Cetuximab是一种单克隆抗体，能够抑制EGFR，SPR方法测得Cetuximab对可溶性EGFR的Kd值为0.201nM；Cetuximab具有高效的抗肿瘤作用。
CAS：205923-56-4
分子式：C6484H10042N1732O2023S36
分子量：145543.35
纯度：98%
存储：Store at -20°C

Background:

Biological Activity
In vitro: Cetuximab 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: Cetuximab 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.

参考文献
[1].Enhancement of Cetuximab-Induced Radiosensitization by JAK-1 Inhibition.
Bonner JA, et al. BMC Cancer. 2015 Oct 12;15:673. PMID: 26458879.
[2].Standard chemotherapy with cetuximab for treatment of colorectal cancer.
Li XX, et al. World J Gastroenterol. 2015 Jun 14;21(22):7022-35. PMID: 26078581.