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Gefetinib

Manufactured by Selleck Chemicals
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Sourced in United States

Gefetinib is a laboratory reagent used in scientific research. It is a tyrosine kinase inhibitor that targets the epidermal growth factor receptor (EGFR). Gefetinib is commonly used in cell culture experiments and preclinical studies.

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Lab products found in correlation

Imatinib, by Selleck Chemicals (1 mentions) Sorafenib, by Selleck Chemicals (1 mentions) Sunitinib, by Selleck Chemicals (1 mentions) Dasatinib, by Selleck Chemicals (1 mentions) Erlotinib, by Selleck Chemicals (1 mentions) Lapatinib, by Selleck Chemicals (1 mentions) Nvp auy922, by Selleck Chemicals (1 mentions) Sgx 523, by Selleck Chemicals (1 mentions)

2 protocols using gefetinib

1

Synthesis and Use of Small Molecule Inhibitors

Cited 1 time
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Erastin was synthesized as described (Yagoda et al., 2007 (link)). Additional erastin and Sorafenib analogs were prepared as described in the Supplementary file 1. Data also available as ‘Extended Materials and Methods’ from Dryad data Repository (Dixon et al., 2014 (link)). The synthesis of (1S, 3R)-RSL3 was described (Yang et al., 2014 (link)). Sorafenib, imatinib, erlotinib, lapatinib, nilotenib, dasatinib, sunitinib, and gefetinib were from SelleckChem (Houston, USA). Unless otherwise indicated, all other compounds were from Sigma-Aldrich (St. Louis, USA).
Dixon S.J., Patel D.N., Welsch M., Skouta R., Lee E.D., Hayano M., Thomas A.G., Gleason C.E., Tatonetti N.P., Slusher B.S, & Stockwell B.R. (2014). Pharmacological inhibition of cystine–glutamate exchange induces endoplasmic reticulum stress and ferroptosis. eLife, 3, e02523.
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2

Synthesis and Preparation of Compounds

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FS-93 was synthesized as previously described [29 (link)]. SGX-523, gefetinib and NVP-AUY922 were obtained from Selleck Chemicals (Houston, USA). All these compounds were dissolved to 10 mM with DMSO as a stock solution and stored at −20°C.
Zhang L., Shen A., Wang L., Liu H., Chen D., Xiong B., Shen J, & Geng M. (2015). FS-93, an Hsp90 inhibitor, induces G2/M arrest and apoptosis via the degradation of client proteins in oncogene addicted and derived resistant cancer cells. Oncoscience, 2(4), 419-427.
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