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

✓ Approved

Dako · EGFR · 辅助诊断

什么是 epidermal growth factor receptor？

epidermal growth factor receptor 是一种辅助诊断，由Dako研发。该药已获批，用于治疗相关适应症，给药途径：Others。

药物档案

商品名EGFR pharmDx, EGFR pharmDx Kit
公司Dako
药物类别辅助诊断
分子靶点EGFR
给药途径Others
状态Approved
来源： ClinicalTrials.gov, Dako

作用机制

分子靶点

epidermal growth factor receptor 作用于 1 个分子靶点：

EGFRepidermal growth factor receptor (ERBB1, NNCIS)
需要更深入的分析？Noah AI 可解释复杂机制并与同类药物比较。

治疗适应症

epidermal growth factor receptor 针对 1 个适应症，涉及 1 个治疗领域。

治疗领域疾病/病症分期
Neoplasms benign, malignant and unspecified (incl cysts and polyps)Uterine cancer✓ Approved

相关研究文献

PubMedFuture medicinal chemistry2026-07-27

Isatin as a privileged scaffold for kinase inhibition: recent advances in anti-cancer research.

Mushtaq Alia A, Khan Azmat Ullah AU, Maqbool Akasha A, Shahzad Muhammad M et al.

Protein kinases are key therapeutic targets in anticancer drug discovery due to their central roles in regulating cell proliferation, survival, and signaling pathways. Among diverse heterocyclic scaffolds, isatin (indole-2,3-dione) has emerged as a privileged framework for the development of potent kinase inhibitors due to its structural versatility and favorable interaction profile within binding pockets. This review provides a comprehensive overview of recent advances in isatin-based kinase inhibitors, highlighting their design strategies, structure-activity relationships (SAR), and key molecular determinants of potency and selectivity. Particular emphasis is placed on structural optimization at the N-1 and C-5/C-7 positions, as well as hybridization with heterocyclic pharmacophores has yielded compounds with nanomolar inhibitory activity against clinically relevant targets, including cyclin dependent kinases (CDKs), vascular-endothelial growth factor receptor (VEGFR), epidermal growth factor receptor (EGFR) and other kinases. In addition, ligand-kinase interactions are critically analyzed, with focus on hinge-region hydrogen bonding and hydrophobic complementarity within the ATP-binding site. Computational approaches, including molecular docking studies, are integrated to rationalize binding modes and support SAR interpretations. Collectively, this review underscores isatin as a versatile and promising scaffold for the rational design of next generation multitarget kinase inhibitors with potential applications in anticancer therapy.

PMID 42504730
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PubMedCells2026-07-27

Rasgrp1-Mediated Dampening of EGFR Signals Supports Coordinated Mammary Gland Development.

Samocha Alexandr A, Shechtman Lauren L, Tapia Eunice Bonfil EB, Doh Hanna M HM et al.

Mammary gland development during puberty requires tightly coordinated epithelial proliferation, lineage specification, and branching morphogenesis, processes critically regulated by growth factor signaling. While epidermal growth factor receptor (EGFR) signaling is essential for ductal development, how its activity is quantitatively controlled within mammary epithelial cells (MECs) remains incompletely understood. Here, we identify Rasgrp1, a Ras guanine nucleotide exchange factor, as a key modulator of EGFR signaling in the mammary epithelium. Using Rasgrp1-deficient mice, primary MEC assays, and organoid models, we demonstrate that loss of Rasgrp1 leads to elevated EGFR-Ras-PI3K-AKT and mTORC1-S6 signaling, resulting in enhanced proliferative capacity and aberrant EGF-driven branching. Transcriptomic analysis of organoids reveals that EGF signaling suppresses Wnt/R-spondin-dependent stem-cell gene programs, suggesting that excessive EGFR activity disrupts stem cell maintenance. In vivo, Rasgrp1 deficiency causes impaired ductal elongation, persistent terminal end buds, and increased epithelial proliferation, indicating a breakdown in the spatial and temporal coordination of mammary morphogenesis. Together, our findings establish Rasgrp1 as a signaling rheostat that dampens EGFR pathway activity to support coordinated mammary gland development. These results highlight the importance of precise signaling calibration in epithelial development and suggest broader implications for Ras pathway regulation in tissue homeostasis and disease.

