Ranolazine dihydrochloride

English synonyms

(+/-)-4-[2-HYDROXY-3-(O-METHOXYPHENOXY)PROPYL]-1-PIPERAZINEACETO-2',
6'-XYLIDIDEDIHYDROCHLORIDE;n-(2,6-dimethylphenyl)-2-[4-[2-hydroxy-3-(2-methoxyphenoxy)propyl]
piperazin-1-yl]acetamidedihydrochloride;
(+/-)-N-(2,6-DIMETHYLPHENYL)-4-[2-HYChemicalbookDROXY-3-(2-METHOXYPHENOXY)PROPYL]-1-PIPERAZINEACETAMIDEDIHYDROCHLORIDE;RANOLAZINEDIHYDROCHLORIDE;
RANOLAZINEHCL;RanolazineDiHCI;Ranolazineandsalt;
N-(2,6-Dimethylphenyl)-2-(4-(2-hydroxy-3-(2-methoxyphenoxy)-propyl)piperazin-1-yl)acetamidedi

CAS number

95635-56-6

Molecular formula

C24H35CI2N304

Molecular weight

500.46

Melting point

222-229.5°C(lit.

Storage conditions

Desiccate at RT

Solubility

H₂O:10 mg/mL, soluble

Form

Solid

Color

Off-white

Water solubility

H2O:soluble≥10mg/mL

Merck

148111

Stability

Hygroscopicity

CAS database

95635-56-6(CAS DataBase Reference)

Biological Activity

Ranolazine 2HCl (RS-43285) is an antianginal drug that is an inhibitor of calcium ion uptake through the sodium/calcium channal, used for the treatment of chronic angina pectoris.

Target

Target

Value

Calcium channel

In vitro studies

In cardiomyocytes, Ranolazine selectively inhibits late phase I(sodium), reduces sodium-dependent calcium overload, and attenuates ventricular repolarization and contraction,
which are associated with abnormalities in ischemia/reperfusion injury and heart failure. In dog left ventricular myocytes,
Ranolazine concentration-dependently and reversibly shortened the action potential duration (APD) of myocytes stimulated at 0.5 Hz or 0.25 Hz. Ranolazine
reversibly shortened the duration of twitch contractions (TC) at 5mM and 10mM and abolished aftercontractions.
Ranolazine was found to bind more to the inactivated state of sodium channels.

In vivo studies

Ranolazine (10 mM) significantly increased glucose oxidation by 1.5-fold to 3-fold in working hearts,
where the contribution of glucoseto overall ATP production was low (low calcium, high FA, insulin), high (high calcium, low FA), or intermediate.
Ranolazine also increased glucose oxidation in Langendorff hearts (high calcium, low FA; 15 ml/min).
Ranolazine also increased glucose oxidation with flow rates reduced to 7 ml/min, 3 ml/min, and 0.5 ml/min. Ranolazine significantly improved functional output,
which was associated with a significant increase in glucoseoxidation, reversing the increase in fatty acid oxidation in controls,
and significantly increasing glycolysis in reperfusedischemic working hearts.