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

PubMedPharmacological research2026-08-09

Biomimetic exosomal delivery of Ginsenoside Rd reduces post-stroke depression via microglial reprogramming in a pathway involving EGFR/JAK2/STAT3.

Chen Jiaxin J, Yin Xuanying X, Yan Dong D, Shi Qing Q et al.

Post-stroke depression (PSD) represents a complex neuropsychiatric challenge characterized by persistent neuroinflammation and synaptic dysfunction, yet effective therapeutic interventions are constrained by the blood-brain barrier (BBB) and the lack of specific targets. Using a multidimensional screening strategy for Chaihu-Jia-Longgu-Muli Decoction (CLM), we identified ginsenoside Rd (Rd) as a key blood-absorbed bioactive constituent associated with Epidermal Growth Factor Receptor (EGFR) signaling. To overcome the bioavailability bottleneck, a biomimetic nanodelivery system is engineered by encapsulating Rd into microglia-derived exosomes (Exos@Rd). Based on the reported lesion-homing properties of microglia-derived exosomes, we developed a biomimetic Exos@Rd delivery system. Exosomal loading markedly enhanced the brain accumulation of Rd compared with free Rd. Mechanistically, it is demonstrated that aberrant EGFR activation functions as an upstream regulator of the JAK2/STAT3 cascade in microglia. Exos@Rd effectively suppressed this pathway and promoted anti-inflammatory microglial reprogramming, characterized by a shift from an M1-associated pro-inflammatory state toward an M2-associated anti-inflammatory profile. This microglia-centered anti-inflammatory regulation was accompanied by reduced oxidative stress and restoration of brain-derived neurotrophic factor (BDNF), postsynaptic density protein 95 (PSD95) and Synapsin I (SYN1) expression. In a PSD mouse model, Exos@Rd significantly restores cerebral perfusion and alleviates depressive-like behaviors. Collectively, this study elucidates a novel EGFR-driven neuroinflammatory mechanism and presents a bio-inspired strategy for precision CNS drug delivery, offering a promising therapeutic paradigm for PSD.

PMID 42570766
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PubMedVeterinary research forum : an international quarterly journal2026-08-09

Protective effects of melatonin against hypoxia-induced TM3 cell damage via suppression of the TGF-β pathway.

Rashidi Sahar S, Saberivand Adel A, Gholami Mohammadreza M, Assadollahi Vahideh V et al.

This study aimed to explore whether melatonin protects TM3 Leydig cells from cobalt (II) chloride (CoCl2)-induced hypoxia through the transforming growth factor beta (TGF-β) signaling pathway. Cells were divided into four groups: a control group without treatment (Group 1), a melatonin group (10.00 ng mL-1; Group 2), a group treated with CoCl2 (100 µM) to induce hypoxia (Group 3), and a melatonin + CoCl2 group (Group 4). After 96 hr of incubation, cell viability was assessed using the MTT assay, and transforming growth factor beta 1, activin receptor-like kinase-5, and bone morphogenetic protein 4 gene and protein expressions were measured through RT‑PCR and western blotting. The CoCl2 and melatonin + CoCl2 groups exhibited significantly diminished cell viability compared to the control. However, melatonin treatment enhanced survival in the CoCl2-exposed cells. Notably, transforming growth factor beta 1 expression was elevated in all groups. Activin receptor-like kinase-5 (gene and protein expression increased in CoCl2-treated groups but was lower in the melatonin + CoCl2 group. Melatonin treatment reduced bone morphogenetic protein 4 expression compared to the control, while CoCl2 groups showed increased bone morphogenetic protein 4 levels. These findings suggest melatonin's potential as a therapeutic agent against oxidative stress and hypoxia in TM3 cells through its antioxidant properties.

PMID 42571600
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PubMedVeterinary research forum : an international quarterly journal2026-08-09

Molecular investigation of biofilm-forming genes in staphylococci isolated from dogs in Ilam, Iran.

Soltani Negar N, Nemati Mostafa M, Pourahmad Fazel F

Biofilm formation is a key virulence factor in Staphylococcus aureus, contributing to bacterial persistence, antimicrobial resistance, and chronic infections. This study aimed to investigate the presence of biofilm-associated genes (fib, fnbA, fnbB, clfA, and clfB) in S. aureus isolates from dogs in Ilam, Iran. From December 2022 to September 2023, 250 swab samples were collected from nasal, oral, and rectal sites of dogs, yielding 81 S. aureus isolates confirmed by PCR amplification of the nuc gene. The prevalence of biofilm-associated genes varied, with clfA, clfB, and fnbA detected in 98.80% of isolates, fib in 63.00%, and fnbB in 16.00%. Notably, fnbA, clfA, and clfB were present in all rectal isolates, while fnbB was absent in this group. The findings highlighted the widespread presence of biofilm-related genes in S. aureus from dogs, suggesting their potential role in colonization and zoonotic transmission. The high prevalence of adhesion-associated genes underscored the need for monitoring biofilm-forming S. aureus in companion animals to mitigate antimicrobial resistance and public health risks.

PMID 42571553
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PubMedIranian journal of medical sciences2026-08-09

Insulin Resistance and Cutaneous Squamous Cell Carcinoma: A Narrative Review of Molecular Mechanisms.

