Ranolazine dihydrochloride
Chemical Name: N-(2,6-Dimethylphenyl)-4-[2-hydroxy-3-(2-methoxyphenoxy)propyl]-1-piperazineacetamide dihydrochloride
Purity: ≥98%
Biological Activity
Ranolazine dihydrochloride is an antianginal agent with antiarrhythmic properties that acts as a partial fatty acid oxidation inhibitor. Activates pyruvate dehydrogenase in ischemic myocytes to promote glucose oxidation, switching substrate utilization from fatty acids to glucose. Also shown to inhibit late INa and IKr currents.Technical Data
The technical data provided above is for guidance only.
For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
Background References
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Ranolazine, a partial fatty acid oxidation inhibitor, reduces myocardial infarct size and cardiac troponin T release in the rat.
Zacharowski et al.
Eur.J.Pharmacol., 2001;418:105 -
Inhibition of late sodium current to reduce electrical and mechanical dysfunction of ischaemic myocardium.
Shryock and Belardinelli
Br.J.Pharmacol., 2008;153:1128 -
Antitorsadogenic effects of (+/-)-N-(2,6-dimethyl-phenyl)-4[2-hydroxy-3-(2-methoxyphenoxy)propyl]-1-piperazine (ranolazine) in anesthetized rabbits.
Wang et al.
J.Pharmacol.Exp.Ther., 2008;325:875
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Citations for Ranolazine dihydrochloride
The citations listed below are publications that use Tocris products. Selected citations for Ranolazine dihydrochloride include:
3 Citations: Showing 1 - 3
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Effects of UK 68798 and RS 43285 on atrial fibrillatory rate in a horse model of acutely induced atrial fibrillation.
Authors: Carstensen Et al.
J Cardiovasc Electrophysiol 2019;30:596
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An Automated Platform for Assessment of Congenital and Drug-Induced Arrhythmia with hiPSC-Derived Cardiomyocytes.
Authors: McKeithan Et al.
Front Physiol 2017;8:766
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Slowly inactivating component of Na+ current in peri-somatic region of hippocampal CA1 pyramidal neurons.
Authors: Park Et al.
J Neurophysiol 2013;109:1378
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Guinea pig ventricular cardiomyocytes were treated (12-16 h) with HOCl-LDL (250 µg/ml). Cells were patched and stimulated at a frequency of 1 Hz. Representative action potentials (shown in Image) recorded in the same cell are shown before (A) and after (B) superfusion with Ranolazine (10 µM, 5 min). For comparative purpose representative APs of a control cardiomyocyte are shown (C).
Application of Ranolazine on acute brain slices to verify for fatty acid oxidation involvement in studied process. It had the same effect as etomoxir (CPT1 blocker), as expected per hypothesis.
