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(Synonyms: N-(3-溴苯基)-6,7-二甲氧基-N-甲基-4-喹唑啉胺) 目录号 : GC35959

EBE-A22 is a derivative of PD 153035 which can inhibit ErbB-1-phosphorylation, whereas EBE-A22 is inactive.

EBE-A22 Chemical Structure

Cas No.:229476-53-3

规格 价格 库存 购买数量
10mM (in 1mL DMSO)
¥1,723.00
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2mg
¥1,080.00
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5mg
¥2,092.00
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10mg
¥3,181.00
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50mg
¥7,533.00
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100mg
¥11,718.00
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200mg 待询 待询
500mg 待询 待询

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产品描述

EBE-A22 is a derivative of PD 153035 which can inhibit ErbB-1-phosphorylation, whereas EBE-A22 is inactive.

[1] Thomas W Grunt, et al. J Cell Physiol . 2007 Jun;211(3):803-15.

Chemical Properties

Cas No. 229476-53-3 SDF
别名 N-(3-溴苯基)-6,7-二甲氧基-N-甲基-4-喹唑啉胺
Canonical SMILES BrC1=CC(N(C)C2=NC=NC3=CC(OC)=C(OC)C=C23)=CC=C1
分子式 C17H16BrN3O2 分子量 374.23
溶解度 DMSO: 50 mg/mL (133.61 mM); Water: < 0.1 mg/mL (insoluble) 储存条件 Store at -20°C
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溶解性数据

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1 mg 5 mg 10 mg
1 mM 2.6722 mL 13.3608 mL 26.7215 mL
5 mM 0.5344 mL 2.6722 mL 5.3443 mL
10 mM 0.2672 mL 1.3361 mL 2.6722 mL
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Research Update

DNA interaction of the tyrosine protein kinase inhibitor PD153035 and its N-methyl analogue

Biochemistry 2001 Apr 17;40(15):4663-71.PMID:11294633DOI:10.1021/bi002777a.

The brominated anilinoquinazoline derivative PD153035 exhibits a very high affinity and selectivity for the epidermal growth factor receptor tyrosine kinase (EGF-R TK) and shows a remarkable cytotoxicity against several types of tumor cell lines. In contrast, its N-methyl derivative, designated EBE-A22, has no effect on EGF-R TK but maintains a high cytotoxic profile. The present study was performed to explore the possibility that PD153035 and its N-methyl analogue might interact with double-stranded DNA, which is a primary target for many conventional antitumor agents. We studied the strength and mode of binding to DNA of PD153035 and EBE-A22 by means of absorption, fluorescence, and circular and linear dichroism as well as by a relaxation assay using human DNA topoisomerases. The results of various optical and gel electrophoresis techniques converge to show that both drugs bind to DNA and behave as typical intercalating agents. In particular, EBE-A22 unwinds supercoiled plasmid, stabilizes duplex DNA against heat denaturation, and produces negative CD and ELD signals, as expected for an intercalating agent. Extensive DNase I footprinting experiments performed with a large range of DNA substrates show that EBE-A22, but not PD153035, interacts preferentially with GC-rich sequences and discriminates against homooligomeric runs of A and T which are often cut more readily by the enzyme in the presence of the drug compared to the control. Altogether, the results provide the first experimental evidence that DNA is a target of anilinoquinazoline derivatives and suggest that this N-methylated ring system is a valid candidate for the development of DNA-targeted cytotoxic compounds. The possible relevance of selective DNA binding to activity is considered. The unexpected GC-selective binding properties of EBE-A22 entreat further exploration into the use of N-methylanilinoquinazoline derivatives as tools for designing sequence-specific DNA binding ligands.

Upregulation of retinoic acid receptor-beta by the epidermal growth factor-receptor inhibitor PD153035 is not mediated by blockade of ErbB pathways

J Cell Physiol 2007 Jun;211(3):803-15.PMID:17286282DOI:10.1002/jcp.20990.

Inhibiting epidermal growth factor-receptor (ErbB-1) represents a powerful anticancer strategy. Activation of retinoid pathways is also in development for cancer treatment. Retinoic acid receptor-beta-the tumor suppressor and main retinoid mediator--is silenced in many tumors. The ErbB-1 inhibitor PD153035 cooperates with retinoic acid during growth inhibition and induces retinoic acid receptor-beta suggesting that ErbB-1 controls retinoic acid receptor-beta. However, here we demonstrate that ErbB pathways are not involved in PD153035-mediated retinoic acid receptor-beta-upregulation. PD153035 inhibits ErbB-1-phosphorylation, whereas its derivative EBE-A22 is inactive. Yet both inhibit cell growth and upregulate retinoic acid receptor-beta in ErbB-1-overexpressing (MDA-MB-468), moderately expressing (OVCAR-3), ErbB-1-negative (MDA-MB-453) or ErbB-negative cells (CEM, Jurkat). Both bind DNA, whereas the closely related ErbB-1 inhibitors AG1478 and ZD1839, which are inactive on retinoic acid receptor-beta, do not significantly bind DNA. None of the other ErbB-1/ErbB-2 inhibitors tested (RG-14620, LFM-A12, AG879, AG825) affect retinoic acid receptor-beta. PD153035 decreases methylation of the retinoic acid receptor-beta2 promoter. In OVCAR-3, it stimulates dislodgement of histone deacetylase 1 from the promoter and acetylation of histones H3 and H4. Consequently, PD153035 facilitates recruitment of RNA polymerase II to the promoter and stimulates transcriptional activity. Moreover, PD153035 increases the retinoic acid receptor-beta mRNA half-life. No other retinoid receptor, nor estrogen receptor-alpha, nor RASSF1A is upregulated by PD153035. Thus PD153035 induces retinoic acid receptor-beta by ErbB-independent transcriptional and post-transcriptional mechanisms. This report highlights a triple action for an ErbB-1 inhibitor (ErbB-1 inhibition, DNA intercalation, retinoic acid receptor-beta-induction). Such multitargeting drugs bear great potential for cancer treatment.