Ardinata Dedi D, Alferraly Tengku Ibnu TI, Yosi Ariyati A, Pase Muhammad Aron MA

Although the association between diabetes and cutaneous squamous cell carcinoma (cSCC) is well recognized, the specific role of insulin resistance (IR) as an independent driver of cSCC pathogenesis remains underexplored. This review synthesized emerging evidence on the ultraviolet (UV)-independent molecular mechanisms by which IR promotes cSCC initiation and progression. Hyperinsulinemia activates the insulin-like growth factor-1 receptor (IGF-1R), which triggers both the mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) and phosphoinositide 3-kinase/protein kinase B (PI3K/Akt) pathways, stimulating keratinocyte proliferation and suppressing apoptosis. In parallel, hyperglycemia-driven formation of advanced glycation end products (AGEs) and oxidative stress cause deoxyribonucleic acid (DNA) damage and impair tumor suppressor functions, notably that of tumor protein p53 (TP53). The resulting reactive oxygen species (ROS) activate nuclear factor-kappa B (NF-κB), establishing a chronic inflammatory milieu that remodels the tumor microenvironment through cytokines, including interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α), and by upregulating matrix metalloproteinases (MMPs). These processes collectively facilitate the malignant transformation of actinic keratosis (AK) to invasive cSCC. The analysis in the present study identified novel therapeutic targets and reaffirmed the importance of further studies on microbiome interactions and lifestyle interventions for IR-associated cSCC.

PMID 42571124
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PubMedAnnals of Saudi medicine2026-08-09

Clinical characteristics of lung cancer in never-smokers: a multicenter Saudi cohort.

Ternati Mohammed M, Qashqari Abdulmajeed A, Alshelli Ihab I, Alrasheed Sarah S et al.

Lung cancer in never-smokers represents a distinct clinical and biologic entity. However, its epidemiologic characteristics remain incompletely described in the Middle East. To characterize lung cancer in never-smokers and compare it with ever-smokers in a multicenter Saudi cohort. Retrospective multicenter cohort study. Three tertiary-care centers of King Faisal Specialist Hospital & Research Centre system in Saudi Arabia. Adults with histologically confirmed primary lung cancer diagnosed between January 2020 and December 2024 were classified as never- or ever-smokers. Carcinoid tumors were excluded from the comparative analysis. Demographic, histologic, stage, and molecular characteristics were compared. Multivariable logistic regression identified factors independently associated with never-smoker status. Clinical, histologic, stage, and molecular differences between never-smokers and ever-smokers expressed as crude and adjusted odds ratios (95% confidence interval). 301 patients reviewed; 253 in the primary analytic cohort (92 never-smokers, 161 ever-smokers). Among 280 patients with available smoking history, 253 were included after excluding 27 carcinoid tumors (92 never-smokers [36%] and 161 ever-smokers [63.6%]). Never-smokers were mostly females (64/92 (70%) vs 12/161 (7.5%); P<.001) and younger than ever-smokers [mean age 59.2 (standard deviation 13.5) vs 62.3 (11.1) years; P=.065]. Adenocarcinoma predominated among never-smokers (81/92 (88%) vs 108/161 (67.1%); P<.001). Among patients tested, Epidermal growth factor receptor (EGFR) mutations(34/86 (39.5%) vs 12/128 (9.4%); P<.001) and Anaplastic lymphoma kinase (ALK) rearrangements [17/86 (20%) vs 9/128 (7.0%); P=.01] were significantly more frequent in never-smokers, whereas KRAS alterations were more common in ever-smokers [6/86 (7%) vs 21/128 (16.4%); P=.068]. Stage III-IV disease was common in both groups (70% vs 72%; P=.783). In multivariable analysis, female sex [adjusted odds ratio (OR) 31.9, 95% CI 14.2-71.6; P<.001] and adenocarcinoma histology (adjusted OR 5.3, 95% CI 2.0-14.2; P<.001) were independently associated with never-smoker status. In this multi-center Saudi cohort, more than one-third of lung cancers occurred in never-smokers, characterized by female predominance, adenocarcinoma histology, and frequent EGFR and ALK alterations. These findings support comprehensive molecular testing regardless of smoking history and underscore the need for strategies to improve early recognition of lung cancer in never-smokers. Retrospective design, incomplete molecular testing, tertiary-referral setting, and potential misclassification of smoking exposure, including unrecorded waterpipe and electronic-cigarette use.

PMID 42571038
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PubMedVeterinary and animal science2026-08-09

Antiepileptic drug therapy in companion animals: New perspectives on clinical pathology monitoring.

Lotfalizadeh Narges N, Nazifi Saeed S

Antiepileptic drugs (AEDs) are widely used in companion animal medicine and are used long-term to treat a variety of epilepsy conditions. The use of these drugs can cause changes in routine tests. This study aimed to investigate the broad dimensions of hematological and biochemical changes induced by various AEDs in dogs and cats. Also, the distinction of these changes from actual pathologic alterations was considered. In this review, relevant articles were searched and selected from PubMed, Scopus, and Web of Science databases. Then, data related to the type of AEDs and hematological and biochemical changes in dogs and cats were extracted and qualitatively analyzed. AEDs in dogs and cats can cause significant changes in laboratory parameters. The most common biochemical changes were liver-related, especially elevated liver enzymes, which in dogs were often adaptive. In contrast, in cats, these changes were less common but were of greater clinical significance. Hematological changes were less common, but in some cases, they included anemia or cytopenias. It was also found that the severity and type of changes depended on the drug type, treatment duration, and animal species. Ultimately, most of these changes were mild and manageable, but in some cases, they required further investigation or adjustment of treatment. Based on the pattern of changes, their severity, the type of drug used, and the patient's clinical status, it is possible to distinguish between true pathological changes and drug-induced changes to a large extent. Conducting targeted studies and developing more precise protocols could improve this distinction and increase the accuracy of clinical decisions.

PMID 42571377
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