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Cardiovascular Research 2007 76(2):199-201; doi:10.1016/j.cardiores.2007.08.013
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Copyright © 2007, European Society of Cardiology

Inhibition of SR Ca2+ uptake: A novel action of the RyR2–FKBP12.6 antagonist K201

Andrew F. James*

Department of Physiology and Pharmacology, and Bristol Heart Institute Cardiovascular Research Laboratories, School of Medical Sciences, University of Bristol, Bristol, BS8 1TD, UK
Department of Cell Physiology, National Institute for Physiological Sciences, Nishigonaka 38, Myodaiji-cho, Okazaki 444-8585, Japan

*Department of Physiology and Pharmacology, and Bristol Heart Institute Cardiovascular Research Laboratories, School of Medical Sciences, University of Bristol, Bristol, BS8 1TD, UK. Tel.: +44 117 331 2297; fax: +44 117 331 2288. a.james@bristol.ac.uk

Received 20 August 2007; revised 28 August 2007; accepted 28 August 2007

The first 10% of the full text of this article appears below.

See article by Loughrey et al. [13] (pages 236–246) in this issue.

K201, also known as JTV519 or JTV-519, is a 1,4-benzothiazepine derivative that was developed for its protective action against Ca2+-induced myocardial damage [1]. It was subsequently shown to be protective in models of ischaemia-reperfusion injury [2,3] and heart failure (HF) [4], has been in phase II clinical trials as a protective agent against acute myocardial infarction since 2000, and is suggested to reduce reperfusion injury following percutaneous transluminal coronary angioplasty (see http://www.jti.co.jp/JTI_E/IR/FR/0111/0111-Supplementary.pdf). Although like diltiazem, to which . . . [Full Text of this Article]


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