Anti-Human EGFR (Clone EGFR.1) – Purified in vivo GOLD™ Functional Grade

Clone EGFR.1 is a monoclonal antibody that targets human EGFR and is most commonly used for detection, imaging, or experimental targeting of human EGFR expressed in mouse models, typically in the context of xenografts or transgenic mice engineered to express human EGFR.

Key in vivo applications in mice include:

• Detection and imaging of human EGFR in tumors engineered to express the human protein (e.g., xenografted human cancer cells or engineered murine tumor cell lines).
• Antibody validation and biodistribution studies to characterize specificity and pharmacokinetics in settings where human EGFR is present.

Important context and limitations:

• EGFR.1 does not recognize endogenous mouse EGFR and therefore is not suitable for studies targeting the native murine receptor in wild-type mice.
• In vivo use is limited to immunodeficient mouse models, such as those bearing human tumor xenografts or expressing human EGFR transgenes.
• Not therapeutically relevant in immunocompetent mice: The antibody is not generally used as a therapeutic in standard immunocompetent mouse models because it lacks cross-reactivity with mouse EGFR and would not model anti-tumor effects mediated by EGFR blockade in the mouse.

Summary of uses:

• In vivo tracking, detection, or imaging of human EGFR-positive xenografts or transgenic tissues in mice.
• Experimental validation of antibody specificity and function in murine models with engineered human EGFR.
• Preclinical testing of anti-EGFR strategies in murine models of human disease when human EGFR is artificially expressed.

Not used for:

• Targeting endogenous mouse EGFR in wild-type mice.
• Therapeutic studies pertaining to mouse EGFR-mediated biology or disease in standard mice.

In summary, clone EGFR.1 is used in mice primarily for detection and experimental manipulation of human EGFR in engineered or xenograft models, not for studies on native mouse EGFR.

Other commonly used antibodies or proteins in the literature with EGFR.1 (an anti-EGFR antibody) include other anti-EGFR monoclonal antibodies such as cetuximab, panitumumab, nimotuzumab, matuzumab, zalutumumab, and depatuxizumab. Combinations of anti-EGFR antibodies with small molecule EGFR tyrosine kinase inhibitors (TKIs)—such as gefitinib and erlotinib—are also widely studied.

Essential details and commonly used reagents:

• Other anti-EGFR monoclonal antibodies:

  • Cetuximab (IMC-C225): Binds EGFR extracellular domain and is often used in research and clinical settings.
  • Panitumumab: Fully human monoclonal antibody targeting EGFR.
  • Nimotuzumab: Humanized monoclonal antibody, particularly used in various cancer types.
  • Matuzumab, zalutumumab, depatuxizumab: Additional anti-EGFR mAbs with distinct epitope specificities, sometimes used in preclinical or clinical studies and often compared or combined for synergy.
  • Duligotuzumab: Dual EGFR/HER3 antibody.

• EGFR Tyrosine Kinase Inhibitors (TKIs):

  • Gefitinib (Iressa) and Erlotinib (Tarceva): Small molecules that target the intracellular portion of EGFR and are often used in combination with antibodies to achieve dual inhibition.

• Other receptor family members or relevant proteins:

  • HER2 (ERBB2): Sometimes included in studies since EGFR (HER1) and HER2 can heterodimerize, and dual targeting is investigated in certain cancers (though HER2-specific antibodies are different from EGFR.1).
  • EGFRvIII: A common mutant form of EGFR found in some tumors; anti-EGFR.1 may be used alongside antibodies specific to EGFRvIII in mechanistic studies.

• Combinatorial antibody approaches:

  • Using multiple non-competing anti-EGFR mAbs (e.g., combination of EGFR.1 with H11 or 225) can downregulate EGFR more effectively than single agents.
  • Dual targeting or bispecific antibodies (e.g., duligotuzumab, which targets both EGFR and HER3).

