Drug Database
EP

epidermal growth factor receptor (EGFR pharmDx / EGFR pharmDx Kit)

✓ Approved

Dako · EGFR · Companion diagnostic

What is epidermal growth factor receptor?

epidermal growth factor receptor is a companion diagnostic developed by Dako. It is approved for therapeutic indications via others.

Drug Profile

Brand NamesEGFR pharmDx, EGFR pharmDx Kit
CompanyDako
Drug ClassCompanion diagnostic
Molecular TargetEGFR
RouteOthers
StatusApproved
Sources: ClinicalTrials.gov, Dako

Mechanism of Action

Molecular Targets

epidermal growth factor receptor acts on 1 molecular target:

EGFRepidermal growth factor receptor (ERBB1, NNCIS)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

epidermal growth factor receptor is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Uterine cancer✓ Approved

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An immunogenic cell death-based signature predicts prognosis and immune landscape in triple-negative breast cancer.

Zhang Xiyao X, Cao Miao M, Wu Lulu L, Zhao Yang Y

Triple-negative breast cancer (TNBC) represents a breast cancer subtype lacking three essential biomarkers: estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2). This biological signature differentiates TNBC from other breast cancer subtypes and acts as an essential diagnostic criterion for clinical identification and constitutes essential diagnostic criteria for clinical identification. Among all subtypes of breast cancer, TNBC exhibits an exceptionally high level of aggressiveness. Its aggressive behavior and paucity of effective treatment options contribute to its notoriously poor prognosis. The immunogenic cell death (ICD) emergence has raised hopes to create fresh treatment approaches to strengthen TNBC patients' immune responses against tumors. However, the correlation between ICD and TNBC prognosis is still unclear. By analyzing transcriptomic data through the Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA), we discovered the differentially expressed genes (DEGs) and linked to ICD in TNBC. A prognostic model utilizing ICD was developed through LASSO regression. Then, we conducted multivariate Cox proportional hazards analysis on the identified DEGs. We used receiver operating characteristic (ROC) curves and Kaplan-Meier (KM) analysis to evaluate the model's predictive accuracy. To comprehensively evaluate the clinical relevance of the ICD signature, we investigated its associations with genomic alterations, tumor microenvironment (TME) characteristics, and therapeutic responses to both chemotherapy and immunotherapy. Furthermore, functional validation was performed using MDA-MB-231 and BT-549 through various in vitro assays, including CCK-8 proliferation tests, colony formation assays, and Transwell migration experiments to assess HEYL's biological role. A 4-gene ICD signature (HEYL, CXCL13, GBP2, and IL22RA2) was developed and stratified TNBC patients into two categories, showing major distinctions in overall survival (OS). We found that higher-risk patients had less favorable results. Meanwhile, they usually had different TMEs with less immune cell infiltration. By contrast, the low-risk group appeared to react better to immunotherapy, as evidenced by their increased immune cell infiltration level and more favorable outcomes. Analysis via the Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) uncovered that DEGs were predominantly involved in immune-related pathways, for example, the receptors on the plasma membrane. Additionally, a lower immunological phenotype score (IPS) and increased susceptibility to various chemotherapeutic medicines, including A-443,654, BAY 61-3606, and CP466722, were detected in the low-risk category. Additionally, HEYL knockdown markedly suppressed TNBC cell growth and metastatic capability, whereas its overexpression produced the opposite outcome, promoting both traits. The prognosis and responsiveness to treatment for TNBC can be anticipated by the ICD-related gene profile, highlighting the significance of the immune microenvironment. It might provide insight into the design of tailored immunotherapies for TNBC.

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PubMedACS nano2026-07-17

A Screening-Guided Biomimetic Exosome-Liposome Hybrid Nanoplatform Enables Pyroptosis-Enhanced Immune Reprogramming in Glioblastoma.

Yu Wang W, Zhao Ru R, Miao Liming L, Bian Jie J et al.

