Cetuximab (anti-EGFR)

Catalog No.A2000 Synonyms: C225

For research use only.
Not for use in humans.

Cetuximab, 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)

Selleck's Cetuximab (anti-EGFR) has been cited by 17 publications

Purity & Quality Control

Choose Selective EGFR Inhibitors

Biological Activity

Description Cetuximab, 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.
EGFR [4]
(Cell-free assay)
0.39 nM(Kd)
In vitro

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[5]. 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)[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[2]. 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[3].

In vivo

C225 enhanced the antitumor activity of several chemotherapeutic drugs in mouse xenograft models[1]. 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[3].

Protocol (from reference)

Cell Research:
  • Objective: Cell Viability Assay
    Cells: HNE1 and CNE2 (Nasopharyngeal carcinoma cell lines)
    Concentrations: 62.5, 125, 250, 500, 1000, or 2000 µg/ml
    Incubation Time: 48 h
    Method: Cells were cultured at a density of 5 × 103 cells per well in flat bottomed 96-well plates. After 24 h of incubation at 37℃ in 5% CO2, 200 μL of cetuximab (62.5, 125, 250, 500, 1000, or 2000 μg/mL) and/or cisplatin (0.25, 0.5, 1, 2, 4, or 8 μg/mL) diluted with the medium to various concentrations were added to each well. After being incubated for 48 h, 10 μL of CCK-8 was added to each well. After 2 h, cell viability was quantified via reading the absorbance at 450 nm. The percentage growth inhibition was calculated as (ODcontrol - ODdrug)/ODcontrol × 100. The half maximal inhibitory concentration (IC50) values were calculated.
    Reference: https://www.ncbi.nlm.nih.gov/pubmed/27313893

    Objective: To analyze the apoptosis of CRC cells
    Cells: human DiFi CRC (Colorectal Cancer) cells
    Concentrations: 10 μg/ml
    Incubation Time: 72h
    Method: To analyze the apoptosis, cells were seeded into 6-well plates (3 × 105 cells per well). After 24 h, cells were cultured both in the absence and presence of drugs. Cell death and apoptosis were assessed by cytofluorimetric analysis using PE-annexin V and 7-aminoactinomycin D (7-AAD) according to the manufacturer's instructions at different time points.
    Reference: https://www.ncbi.nlm.nih.gov/pubmed/27135741

    Cetuximab can apply to nude mice, various cancer cell lines and other related assays (Only for Reference)

Animal Research:
  • Objective: Antitumor activity of cetuximab in murine gastric cancer model
    Animal Models: Nude mouse model for human gastric cancer (CD-1/nu-nu mice)
    Formulation: 0.9% NaCl
    Dosages: 1 mg/kg
    Administration: i.p.
    Reference: https://www.ncbi.nlm.nih.gov/pubmed/22011788

    Objective: To investigate the relationship between the EGFR levels and the responsiveness to cetuximab treatment in human cancer xenograft models
    Animal Models: Female athymic, nude mice were implanted s.c. with ~1 mm3 tumor fragments
    Formulation: PBS
    Dosages: 0.25, 0.5 or 1 mg/mouse
    Administration: i.p.
    Reference: https://www.ncbi.nlm.nih.gov/pubmed/27186886

    Cetuximab can apply to nude mice, various cancer cell lines and other related assays (Only for Reference)

Product Details

CAS No. 205923-56-4
Formulation PBS buffer, pH 7.2
Isotype Human IgG1
Source CHO cells
Storage Store the undiluted solution at 4°C in the dark to avoid freeze-thaw cycles

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Frequently Asked Questions

Question 1:
How to store the antibody?

Store the undiluted solution at 4 °C in the dark. Freezing antibodies can result in a loss of activity caused by the freezing/thawing process. Diluting antibodies to working concentrations and storing at 4°C for more than a day should be avoided. Additionally, make sure to keep the antibody sterile. Under these storage conditions, your antibodies should remain active for up to one year and oftentimes longer.

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