EGFR/VEGFR Mutation Colorectal Cancer

EGFR/VEGFR mutation colorectal cancer is characterized by dysregulated EGFR signaling due to overexpression of EGFR protein or kinase-activating mutations, leading to enhanced cell proliferation, angiogenesis, migration, and survival. ADAM17 plays a key role in releasing EGFR ligands such as EGF, amphiregulin, and heparin-binding EGF, which activate downstream signaling pathways upon binding. These pathways are critical for tumor progression and metastasis, making EGFR a valuable therapeutic target. Resistance mechanisms, including acquired kinase-activating mutations, can emerge during anti-EGFR therapy. Molecular differences between colonic and rectal tumors influence their behavior and response to treatment, with diagnosis relying on colonoscopy and stool-based tests. Response to chemotherapy and anti-EGFR monoclonal antibodies guides clinical management, highlighting the importance of molecular profiling in personalized therapy.

References:

[1]. Balakarthikeyan Janani, et al. EGFR-Based Targeted Therapy for Colorectal Cancer-Promises and Challenges. Review Vaccines (Basel). 2022 Mar 24;10(4):499.

EGFR/VEGFR Mutation Colorectal Cancer (1):

Targets:	Bcl-2 Family (1) Raf (1) Caspase (1) EGFR (1) Apoptosis (1)

Cat. No.	Product Name	CAS No.	Purity	Chemical Structure

HY-180154

EGFR/BRAFV600E-IN-6
EGFR/BRAFV600E-IN-6 (Compound 7c) is a dual EGFR/BRAF^V600E inhibitor with IC₅₀ values of 0.12 and 0.05 μM. EGFR/BRAFV600E-IN-6 can activate caspase-3/8/9, unregulate Bax expression and downregulate Bcl-2 levels. EGFR/BRAFV600E-IN-6 can induce apoptosis and shows antioxidant activity. EGFR/BRAFV600E-IN-6 can be used for the research of cancer, such as colon cancer.

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