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Erlotinib

Manufactured by Roche
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Sourced in Switzerland, Germany, United States, United Kingdom

Erlotinib is a laboratory reagent used in research and development applications. It functions as a tyrosine kinase inhibitor. The core function of Erlotinib is to inhibit the activity of the epidermal growth factor receptor (EGFR) protein.

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Lab products found in correlation

Gefitinib, by AstraZeneca (6 mentions) Gemcitabine, by Eli Lilly (3 mentions) Lapatinib, by Selleck Chemicals (2 mentions) Dimethyl sulfoxide (dmso), by Merck Group (2 mentions) Lipofectamine 2000, by Thermo Fisher Scientific (2 mentions) β actin, by Merck Group (2 mentions) Bevacizumab, by Roche (2 mentions) Axiovert 200m, by Zeiss (2 mentions) Epidermal growth factor (egf), by Merck Group (2 mentions) Sorafenib, by LGC (1 mentions) Osimertinib, by Selleck Chemicals (1 mentions) Anti igf1rβ, by Cell Signaling Technology (1 mentions) Anti p c met, by Cell Signaling Technology (1 mentions) Anti src, by Cell Signaling Technology (1 mentions) Anti lck, by Cell Signaling Technology (1 mentions) Anti akt, by Cell Signaling Technology (1 mentions) Anti p stat3, by Cell Signaling Technology (1 mentions) Anti p akt, by Cell Signaling Technology (1 mentions) Anti fgfr1, by Cell Signaling Technology (1 mentions) Sb203580, by Cayman Chemical (1 mentions)

37 protocols using erlotinib

1

Anticancer Compounds Characterization

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Erlotinib was kindly provided by F. Hoffman-La Roche Ltd, gefitinib was provided by AstraZeneca Inc; VS-4718 was provided by Verastem Inc; afatinib, osimertinib, lapatinib, AZD4547, and BIBF1120 were purchased from Selleck Chemicals; SU11274 and picropodophyllin were from Carbiochem; dasatinib was from Bio Vision; SB203580 was from Cayman Chemical; sorafenib was acquired from Toronto Research Chemicals Inc, cisplatin was from Bristol-Myers Squibb Company; and PD173074 was from Sigma-Aldrich.
Anti-HER2 and anti-pHER2 antibodies were purchased from Merck Millipore Corporation, anti-EGFR, anti-pEGFR, anti-pHER3, anti-HER4, anti-pHER4, anti-pc-Met, anti-IGF1Rβ, anti-pIGF1Rβ, anti-PDGFRβ, anti-pPDGFRβ, anti-FGFR1, anti-pFGFR, anti-ERK1/2, anti-pERK1/2, anti-AKT, anti-pAKT, anti-STAT3, anti-pSTAT3, anti-PTEN, anti-SRC, anti-FYN, anti-LYN, anti-YES, anti-LCK, anti-pSRC family (Y416), anti-pSRC (Y527), anti-FAK, anti-pFAK (Y397), anti-pFAK (Y576/577), anti-pFAK (Y925) and anti- EGFR (del E746-A750) antibody were from Cell Signaling Technology, anti-HER3 and anti-c-Met were from Santa Cruz Biotechnology Inc, anti-β-actin was from Abcam, Inc., and anti-α-tubulin was from Sigma-Aldrich.
Murakami Y., Sonoda K., Abe H., Watari K., Kusakabe D., Azuma K., Kawahara A., Akiba J., Oneyama C., Pachter J.A., Sakai K., Nishio K., Kuwano M, & Ono M. (2017). The activation of SRC family kinases and focal adhesion kinase with the loss of the amplified, mutated EGFR gene contributes to the resistance to afatinib, erlotinib and osimertinib in human lung cancer cells. Oncotarget, 8(41), 70736-70751.
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2

Raman Spectroscopy Analysis of Erlotinib Effect on Colon Cancer Cells

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The colon cancer cell lines SW-48, HT-29, and SW-480 were purchased from American Type Culture Collection. Cells were cultured in Dulbecco’s modified Eagle’s medium (Life Technologies, Darmstadt, Germany) supplemented with 10 % fetal bovine serum (Life Technologies, Darmstadt, Germany), 2 mM l-glutamine, and 5 % penicillin–streptomycin, and were incubated at 37 °C in a 10 % CO2 atmosphere. Cells were subcultured to 80 % confluence, detached by trypsin–EDTA (0.25 %) (Gibco trypsin solution, Life Technologies, Darmstadt, Germany), centrifuged at 1500 rpm for 3 min and diluted to 10 %, then seeded again in culture medium. Raman measurements were performed on cells grown on CaF2 windows (Korth Kristalle, Kiel, Germany) to avoid Raman scattering from regular glass slides. Cells were incubated with erlotinib (Tarceva; Roche, Switzerland) at 10 μg/ml at 37 °C in 10 % CO2 for 12 h. Subsequently, cells were fixed in 4 % paraformaldehyde (VWR International, Darmstadt, Germany) and then submerged in phosphate-buffered saline (Life Technologies, Darmstadt, Germany).
Yosef H.K., Mavarani L., Maghnouj A., Hahn S., El-Mashtoly S.F, & Gerwert K. (2015). In vitro prediction of the efficacy of molecularly targeted cancer therapy by Raman spectral imaging. Analytical and Bioanalytical Chemistry, 407(27), 8321-8331.
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3

