Erbitux

Manufactured by Merck Group

Sourced in Germany, China

Erbitux is a monoclonal antibody laboratory product developed by Merck Group. Its core function is to bind to and inhibit the epidermal growth factor receptor (EGFR) in cellular samples.

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Lab products found in correlation

Herceptin, by Roche (8 mentions) Cetuximab, by Merck Group (6 mentions) Mabthera, by Roche (6 mentions) Herceptin, by Merck Group (2 mentions) Xolair, by Novartis (2 mentions) Vectibix, by Amgen (2 mentions) Expi293 expression system, by Thermo Fisher Scientific (1 mentions) Prosep a media, by Merck Group (1 mentions) Amicon ultra 15, by Merck Group (1 mentions) Rad001, by Bio-Techne (1 mentions) Nap 5 column, by GE Healthcare (1 mentions) Omnitarg, by Genentech (1 mentions) Powerplex 21 pcr kit, by Promega (1 mentions) Tnf α, by ProSpec (1 mentions) Epidermal growth factor (egf), by ProSpec (1 mentions) Mouse igg1k, by BD (1 mentions) Golgi stop monesin, by BD (1 mentions) Dimethyl sulfoxide (dmso), by Roche (1 mentions) Rnase a, by Serva Electrophoresis (1 mentions) Staurosporine, by Merck Group (1 mentions)

Close spelling variants of this product

Cetuximab (Erbitux) (21 citations)

45 protocols using erbitux

Effects of Endostar and Erbitux on MGC803 Cells

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The expressions of EGF, EGFR, VEGF and VEGFR in MGC803 cells were evaluated using semi-quantitative PCR. The MGC803 cells were treated with 1.75 mg/ml Endostar (Endostatin, Simcere-Medgenn BioPharmaceutical Co., Ltd, Shandong, China) or 162 mg/ml Erbitux (Cetuximab, Merck-China, Beijing, China) for 12 h. The drug concentration is calculated according to this formula:
Erbitux (Cetuximab, Merck-China, Beijing, China) for 12 h was evaluated using semi-quantitative PCR. To test the effect of 1.75 μg/ml Endostar or 162 μg/ml Erbitux on the proliferation of MGC803 cells, MGC803 cells (6 × 10³/well) were plated in a 96-well plate, followed by 4 h incubation at 37°C. Then, 1.75 μg/ml Endostar or 162 μg/ml Erbitux in 0.9% NaCl was added to MGC803 cells, with 0.9% NaCl as a negative control and oxaliplatin as a positive control. The proliferation was evaluated using MTT assay. To measure the effect of Endostar or Erbitux on the ability of migration, adhesion and invasion, MGC803 cells were plated into a culture flask, followed by 24 h incubation. Then, 1.75 μg/ml Endostar or 162 μg/ml Erbitux in 0.9% NaCl was added to culture medium for 12 with 0.9% NaCl as a control. The attached cells were used for migration, adhesion and invasion assays.

Li C., Zheng J, & Xue Y. (2019). Effects of vascular endothelial growth factor and epidermal growth factor on biological properties of gastric cancer cells. Archives of Medical Science : AMS, 15(6), 1498-1509.

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Fc-Fusion Antibody Constructs

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IgG1 Fc (pEXPR-IgG1 Fc) was fused to either SpyTag (AHIVMVDAYKPTK) or KTag (ATHIKFSKRD) with additional GY-dipeptide at the C-terminus by using standard molecular cloning techniques. Native IgG1 glycosylation at position N297 was eliminated by introducing a N297A mutation by Quick Change Side-Directed Mutagenesis. Plasmids coding for chimeric cetuximab (C225, Erbitux^®) and trastuzumab (Herceptin^®) were kindly provided by Merck KGaA (Darmstadt). Cetuximab and trastuzumab variants containing SpyTag at the C-terminus of either the heavy chains, the light chains, or at both chains were prepared by standard molecular cloning techniques. A (GSG)₂-linker was introduced between the C-terminus of the antibody and SpyTag. IgG1 Fc and full-length antibodies were transiently expressed from HEK293F cells using the Expi293 Expression System (Life Technologies). Supernatants containing secreted proteins were conditioned and applied to spin columns with PROSEP-A Media (Montage, Merck Millipore). Columns were washed with 1.5 M Glycine/NaOH, 3 M NaCl, pH 9.0 and proteins eluted with 0.2 M Glycine/HCl pH 2.5 into 1 M Tris/HCl pH 9.0. Eluted proteins were dialyzed in 1 × DPBS (Life Technologies) using Amicon Ultra-15 (Merck Millipore, NMWL 10000 Da) and stored at 4 °C.

Siegmund V., Piater B., Zakeri B., Eichhorn T., Fischer F., Deutsch C., Becker S., Toleikis L., Hock B., Betz U.A, & Kolmar H. (2016). Spontaneous Isopeptide Bond Formation as a Powerful Tool for Engineering Site-Specific Antibody-Drug Conjugates. Scientific Reports, 6, 39291.

