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

Clone EGFR.1 is an antibody that specifically targets human EGFR, not mouse EGFR, and its in vivo use in mice is generally limited to models where human EGFR is present, such as xenografts or transgenic mice expressing human EGFR.

Key in vivo applications of clone EGFR.1 in mice include:

• Detection or imaging of human EGFR-expressing tumors in murine models, particularly in xenograft studies where human tumor cell lines expressing EGFR are engrafted into immunodeficient mice.
• Functional and mechanistic studies: As a blocking or neutralizing reagent to study the impact of EGFR signaling inhibition in tumors or tissues expressing the human receptor. However, this only applies if the model expresses human EGFR (either through xenografts or genetic modification), since EGFR.1 does not bind to endogenous mouse EGFR.

EGFR.1 is not suitable for studies targeting mouse EGFR in standard immunocompetent mice because it lacks cross-reactivity with murine EGFR. There is no evidence in the literature for its use as a therapeutic antibody in mice outside of humanized or xenograft models. For applications in endogenous mouse EGFR, other antibodies such as those specifically developed against mouse EGFR should be used.

Summary Table: In Vivo Uses of Clone EGFR.1 in Mice

In summary, clone EGFR.1’s in vivo use in mice is largely restricted to imaging or functional studies in models expressing human EGFR; it is not effective for studies involving endogenous mouse EGFR.

In the context of EGFR (Epidermal Growth Factor Receptor) research, several antibodies and proteins are commonly used alongside EGFR.1:

Monoclonal Antibodies Targeting EGFR

1. Cetuximab (C225): A chimeric monoclonal antibody that competes with EGFR ligands, preventing receptor activation. It is used to treat colorectal cancer and head and neck cancer.
2. Panitumumab: A fully human monoclonal antibody targeting EGFR, used in the treatment of colorectal cancer.
3. Nimotuzumab: A humanized monoclonal antibody that targets EGFR and is used in several cancer types.
4. Depatuxizumab (ABT 806): An antibody drug conjugate targeting EGFR, particularly noted for its use in glioblastoma trials.

Other Proteins and Antibodies

1. EGFR Tyrosine Kinase Inhibitors (EGFR-TKIs): These include drugs like gefitinib and erlotinib, which are used in combination with monoclonal antibodies in some cancer treatments.
2. Bifunctional Antibodies: Such as MaAbNA, which targets EGFR1 and HER2, providing a dual targeting approach for cancer therapy.
3. Dual-Targeting Antibodies: Examples include duligotuzumab, which inhibits both EGFR and HER3.

These antibodies and proteins are often used in combination or individually to target EGFR in various cancer therapies, offering a range of treatment options depending on the specific cancer type and patient profile.

Key Findings on Clone EGFR.1 in the Scientific Literature

There is no direct scientific literature on "clone EGFR.1" as a specific biological or cancer research topic in the provided search results—rather, the term "clone" in your query may refer to either (a) a monoclonal antibody clone (such as "EGFR.1" used for laboratory detection), or (b) the concept of tumor cell clones with altered EGFR status (e.g., EGFR mutations, amplification, or clonal evolution). I will summarize key findings from both relevant contexts.

Monoclonal Antibody EGFR.1

The term "EGFR.1" appears as a monoclonal antibody clone engineered to target the human EGFR protein, used in laboratory research and diagnostics. For example, Leinco Technologies markets an "Anti-Human EGFR, Clone EGFR.1" for in vivo and in vitro applications. However, the provided scientific literature does not describe experimental findings specifically related to the use or effects of this clone in research, but it is evident that monoclonal antibodies like EGFR.1 (and, e.g., "EGFR1" clone ab30 from Abcam) are used to detect EGFR protein expression, binding specifically to the external domain of EGFR without affecting tyrosine kinase activity.

EGFR Clonal Evolution and Tumor Biology

Intratumor Heterogeneity of EGFR Expression
A study in non-small cell lung cancer (NSCLC) found that EGFR-mutant tumors can contain subclones with low expression of both wild-type and mutant EGFR protein, which may influence responses to targeted therapies. This highlights the complexity of EGFR signaling within tumors and the potential for therapeutic resistance due to clonal diversity.

EGFR Copy Number Gain
EGFR gene copy number gain (amplification) is more common in EGFR-mutant NSCLC (27.9%) than in wild-type EGFR tumors (7.4%). EGFR copy number gain is associated with worse overall survival in EGFR-mutant patients treated with first-line EGFR tyrosine kinase inhibitors (TKIs), but not with progression-free survival. This suggests that EGFR amplification may be a marker of aggressive biology rather than primary TKI resistance.

Clonal Evolution Under Treatment Pressure
Phylogenetic analysis of metastases from a patient with EGFR-mutant lung cancer treated with osimertinib and a personalized neoantigen vaccine revealed that different metastases originated from distinct subclones, some of which had lost the original EGFR driver mutation. Clonal selection and evolution—including loss of EGFR driver mutations and acquisition of other driver alterations (e.g., RB1 and TP53 loss)—drive therapeutic resistance and transformation to small cell lung cancer (SCLC) histology.

Acquired Resistance and Clonal Decay
In colorectal cancer, anti-EGFR-resistant clones (often with RAS or EGFR extracellular domain mutations) decay exponentially after therapy is stopped, as demonstrated by circulating tumor DNA (ctDNA) analysis. This decay pattern can guide the optimal timing for re-challenge with anti-EGFR therapies, providing a predictive model for treatment sequencing.

Summary Table: Key EGFR Clonal Findings

Clinical and Translational Implications

• Detection of EGFR status (mutations, amplification) is critical for selecting patients for EGFR-targeted therapies and understanding prognosis.
• Clonal evolution under therapy can lead to loss of targetable mutations and histologic transformation, necessitating re-biopsy and molecular profiling at progression.
• Dynamic monitoring of clonal populations via ctDNA can help predict the optimal timing for therapy re-challenge in metastatic cancers.
• Intratumor heterogeneity in EGFR expression underscores the challenges of achieving durable responses with single-agent targeted therapies.

Conclusion

While there is no direct citation of findings from "clone EGFR.1" as a research model in the provided literature, the broader context of EGFR clonal biology in cancer reveals significant insights into tumor evolution, therapeutic resistance, and the importance of genomic profiling for personalized oncology. Monoclonal antibodies like EGFR.1 are tools for research and diagnostics, but the most impactful scientific findings concern the behavior of tumor cell clones with altered EGFR status under selective pressure from targeted therapies.

The dosing regimens for clone EGFR.1, an anti-human EGFR monoclonal antibody, are generally based on standard antibody practices in mouse models. While specific details on variability across different models are not provided in the available literature, typical dosing for such antibodies often ranges from 5 to 20 mg/kg and can be administered once or twice weekly.

In general, dosing regimens for EGFR inhibitors can vary based on factors like the specific mutation type, the model's sensitivity to the drug, and the desired clinical outcome. For instance, in some studies involving EGFR mutant mouse models, other EGFR inhibitors are dosed at 20 to 100 mg/kg daily to achieve significant tumor growth inhibition. However, direct comparisons for clone EGFR.1 across various mouse models are not detailed in the provided sources.