Epidermal Keratinocyte Inflammatory Response

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Human primary epidermal keratinocytes were isolated and cultured in keratinocyte serum-free medium (SFM, Invitrogen) at 37°C, 5% CO2. Cells were treated with erlotinib (500 nM and 1000 nM; Roche Pharmaceuticals) or medium (vehicle control), either in the presence or absence of TNF-α (10 ng/ml; AbD Serotec) and IL-1β (5 ng/ml; R&D Systems) for 24 hours, following which the cells were harvested for RNA extraction.
Gerber P.A., Buhren B.A., Schrumpf H., Hevezi P., Bölke E., Sohn D., Jänicke R., Belum V.R., Robert C., Lacouture M.E, & Homey B. (2016). Mechanisms of skin aging induced by EGFR inhibitors. Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer, 24(10), 4241-4248.
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4

Assessing Cellular Senescence via SA β-Gal

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Cellular senescence was examined by measuring senescence-associated beta-galactosidase (SA β-Gal) activity (BioVision, Milpitas, CA). Human primary epidermal keratinocytes were grown for 24 hours in 6-well plates either with erlotinib (1000 nM; Roche Pharmaceuticals) or medium (vehicle control). The culture media was then decanted and the cells were stained for SA β-Gal activity as directed by the supplier (BioVision). Histologic images were acquired with a Zeiss microscope (Axiovert 200 M) (Zeiss, Jena, Germany) using Axiovision 4.7 software (Zeiss).
Gerber P.A., Buhren B.A., Schrumpf H., Hevezi P., Bölke E., Sohn D., Jänicke R., Belum V.R., Robert C., Lacouture M.E, & Homey B. (2016). Mechanisms of skin aging induced by EGFR inhibitors. Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer, 24(10), 4241-4248.
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5

EGFR-TKI and Chinese Herbal Medicine

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Patients assigned to TKI+CHM received oral EGFR-TKI [erlotinib (Roche, Switzerland) 150 mg, gefitinib (AstraZeneca, UK) 250 mg, or icotinib (Beta, China) 125 mg per dose, three times per day; the drug was chosen by the patients] plus oral CHM.
Jiao L., Xu J., Sun J., Chen Z., Gong Y., Bi L., Lu Y., Yao J., Zhu W., Hou A., Feng G., Jia Y., Shen W., Li Y., Zhang Z., Chen P, & Xu L. (2019). Chinese Herbal Medicine Combined With EGFR-TKI in EGFR Mutation-Positive Advanced Pulmonary Adenocarcinoma (CATLA): A Multicenter, Randomized, Double-Blind, Placebo-Controlled Trial. Frontiers in Pharmacology, 10, 732.
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6

Evaluating Anti-Cancer Drug Efficacy

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The following materials were commercially obtained: Gefitinib (Biaffin, Kassel, Germany); Erlotinib (kindly provided from Roche Diagnostics, Mannheim, Germany); Cisplatin (Wako Pure Chemical Industries, Osaka, Japan); Pemetrexed (Wako Pure Chemical Industries); TGF-β1 (PeproTech, Rocky Hill, USA).
Antibodies were obtained from the following sources: p22phox [E-11] (Santa Cruz Biotechnology, Santa Cruz, CA, USA); HIF-1α [h1alpha67] (Abcam, Cambridge, UK), E-cadherin [4A2C7] (Thermo Fisher Scientific, Rockford, USA), Vimentin [V9] (Acris, San Diego, USA), β-actin [AC-15] (Sigma-Aldrich, St. Louis, MO, USA).
Kobayashi M., Saito R., Miki Y., Nanamiya R., Inoue C., Abe J., Sato I., Okada Y, & Sasano H. (2019). The correlation of p22phox and chemosensitivity in EGFR-TKI resistant lung adenocarcinoma. Oncotarget, 10(10), 1119-1131.
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7

Preparation of Erlotinib Solutions

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Erlotinib was obtained from Roche Diagnostics (Basel, Switzerland) and dissolved in DMSO (50 mmol/l stock solution). Erlotinib was stored at −40°C as frozen aliquots and the solution was thawed directly prior to the experiments. The chemical structure of Erlotinib is presented in Fig. 1A.
Chen X., Yang S., Pan Y., Li X, & Ma S. (2017). Mitochondrial pathway-mediated apoptosis is associated with erlotinib-induced cytotoxicity in hepatic cells. Oncology Letters, 15(1), 783-788.
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8

