Quinidine Sulfate (Quinidine Sulfate)

Trade Name : Quinidine Sulfate

Eon Labs, Inc.

TABLET

Strength 300 mg/1

QUINIDINE SULFATE Antiarrhythmic [EPC],Cytochrome P450 2D6 Inhibitor [EPC],Cytochrome P450 2D6 Inhibitors [MoA]

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GNH India is WHO GDP and ISO 9001 2015 Certified Pharmaceutical Wholesaler/ Supplier/ Exporters/ Importer from India of Quinidine Sulfate (Quinidine Sulfate) which is also known as Quinidine Sulfate and Manufactured by Eon Labs, Inc.. It is available in strength of 300 mg/1 per ml. Read more

Quinidine Sulfate (Quinidine Sulfate) is supplied for Tenders/ Emergency imports/ Un - licensed, Specials, Orphan drug/ Name patient line/ RLD supplies/ Reference listed drugs/ Comparator Drug/ Bio-Similar/ Innovator samples For Clinical trials.  Click to know price.     Read less

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We deliver your medicines through a validated cold chain shipment process. This process is used as these medicines need to manufactured, transported and stored at very specific temperatures, utilizing thermal and refrigerated packaging methods.

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  • No data
  • Quinidine is an antimalarial schizonticide and an antiarrhythmic agent with class 1A activity; it is the isomer of quinine, and its molecular weight is 324.43. Quinidine sulfate is the sulfate salt of quinidine; its chemical name is cinchonan-9-ol,6u2019- methoxy-,(9)-, sulfate(2:1) dihydrate; its structural formula is:
  • Its molecular formula is: CHNOu2022HSOu20222HO; and its molecular weight is 782.96, of which 82.9% is quinidine base.
  • Quinidine sulfate occurs as fine needle-like, white crystals, frequently cohering in masses, or fine, white powder. It is odorless, has a very bitter taste, and darkens on exposure to light. It is slightly soluble in water, soluble in alcohol and in chloroform, and insoluble in ether.
  • Each tablet, for oral administration, contains 200 mg of quinidine sulfate (equivalent to 166 mg of quinidine base) 300 mg of quinidine sulfate (equivalent to 249 mg of quinidine base). In addition, each tablet contains the following inactive ingredients: confectioneru2019s sugar, corn starch, microcrystalline cellulose, pregelatinized starch and zinc stearate.
  • Pharmacokinetics and Metabolism
  • The absolute bioavailability of quinidine from quinidine sulfate tablets is about 70%, but this varies widely (45 to 100%) between patients. The less-than-complete bioavailability is the result of first-pass metabolism in the liver. Peak serum levels generally appear about 2 hours after dosing; the rate of absorption is somewhat slowed when the drug is taken with food, but the extent of absorption is not changed.
  • The of quinidine is 2 to 3 L/kg in healthy young adults, but this may be reduced to as little as 0.5 L/kg in patients with congestive heart failure, or increased to 3 to 5 L/kg in patients with cirrhosis of the liver. At concentrations of 2 to 5 mg/L (6.5 to 16.2 u03bcmol/L), the fraction of quinidine bound to plasma proteins (mainly to u03b1-acid glycoprotein and to albumin) is 80 to 88% in adults and older children, but it is lower in pregnant women, and in infants and neonates it may be as low as 50 to 70%. Because u03b1-acid glycoprotein levels are increased in response to stress, serum levels of total quinidine may be greatly increased in settings such as acute myocardial infarction, even though the serum content of unbound (active) drug may remain normal. Protein binding is also increased in chronic renal failure, but binding abruptly descends toward or below normal when heparin is administered for hemodialysis.
  • Quinidine typically proceeds at 3 to 5 mL/min/kg in adults, but clearance in children may be twice or three times as rapid. The elimination half-life is 6 to 8 hours in adults and 3 to 4 hours in children. Quinidine clearance is unaffected by hepatic cirrhosis, so the increased volume of distribution seen in cirrhosis leads to a proportionate increase in the elimination half-life.
  • Most quinidine is eliminated hepatically via the action of cytochrome P450; there are several different hydroxylated metabolites, and some of these have antiarrhythmic activity.
  • The most important of quinidineu2019s metabolites is 3-hydroxyquinidine (3HQ), serum levels of which can exceed those of quinidine in patients receiving conventional doses of quinidine sulfate. The volume of distribution of 3HQ appears to be larger than that of quinidine, and the elimination half-life of 3HQ is about 12 hours.
  • As measured by antiarrhythmic effects in animals, by QTc prolongation in human volunteers, or by various techniques, 3HQ has at least half the antiarrhythmic activity of the parent compound, so it may be responsible for a substantial fraction of the effect of quinidine sulfate in chronic use.
  • When the urine pH is less than 7, about 20% of administered quinidine appears unchanged in the urine, but this fraction drops to as little as 5% when the urine is more alkaline. Renal clearance involves both glomerular filtration and active tubular secretion, moderated by (pH-dependent) tubular reabsorption. The net renal clearance is about 1 mL/min/kg in healthy adults. When renal function is taken into account, quinidine clearance is apparently independent of patient age.
  • Assays
  • Mechanisms of Action
  • In patients with malaria, quinidine acts primarily as an intra-erythrocytic schizonticide, with little effect upon sporozites or upon pre-erythrocytic parasites. Quinidine is gametocidal to and but not to .
