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CHD-5

目录号 : GC67892

CHD-5 是一种有效的 AhR (芳香烃受体)拮抗剂。

CHD-5 Chemical Structure

Cas No.:289494-16-2

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10mg
¥5,040.00
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Sample solution is provided at 25 µL, 10mM.

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产品描述

CHD-5 is a potent AhR (aryl hydrocarbon receptor) antagonist[1].

[1]. Choi EY, et al. Development of novel CH223191-based antagonists of the aryl hydrocarbon receptor. Mol Pharmacol. 2012 Jan;81(1):3-11.

Chemical Properties

Cas No. 289494-16-2 SDF Download SDF
分子式 C19H17N3O2 分子量 319.36
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1 mM 3.1313 mL 15.6563 mL 31.3126 mL
5 mM 0.6263 mL 3.1313 mL 6.2625 mL
10 mM 0.3131 mL 1.5656 mL 3.1313 mL
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Research Update

Development of novel CH223191-based antagonists of the aryl hydrocarbon receptor

Mol Pharmacol 2012 Jan;81(1):3-11.PMID:21967751DOI:PMC3250110

Aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor that regulates genes involved in drug/xenobiotic metabolism, cell cycle progression, cell fate determination, immune function, and inflammatory response. Increasing evidence that AHR plays a role in the pathophysiology of a number of human disease states is driving the need for improved pharmacological tools to be used for understanding the in vivo impact of AHR modulation. In this study, we have characterized and used structure-activity relationship analyses of a newly synthesized library of derivatives of the potent AHR antagonist 2-methyl-2H-pyrazole-3-carboxylic acid (2-methyl-4-o-tolylazo-phenyl)-amide (CH223191). Initial screening of these compounds revealed that those bearing groups with strong electronegativity at the R1 position (i.e., CHD-5, CHD-11, and CHD-12) versus those that are more electron-poor at this position (i.e., CHD-7 and CHD-8) elicited the most potent AHR antagonistic properties. The ability of these derivatives to inhibit agonist (2,3,7,8-tetrachlorodibenzo-p-dioxin) binding, nuclear translocation of AHR, and agonist-induced enzyme activity also were determined and support the initial findings. Furthermore, CH223191, but not CHD-5, CHD-11, or CHD-12, was found to exhibit AHR-independent proproliferative properties. These results contribute to our understanding of the structural requirements of potent AHR antagonists and the development of effective pharmacological tools to be used for studying the pathophysiological role of AHR.