ArticlemAbs2017
Fc-mediated activity of EGFR x c-Met bispecific antibody JNJ-61186372 enhanced killing of lung cancer cells.
Article in mAbs, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
50 citing papers in PubMed, 2 syntheses or guidelines pooled it, 85 citations in OpenAlex.
- Therapeutic exploration of uncommon EGFR exon 20 insertion mutations in advanced non-small cell lung cancer: breaking through brambles and thorns.Journal of cancer research and clinical oncology · 2022Pooled it
- Bispecific Antibodies: From Research to Clinical Application.Frontiers in immunology · 2021Pooled it
- Review
- Amivantamab Induces Immune-Mediated Cytotoxicity in Mesothelioma Through EGFR and MET Engagement.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2026Article
- A tri-specific EGFR/cMet/VEGF antibody demonstrates potent multi-mechanistic activity in preclinical triple-negative breast cancer models.The Journal of biological chemistry · 2026Article
- Immunological effects of amivantamab in EGFR or MET-expressing non-small cell lung cancer.Cancer immunology, immunotherapy : CII · 2026Article
- EMB-01, a Tetravalent Bispecific Antibody, Inducing Co-Degradation of EGFR and c-Met for Enhanced Anti-Tumor Efficacy.Cancer science · 2026Article
- A combined strategy of EGFR-MET bispecific antibody and HER3 ADC to overcome osimertinib resistance in NSCLC.Cellular oncology (Dordrecht, Netherlands) · 2026Article
- MET Enhances Amivantamab Binding to EGFR and Antibody-Dependent Cellular Toxicity.Cancer science · 2026Article
- Technological advancements in antibody-based therapeutics for treatment of diseases.Journal of biomedical science · 2025Review
- The application of antibody-based agents in cancer therapy based on their mechanisms of action.Fundamental research · 2025Review
- Identification of potent biparatopic antibodies targeting FGFR2 fusion-driven cholangiocarcinoma.The Journal of clinical investigation · 2025Article
- Pancreatic Cancer: Pathogenesis and Clinical Studies.MedComm · 2025Review
- The changing treatment landscape of EGFR-mutant non-small-cell lung cancer.Nature reviews. Clinical oncology · 2025Review
- Review
- Advances in cancer immunotherapy: Strategies and innovations strategies for adoptive immunotherapy of cancer.Iranian journal of basic medical sciences · 2025Review
- Evolving treatment strategies for EGFRex20ins-mutated NSCLC: a comprehensive review of Amivantamab's role and future directions.Ecancermedicalscience · 2025Review
- A trispecific antibody targeting EGFR/cMET/VEGF-A demonstrates multiple mechanisms of action to inhibit wild-type and mutant NSCLC animal models.Frontiers in oncology · 2025Article
- Amivantamab efficacy in wild-type EGFR NSCLC tumors correlates with levels of ligand expression.NPJ precision oncology · 2024Article
- c-MET and the immunological landscape of cancer: novel therapeutic strategies for enhanced anti-tumor immunity.Frontiers in immunology · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epidermal growth factor receptor (EGFR) mutant non-small cell lung cancers acquire resistance to EGFR tyrosine kinase inhibitors through multiple mechanisms including c-Met receptor pathway activation. We generated a bispecific antibody targeting EGFR and c-Met (JNJ-61186372) demonstrating anti-tumor activity in wild-type and mutant EGFR settings with c-Met pathway activation. JNJ-61186372 was engineered with low fucosylation (<10 %), resulting in enhanced antibody-dependent cell-mediated cytotoxicity and FcγRIIIa binding. In vitro and in vivo studies with the single-arm EGFR or c-Met versions of JNJ-61186372 identified that the Fc-activity of JNJ-61186372 is mediated by binding of the anti-EGFR arm and required for inhibition of EGFR-driven tumor cells. In a tumor model driven by both EGFR and c-Met, treatment with Fc-silent JNJ-61186372 or with c-Met single-arm antibody reduced tumor growth inhibition compared to treatment with JNJ-61186372, suggesting that the Fc function of JNJ-61186372 is essential for maximal tumor inhibition. Moreover in this same model, downregulation of both EGFR and c-Met receptors was observed upon treatment with Fc-competent JNJ-61186372, suggesting that the Fc interactions are necessary for down-modulation of the receptors in vivo and for efficacy. These Fc-mediated activities, in combination with inhibition of both the EGFR and c-Met signaling pathways, highlight the multiple mechanisms by which JNJ-61186372 combats therapeutic resistance in EGFR mutant patients.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.