficacy by modulating the tumor microenvironment and migratory potential of resistant cells. Taken together, this study supports the potential of cilengitide as an adjuvant therapeutic strategy in treating EGFR-TKI-resistant NSCLC. Further validation through preclinical animal models and pharmacokinetic studies will be crucial for future clinical translation.

01 May 2026·Advances in biological regulation

Afatinib alters DNA methylation and Paneth-like differentiation markers in Caco-2 cells

Article

Author: Uemura, Ippei ; Takahashi-Suzuki, Natsuko ; Satoh, Takashi

Afatinib is an irreversible epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) used to treat EGFR-mutant non-small cell lung cancer. It frequently causes gastrointestinal toxicity that perturbs intestinal homeostasis, and its impact on Paneth-like lineage differentiation along the crypt-villus axis remains unclear. Using a controlled differentiation-stage framework in Caco-2 cells, we examined how afatinib affects Paneth-like differentiation markers. We incubated undifferentiated Caco-2 cells with afatinib (10-5000 nM) for 24 h during early culture and evaluated downstream DNA methylation and differentiation-associated readouts up to day 14. We quantified proteins (western blotting), mRNAs (RT-qPCR), and promoter methylation (methylation-sensitive restriction enzyme-qPCR). Afatinib increased DNA methylation at the SRY-box transcription factor 9 (SOX9) and defensin alpha 5 (DEFA5) promoters and reduced their protein expression. Immunostaining indicated reduced expression of Paneth-like differentiation markers in Caco-2 cells. In contrast, mRNA levels of the SOX9 regulators odd-skipped related transcription factor 1 (OSR1) and receptor-interacting protein 140 (RIP140) were upregulated without changes in promoter methylation at the analyzed sites, indicating DNA methylation-independent regulation at these promoters. These findings suggest that DNMT1/3B-skewed methylation at the SOX9/DEFA5 promoters may be counteracted by ten-eleven translocation-mediated counter-demethylation. Collectively, our data indicate that afatinib modulates Paneth-like differentiation markers via DNA methylation-dependent repression of SOX9/DEFA5 and DNA methylation-independent induction of OSR1/RIP140 in Caco-2 cells, which may be relevant to crypt-associated epithelial function and gastrointestinal safety.

63

News (Medical) associated with Afatinib Dimaleate

23 Mar 2026

·allsci.com

Dizal’s Zegfrovy beats chemotherapy in Phase III first-line EGFR exon 20 insertion NSCLC trial

Dizal (SSE:688192) reported that its Phase III WU-KONG28 trial of sunvozertinib (Zegfrovy) met its primary endpoint in first-line NSCLC harboring EGFR exon 20 insertion mutations, with the oral EGFR inhibitor delivering a statistically significant improvement in progression-free survival over platinum-based chemotherapy. The result positions sunvozertinib as the first targeted oral, chemo-free monotherapy regimen to generate Phase III data showing PFS benefit against chemotherapy in this mutation-defined population. WU-KONG28 is a multinational, open-label, randomized Phase III trial conducted across 16 countries comparing once-daily oral sunvozertinib monotherapy to investigator-choice platinum-containing doublet chemotherapy in treatment-naive patients with advanced NSCLC driven by EGFR exon 20 insertion mutations. PFS, assessed by blinded independent central review, served as the primary endpoint. Dizal disclosed that sunvozertinib achieved a statistically significant and clinically meaningful PFS advantage over chemotherapy. The company also stated that all prespecified secondary endpoints, including confirmed objective response rate, duration of response, and disease control rate, favored the sunvozertinib arm. Specific numerical results for PFS and secondary endpoints were not disclosed – the company said detailed data will be submitted for presentation at an upcoming scientific congress. Sunvozertinib was generally well tolerated, with a safety profile consistent with earlier studies. The most common treatment-emergent adverse events were Grade 1 or 2 in severity, according to the company. Sunvozertinib is an irreversible, oral small-molecule EGFR tyrosine kinase inhibitor designed to selectively target mutant EGFR while sparing wild-type receptor activity. EGFR exon 20 insertion mutations represent approximately 1-2% of all NSCLC cases and have historically been resistant to first- and second-generation EGFR inhibitors such as erlotinib and afatinib. The structural heterogeneity of these insertions, with over 100 identified subtypes, has made drug design against this target class particularly difficult, and patients have until now relied on platinum-based chemotherapy as first-line treatment. Sunvozertinib already holds approvals in both the United States and China for adult patients with locally advanced or metastatic NSCLC with EGFR exon 20 insertion mutations whose disease has progressed on or after platinum-based chemotherapy. The US approval was supported by the multinational WU-KONG1 Part B study, while the China approval drew on the WU-KONG6 trial. Johnson & Johnson’s amivantamab (Rybrevant), a bispecific antibody targeting EGFR and MET, and Takeda’s mobocertinib were both approved in the second-line exon 20 insertion setting, though Takeda voluntarily withdrew mobocertinib from the US market in 2023 after a confirmatory trial failed to meet its primary endpoint. Amivantamab in combination with chemotherapy has been studied in earlier lines of therapy for broader EGFR-mutant populations, but no targeted oral agent had previously demonstrated a Phase III PFS benefit as monotherapy versus chemotherapy in the first-line exon 20 insertion setting specifically. Cross-trial comparisons are limited by differences in study design, patient populations, and endpoints. The WU-KONG28 result is therefore notable for establishing, in a controlled setting, that a chemotherapy-free oral regimen can outperform the existing standard of care for a patient population with limited targeted treatment options. Sunvozertinib has received Breakthrough Therapy Designation from both the US FDA and China’s Center for Drug Evaluation for the first-line exon 20 insertion indication, which may facilitate regulatory review timelines. Dizal said it plans to engage with regulatory authorities regarding potential new drug applications based on the WU-KONG28 data. Your email address will not be published. Required fields are marked * Comment * Name * Email * Website

