Catalog No.A2000 Synonyms: C225 Non-humanized mouse model applicable
For research use only. Not for use in humans.
Cetuximab (anti-EGFR), a novel molecular-targeted agent,is an inhibitor of EGFR monoclonal humanized antibody interacting with the extracellular binding site of EGFR to block ligand stimulation. MW : 145.781 KD.
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Mice showed progression disease to first-line treatment were randomized 1:1 to the two arms of treatment and were treated until onset of progression disease or until the end-time of experiment in case of response (fixed to 52 weeks from the start of first-line therapy ), as indicated in in the Materials and Methods section. Growth curves of HCC827 xenografts treated in secondline with osimertinib plus selumetinib or cetuximab are represented as changes in the values of volumes as percentage compared to baseline tumor volume at the time of progression diasease to first-line (defined as 100%) for each case. Median tumor volume at PD2 was of 348 mm3.
J Thorac Oncol, 2018, 13(6):810-820. Cetuximab (anti-EGFR) purchased from Selleck.
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|Description||Cetuximab (anti-EGFR), a novel molecular-targeted agent,is an inhibitor of EGFR monoclonal humanized antibody interacting with the extracellular binding site of EGFR to block ligand stimulation. MW : 145.781 KD.|
Cetuximab (anti-EGFR) is a recombinant chimeric monoclonal antibody that binds to the human epidermal growth factor receptor (EGFR) with high affinity. Binding to EGFR blocks phosphorylation and activation of receptor-associated kinases which results in cell growth inhibition, induction of apoptosis, and decreased vascular endothelial growth factor production. C225 showed a significant single agent antitumor effect and an additive effect with cisplatin or paclitaxel in NPC cell lines with high EGFR protein expression (HK-1 and HONE-1) but a minimal activity in NPC cell lines with a low expression (CNE-2 and C666-1). Cetuximab blocks epidermal growth factor receptor (EGFR)-ligand interaction and inhibits downstream RAS-ERK activation. Cetuximab fostered an ER stress response and the translocation of ER proteins to the cell membrane. Cetuximab promotes phagocytosis by dendritic cells. Cetuximab is effective in K-ras wild-type, EGFR-expressing gastric cancer cell lines and xenografts. It binds to the extracellular domain of EGFR with high affinity. It competitively blocks ligand binding and inhibits tyrosine kinase activation, resulting in receptor downregulation. Apart from this competitive inhibition, cetuximab binding with EGFR might trigger internalization and destruction of the receptor.
|In vivo||C225 enhanced the antitumor activity of several chemotherapeutic drugs in mouse xenograft models. Cetuximab, exerts its antitumor efficacy by multiple mechanisms that include the inhibition of cell cycle progression by arrest in the G1- phase and decreased cell number in the S-phase. Cell cycle arrest in the G1-phase also induces apoptosis by the induction and activation of proapoptotic molecules. cetuximab alone and in synergy with carboplatin resulted in decreases of tumor size, metastatic spread, and MVD in NCI-N87 tumors with EGFR cell surface expression and absence of mutations in BRAF and K-ras, whereas cetuximab had minimal in vitro effect and no in vivo treatment efficacy in tumors derived from MKN-45, in which the phenotype was also BRAF and K-ras wildtype, but which had only weak cytoplasmic EGFR protein expression.|
|Formulation||PBS buffer, pH 7.2|
|Storage||Store at -80°C and avoid freeze-thaw cycles.|
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