PMID 42505397
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PubMedCells2026-07-27

Necroptosis: The Regulation Between EGFR and TNFR in Cancer.

Kim Jin Gyeom JG, Jin Wook W

Most cancers are fatal and remain challenging to cure due to changes in tumorigenesis and therapeutic resistance. Despite significant advancements in cancer therapy, a substantial proportion of malignancies exhibit resistance to conventional therapies, driven primarily by cancer plasticity and the emergence of multidrug resistance. Recent cancer treatments include cytotoxic chemotherapy, molecular targeted therapy, and immune checkpoint inhibitors. A major hallmark of cancer cells is their ability to develop sophisticated evasion mechanisms that bypass programmed cell death when exposed to anti-cancer drugs. In addition, malignant cells evade the efficacy of anti-cancer drugs by altering cell proliferation, survival, and metastasis. To suppress oncogenic characteristics, necroptosis-based therapies have attracted substantial attention, as they can inhibit tumorigenesis and improve treatment outcomes across many cancer types. Furthermore, an increasing body of research focuses on suppressing tumorigenesis by targeting receptors that are overexpressed in cancer cells. In this review, we elucidate how tumorigenesis is inhibited by regulating the epidermal growth factor receptor (EGFR)-tumor necrosis factor receptor (TNFR) signaling pathway in necroptosis. By delineating the underlying mechanisms of these receptors, we propose that the induction of necroptosis via EGFR and TNFR represents an innovative paradigm for targeted therapy, offering a strategy to enhance clinical outcomes in treatment-resistant cancers.

PMID 42505417
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PubMedCurrent oncology (Toronto, Ont.)2026-07-27

Evolving First-Line Endocrine Therapy in HR+/HER2- Metastatic Breast Cancer: CDK4/6 Inhibition, Biomarker-Guided Strategies and Emerging Therapeutic Paradigms.

Abdel-Razeq Hikmat H, Sharaf Baha B

Hormone receptor-positive (HR+), human epidermal growth factor receptor 2-negative (HER2-) metastatic breast cancer (MBC) is the most prevalent subtype of advanced breast cancer and is predominantly driven by estrogen receptor (ER) signaling. Endocrine therapy (ET) has become the backbone of first-line treatment; however, both intrinsic and acquired resistance limit long-term disease control. The introduction of cyclin-dependent kinase 4/6 (CDK4/6) inhibitors has fundamentally reshaped the therapeutic landscape even in subsets of patients with aggressive or symptomatic visceral metastatic disease. Advances in molecular profiling have also enabled more precise, adaptive therapy. Circulating tumor DNA (ctDNA)-based liquid biopsy now allows real-time detection of emerging resistance mutations, particularly in ESR1. Additionally, patients with PIK3CA-mutated tumors who had progressed on or within 12 months of completing adjuvant ET and had no prior systemic therapy for metastatic disease had better treatment outcomes when treated with the PI3K inhibitor inavolisib in combination with palbociclib and fulvestrant. Together, these developments mark a shift from fixed treatment sequencing toward a more dynamic, biomarker-driven approach in first-line HR+/HER2- MBC. Integration of CDK4/6 inhibitors with next-generation endocrine agents and liquid biopsy-guided therapy offers the potential to delay resistance, improve survival outcomes, and individualize treatment.

PMID 42505223
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PubMedCureus2026-07-27

Evaluation of Serum Vascular Endothelial Growth Factor (VEGF) and Placental Growth Factor (PlGF) Levels in Unexplained Early Pregnancy Loss: A Case-Control Study.

