Pharmacology of SEA0400, a Specific Inhibitor of the Na〔+〕-Ca〔2+〕 Exchanger
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- Matsuda Toshio
- Laboratory of Medicinal Pharmacology, Graduate School of Pharmaceutical Sciences, Osaka University
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- Koyama Yutaka
- Laboratory of Medicinal Pharmacology, Graduate School of Pharmaceutical Sciences, Osaka University
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- Baba Akemichi
- Laboratory of Molecular Neuropharmacology, Graduate School of Pharmaceutical Sciences, Osaka University
書誌事項
- タイトル別名
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- Functional Proteins Involved in Regulation of Intracellular Ca2+ for Drug Development: Pharmacology of SEA0400, a Specific Inhibitor of the Na+-Ca2+ Exchanger
- Pharmacology of SEA0400 a Specific Inhibitor of the Na Ca 2 Exchanger
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説明
The Na+-Ca2+ exchanger (NCX) is involved in regulation of intracellular Ca2+ concentration. A specific inhibitor of NCX has been required for clarification of the physiological and pathological roles of NCX. We have developed 2-[4-[(2,5-difluorophenyl)methoxy]phenoxy]-5-ethoxyaniline (SEA0400), a highly potent and selective inhibitor of NCX. SEA0400 in the concentration range that inhibits NCX exhibits negligible affinities for the Ca2+ channels, Na+ channels, K+ channels, noradrenaline transporter, and 14 receptors; and it does not affect the activities of the store-operated Ca2+ channel, Na+-H+ exchanger, and several enzymes including Na+,K+-ATPase and Ca2+-ATPase. Furthermore, recent studies show that SEA0400 attenuates ischemia-reperfusion injury in the brain, heart, and kidney and radiofrequency lesion-induced edema in rat brain. These findings suggest that NCX plays a key role in ischemia-reperfusion injury and may be a target molecule for treatment of reperfusion injury-related diseases.<br>
収録刊行物
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- Journal of Pharmacological Sciences
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Journal of Pharmacological Sciences 97 (3), 339-343, 2005
公益社団法人 日本薬理学会
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詳細情報 詳細情報について
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- CRID
- 1390282680154223104
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- NII論文ID
- 10025726628
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- NII書誌ID
- AA11806667
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- ISSN
- 13478648
- 13478613
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- NDL書誌ID
- 7289018
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- PubMed
- 15764845
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- NDL
- Crossref
- PubMed
- CiNii Articles
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- 抄録ライセンスフラグ
- 使用不可