Erlotinib metabolite M12 - CAS 183321-84-8
Molecular Formula:
C20H19N3O4
Molecular Weight:
365.389
COA:
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Description:
A metabolite of Erlotinib. Erlotinib is a tyrosine kinase inhibitor which acts on the epidermal growth factor receptor (EGFR), inhibiting EGFR-associated kinase activity.
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Synonyms:
4-[(3-Ethynylphenyl)amino]-6,7-bis(2-hydroxyethoxy)quinazoline; 2-(4-(3-Ethynylanilino)-7-(2-hydroxyethoxy)quinazolin-6-yl)oxyethanol; 2-[4-(3-ethynylanilino)-7-(2-hydroxyethoxy)quinazolin-6-yl]oxyethanol
MSDS:
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InChIKey:
YWSAEKIQJPQSDJ-UHFFFAOYSA-N
InChI:
InChI=1S/C20H19N3O4/c1-2-14-4-3-5-15(10-14)23-20-16-11-18(26-8-6-24)19(27-9-7-25)12-17(16)21-13-22-20/h1,3-5,10-13,24-25H,6-9H2,(H,21,22,23)
Canonical SMILES:
C#CC1=CC(=CC=C1)NC2=NC=NC3=CC(=C(C=C32)OCCO)OCCO
1.[Gefitinib therapy in advanced non-small cell lung cancer in patients with EGFR mutations: cost-effectiveness analysis].
Protsenko SA, Rudakova AV. Vopr Onkol. 2015;61(4):676-80.
Therapy for advanced non-small cell lung cancer (NSCLC) is very complex clinical problem. The optimal choice of therapy demands not only the analysis of data on clinical effectiveness, but also an assessment of cost-effectiveness of the applied drugs. The current options for first- or second/third-line of lung cancer treatment are tirosine kinase inhibitors (TKI)--gefitinib, erlotinib and afatinib. According to the received results TKI first-line therapy for NSCLC in patients with EGFR mutations is not only clinically effective but also is economically acceptable from a position of the Russian budgetary health care. TKI second-line therapy for NSCLC patients who fail first-line therapy also provides improvement of the quality of life and prolonged time to progression. Comparable clinical effectiveness and safety of erlotinib and gefitinib in patients with EGFR mutations allows making drug choice on the basis of regional price characteristics.
2.Epidermal growth factor receptor-inhibition (EGFR-I) in the treatment of neuropathic pain.
Kersten C1, Cameron MG2, Laird B3, Mjåland S2. Br J Anaesth. 2015 Nov;115(5):761-7. doi: 10.1093/bja/aev326.
BACKGROUND: Neurobiological work has demonstrated that expression of mitogen-activated protein kinases (MAPK) is upregulated on neurones and glial cells after nerve damage. Furthermore, the epidermal growth factor receptor (EGFR) has been identified as having a key role in this process and subsequent interruption of this using EGFR-Inhibitors (EGFR-I), may improve neuropathic pain. The aim of this report was to explore if EGFR-I attenuated neuropathic pain in humans.
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CAS 183321-84-8 Erlotinib metabolite M12

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