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)
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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

Related Research Articles

PubMedNPJ breast cancer2026-08-30

Genomic characterization of ER-positive primary tumors and corresponding relapses identifies potentially targetable alterations.

Schagerholm Stanev Caroline C, Robertson Stephanie S, Toosi Hosein H, Sifakis Emmanouil G EG et al.

The majority of breast cancer patients have tumors expressing estrogen receptor α (ER) and receive endocrine therapy. However, around one-third relapse in their disease, predominantly with retained ER expression. Molecular alterations are proposed to be contributors to the resistance mechanisms. Patients with ER-positive, human epidermal growth factor receptor 2 (HER2)-negative primary breast cancer with an ER-positive relapse < 5 years of ongoing endocrine therapy were retrospectively assessed. Extracted DNA was analyzed through panel sequencing, and RNA by microarray, from patients' primary (n = 58), and paired relapse tumors (n = 54), and tumor-free lymph nodes (DNA germline controls, n = 62). Several single-nucleotide variations and copy number variations showed nominal exploratory associations with worse overall survival. Copy number correlations with intrinsic subtypes and individual gene expression supported the findings. These results identify hypothesis-generating genomic and transcriptomic features, including potentially targetable alterations, in a clinically defined cohort of endocrine-resistant breast cancer patients.

PMID 42668305
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PubMedJournal of chromatography. B, Analytical technologies in the biomedical and life sciences2026-08-30

Development and ICH M10-compliant validation of an LC-MS/MS method for quantification of atirmociclib in mouse plasma and its application to preclinical pharmacokinetic studies.

Gaur Ashwani A, Patel Urvesh U, Gavali Ashutosh A, Sekar Sasikumar S et al.

Atirmociclib is a selective cyclin-dependent kinase 4 (CDK4) inhibitor currently under clinical investigation for the treatment of advanced malignancies, particularly hormone receptor positive (HR+) or human epidermal growth factor receptor 2 negative (HER2-) breast cancer. Here, we report the first validated liquid chromatography tandem mass spectrometry (LC-MS/MS) bioanalytical method for the quantification of atirmociclib in mouse plasma, validated in compliance with international council for harmonisation-M10 (ICH-M10) guidelines. Sample preparation involved a rapid and straightforward protein precipitation approach using acetonitrile, yielding consistent recovery (>80%) across low to high concentration levels. Chromatographic separation was achieved on a Kinetex C18 column (50 mm length × 2.1 mm internal diameter, 5 μm particle size) using gradient elution with 5 mM ammonium acetate in water (mobile phase A) and 0.1% v/v formic acid in acetonitrile (mobile phase B). The analyte (atirmociclib) and internal standard (warfarin) were detected using Q1/Q3 (m/z) mass transitions 464.2/303.9 and 309.0/163.0 respectively. The method demonstrated excellent selectivity, accuracy, precision, and linearity over a concentration range of 1-1000 ng/mL. Additionally, reliable quantification was maintained for samples exceeding the upper limit of quantification following up to 10-fold dilution. All validation parameters, including stability in biological matrices and solution, met the predefined acceptance criteria. This sensitive, and reproducible method was successfully applied to support preclinical pharmacokinetic study of atirmociclib in mouse, providing a valuable analytical tool.

PMID 42669270
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PubMedAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026-08-30

Hyper-Intense Tumor Peripheral Accumulation of Antibody-Conjugated Iron Oxide Nanoparticles can Enable Breast Cancer Detection by Magnetic Particle Imaging.

Korangath Preethi P, Carlton Hayden H, Wong Theresa T, Healy Sean S et al.

Targeting nanoparticles to cancer cells in vivo remains a challenge for cancer imaging. We assessed nanoparticle distribution after injecting iron oxide nanoparticles conjugated with either a monoclonal anti-HER2 (human epidermal growth factor 2), or a non-specific IgG antibody into a human HER2 overexpressing murine breast cancer model. We used Magnetic Particle Imaging (MPI) and histopathology to assess particle localization at 72 h after injection. MPI detects magnetic moments produced by magnetic particles, and histology enables spatial quantification of nanoparticles. Intratumor iron content measured by MPI correlated with inductively coupled plasma mass spectrometry (ρ = 0.868, p < 0.0001). We detected nanoparticle accumulation in tumors, and organs and tissues associated with inflammation. MPI showed higher uptake of nanoparticles in tumors, regardless of their performance in vitro. Spatial analysis showed that 43 ± 7% of nanoparticles that reached the tumor accumulated in the peripheral quartile of the tumor, with decreasing amounts toward the center. Immunohistochemical analysis showed the nanoparticles were strongly associated with inflammatory immune and stromal cells in the tumor microenvironment. This hyperintense peripheral accumulation, or ring pattern, observed with MPI enabled us to distinguish tumors from general inflammation. Iron oxide nanoparticle-mediated MPI has the potential to detect tumors, providing another powerful diagnostic tool.

PMID 42669153
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PubMedBiochimica et biophysica acta. Molecular basis of disease2026-08-30

EGFR and PGE2 signaling pathways mutually cooperate to promote pro-tumorigenic effects in cervical cancer.

de Azevedo Vitória R VR, Guimarães Isabella Dos S IDS, Farrapo Mario J MJ, Martins-Cardoso Karina K et al.

