NIZACARD 500
RANOLAZINE
What it does
Ranolazine is a medication used to manage chest pain associated with heart problems.
Commonly used for: chest pain (angina)
Read more in plain English ↓Plain-language summary for general understanding - not medical advice. Always follow your pharmacist/doctor.
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Answers come only from this medicine's registration record, BNF monograph and interaction data - not medical advice.
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Sourcing - Kenya onlyRegistration & product details
Source: Medicines Control Authority of Zimbabwe · fetched 2026-04-18 08:22:09 · updated 2026-09-16 04:30:08
Drug Interactions
54Pharmacodynamic Warnings
Ranolazine appears in TABLE 9: Drugs that prolong the QT interval
Severe (4)
Fidaxomicin - increases exposure
Ranolazine is predicted to increase the exposure to fidaxomicin. Avoid.
Ranolazine - increases concentration
Grapefruit juice is predicted to increase the concentration of ranolazine. Avoid.
Ranolazine - increases exposure
Clarithromycinispredictedtoincreasetheexposureto ranolazine.Avoid.rStudy →AlsoseeTABLE9p.1519 https://www.facebook.c (Books-Courses-Medic
Ranolazine - decreases exposure
St John’s wort is predicted to decrease the exposure to ranolazine. Avoid.
Moderate (5)
Bictegravir - increases exposure
Ranolazine is predicted to increase the exposure to bictegravir. Use with caution or avoid.
Dopamine Receptor Agonists - increases exposure
Ranolazine is predicted to increase the exposure to dopamine receptor agonists (pramipexole). Adjust dose.
Panobinostat - increases exposure
Ranolazine is predicted to increase the exposure to panobinostat. Adjust dose. Also see TABLE 9 p. 1519
Pramipexole - increases exposure
Ranolazine is predicted to increase the exposure to pramipexole. Adjust dose.
Ticagrelor - increases exposure
Ranolazine is predicted to increase the exposure to ticagrelor. Use with caution or avoid.
Unknown (45)
Afatinib - increases exposure
Ranolazine is predicted to increase the exposure to afatinib.
Aliskiren - increases exposure
Ranolazineispredictedtoincreasetheexposuretoaliskiren. oTheoretical
Apixaban - increases exposure
Ranolazineispredictedtoincreasetheexposuretoapixaban. oTheoretical
Atorvastatin - increases exposure
Ranolazineispredictedtoincreasetheexposuretostatins (atorvastatin).oTheoretical
Berotralstat - increases exposure
Ranolazineispredictedtoincreasetheexposureto berotralstat.rStudy com/codemedicalapps/ cal Applications)
Data from BNF 85 (British National Formulary). This is not a substitute for professional medical advice. Matched via: exact
About this medicine
Ranolazine is a medication used to manage chest pain associated with heart problems.
What it treats
- chest pain (angina)
How it works
It helps improve blood flow to the heart, allowing it to work more efficiently and reducing pain.
Who it's for
This medication is for adults experiencing chest pain due to heart disease.
Cautions
- • Avoid using with medications that prolong the QT interval, which can affect heart rhythm.
AI-assisted summary grounded in BNF data - general information only, not medical advice. Always confirm with your pharmacist or doctor.
Clinical monograph: Ranolazine
BNF-referencedRanolazine is an antianginal medication primarily used for the treatment of stable angina pectoris. It functions by altering the ionic currents associated with cardiac contractility and energy metabolism, thereby improving myocardial ischemia without significant effects on heart rate or blood pressure. Its unique mechanism allows it to relieve angina symptoms by addressing the underlying ionic imbalances in myocardial cells.
Indications
- Chronic stable angina pectoris
- Myocardial ischemia
Dosage
Adults: Initially, 375 mg twice daily for 2–4 weeks, then increased to 500 mg twice daily. Adjust based on response, maximum 750 mg twice daily, and reduce if not tolerated.
Mechanism of action
Ranolazine inhibits the late sodium current (I_Na) in cardiac myocytes, which helps restore the balance of sodium and potassium ions essential for normal heart function. This inhibition reduces intracellular calcium overload and improves myocardial energy metabolism, thereby alleviating symptoms of angina. Additionally, ranolazine has weak activity on L-type calcium channels and can exert minimal vasodilatory effects. It also antagonizes alpha 1 and beta 1 adrenergic receptors and inhibits fatty acid oxidation.
Pharmacodynamics
Ranolazine has antianginal and ischemic effects that are independent of its impact on heart rate or blood pressure. It blocks the rapid component of the delayed rectifier potassium current (I_Kr), which prolongs the QTc interval in a dose-dependent manner without causing negative chronotropic or inotropic effects during rest or exercise. This allows it to effectively manage angina symptoms without exacerbating heart failure or causing bradycardia.
Pharmacokinetics
Ranolazine is well absorbed from the gastrointestinal tract, with peak plasma concentrations occurring approximately 2 to 4 hours after administration. It undergoes extensive hepatic metabolism primarily via CYP3A4 and has a half-life of about 7 hours. The presence of food can increase the bioavailability of ranolazine. It is primarily excreted in the urine, with a significant portion of the drug metabolized to its active metabolites.
