The solubility of this product in water is not determined. However, various sources state that is it poorly soluble in water.
SML3621
Erlotinib
≥98% (HPLC)
同義詞:
4-[(3-Ethynylphenyl)amino]-6,7-bis(2-methoxyethoxy)quinazoline, 6,7-Bis(2-methoxy-ethoxy)-quinazolin-4-yl]- (3-ethynyl-phenyl)amine, Erlotinib free base, N-(3-Ethynylphenyl)-6,7-bis(2-methoxyethoxy)-4-quinazolinamine, NSC 718781, OSI-774
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About This Item
暫時無法取得訂價和供貨情況
推薦產品
品質等級
化驗
≥98% (HPLC)
形狀
powder
顏色
white to beige
溶解度
DMSO: 2 mg/mL, clear
儲存溫度
-10 to -25°C
SMILES 字串
N(c3cc(ccc3)C#C)c1ncnc2c1cc(c(c2)OCCOC)OCCOC
InChI 密鑰
AAKJLRGGTJKAMG-UHFFFAOYSA-N
生化／生理作用
Erlotinib is an orally available, potent, and specific inhibitor of epidermal growth factor receptor (EGFR) tyrosine kinase. Erlotinib binds to the ATP binding site of the receptor. It is used to treat lung and pancreatic cancer.
orally available, potent, and specific inhibitor of epidermal growth factor receptor (EGFR) tyrosine kinase
訊號詞
Warning
危險聲明
危險分類
Acute Tox. 4 Oral
儲存類別代碼
11 - Combustible Solids
水污染物質分類（WGK）
WGK 3
閃點（°F）
Not applicable
閃點（°C）
Not applicable
從最近期的版本中選擇一個：
分析證明 (COA)
Lot/Batch Number
Jennifer Stamos et al.
The Journal of biological chemistry, 277(48), 46265-46272 (2002-08-28)
The crystal structure of the kinase domain from the epidermal growth factor receptor (EGFRK) including forty amino acids from the carboxyl-terminal tail has been determined to 2.6-A resolution, both with and without an EGFRK-specific inhibitor currently in Phase III clinical
Xiaoping He et al.
Scientific reports, 12(1), 8007-8007 (2022-05-15)
Hepatocellular carcinoma (HCC) is a leading cause of cancer-related death worldwide. Lenvatinib is approved as a first-line treatment for unresectable HCC. The therapeutic duration of lenvatinib is limited by resistance, but the underlying mechanism is unclear. To establish lenvatinib-resistant cells
Chike Osude et al.
Cells, 11(10) (2022-05-29)
NSCLC treatment includes targeting of EGFR with tyrosine kinase inhibitors (TKIs) such as Erlotinib; however, resistance to TKIs is commonly acquired through T790M EGFR mutations or overexpression of vascular endothelial growth factor receptor-2 (VEGFR-2). We investigated the mechanisms of EGFR-TKI
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