research use only
Cat.No.S1425
| Related Targets | CFTR CRM1 CD markers AChR Sodium Channel Potassium Channel GABA Receptor TRP Channel ATPase GluR |
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| Other Calcium Channel Inhibitors | Bay K 8644 Tetrandrine Nilvadipine Flunarizine 2HCl Cilnidipine YM-58483 (BTP2) Ionomycin Imperatorin Manidipine 2HCl Astragaloside A |
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In vitro |
DMSO
: 100 mg/mL
(199.81 mM)
Water : Insoluble Ethanol : Insoluble |
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In vivo |
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| Molecular Weight | 500.46 | Formula | C24H33N3O4.2HCl |
Storage (From the date of receipt) | |
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| CAS No. | 95635-56-6 | Download SDF | Storage of Stock Solutions |
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| Synonyms | RS-43285,RS 43285-193,Ranexa, renolazine,Ranolazine dihydrochloride | Smiles | CC1=C(C(=CC=C1)C)NC(=O)CN2CCN(CC2)CC(COC3=CC=CC=C3OC)O.Cl.Cl | ||
| Targets/IC50/Ki |
Calcium channel
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| In vitro |
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). |
| 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. |
References |
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(data from https://clinicaltrials.gov, updated on 2024-05-22)
| NCT Number | Recruitment | Conditions | Sponsor/Collaborators | Start Date | Phases |
|---|---|---|---|---|---|
| NCT03486561 | Unknown status | Chronic Stable Angina |
OBS Pakistan |
April 1 2018 | Phase 4 |
| NCT03044964 | Unknown status | Angina |
Amit Malhotra MD|Gilead Sciences|Stern Cardiovascular Foundation Inc. |
January 10 2017 | Phase 4 |
| NCT02252406 | Completed | Stable Angina|Metabolic Syndrome |
University of Florida |
September 2015 | Phase 4 |
| NCT02360397 | Completed | Ventricular Premature Complexes|Myocardial Ischemia |
Kent Hospital Rhode Island|Gilead Sciences |
December 2014 | Phase 2 |
| NCT02156336 | Terminated | Diabetic Peripheral Neuropathic Pain |
Horizons International Peripheral Group|Gilead Sciences |
May 2014 | Phase 4 |
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