• Other relevant reagents:

  • Downstream signaling proteins (e.g., antibodies against phosphorylated MAPK, AKT) are often included to assess EGFR pathway activity changes upon treatment.

These combinations are frequently selected to improve efficacy, overcome resistance, or study signaling pathway modulation in various cell lines and cancer models.

The key findings from citations in scientific literature concerning clone EGFR.1 focus on its use as an antibody for detecting and quantifying EGFR (epidermal growth factor receptor), with implications for cancer research and therapy assessment.

Essential context and details:

• Clone EGFR.1 is a monoclonal antibody against human EGFR. It is frequently referenced in the literature as a tool for detecting EGFR expression in various assays, including flow cytometry, immunohistochemistry, and functional studies.

• Applications in cancer research: EGFR.1 is used to study EGFR's role in tumor biology, particularly in cancers where EGFR overexpression or mutation drives oncogenesis (such as lung, colon, and breast cancers). Detection of EGFR expression with EGFR.1 helps to stratify tumors, predict therapeutic response, and assess prognosis, since high EGFR expression or gene amplification is often associated with poor outcomes.

• Utility for functional and binding studies: EGFR.1 is described as "functional grade," indicating it can block ligand binding or downstream signaling, enabling researchers to study anti-EGFR therapeutics and resistance mechanisms directly.

• Usage in cell sorting and in vivo studies: The antibody is also utilized in cell sorting platforms (e.g., CTC chips) to selectively capture EGFR-expressing cells from blood samples, aiding in liquid biopsy and minimal residual disease detection in cancer patients.

Additional relevant points:

• Role in resistance and clonal evolution: Studies using anti-EGFR antibodies (not always clone EGFR.1 specifically, but often referencing similar clones) demonstrate that resistance mutations in EGFR can arise during therapeutic antibody treatment, and monitoring these with specific antibodies is vital for treatment strategy adaptation.

• Concordance with genetic findings: The presence and quantification of EGFR protein (as assessed by clone EGFR.1) are frequently aligned with genetic alterations such as EGFR amplification or mutations, underscoring its diagnostic and prognostic significance.

In summary, the literature broadly recognizes clone EGFR.1 as a validated tool for studying EGFR expression, understanding cancer biology, predicting prognosis, guiding therapy, and advancing biomarker research.

Dosing regimens for clone EGFR.1, an anti-human EGFR antibody, typically follow standard antibody practices in mouse models, with doses ranging from 5–20 mg/kg, often administered once or twice weekly. However, the specific dosing strategies can vary considerably depending on the experimental context and the mouse model being used.

Dosing Considerations in EGFR-Targeted Therapies

The variation in dosing regimens across different mouse models reflects the need to balance therapeutic efficacy with safety profiles. While clone EGFR.1 follows the general 5–20 mg/kg range, related EGFR-targeted therapeutic approaches in mouse models demonstrate considerable flexibility in dosing strategies.

For EGFR inhibitors in mouse lung tumor models, doses have been tested at 25–50 mg/kg per day for periods ranging from 1 to 30 days, with these doses proven effective at inducing tumor regressions. In osimertinib studies using EGFR mutant lung adenocarcinoma models, researchers initially used 5 mg/kg daily but later determined that 25 mg/kg once daily was approximately equivalent to the 80 mg daily human clinical dose. This demonstrates how dosing strategies must be calibrated to achieve human-relevant drug exposures.

Frequency and Duration Variations

The frequency of administration appears to be a critical variable. Daily dosing regimens have shown superior efficacy compared to weekly dosing in certain contexts. In erlotinib studies, daily pretreatment significantly prevented tumor cell homing compared to weekly administration at the same dose, suggesting that continuous drug exposure may be more effective than intermittent dosing for some EGFR-targeted therapies.

For other anti-EGFR monoclonal antibodies in mouse models, dosing schedules such as 100 µg administered intraperitoneally on days 1, 7 have been employed in xenograft studies, indicating that the route of administration and specific timing can be adapted based on the experimental design and therapeutic goals.