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Submit ReviewSEA 0400
Discontinued Product
6164 has been discontinued.
说明： Potent Na+/Ca2+ exchanger (NCX) inhibitor
化学名： 2-[4-[(2,5-Difluorophenyl)methoxy]phenoxy]-5-ethoxybenzenamine
纯度： ≥98% (HPLC)
生物活性 for SEA 0400
SEA 0400 is a potent Na+/Ca2+ exchanger (NCX) inhibitor. Inhibits NCX activity in rat astrocytes, microglia and cultured neurons, canine cardiac sarcolemmal vesicles and rat cardiomyocytes (IC50 values are 5 and 8.3, 33, 90 and 92 nM, respectively). Reduces infarct volumes and exhibits protective effects against myocardial ischemia in rats.
化合物库 for SEA 0400
SEA 0400 is also offered as part of the Tocriscreen 2.0 Max. 了解 Tocris 化合物库的更多信息。
技术数据 for SEA 0400
| 分子量 | 371.38 |
| 公式 | C21H19F2NO3 |
| 储存 | Store at -20°C |
| 纯度 | ≥98% (HPLC) |
| CAS Number | 223104-29-8 |
| PubChem ID | 644100 |
| InChI Key | YSUBLPUJDOWYDP-UHFFFAOYSA-N |
| Smiles | CCOC1=CC(N)=C(C=C1)OC2=CC=C(C=C2)OCC3=C(C=CC(F)=C3)F |
上方提供的技术数据仅供参考。批次相关数据请参见分析证书。
Tocris products are intended for laboratory research use only, unless stated otherwise.
产品说明书 for SEA 0400
参考文献 for SEA 0400
参考文献是支持产品生物活性的出版物。
Takahashi et al (2003) Protective effects of SEA0400, a novel and selective inhibitor of the Na+/Ca2+ exchanger, on myocardial ischemia-reperfusion injuries. Eur.J.Pharmacol. 458 155 PMID: 12498920
Christ et al (2016) Block of Na(+)/Ca(2+) exchanger by SEA0400 in human right atrial preparations from patients in sinus rhythm and in atrial fibrillation. Eur.J.Pharmacol. 788 286 PMID: 27373849
Karashima et al (2007) Involvement of Na+-Ca2+ exchanger in cAMP-mediated relaxation in mice aorta: evaluation using transgenic mice. Br.J.Pharmacol. 150 343 PMID: 17220909
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关键词: SEA 0400, SEA 0400 supplier, SEA0400, Inhibitors, Inhibits, NCX, Na+/Ca2+, exchanger, cardioprotectant, Exchanger, 6164, Tocris Bioscience
3 篇 SEA 0400 的引用文献
引用文献是使用了 Tocris 产品的出版物。 SEA 0400 的部分引用包括：
Neubert et al (2020) NCX1 Represents an Ionic Na+ Sensing Mechanism in Macrophages. PLoS Biol 18 PMID: 32569301
Yan et al (2019) Blockade of the forward Na+ /Ca2+ exchanger suppresses the growth of glioblastoma cells through Ca2+ -mediated cell death. Br J Pharmacol 176 2691-2707 PMID: 31034096
Bradley J et al (2019) Intracellular Ca2+ Homeostasis and Nuclear Export Mediate Exit from Naive Pluripotency. Cell Stem Cell 25 210-224.e6 PMID: 31104942
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