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

Related Research Articles

PubMedNature metabolism2026-11-11

Microbiota-based modulation of intratumoral cholesterol metabolism for colorectal cancer treatment.

Wu Jiayan J, Li Liguo L, Lai Yingyao Y, Li Jinming J et al.

Excess cholesterol accumulates in colorectal cancer (CRC) and promotes its progression, yet systemic cholesterol-lowering has limited benefits and safety concerns. Here we show that redirecting intestinal cholesterol metabolism through the gut microbiota generates a metabolite, 4-cholesten-3-one (4-C-3), which suppresses CRC growth. A screen of microbial cholesterol metabolites showed that 4-C-3 is depleted in faecal and tumour samples from patients with CRC. 4-C-3 suppresses tumour growth in CRC cell lines, patient-derived organoids and xenografts. Mechanistically, 4-C-3 suppresses two major oncogenic drivers of CRC by inhibiting epidermal growth-factor receptor activation and stabilizing mutant oncogenic KRAS in an inactive state, thereby overcoming KRAS-driven resistance to anti-epidermal growth-factor receptor therapy. As proof of concept, restoring 4-C-3 using either Oscillibacter ruminantium, a natural 4-C-3 producer reduced in CRC, or a non-pathogenic Escherichia coli engineered to convert intestinal cholesterol into 4-C-3, lowered intratumoral cholesterol and induced tumour regression in preclinical models without overt toxicity. These findings uncover a microbiota-cholesterol metabolic pathway that can be harnessed through microbiome engineering to selectively target CRC and overcome therapy resistance.

PMID 43009614
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PubMedBMC women's health2026-11-11

Breast metastasis from BRCA1-mutated ovarian cancer: response to parp inhibition and a potential lymphatic route.

Xie Weiwei W, Liu Riqiang R, Xu Zhiyong Z, Xie Yanyan Y

Breast metastasis from extramammary malignancies is rare, with ovarian cancer being an exceptionally uncommon primary source. These metastases frequently mimic primary breast carcinoma, posing substantial diagnostic and therapeutic challenges. A 44-year-old woman presented with a breast mass initially suspected to be a primary breast carcinoma based on estrogen receptor (ER) (+, 80%), progesterone receptor (PR) (+, 5%), and Human Epidermal Growth Factor Receptor 2 (HER2) (0) staining. However, subsequent workup revealed a synchronous ovarian high-grade serous carcinoma (PAX8+/WT1+), raising the question of dual primary versus metastatic disease and prompting re-review of the breast biopsy, which ultimately confirmed the metastatic ovarian origin of the breast lesion. A pathogenic germline BRCA1 mutation c.964del (p.Ala322Leufs*19) was identified. After neoadjuvant chemotherapy and cytoreductive surgery, the patient received olaparib maintenance therapy, achieving 27 months of progression-free survival before platinum-resistant recurrence. Repeat HER2 testing of the breast lesion at recurrence showed conversion to IHC 2 + with FISH amplification, prompting enrollment in a clinical trial evaluating an anti-HER2 antibody-drug conjugate (ADC). This case highlights three key points. First, the PAX8/WT1/GATA3 immunohistochemical panel is critical for distinguishing ovarian metastasis from primary breast carcinoma. Second, the route of spread from the ovary to the breast, possibly transdiaphragmatic via the cardiophrenic and internal mammary nodes, requires further investigation. Third, PARP inhibitor maintenance in the context of a germline BRCA1 mutation provided sustained disease control, and HER2 status conversion at recurrence opened a therapeutic window for sequential antibody-drug conjugate (ADC) therapy.

PMID 43009943
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PubMedJournal of ovarian research2026-11-11

Advances in the application of fluorescent probes for ovarian cancer.

Qi Long L, Chen Mingjie M, Wang Chao C, Feng Shuo S et al.

Ovarian cancer remains a major challenge among gynecologic malignancies because it often develops with vague or nonspecific symptoms and frequently disseminates within the peritoneal cavity before detection. Currently, no screening strategy has been proven to effectively reduce mortality in the general population, so many patients are diagnosed at an advanced stage. Therefore, improving diagnostic accuracy and treatment precision is important for better clinical outcomes. Fluorescent probe-based imaging has gained increasing attention in ovarian cancer diagnosis, surgical navigation, and treatment monitoring. Owing to their molecular targeting ability, these probes can help visualize small peritoneal implants, micrometastases, and tumor margins that may be difficult to identify under conventional white-light observation. This may improve lesion detection and support more complete cytoreductive surgery. In addition, some probe systems are being investigated for drug-delivery tracking and theranostic applications, combining imaging with therapeutic functions. In recent years, probes targeting ovarian cancer-associated biomarkers such as folate receptor(FR), epidermal growth factor receptor(EGFR), γ-glutamyl transpeptidase(γ-GGT), gonadotropin-releasing hormone receptor(GnRHR), and β-galactosidase(β-Gal) activity have been developed. Some of these platforms incorporate activatable fluorescence, photothermal effects, or drug-loading capacity, providing potential strategies for image-guided surgery and targeted therapy. However, several limitations remain. Conventional fluorescent dyes may have limited tissue penetration, photobleaching, background autofluorescence, and dependence on specialized imaging equipment. Off-target accumulation or biomarker expression in normal tissues can also reduce tumor-to-background contrast.Future studies should integrate nanotechnology, chemical probe design, and genetic engineering to improve penetration depth, signal stability, and tumor specificity. Before clinical application, these probes require rigorous validation in standardized trials to assess their safety, reproducibility, imaging performance, and therapeutic value.