Contra-indications
- Severe hepatic impairment
- Concurrent use of strong CYP3A4 inhibitors (except diltiazem, erythromycin)
- Hypersensitivity to ranolazine or any of its components
Adverse effects
- Dizziness
- Nausea
- Constipation
- Headache
- QT interval prolongation
- Palpitations
- Abdominal pain
- Fatigue
Interactions
- Severe: fidaxomicin, grapefruit juice, clarithromycin, St. John's Wort
- Moderate: bictegravir, pramipexole, panobinostat, dopaminergic receptor agonists, ticagrelor, afatinib
Precautions
- Monitor heart rate and blood pressure
- Caution in patients with moderate to severe renal impairment
- Avoid in patients with body weight less than 60 kg
- Use with caution in elderly patients
Pregnancy
Manufacturer advises to avoid unless essential, no information available.
Breast-feeding
Manufacturer advises to avoid, no information available.
Storage
Store in a cool, dry place, away from light, at room temperature.
Formulations
- Modified-release tablet 375 mg
- Modified-release tablet 500 mg
- Modified-release tablet 750 mg
- Infusion 12.5 mg/250 ml
- Infusion 60 mg/250 ml
AI-synthesized from BNF references - general information only, not a substitute for professional medical advice or the current BNF. Verify doses with a pharmacist.
Molecular reference: Ranolazine
PubChem CID 56959Molecular formula: C24H33N3O4
Mechanism of action
Myocardial ischemia exerts effects on adenosine triphosphate flux, leading to a decrease in the energy available for contraction and relaxation of the heart muscle. Electrolyte balance of sodium and potassium is necessary for maintaining normal cardiac contraction and relaxation. Disruption of adequate sodium and potassium electrolyte balance leads to excessively high concentrations of sodium and calcium, which likely interferes with oxygen supply to the heart muscle. This imbalance eventually leads to angina symptoms of chest pain or pressure, nausea, and dizziness, among others. The mechanism of action for ranolazine is not fully understood. At therapeutic concentrations, it can inhibit the cardiac late sodium 205 current (INa), which may affect the electrolyte balance in the myocardium, relieving angina symptoms. The clinical significance this inhibition in the treatment of angina symptoms is not yet confirmed. Ranolazine inhibits sodium and potassium ion channel currents. It has been shown to exert weak activity on L-type calcium channels making it a weak direct vasodilator and exerts minimal direct effects on atrioventricular nodal conduction. Some additional mechanisms have been elucidated. Ranolazine exerts antagonistic activity towards the alpha 1 and beta 1 adrenergic receptors and inhibition of fatty acid oxidation. Ranolazine, a piperazine derivative, is an antianginal agent. Although the exact mechanism of antianginal activity of ranolazine has not been fully elucidated, results of early studies suggested that ranolazine shifted adenosine triphosphate (ATP) production away from fatty acid oxidation (ie, partial inhibition of fatty acid oxidation) in favor of more oxygen-efficient glucose oxidation, especially when free fatty acid concentrations were elevated (eg, during ischemia), leading to reduced oxygen demand and symptoms of ischemia without affecting cardiac work. However, these pharmacologic effects generally were observed at concentrations exceeding therapeutic plasma concentrations in clinical studies. Recent data suggest that ranolazine may exert its antianginal and anti-ischemic effects through concentration-, voltage-, and frequency-dependent inhibition of the late (ie, sustained, persistent) sodium current and other cardiac ion channels and transporters. The late sodium current is created by inactivation of the sodium channel protein. However, angina (ie, ischemia, hypoxia) impairs sodium channel inactivation and increases the amount of sodium in cardiac cells, which facilitates calcium overload via the sodium-calcium exchange pump. Increased intracellular calcium may result in myocyte hyperexcitability and electrical instability, impaired diastolic relaxation, reduced coronary artery perfusion, impaired myocardial oxygen supply, increased oxygen demand, and ventricular dysfunction. Thus, ranolazine may decrease the magnitude of the late sodium current resulting in a net reduction in intracellular sodium concentrations, reversal of calcium overload, restoration of ventricular pump function, and prevention of ischemia-induced arrhythmias. Unlike other antianginal agents, the antianginal effects of ranolazine are not dependent upon reductions in heart rate or blood pressure. The QT prolongation effect of ranolazine on the surface electrocardiogram is the result of inhibition of IKr, which prolongs the ventricular action potential. /The authors/ investigated changes in Na(+) currents (I(Na)) in permanent (or chronic) atrial fibrillation (AF) and the effects of I(Na) inhibition using ranolazine (Ran) on arrhythmias and contractility in human atrial myocardium. Electrical remodeling during AF is typically associated with alterations in Ca(2+) and K(+) currents. It remains unclear whether I(Na) is also altered. Right atrial appendages from patients with AF (n = 23) and in sinus rhythm (SR) (n = 79) were studied. Patch-clamp experiments in isolated atrial myocytes showed significantly reduced peak I(Na) d
Pharmacodynamics
Ranolazine exerts both antianginal and ischemic effects independent from lowering heart rate or blood pressure. It blocks IKr, the rapid portion of the delayed rectifier potassium current, and prolongs the QTc interval in a dose-dependent fashion. The Ikr is important for cardiac repolarization. Ranolazine exerts its therapeutic effects without negative chronotropic, dromotropic, or inotropic actions neither at rest, nor during exercise.
Source: PubChem (NCBI) · pathways from PathBank, Reactome, WikiPathways & PharmGKB.
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