Glioblastoma (GBM) is a highly lethal brain tumor, with therapeutic efforts hampered by the restrictive blood-brain barrier (BBB) and a profoundly immunosuppressive tumor microenvironment (TME). Driven by bioinformatics analysis identifying epidermal growth factor receptor (EGFR) and caspase-3 as key regulators of an immune-evasive pyroptosis pathway, we screened natural compounds and identified quercetin (Q) and chlorogenic acid (C) as dual-targeting agents, thereby laying a therapeutic foundation for amplifying pyroptosis in GBM treatment. The compounds were conjugated into a glutathione-responsive prodrug (QSSC) and encapsulated in a tumor-derived exosome-liposome nanoplatform (QSSC@Exo-LNP), enabling enhanced BBB penetration and intracranial targeting. Mechanistic studies revealed a dual-pathway amplification of pyroptosis, in which C directly activates caspase-8 to initiate gasdermin E (GSDME)-mediated pyroptosis, while Q/C-mediated EGFR inhibition activates mitochondrial pro-apoptotic protein, thereby augmenting caspase-3 and intensifying pyroptotic cell death. Upon intravenous injection, QSSC@Exo-LNP triggers robust pyroptosis, releasing DAMPs and tumor antigens for immune activation and macrophage reprogramming, converting the TME from "cold" to "hot" state. Moreover, this treatment strategy can significantly inhibit the distant tumors in the primary-distal orthotopic GBM model. This study proposes a strategy for the precise immunotherapy of GBM by exploiting natural products to target overexpressed GSDME and induce the pyroptotic cascade.

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PubMedOncogene2026-07-17

Multiparatopic antibodies overcome tyrosine kinase inhibitor resistance by inducing lysosomal degradation of EGFR mutants.

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Acquired resistance to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) remains a major challenge in the treatment of non-small cell lung cancer (NSCLC). To address this issue, we developed a novel therapeutic strategy based on multiparatopic antibodies that induce targeted degradation of EGFR, independent of driver mutations typically residing in the cytosolic domain. We engineered nanobodies (Nbs) recognizing four distinct epitopes within the EGFR extracellular domain into biparatopic and triparatopic antibody formats. These antibodies effectively promoted EGFR clustering, endocytosis, and lysosomal degradation, resulting in potent suppression of downstream signaling and cell proliferation in NSCLC cell lines carrying diverse EGFR mutations, including those resistant to osimertinib. The degradation process was epitope-dependent and mediated through a dynamin-dependent endocytic pathway. Triparatopic antibodies exhibited superior antitumor efficacy compared to both biparatopic antibodies and osimertinib in xenograft models of TKI-sensitive and TKI-resistant NSCLC cells. Moreover, these antibodies displayed additive effects when combined with osimertinib. We further demonstrated that this degradation mechanism extends beyond EGFR, as antibody-mediated crosslinking similarly triggered PD-L1 degradation. Collectively, this study indicates multiparatopic antibodies as a potent and mechanistically distinct strategy to overcome TKI resistance by directly degrading the target oncoprotein, with broad applicability to other pathogenic cell surface proteins.

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PubMedBioorganic chemistry2026-07-17

Structure-based design, synthesis, and biological evaluation of benzofuran derivatives as dual TGF-βR1 and VEGFR2 inhibitors for potent antitumor therapy.

Hu Liming L, Xu Yanan Y, Yao Keke K, Wang Xiaoli X et al.

The transforming growth factor-beta receptor type I (TGF-βR1) and vascular endothelial growth factor receptor 2 (VEGFR-2) signaling pathways are crucial for tumorigenesis across multiple cancer types. Evidence indicates that simultaneously targeting these pathways can offer an effective anticancer strategy, potentially overcoming resistance and the inconsistent responses often observed with single-target agents or standard combination therapies. We applied a structure-based design strategy that combined virtual screening, molecular docking, and molecular dynamics (MD) simulations. Using this approach, a series of benzofuran-pyrazole derivatives was designed and synthesized as dual inhibitors of TGF-βR1 and VEGFR-2 signaling. Additionally, in vitro testing identified compound 3b5 as the most potent dual inhibitor, displaying strong antiproliferative effects across various human cancer cell lines. Its impressive performance in the HT-29 colorectal cancer model makes 3b5 a promising candidate for further development.