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PubMedBMC pulmonary medicine2026-11-11

Afatinib-associated pancreatitis in a patient with lung cancer- A rare case report.

Chu Ko-Hsin KH, Lin Meng-Jiong MJ, Chen Guan-Liang GL

Afatinib is an epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor used in EGFR-mutant non-small cell lung cancer (NSCLC). Although gastrointestinal adverse effects are common, pancreatitis is rarely reported. A 63-year-old woman with EGFR exon 21 L858R-mutant lung adenocarcinoma developed progressive gastrointestinal symptoms one month after starting afatinib. Laboratory tests showed markedly elevated pancreatic enzyme levels, while abdominal imaging revealed no typical findings of pancreatitis. Other common etiologies were excluded. Afatinib was discontinued, and supportive treatment resulted in clinical improvement and normalization of pancreatic enzymes. She was subsequently switched to erlotinib with stable disease. Afatinib-associated pancreatitis is an extremely rare adverse event that may occur without characteristic imaging abnormalities. Early recognition and discontinuation of the offending agent are essential.

PMID 43009907
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PubMedBiomedical chromatography : BMC2026-11-11

Exploring Material Basis and Q-Markers for Treatment of Alcoholic Liver Disease With Tetracera asiatica Tablets Based on In Vitro Components-In Vivo Transferring Components-Efficacy Targets.

Fangfang Da D, Ziwan Yuan Y, Ying Liu L, Yufeng Chen C et al.

This study aimed to clarify the therapeutic material basis of Tetracera asiatica (TA) against alcoholic liver disease (ALD) and predict its potential quality markers (Q-markers). UPLC-Q-Exactive Orbitrap HRMS, Progenesis QI 3.0 and reference compound database were adopted to characterize in vitro constituents, in vivo prototypes and postintragastric metabolites. Targets retrieved from multiple databases were used to construct a component-target-disease network, and molecular docking was performed to evaluate binding affinity. The ethanol extract of TA alleviated ethanol-induced increases in aspartate aminotransferase (AST) and alanine aminotransferase (ALT). Among 170 characterized constituents, 49 were detected in mouse serum and liver, and 350 overlapping targets between TA and ALD were screened. Kaempferol, eriodictyol, ellagic acid, catechin, quercetin, and naringenin were key active constituents, functioning through HIF-1, AGE-RAGE, and JAK-STAT pathways and showing strong binding to SRC proto-oncogene, non-receptor tyrosine kinase (SRC), B-cell lymphoma-2 (BCL2), and epidermal growth factor receptor (EGFR). These six compounds constitute the core pharmacodynamic material basis of TA against ALD and are promising candidate Q-markers based on specificity, detectability, efficacy correlation, bioavailability, and TCM theory.

PMID 43012167
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PubMedFrontiers in pharmacology2026-11-11

Cost-effectiveness of inavolisib plus palbociclib/fulvestrant versus palbociclib/fulvestrant for PIK3CA-mutated advanced breast cancer in China.

Xiang Zuojuan Z, Chen Xiaojuan X, Ma Ling L

Based on the positive findings of the INAVO120 study, inavolisib is the only phosphatidylinositol 3-kinase alpha (PI3Kα) inhibitor approved for breast cancer treatment in China and has been included in the National Reimbursement Drug List following national medical insurance price negotiations. A partitioned survival model with a 30-year time horizon was constructed to assess the cost-effectiveness of inavolisib plus palbociclib/fulvestrant versus palbociclib/fulvestrant alone in patients with phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha (PIK3CA)-mutated, hormone receptor (HR)+, human epidermal growth factor receptor 2 (HER2)-, locally advanced or metastatic breast cancer (a/m BC). Clinical data were extracted from the Asian cohort of the INAVO120 trial. Drug prices were sourced from the government procurement platform, while additional cost and utility parameters were derived from the published literature. The primary model outcome was the incremental cost-effectiveness ratio (ICER). To assess the robustness of the results, scenario and sensitivity analyses were performed. Additionally, a price simulation analysis was conducted for inavolisib. The ICER was determined to be $36,932.91/quality-adjusted life-year (QALY), which exceeded the willingness-to-pay (WTP) threshold of $27,906/QALY. To attain cost-effectiveness, a further price reduction of 27.02% for inavolisib would be necessary. Scenario and sensitivity analyses confirmed the robustness of the results. The addition of inavolisib to palbociclib plus fulvestrant for PIK3CA-mutated HR+/HER2-a/m BC is not a cost-effective treatment strategy at the national level in China. However, this triple therapy may achieve cost-effectiveness in economically affluent regions with higher local WTP thresholds.

PMID 43011102
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