Cervical cancer (CC) remains a public health challenge in developing countries. Epidermal growth factor receptor (EGFR) is a receptor tyrosine kinase highly expressed in CC. Studies showed that PGE2 may transactivate EGFR in some models. However, understanding the interaction between the EGFR and PGE2 signaling pathways in CC is a key area for investigation. The Cancer Genome Atlas (TCGA) was used to evaluate gene expression correlation and clinical outcomes. Panitumumab and aspirin were employed to inhibit EGFR and COX-1/2, respectively. Cell migration was evaluated using Boyden chamber. MTT and clonogenic assays determined cell viability and clonogenicity. Western Blotting analyzed protein expression. PGE2 was measured in the supernatants of cell lines using ELISA. Flow cytometry was used for cell death assays. TCGA analysis revealed a significant positive correlation between EGFR and COX-1, COX-2, and microsomal prostaglandin E synthase-1 (mPGES-1). CC patients showed decreased overall survival upon overexpression of EGFR or COX-2. CASKI and HeLa cells were cisplatin-resistant, whereas C33A cells were chemosensitive. CASKI cells exhibited the highest EGFR levels, while HeLa cells showed highest levels of COX-2 and mPGES-1. HeLa cells showed marked upregulation of COX-2 and mPGES-1 and increased PGE2 secretion upon EGF stimulation. Moreover, PGE2 activated ERK signaling and promoted cell migration through an EGFR-dependent mechanism. Panitumumab plus aspirin impaired cell viability, clonogenicity and chemoresistance. Simultaneous stimulation with EGF and PGE2 mitigated cisplatin-induced apoptosis in CASKI cells. The interactions between EGFR and PGE2 signaling pathways link inflammation and oncogenic signaling, promoting tumor aggressive behavior.

PMID 42669370
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PubMedAnti-cancer drugs2026-08-30

Estrogen-related receptor α promotes breast cancer cell migration and invasion by activating transforming growth factor β signaling.

Prusty Monica M, Muduli Kartik K, Pradhan Jagannath J, Samal Archana Priyadarshini AP et al.

Breast cancer is a major cause of cancer-related mortality among women, and many patients eventually experience recurrence and progression to metastasis, despite advances in treatment. Estrogen-related receptor α (ERRα), an orphan nuclear receptor, is frequently overexpressed in aggressive breast cancer subtypes and is associated with poor prognosis and an increased risk of recurrence. This study aimed to investigate the role of transforming growth factor β (TGFβ) signaling in ERRα-mediated epithelial-mesenchymal transition (EMT), migration, and invasion in breast cancer cells. ERRα expression was modulated in breast cancer cells using XCT790-mediated inhibition, shRNA-mediated knockdown, and overexpression. Cell viability, clonogenicity, migration, invasion, EMT marker expression, and matrix metalloproteinase (MMP) activity were evaluated. TGFβ1 secretion and Smad signaling were also evaluated. XCT790-mediated inhibition or shRNA-mediated silencing of ERRα significantly reduced cell viability, migration, invasion, and MMP secretion in breast cancer cell lines, whereas ERRα overexpression upregulated migration, invasion, and MMP levels. ERRα suppression also upregulated the epithelial marker ZO-1 and downregulated mesenchymal markers, such as vimentin and β-catenin. This effect was associated with a significant decrease in TGFβ secretion, downregulation of TGFβ-mediated Smad signaling, and reduced expression of its downstream target ANGPTL4. These findings indicate that ERRα promotes EMT, migration, and invasion in breast cancer by upregulating TGFβ secretion and its signaling, underscoring its potential as a therapeutic target.

PMID 42669034
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PubMedCancer pathogenesis and therapy2026-08-30

Efficacy and safety of SCT200 in patients with recurrent or metastatic head and neck squamous cell carcinoma after platinum failure: A phase 2 study.

Shi Yuankai Y, Zhang Qingyuan Q, Wang Wei W, Shi Jianhua J et al.

There are limited treatment options for patients with recurrent or metastatic head and neck squamous cell carcinoma (R/M HNSCC) progressing after platinum-based therapy. Epidermal growth factor receptor (EGFR)-targeting monoclonal antibodies (mAbs) have demonstrated efficacy in R/M HNSCC. This phase 2 study evaluated the efficacy and safety of SCT200, a novel fully humanized EGFR mAb, in Chinese patients with R/M HNSCC progressing after platinum-based therapy. This was a single-arm, multi-center phase 2 study, which enrolled patients with R/M HNSCC who had progressed after ≥2 cycles of platinum-based therapy. All patients received SCT200 at 6.0 mg/kg weekly for the first 6 weeks, followed by 8.0 mg/kg every 2 weeks until disease progression or unacceptable toxicity. The primary endpoint was the objective response rate (ORR). Between November 14, 2018, and April 2, 2020, 36 patients were enrolled. The ORR was 13.9% (5/36, 95% confidence interval [CI]: 4.7-29.5), the complete response rate was 2.8% (1/36), while the partial response rate was 11.1% (4/36). The disease control rate was 69.4% (25/36, 95% CI: 51.9-83.7). The median time to response was 1.38 months (95% CI: 0.99-2.60). The median duration of response was 5.95 months (95% CI: 2.60-not reached [NR]). The median progression-free survival and overall survival were 3.98 months (95% CI: 2.76-5.32) and 8.77 months (95% CI: 6.64-NR), respectively. Grade ≥3 treatment-related adverse events occurred in 44.4% (16/36) of patients, with the most common being hypomagnesemia (7/36, 19.4%, 95% CI: 8.2-36.0), hypokalemia (3/36, 8.3%, 95% CI: 1.8-22.5), rash (2/36, 5.6%, 95% CI: 0.7-18.7), and anemia (2/36, 5.6%, 95% CI: 0.7-18.7). This study demonstrated promising efficacy and a manageable safety profile of SCT200 in patients with R/M HNSCC progressing after platinum-based chemotherapy. Clinical Trials.gov, NCT03713372; https://www.clinicaltrials.gov.

PMID 42668534
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