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Radiochemical Purity Evaluation of PSMA-Targeted Ligands

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To evaluate the quality of the extracted ²¹²Pb, the tumor-targeting ligand NG001 (PSMA617-TCMC TFA; MedKoo Biosciences Inc.) and the S-2-(4-Isothiocyanatobenzyl)-1,4,7,10-tetraaza-1,4,7,10-tetra(2-carbamoylmethyl)cyclododecane (TCMC)–conjugated cetuximab (Erbitux; Merck Group) and rituximab (MabThera; Roche) were radiolabeled and the radiochemical purity was measured as described in Supplemental Section 3.

Li R.G., Stenberg V.Y, & Larsen R.H. (2023). An Experimental Generator for Production of High-Purity 212Pb for Use in Radiopharmaceuticals. Journal of Nuclear Medicine, 64(1), 173-176.

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Randomized Trial of Paclitaxel-Cisplatin with Cetuximab

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Randomization was performed by the stratified block randomization method, according to previous treatment (previous surgery or radiotherapy versus no previous treatment), ECOG performance status (0 versus 1), and the number of metastatic sites (one versus greater than or equal to two affected organs). Patients were randomly assigned (1:1) to the TP (paclitaxel [175 mg/m² i.v. on day 1 of every 3-week cycle] and cisplatin [75 mg/m² i.v. on day 1 of every 3-week cycle]) and CTP (Erbitux; Merck KGaA, Darmstadt, Germany) arms. Cetuximab was administered at a dose of 400 mg/m² (i.v. on day 1 of week 1), followed by 250 mg/m² weekly. Cisplatin was replaced by carboplatin (area under the plasma concentration-time curve [AUC] 5) in case of intolerance. All patients received a maximum of six cycles of chemotherapy. After six cycles of treatment, the patients in the CTP arm who had clinical benefits continued treatment with cetuximab as monotherapy. Tumor assessment was performed by computed tomography (CT) or magnetic resonance imaging (MRI) at baseline and every 6 weeks. Treatment was continued until disease progression (defined according to RECIST version 1.1), unacceptable toxicity, patient withdrawal, or investigator decision, whichever occurred first. Further details regarding study design, procedures, and assessment are summarized in the supplement.

Lu Z., Zhang Y., Fan Q., Pan Y., Jiang D., Lu P., Zhang J., Yuan X., Feng J., Yang S., Yue W., Zhao L., Xu Y., Luo J, & Shen L. (2022). Paclitaxel and cisplatin with or without cetuximab in metastatic esophageal squamous cell carcinoma: a randomized, multicenter phase II trial. The Innovation, 3(3), 100239.

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3D Integrin and EGFR Modulation in Radiation

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For β1 integrin blocking, 10 μg/ml of the inhibitory monoclonal antibody AIIB2 was used as published [12 ]. Epidermal growth factor receptor inhibition was accomplished using Erbitux^® (Cetuximab; 5 μg/ml; Merck). 3D lrECM cell cultures were treated with AIIB2, Cetuximab or IgG isotype control for 1 h prior to irradiation. Where indicated, cells were additionally treated with Rad001 (Everolimus; 0.01–14 μM, Tocris) or ML334 (3–50 μM, Axon Medchem) 1 h prior to irradiation. DMSO was used as control. After 24 h, cells were washed with fresh culture medium.

Klapproth E., Dickreuter E., Zakrzewski F., Seifert M., Petzold A., Dahl A., Schröck E., Klink B, & Cordes N. (2018). Whole exome sequencing identifies mTOR and KEAP1 as potential targets for radiosensitization of HNSCC cells refractory to EGFR and β1 integrin inhibition. Oncotarget, 9(26), 18099-18114.

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Fluorescent Labeling of Therapeutic Antibodies

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Pertuzumab (purified from Omnitarg™; Genentech, Inc., South San Francisco, CA, USA) was labeled with Texas Red^® label (Invitrogen; Thermo Fisher Scientific, Inc.), the targets of which are primary amines, i.e., lysines. For this purpose, the clinical mAb was labeled as described by Bondza et al (22 (link)). Additionally, cetuximab (purified from Erbitux^®; Merck KGaA) was labeled with fluorescein isothiocyanate (FITC; cat. no. F3651; Sigma-Aldrich; Merck KGaA) as described by Stenberg et al (13 (link)). The labeled proteins were purified through a NAP-5 column (GE Healthcare Life Sciences, Little Chalfont, UK) for the removal of unbound fluorophore.

Encarnação J.C., Barta P., Fornstedt T, & Andersson K. (2017). Impact of assay temperature on antibody binding characteristics in living cells: A case study. Biomedical Reports, 7(5), 400-406.