Clinical ResultPhase 3Drug ApprovalBreakthrough TherapyPriority Review

18 Mar 2026

·www.adalvo.com

Adalvo receives EU marketing authorisation via DCP for Afatinib

Adalvo has received marketing authorisation via the DCP for its generic Afatinib film-coated tablets in Europe. The approval covers all strengths: 20, 30, 40 and 50 mg. Afatinib is indicated for the first-line treatment of adult patients with advanced non-small cell lung cancer (NSCLC) harbouring activating EGFR mutations and belongs to the established class of EGFR tyrosine kinase inhibitors. Afatinib works by irreversibly blocking the ErbB family of proteins involved in tumour growth and progression in EGFR-mutated NSCLC. Unlike first-generation EGFR inhibitors, it binds covalently, resulting in prolonged inhibition of ErbB signalling. NSCLC accounts for approximately 85% of all lung cancer cases globally. EGFR mutations occur in around 10–35% of NSCLC adenocarcinomas, with higher prevalence observed in Asian populations. According to IQVIA, MAT sales for Afatinib reached $229M in Q4 2025. With marketing authorisations now in place across EU markets, Adalvo can offer partners licensing opportunities to bring this approved generic to patients. The successful development of Afatinib further strengthens Adalvo’s oncology portfolio and demonstrates its capabilities in developing and delivering complex solid oral oncology therapies. To discuss partnership opportunities or to explore Adalvo's full oncology pipeline, contact us today.