Bb Mahantesh M, Dongre Nilima N, Mallapur Ashalata A

Early pregnancy loss, defined as spontaneous termination of pregnancy before 20 weeks of gestation or fetal weight below 500 g, remains a common obstetric complication. While several etiological factors, such as genetic abnormalities and uterine defects, are established, nearly half of the cases remain unexplained, necessitating exploration of underlying biochemical mechanisms. To evaluate and compare serum levels of vascular endothelial growth factor (VEGF) and placental growth factor (PlGF) in women with early pregnancy loss and healthy pregnant controls of similar gestational age and to assess the association and diagnostic performance of these angiogenic markers. A hospital-based case-control study was conducted involving 60 pregnant women aged 19-45 years with pregnancies of less than 20 weeks' gestation, including 30 cases of early pregnancy loss and 30 healthy pregnant controls with viable intrauterine pregnancies of comparable gestational age. Participants were recruited from the Department of Obstetrics and Gynecology of HSK Hospital, Bagalkot, and biochemical analysis was performed at Bharatiya Lingayat Development Educational Association (Deemed to be University) (BLDE [DU]), Vijayapura. Serum VEGF and PlGF levels were measured using enzyme-linked immunosorbent assay (ELISA). Statistical analysis was performed using IBM Corp. Released 2014. IBM SPSS Statistics for Windows, Version 20. Armonk, NY: IBM Corp., applying chi-square and independent t-tests, with results expressed as mean ± standard deviation (SD). Receiver operating characteristic (ROC) curve analysis was performed to assess diagnostic performance and derive optimal cut-off values. Serum VEGF and PlGF levels were significantly reduced in cases compared to controls (p < 0.05), indicating impaired angiogenesis in early pregnancy loss. ROC analysis showed adequate diagnostic performance for VEGF and excellent diagnostic performance for PlGF in differentiating cases from controls within this case-control sample. Reduced serum VEGF and PlGF levels are associated with early pregnancy loss and may serve as adjunctive diagnostic biomarkers for identifying altered angiogenic profiles in affected women after validation in larger prospective studies.

PMID 42504346
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PubMedMedicinal research reviews2026-07-27

Hsp90 Inhibition on the Western Blot: N-Terminal Versus C-Terminal Inhibitors in Breast Cancer.

Dernovšek Jaka J, Cingl Jernej J, Fonović Urša Pečar UP, Tomašič Tihomir T

Heat shock protein 90 (Hsp90) is an established and clinically validated anticancer target. By regulating the folding and maturation of diverse client proteins, it is indirectly involved in carcinogenesis. Key breast cancer oncogenic drivers, including estrogen receptor, progesterone receptor, and human epidermal growth factor receptor 2, are established Hsp90 clients, making breast cancer models widely used for Hsp90 inhibitor evaluation. However, N-terminal inhibitors are well known to induce a heat shock response (HSR), representing a major limitation in cancer therapy. This has driven the development of alternative modalities, such as C-terminal inhibitors, which in several cases avoid HSR induction. To evaluate Hsp90 inhibitors and characterize their proteomic effects, most studies employ western blotting (WB) as the primary method. On WB, different inhibitors are tested across various concentrations, time points, and breast cancer cell lines for their effects on client, heat shock, and other proteins. This generates extensive data sets that outline the expected WB performance of Hsp90 inhibitors. In this review, we focus on 10 protein families that are commonly used to assess Hsp90 inhibition in in vitro breast cancer models and represent all 10 cancer hallmarks. We provide basic structural and functional information on these families and comprehensively describe the effects of N- and C-terminal inhibitors on their levels. We summarize WB-based observations for more than 100 Hsp90 inhibitors, outlining the characteristic effects of N- and C-terminal inhibition, highlighting opportunities for future research, and ending with a suggestion for the WB method design based on best practices observed in literature.

PMID 42504391
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