Cetuximab (C225) (Synonyms: C225) |
| Catalog No.GC34217 |
Cetuximab (C225) est un anticorps monoclonal IgG1 humain qui inhibe le récepteur du facteur de croissance épidermique (EGFR), avec une Kd de 0,201 nM pour l'EGFR par SPR. Cetuximab (C225) a une activité antitumorale puissante.
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Cas No.: 205923-56-4
Sample solution is provided at 25 µL, 10mM.
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Cetuximab is a chimeric monoclonal antibody generated from fusion of the variable region of the murine anti-EGFR monoclonal antibody M225 and the human IgG1 constant region. It produced antibody retains high affinity and specificity to EGFR and reduces immunogenicity.[1] Cetuximab bound with high affinity to FcγRI (EC50 = 0.13 nM) and FcγRIIIa (EC50 = 6 nM). It effectively induced ADCC across multiple tumor cell lines.[4] Treatment with 100 μg/ml cetuximab for 24h enhances the cytotoxicity effect of RSL3 treatment on KRAS mutant CRC cells.[2]
In vitro experiment indicated it that radiation enhances cetuximab (0.5 μg/ml)-mediated ADCC and activation of NK cells.[3] Treatment with 20 μg/mL cetuximab inhibited the proliferation of the parental UMSCC1 cell line (UMSCC1-P) ,while the three HNSCC cetuximab-resistant clones (C2, C5, and C11) were completely refractory to cetuximab.[6]
In vivo experiment it shown that cetuximab (13 mg/kg, s.c.) enhances the inhibitory effects of RSL3 and RSL3-induced ferroptosis.[2] In vivo, after i.v. injection of 4 doses of 10 mg/kg body-weight demonstrated that cetuximab markly inhibited tumor growth in SCC1 tumor bearing mice.[5] In vivo experiment it illustrated that cetuximab-treated (50 mg/kg, i.p.) tumors showed delayed growth, when mice were inoculated with the NSCLC H226 cell line individually with 2x106 tumor cells in the dorsal flank.[6]
References:
[1]. Xiong HQ, et al. Cetuximab, a monoclonal antibody targeting the epidermal growth factor receptor, in combination with gemcitabine for advanced pancreatic cancer: a multicenter phase II Trial. J Clin Oncol. 2004 Jul 1;22(13):2610-6.
[2]. Yang J, et al. Cetuximab promotes RSL3-induced ferroptosis by suppressing the Nrf2/HO-1 signalling pathway in KRAS mutant colorectal cancer. Cell Death Dis. 2021 Nov 13;12(11):1079.
[3]. Jin WJ, et al. Tumor-Specific Antibody, Cetuximab, Enhances the In Situ Vaccine Effect of Radiation in Immunologically Cold Head and Neck Squamous Cell Carcinoma. Front Immunol. 2020 Nov 12;11:591139.
[4]. Patel D, et al. IgG isotype, glycosylation, and EGFR expression determine the induction of antibody-dependent cellular cytotoxicity in vitro by cetuximab. Hum Antibodies. 2010;19(4):89-99.
[5]. Niu G, et al. Cetuximab-based immunotherapy and radioimmunotherapy of head and neck squamous cell carcinoma. Clin Cancer Res. 2010 Apr 1;16(7):2095-105.
[6]. Iida M, et al. Targeting the HER Family with Pan-HER Effectively Overcomes Resistance to Cetuximab. Mol Cancer Ther. 2016 Sep;15(9):2175-86.
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