Drug Approval

18 Mar 2026

·www.edisononcology.com

Edison Oncology to Present Two Posters at the 2026 AACR Annual Meeting

Preclinical data for EO1001 an orally bioavailable, irreversible pan-ErbB inhibitor targeting EGFR extracellular domain (ECD) mutant solid tumors. Preclinical data for EO4426 (tezacitabine), an orally bioavailable brain-penetrant, dual inhibitor of DNA polymerase alpha (Pol α) and ribonucleotide reductase (RNR), targeting CDA-mediated resistance in solid tumors and mesenchymal GBM. Presentations’ highlight – Edison Oncology’s expanding precision oncology pipeline focused on biomarker-directed therapies for molecularly-defined patient populations with significant unmet need. MENLO PARK, CA / ACCESS Newswire / March 18, 2026 / Edison Oncology Holding Corp. (“Edison Oncology” or the “Company”) today announced the presentation of two posters at the upcoming American Association for Cancer Research (AACR) Annual Meeting 2026, taking place April 17-22, in San Diego, California. The presentations showcased Edison Oncology’s advancements in precision oncology, including EO1001, an irreversible pan-ErbB TKI with CNS penetration, and EO4426, a brain-penetrant dual inhibitor of DNA polymerase alpha (Pol α) and ribonucleotide reductase (RNR). “We are pleased to present these two programs at the AACR Annual Meeting, which together reflect Edison Oncology’s focus on developing biomarker-directed oncology targeted therapies for molecularly-defined patient populations with significant unmet need,” said Jeffrey A. Bacha, Chief Executive Officer, Edison Oncology Holding Corp. “EO1001 addresses the critical gap in treatment for EGFR extracellular domain mutant cancers and is currently being evaluated in clinical studies, while EO4426 targets the CDA-mediated resistance mechanisms that limit the efficacy of current cytidine-based therapies.” EO1001 EGFR extracellular domain (ECD) mutations, including EGFRvIII, A289 substitutions, R108 variants, and related structural alterations, drive ligand-independent EGFR activation and highly aggressive tumor biology. These mutations occur in head and neck, lung, and gastrointestinal cancers and glioblastoma (GBM), where they are associated with therapeutic resistance and poor patient outcomes. EGFR-ECD mutations are generally resistant to approved EGFR TKIs, including osimertinib, erlotinib, gefitinib, and afatinib, because the structural alterations lie outside the ATP-binding pocket and may preserve receptor signaling despite drug engagement. EO1001 is an orally bioavailable, irreversible pan-ErbB inhibitor designed to inhibit signaling from both wild-type and structurally altered ErbB receptors. Early signals of clinical activity in EGFR-ECD mutant GBM patients have been observed in an ongoing Phase 1-2a study (ANZCTR: ACTRN12620000583943), underscoring the need for mechanistic validation. To further investigate this, Edison Oncology initiated a focused, preclinical program assessing EO1001 activity in patient derived xenograft (PDX) tumor models harboring clinically relevant EGFR-ECD variants. Preliminary preclinical data from the program will be presented at the AACR Annual Meeting. This preclinical program will further explore mechanisms of EO1001’s activity in EGFR-ECD mutant cancers, providing support for biomarker-guided clinical development. EO4426 EO4426 (tezacitabine) is a novel brain-penetrant, deamination-resistant, cytidine analog that exhibits dual inhibition of both DNA polymerase-α (Polα) and ribonucleotide reductase (RNR), resulting in depletion of deoxynucleotide pools, replication-fork collapse, and accumulation of DNA damage in rapidly proliferating tumor cells. Unlike gemcitabine and hydroxyurea, EO4426 resists cytidine deaminase (CDA)-mediated inactivation. Tumors with high CDA expression such as mesenchymal GBM, TNBC, NSCLC, and ovarian cancer are predicted to exhibit heightened dependence on Polα/RNR function and may therefore be particularly susceptible to dual-targeting strategies. Prior nonclinical studies demonstrate that EO4426 retains activity in CDA-high tumor environments and is less susceptible to rapid deamination than gemcitabine. Historically, EO4426 has been evaluated in multiple third-party Phase I and Phase II trials, demonstrating a generally manageable safety profile with reversible myelosuppression reported as the principal dose-limiting toxicity and evidence of clinical activity in heavily pretreated solid-tumor populations. New data are being developed to support further investigation of EO4426 in biomarker guided clinical development strategies for CDA-high solid tumors. Preliminary results of these ongoing non-clinical studies will be presented at the meeting. Additional details on key presentations at AACR are available below and further information on the AACR Annual Meeting 2026 is available here. Title: Preclinical evaluation of EO1001 in EGFR-ECD mutant solid tumor models: Toward biomarker-directed therapy Date/Time: Tuesday April 21, 2026, 2:00-5:00PM PT Session: Poster, Experimental and Molecular Therapeutics, Tyrosine Kinase, Phosphatase, and Other Inhibitors Abstract Number: 5889 Title: Overcoming cytidine deaminase (CDA) mediated resistance via EO4426 dual DNA-replication targeting: Implications for CDA-high solid tumors and mesenchymal GBM Date/Time: Wednesday April 22, 2026, 9:00AM – noon PT Session: Poster, Experimental and Molecular Therapeutics, Novel Antitumor Agents Abstract Number: 7102 About Edison Oncology Holding Corp. Edison Oncology Holding Corp. is a clinical-stage biopharmaceutical company developing a pipeline of first-in-class, small-molecule, biomarker-driven therapies designed to overcome key resistance mechanisms and address critical unmet needs in aggressive and underserved cancers. Leveraging existing clinical data and a modern understanding of cancer biology, the Edison Oncology focuses on genetically defined cancers, advancing its programs through a capital-efficient combination of internal development and strategic partnerships while retaining meaningful development and commercial rights. To learn more, please visit https://www.edisononcology.com/ and follow us for updates on LinkedIn. Contact Hayden IR Brett Maas (646) 536-7331 brett@haydenir.com or James Carbonara (646)-755-7412 james@haydenir.com SOURCE: Edison Oncology Holding Corp. View Original Press Release Here Edison Oncology to Present Two Posters at the 2026 AACR Annual Meeting Society for NeuroOncology: EO-4426: A Brain-Penetrant Dual DNA Polymerase α and Ribonucleotide Reductase Inhibitor for High-Grade Gliomas and Other Aggressive Cancers