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S100A8+S100A9+ transitional macrophages are associated with pulmonary fibrosis progression by integrating immunometabolism and fibrogenic crosstalk.

Lin Censhan C, Wu Mingyue M, Zhang Ziying Z, Zheng Muxu M et al.

Idiopathic pulmonary fibrosis (IPF) is a progressive interstitial lung disease with limited therapeutic options. Although macrophage heterogeneity has been implicated in pathogenesis, the contribution of transitional macrophage states remains poorly understood. We integrated single-cell RNA-seq from 93 human lung specimens (44 IPF, 49 controls) and analyzed peripheral blood single-cell datasets (31 IPF, 17 controls). We examined differentiation trajectories and ligand-receptor networks and assessed metabolic programs. Functional relevance was evaluated in a bleomycin mouse model using histology, immunostaining, qRT-PCR, and tissue glutamine quantification. We identified an S100A8+S100A9+ transitional macrophage population bridging FABP4+MME+ precursors and SPP1+MMP9+ effector macrophages. These cells are associated with fibrogenesis through two interconnected mechanisms: epidermal growth factor (EGF)-mediated signaling to fibroblasts and alveolar epithelial cells, amplifying profibrotic communication; and glutamine metabolic reprogramming, marked by GLUL. In murine bleomycin induced fibrosis, these features emerged early, with elevated S100a8, S100a9, Fcna, Timp1, and coincided with increased lung glutamine at day 14. Peripheral profiling confirmed concordant transcriptional changes in monocytes from IPF patients, supporting translational biomarker potential. S100A8+S100A9+ macrophages might function as a druggable immune-metabolic hub in IPF. Targeting S100A8/A9, GLUL-dependent glutamine flux, or EGFR-axis signaling may enable actionable paths for mechanism-based therapy. Furthermore, their peripheral molecular signature may offer a disease-specific biomarker platform for early diagnosis and therapeutic monitoring.

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PubMedAmerican journal of cancer research2026-07-17

Kang Ru Plus reverses osimertinib resistance in lung adenocarcinoma via suppression of EGFR/PI3K/AKT signaling.

Mhone Thomas G TG, Kuo Wei-Wen WW, Chi Chih-Ying CY, Kuo Chia-Hua CH et al.

Acquired resistance to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors such as osimertinib remains a major challenge in the treatment of EGFR-mutant non-small cell lung cancer (NSCLC). Multi-component natural product therapies may provide complementary strategies capable of modulating multiple signaling pathways involved in therapeutic resistance. This study investigated the pharmacological activity of Kang Ru Plus (KR-Plus), a multi-herb formulation, and evaluated its ability to enhance sensitivity to osimertinib in resistant lung adenocarcinoma models. The anti-proliferative and chemosensitizing effects of KR-Plus were assessed in EGFR-mutant lung adenocarcinoma cells and osimertinib-resistant derivatives using MTT assays, flow cytometry, immunofluorescence, and Western blot. Phytochemical composition was characterized by UHPLC-QTOF-MS-based metabolite profiling. Network pharmacology and molecular docking analyses were performed to predict potential targets and pathways. In vivo efficacy was evaluated in H1975-OSR xenograft mouse models. KR-Plus inhibited cell proliferation across multiple cancer cell lines and significantly enhanced the cytotoxic effects of osimertinib in resistant lung adenocarcinoma cells. Mechanistically, KR-Plus reduced EGFR phosphorylation and suppressed downstream PI3K/AKT, ERK, and mTOR signaling, resulting in cell-cycle arrest and apoptosis. Metabolite profiling identified several flavonoids and phenolic compounds with predicted interactions within EGFR-associated signaling networks. In xenograft models, combined treatment with KR-Plus and osimertinib markedly suppressed tumor growth and improved survival without evident systemic toxicity. KR-Plus exerts multi-target effects that disrupt EGFR-driven survival signaling and enhance responsiveness to osimertinib in resistant lung adenocarcinoma models. These findings support the potential of polyherbal formulations as complementary strategies to overcome resistance to targeted therapies.

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