Chemosensitivity of Ascites-Derived PDAC Cells

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2 × 103 ascites-derived PDAC primary cells per well from 14 different patients were seeded in 96-well plates and cultured for 3–4 days. The cells were treated with different chemotherapeutic agents: gemcitabine 10 μM (Medac, Wedel, Germany), erlotinib 10 μM (Roche, Basel, Switzerland), cisplatin 1 μM (Pharma-Chem, Haarlem, Holland), 5FU 5 μM and oxaliplatin 6 μM (Ebewe, Unterach, Austria), irinotecan 10 μM (Hospira, Melbourne, Australia) and paclitaxel 1 μM (Teva, Petach Tikva, Israel) for 72 h. FOLFIRINOX is a combination of 5FU, irinotecan and oxaliplatin. Cell proliferation was measured using the XTT cell proliferation kit (Biological Industries) according to the manufacturer's protocol.
Golan T., Atias D., Barshack I., Avivi C., Goldstein R.S, & Berger R. (2014). Ascites-derived pancreatic ductal adenocarcinoma primary cell cultures as a platform for personalised medicine. British Journal of Cancer, 110(9), 2269-2276.
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9

Engineered EGFR Mutant Cell Lines

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EGFR -negative CHO cells (CCL-61, ATCC, Wesel, Germany) were chemically transfected with wt, G465R or S492R EGFR encoding vector. Ba/F3 cells (CSC-C2045, Creative Bioarray, New York, USA) kindly provided by Stefan Horn (Research Department Cell and Gene Therapy, Department of Stem Cell Transplantation, University Medical Center Hamburg-Eppendorf, Hamburg, Germany) were maintained in medium containing 10ng/ml murine IL-3 (Peprotech, Rocky Hill, USA, [40 (link)]). Electroporation-transfected cells expressing wt or mutant EGFR were G418-selected (1mg/ml) and subsequently cultured in the absence of IL-3 and in the presence of 10ng/ml EGF. Stable cells transformed to IL-3 independence were screened for EGFR functionality by treatment with EGF or EGF + erlotinib at 5μM (Roche, Basel, Switzerland) and subsequently used for drug-sensitivity experiments.
Braig F., März M., Schieferdecker A., Schulte A., Voigt M., Stein A., Grob T., Alawi M., Indenbirken D., Kriegs M., Engel E., Vanhoefer U., Grundhoff A., Loges S., Riecken K., Fehse B., Bokemeyer C, & Binder M. (2015). Epidermal growth factor receptor mutation mediates cross-resistance to panitumumab and cetuximab in gastrointestinal cancer. Oncotarget, 6(14), 12035-12047.
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10

Evaluating Immune Cell Responses in Lung Cancer

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The following materials were used in this study: recombinant human interleukin-2 (Liaoning Weixing Biological Products Institute, Liaoning, China); interferon-g (Shanghai Clone Bio-Tech Co., Ltd., Shanghai, China); lymphocyte separation medium (Tianjin Haoyang Biological Products Co., Ltd., Tianjin, China) ; RPMI 1640 (Gibco, Grand Island, NY, USA); tetrazolium blue (Sigma, St. Louis, MO, USA); CD3 mAb (ProSpec-Tany TechnoGene, Rehovot, Israel); FITC-CD4/PE-CD8/PerCP-CD3, FITC-CD56, PE-CD3, PerCP-CD3, NKG2D-PE, FITC-IgG1, PE-IgG1, MICA, MICB, ULBP1, ULBP2, ULBP3 monoclonal antibodies, and flow cytometry apparatus (BD Biosciences, Franklin Lakes, NJ, USA); lactate dehydrogenase release assay kit (Promega Corporation, Madison, WI, USA); erlotinib (Roche, Basel, Switzerland), LY294002, SB203580 (Sigma), and signal transduction and transcription 21 (STAT21) (Biomol, Farmingdale, NY, USA). The drugs were dissolved in dimethyl sulfoxide and stored at -20°C. Drugs were thawed before use. The RPMI 1640 culture medium containing 10% fetal bovine serum was diluted to the desired concentration. The final concentration of dimethyl sulfoxide was <0.1%. Human lung adenocarcinoma A549 cells were routinely passaged and stored in our center.
Mei J.Z., Liu G.J., Zhang X.J., Zhao J.Z, & Feng R.T. (2015). Erlotinib enhances the CIK cell-killing sensitivity of lung adenocarcinoma A549 cells. Genetics and molecular research : GMR, 14(2).
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