Phase 1AACR

100 Deals associated with Afatinib Dimaleate

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External Link

KEGG	Wiki	ATC	Drug Bank
D09733	Afatinib Dimaleate	L01XE13	DB08916

R&D Status

Approved

10 top approved records.

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Indication	Country/Location	Organization	Date
metastatic non-small cell lung cancer	United States	Boehringer Ingelheim GmbH	12 Jan 2018
Non-Small Cell Lung Cancer	China	Boehringer Ingelheim International GmbH	21 Feb 2017
EGFR positive non-small cell lung cancer	Japan	Nippon Boehringer Ingelheim Co., Ltd.	17 Jan 2014
Locally Advanced Lung Non-Squamous Non-Small Cell Carcinoma	Australia	Boehringer Ingelheim Pty Ltd.	07 Nov 2013
Metastatic Non-Squamous Non-Small Cell Lung Carcinoma	Australia	Boehringer Ingelheim Pty Ltd.	07 Nov 2013
Squamous non-small cell lung cancer	European Union	Boehringer Ingelheim International GmbH	25 Sep 2013
Squamous non-small cell lung cancer	Iceland	Boehringer Ingelheim International GmbH	25 Sep 2013
Squamous non-small cell lung cancer	Liechtenstein	Boehringer Ingelheim International GmbH	25 Sep 2013
Squamous non-small cell lung cancer	Norway	Boehringer Ingelheim International GmbH	25 Sep 2013
EGFR-mutated non-small Cell Lung Cancer	European Union	Boehringer Ingelheim International GmbH	25 Sep 2013
EGFR-mutated non-small Cell Lung Cancer	Iceland	Boehringer Ingelheim International GmbH	25 Sep 2013
EGFR-mutated non-small Cell Lung Cancer	Liechtenstein	Boehringer Ingelheim International GmbH	25 Sep 2013
EGFR-mutated non-small Cell Lung Cancer	Norway	Boehringer Ingelheim International GmbH	25 Sep 2013
EGFR exon 19 Deletions Mutant Non-small Cell Lung Cancer	United States	Boehringer Ingelheim GmbH	12 Jul 2013
EGFR exon 21 Substitution Mutant Non-small Cell Lung Cancer	United States	Boehringer Ingelheim GmbH	12 Jul 2013

Developing

10 top R&D records.

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Indication	Highest Phase	Country/Location	Organization	Date
Advanced Lung Non-Small Cell Carcinoma	Phase 3	China	Boehringer Ingelheim GmbH	30 Sep 2013
Advanced Lung Non-Small Cell Carcinoma	Phase 3	Hong Kong	Boehringer Ingelheim GmbH	30 Sep 2013
Advanced Lung Non-Small Cell Carcinoma	Phase 3	India	Boehringer Ingelheim GmbH	30 Sep 2013
Advanced Lung Non-Small Cell Carcinoma	Phase 3	Singapore	Boehringer Ingelheim GmbH	30 Sep 2013
Advanced Lung Non-Small Cell Carcinoma	Phase 3	Taiwan Province	Boehringer Ingelheim GmbH	30 Sep 2013
Diarrhea	Phase 3	United States	Boehringer Ingelheim GmbH	01 Apr 2013
Advanced Lung Squamous Cell Carcinoma	Phase 3	Greece	-	10 Jan 2012
Squamous cell carcinoma of head and neck metastatic	Phase 3	United States	Boehringer Ingelheim GmbH	05 Jan 2012
Squamous cell carcinoma of head and neck metastatic	Phase 3	Japan	Boehringer Ingelheim GmbH	05 Jan 2012
Squamous cell carcinoma of head and neck metastatic	Phase 3	Argentina	Boehringer Ingelheim GmbH	05 Jan 2012