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Xenograft Model of Head and Neck Cancer

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20 BALB/c (nu/nu) female nude mice were injected subcutaneously in both flanks with 5 × 10⁶ cells suspended in 0.2 ml of phosphate-buffered saline (PBS) using ethical committee-approved standard protocols and procedures. All procedures were performed at the Linköping University’s animal facility and were approved by the local Animal Use and Care Committee (Dnr 126-10). Ten mice were injected with UT-SCC-14 and the remaining ten with UT-SCC-2. The mice were examined twice a week for development of tumours. Within each group of ten animals five received three intraperitoneal injections of cetuximab (Erbitux^®; 1 mg/injection; Merck KGaA, Darmstadt, Germany) at day 10, 13, and 16 after injection of tumour cells. The size of the tumours was recorded at an interval of 2–3 days. Tumour-bearing mice were sacrificed at day 21, and the tumour tissue was excised, fixed in formalin, and embedded in paraffin. The experiment was repeated twice.

Gustafsson H., Kale A., Dasu A., Lund A., Edqvist P.H, & Roberg K. (2017). EPR Oximetry of Cetuximab-Treated Head-and-Neck Tumours in a Mouse Model. Cell Biochemistry and Biophysics, 75(3), 299-309.

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Caco-2 Cells with Cetuximab Resistance

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Caco-2 cells were maintained in DMEM supplemented with 10% fetal bovine serum and 1% Pen/Strep. For the establishment of CTX resistant Caco-2 clones (Caco-2 CXR) please refer to our previous work [21 (link)]. Caco-2 CXR were maintained in presence of cetuximab (Erbitux, Merck KgaA, Germany) at 10 µg/mL concentration. Caco-2 cells were authenticated by short tandem repeat (STR) profiling (PowerPlex 21 PCR Kit, Promega, Madison, WI, USA) and the certificate was released by the external service Eurofins Medigenomix Forensik GmbH (Ebersberg, Germany). Cells were routinely tested for mycoplasma contamination.

Gelfo V., Pontis F., Mazzeschi M., Sgarzi M., Mazzarini M., Solmi R., D’Uva G, & Lauriola M. (2019). Glucocorticoid Receptor Modulates EGFR Feedback upon Acquisition of Resistance to Monoclonal Antibodies. Journal of Clinical Medicine, 8(5), 600.

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Keratinocyte Migration in Sepsis

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To explore keratinocyte migration, the horizontal wound healing assay was used in which 1% healthy or sepsis serum pools were supplemented with 5, 10 or 50 ng/ml of EGF or TNF-α (both from ProSpec, East Brunswick, NJ, USA) as well as 1, 10 or 50 µg/ml of EGFR inhibitor (Erbitux (cetuximab) 5 mg/ml, Merck, Germany). In this experiment, 1% healthy and sepsis serum samples without supplements served as controls. The migration test was performed three times and the number of wounds was between 4 and 8 in each group.

Jaurila H., Koivukangas V., Koskela M., Gäddnäs F., Salo S., Korvala J., Risteli M., Karhu T., Herzig K.H., Salo T, & Ala-Kokko T.I. (2017). Inhibitory effects of serum from sepsis patients on epithelial cell migration in vitro: a case control study. Journal of Translational Medicine, 15, 11.

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Evaluating NK Cell Cytotoxicity with Nanoparticles

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NK cells express CD107a during degranulation, which also correlates to NK cell-mediated tumor cell lysis (21 (link)). To evaluate natural and antibody-dependent NK cell cytotoxicity purified NK cells and SKOV-3/OVCAR-4 cells were coincubated (1:1 ratio) in a flat-bottom 96-well plate with or without different nanoparticles. For ADCC-experiments Cetuximab 1 μg/ml (Erbitux, 5mg/mL, Merck (Serono)) or Cetuximab-bound nanoparticles in corresponding concentrations were added. NK cells were labelled with anti-CD107a-FITC (25µg/mL, clone H4A3, Mouse IgG1, k, BD Biosciences). After incubation for 1 hour at 37°C and 5% CO2, the protein Golgistop-Monesin (BD Biosciences) was added (1:600). After further 5 hours incubation NK cells were stained with CD56-BV421 (12µg/mL, NCAM 16.2, IgG2b,k, BD Biosciences) and CD107 expression analyzed by flow cytometry.
NK cell degranulation was calculated by the following formula in case of natural cytotoxicity:
NP or NP induced degranulation was calculated as:
For antibody-dependent cell-mediated cytotoxicity the following formula was used:

Hrvat A., Schmidt M., Obholzer M., Benders S., Kollenda S., Horn P.A., Epple M., Brandau S, & Mallmann-Gottschalk N. (2022). Reactivity of NK Cells Against Ovarian Cancer Cells Is Maintained in the Presence of Calcium Phosphate Nanoparticles. Frontiers in Immunology, 13, 830938.

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