product name Ranolazine 2HCl
Description: Ranolazine 2HCl, the HCl salt of ranolzaine, is a calcium uptake inhibitor via the sodium/calcium channel, it is used to treat chronic angina. Ranolazine is an anti-ischemic agent that inhibits late sodium current that results in a reduction of Na+ dependent Ca2+ overload. Ranolazine can cause the shift of ATP production towards glucose oxidation, which is due to the fact that more oxygen is required to phosphorylate the same amount of ATP during fatty acid oxidation than carbohydrate oxidation. These studies indicate that Ranolazine also inhibits oxygen consumption and ketogenesis by fatty acids in liver cells.
References: Heart. 2006 Jul;92 Suppl 4:iv6-iv14; Circulation. 1996 Jan 1;93(1):135-42.
500.46
Formula
C24H33N3O4.2HCl
CAS No.
95635-56-6
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 100 mg/mL (199.8 mM)
Water: 100 mg/mL (199.8 mM)
Ethanol: <1 mg/mL
Solubility (In vivo)
Synonyms
RS-43285
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19403490
| In Vitro |
In vitro activity: Ranolazine selectively inhibits late I(Na), reduces [Na(+)](i)-dependent calcium overload and attenuates the abnormalities of ventricular repolarisation and contractility that are associated with ischaemia/reperfusion and heart failure in myocardial cells. Ranolazine significantly and reversibly shortens the action potential duration (APD) of myocytes stimulated at either 0.5 Hz or 0.25 Hz in a concentration-dependent manner in left ventricular myocytes of dogs. Ranolazine at 5 and 10 mM reversibly shortens the duration of twitch contractions (TC) and abolished the after contraction. Ranolazine is found to bind more tightly to the inactivated state than the resting state of the sodium channel underlying I(NaL). Kinase Assay: Cell Assay: |
|---|---|
| In Vivo | Ranolazine (10 mM) significantly increases glucose oxidation 1.5-fold to 3-fold under conditions in which the contribution of glucoseto overall ATP production is low (low Ca, high FA, with insulin), high (high Ca, low Fa, with pacing), or intermediate in working hearts. Ranolazine similarly increases glucose oxidation in normoxic Langendorff hearts (high Ca, low FA; 15 mL/min). Ranolazine also significantly increases it during flow reduction to 7 mL/min, 3 mL/min, and 0.5 mL/min. Ranolazine significantly improves functional outcome, which is associated with significant increases in glucoseoxidation, a reversal of the increased FA oxidation seen in control reperfusions (versus preischemic), and a smaller but significant increase in glycolysis in reperfuse dischemic working hearts. |
| Animal model | |
| Formulation & Dosage | |
| References | Heart. 2006 Jul;92 Suppl 4:iv6-iv14; Circulation. 1996 Jan 1;93(1):135-42. |
Related Posts
product name Ranolazine 2HCl
Description: Ranolazine 2HCl, the HCl salt of ranolzaine, is a calcium uptake inhibitor via the sodium/calcium channel, it is used to treat chronic angina. Ranolazine is an anti-ischemic agent that inhibits late sodium current that results in a reduction of Na+ dependent Ca2+ overload. Ranolazine can cause the shift of ATP production towards glucose oxidation, which is due to the fact that more oxygen is required to phosphorylate the same amount of ATP during fatty acid oxidation than carbohydrate oxidation. These studies indicate that Ranolazine also inhibits oxygen consumption and ketogenesis by fatty acids in liver cells.
References: Heart. 2006 Jul;92 Suppl 4:iv6-iv14; Circulation. 1996 Jan 1;93(1):135-42.
500.46
Formula
C24H33N3O4.2HCl
CAS No.
95635-56-6
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 100 mg/mL (199.8 mM)
Water: 100 mg/mL (199.8 mM)
Ethanol: <1 mg/mL
Solubility (In vivo)
Synonyms
RS-43285
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19403490
| In Vitro |
In vitro activity: Ranolazine selectively inhibits late I(Na), reduces [Na(+)](i)-dependent calcium overload and attenuates the abnormalities of ventricular repolarisation and contractility that are associated with ischaemia/reperfusion and heart failure in myocardial cells. Ranolazine significantly and reversibly shortens the action potential duration (APD) of myocytes stimulated at either 0.5 Hz or 0.25 Hz in a concentration-dependent manner in left ventricular myocytes of dogs. Ranolazine at 5 and 10 mM reversibly shortens the duration of twitch contractions (TC) and abolished the after contraction. Ranolazine is found to bind more tightly to the inactivated state than the resting state of the sodium channel underlying I(NaL). Kinase Assay: Cell Assay: |
|---|---|
| In Vivo | Ranolazine (10 mM) significantly increases glucose oxidation 1.5-fold to 3-fold under conditions in which the contribution of glucoseto overall ATP production is low (low Ca, high FA, with insulin), high (high Ca, low Fa, with pacing), or intermediate in working hearts. Ranolazine similarly increases glucose oxidation in normoxic Langendorff hearts (high Ca, low FA; 15 mL/min). Ranolazine also significantly increases it during flow reduction to 7 mL/min, 3 mL/min, and 0.5 mL/min. Ranolazine significantly improves functional outcome, which is associated with significant increases in glucoseoxidation, a reversal of the increased FA oxidation seen in control reperfusions (versus preischemic), and a smaller but significant increase in glycolysis in reperfuse dischemic working hearts. |
| Animal model | |
| Formulation & Dosage | |
| References | Heart. 2006 Jul;92 Suppl 4:iv6-iv14; Circulation. 1996 Jan 1;93(1):135-42. |