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Clinical Result

Indication

Phase

Evaluation

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


ESMO_TAT2026	Not Applicable	Head and neck cancer metastatic	25	Afatinib 20mg	hiaxodikcu(xzhtpvblhh) = hbaqlrqkfw mxrqmubiga (jvvuxjbbom ) View more	Positive	16 Mar 2026
NCT02979977 (Phase 2 trial of dual EGFR inhibition with cetuximab and afatinib, CTgov)	Phase 2	Advanced Head and Neck Squamous Cell Carcinoma	50	Afatinib+cetuximab	duazmpxblm(svhsbyqqyi) = alarixyirc ukbbaopytk (ffqbrqytga, ptsrqdbmwr - mfvpxiriad) View more	-	04 Feb 2026
NCT01856478 (LUX-Head & Neck 3, CTgov)	Phase 3	Squamous Cell Carcinoma of Head and Neck	340	Afatinib (Afatinib 40 mg)	gyfjjkcake(ngpxqsgetn) = boftrzpphm czcgwskbet (riamlrjrwo, zwtvdnhdol - nptbfasyjo) View more	-	12 Jan 2026
				Methotrexate (Methotrexate 40 mg)	gyfjjkcake(ngpxqsgetn) = gbkamexery czcgwskbet (riamlrjrwo, unfcoahqrb - zelpnrpjne) View more
NCT04909073 (ESMO_ASIA2025)	Phase 2	EGFR-mutated non-small Cell Lung Cancer First line EGFR mutations	30	Afatinib 30mg daily	mghygjzctm(ccqrhoomdp) = cmnuwbdvax koffesevlo (rkrxzsopqy, 75.5 - 98.3) View more	Positive	05 Dec 2025
WCLC2025	Phase 2	metastatic non-small cell lung cancer EGFR-mutant	91	Afatinib	qzimvndvgf(isqcxufjwp): HR = 0.49 (95.0% CI, 0.25 - 0.94), P-Value = 0.035	Positive	09 Sep 2025
				Afatinib (Primary tumor resection with or without radiotherapy)
NCT04795245 (Pubmed \| Future Oncol)	Not Applicable	Non-squamous non-small cell lung cancer \| Advanced Lung Adenocarcinoma	-	Afatinib	msexkwovxs(xvsricafgg) = xxogtoyefz dntgjzpvfv (tnbrjrfqsh ) View more	-	03 Jul 2025
NCT02191891 (CTgov)	Phase 1	EGFR-mutated non-small Cell Lung Cancer	32	Afatinib+Xentuzumab (Xentuzumab + Afatinib 30 Milligram (mg) - Part A)	ymapfzwerh = qbefgmlntn uhcbrdcsjh (auqkdppybp, oxfobznnyg - vavvsithye)	-	25 Jun 2025
				Afatinib+Xentuzumab (Xentuzumab + Afatinib 40 mg - Part A)	ymapfzwerh = grcpyicjgq uhcbrdcsjh (auqkdppybp, arkfrjuiqs - fptznctmdr)
JPRN-jRCTs031190221 (Heat on Beat, ASCO2025)	Phase 2	First line Th7R \| Th2	95	Afatinib	mgtwxjjhzu(nvfkqyiuhd) = jiclbltzep rdwhxazofi (aqlzzwkprv, 39.4 - 67.7) View more	Positive	30 May 2025
				Osimertinib	mgtwxjjhzu(nvfkqyiuhd) = clowkwasbm rdwhxazofi (aqlzzwkprv, 42.2 - 70.1) View more
NEJ025B (ASCO2025)	Not Applicable	EGFR-mutated non-small Cell Lung Cancer Second line EGFR mutations \| p53 mutations \| MET gene amplification	35	Afatinib + Carboplatin + Pemetrexed	gmglxbwsdq(aqbvgeepem) = pfqhgboalz vudhgxeomj (cdkrhaqfag, 39.3 - 71.5) View more	Positive	30 May 2025
NCT03088059 (EORTC-HNCG-1559, ASCO2025)	Phase 2	Squamous Cell Carcinoma of Head and Neck EGFR \| HER2 \| PTEN ... View more	250	Afatinib in pts with EGFR amp/mut and/or HER2 amp/mut and/or PTEN high	fdnasmlach(aazpqzigsl) = pkmlltimzf srdgbypjdw (zhgsmjgubd )	Negative	30 May 2025
				Afatinib in cetuximab-naïve pts	fdnasmlach(aazpqzigsl) = rkivmcpkbm srdgbypjdw (zhgsmjgubd )