  • In cardiac muscle and in Purkinje fibers, quinidine depresses the rapid inward depolarizing sodium current, thereby slowing phase-0 depolarization and reducing the amplitude of the action potential without affecting the resting potential. In normal Purkinje fibers, it reduces the slope of phase-4 depolarization, shifting the threshold voltage upward toward zero. The result is slowed conduction and reduced automaticity in all parts of the heart, with increase of the effective refractory period relative to the duration of the action potential in the atria, ventricles, and Purkinje tissues. Quinidine also raises the fibrillation thresholds of the atria and ventricles, and it raises the ventricular fibrillation threshold as well. Quinidineu2019s actions fall into class 1A in the Vaughan-Williams classification.
  • By slowing conduction and prolonging the effective refractory period, quinidine can interrupt or prevent reentrant arrhythmias and arrhythmias due to increased automaticity, including atrial flutter, atrial fibrillation, and paroxysmal supraventricular tachycardia. In patients with the sick sinus syndrome, quinidine can cause marked sinus node depression and bradycardia. In most patients, however, use of quinidine is associated with an increase in the sinus rate.
  • Quinidine prolongs the QT interval in a dose-related fashion. This may lead to increased ventricular automaticity and polymorphic ventricular tachycardias, including (see ).
  • In addition, quinidine has anticholinergic activity, it has negative inotropic activity, and it acts peripherally as an u03b1-adrenergic antagonist (that is, as a vasodilator).
  • Maintenance of sinus rhythm after conversion from atrial fibrillation:
  • In six clinical trials (published between 1970 and 1984) with a total of 808 patients, quinidine (418 patients) was compared to nontreatment (258 patients) or placebo (132 patients) for the maintenance of sinus rhythm after cardioversion from chronic atrial fibrillation. Quinidine was consistently more efficacious in maintaining sinus rhythm, but a metaanalysis found that mortality in the quinidine-exposed patients (2.9%) was significantly greater than mortality in the patients who had not been treated with active drug (0.8%). Suppression of atrial fibrillation with quinidine has theoretical patient benefits (improved exercise tolerance; reduction in hospitalization for cardioversion; lack of arrhythmiarelated palpitations, dyspnea, and chest pain; reduced incidence of systemic embolism and/or stroke), but these benefits have never been demonstrated in clinical trials. Some of these benefits (reduction in stroke incidence) may be achievable by other means (anticoagulation).
  • By slowing the rate of atrial flutter/fibrillation, quinidine can decrease the degree of atrioventricular block and cause an increase, sometimes marked, in the rate at which supraventricular impulses are successfully conducted by the atrioventricular node, with a resultant paradoxical increase in ventricular rate (see ).
  • Non-life-threatening ventricular arrhythmias:
  • u00a0
  • At therapeutic doses, quinidineu2019s only consistent effect upon the surface electrocardiogram is an increase in the QT interval. This prolongation can be monitored as a guide to safety, and it may provide better guidance than serum drug levels (see ).
  • Conversion of atrial fibrillation/flutter
  • In patients with symptomatic atrial fibrillation/flutter whose symptoms are not adequately controlled by measures that reduce the rate of ventricular response, quinidine sulfate is indicated as a means of restoring normal sinus rhythm. If this use of quinidine sulfate does not restore sinus rhythm within a reasonable time (see ), then quinidine sulfate should be discontinued.
  • Reduction of frequency of relapse into atrial fibrillation/flutter
  • Chronic therapy with quinidine sulfate is indicated for some patients at high risk of symptomatic atrial fibrillation/flutter, generally patients who have had previous episodes of atrial fibrillation/flutter that were so frequent and poorly tolerated as to outweigh, in the judgement of the physician and the patient, the risks of prophylactic therapy with quinidine sulfate. The increased risk of death should specifically be considered. Quinidine sulfate should be used only after alternative measures (use of other drugs to control the ventricular rate) have been found to be inadequate.
  • In patients with histories of frequent symptomatic episodes of atrial fibrillation/flutter, the goal of therapy should be an increase in the average time between episodes. In most patients, the tachyarrhythmia during therapy, and a single recurrence should not be interpreted as therapeutic failure.
  • Suppression of ventricular arrhythmias
  • Quinidine sulfate is also indicated for the suppression of recurrent documented ventricular arrhythmias, such as sustained ventricular tachycardia, that in the judgement of the physician are lifethreatening. Because of the proarrhythmic effects of quinidine, its use with ventricular arrhythmias of lesser severity is generally not recommended, and treatment of patients with asymptomatic ventricular premature contractions should be avoided. Where possible, therapy should be guided by the results of programmed electrical stimulation and/or Holter monitoring with exercise.
  • Antiarrhythmic drugs (including quinidine sulfate) have not been shown to enhance survival in patients with ventricular arrhythmias.
  • Treatment of malaria
  • Quinidine sulfate is also indicated in the treatment of life-threatening malaria.
  • Quinidine is contraindicated in patients who are known to be allergic to it, or who have developed thrombocytopenic purpura during prior therapy with quinidine or quinine.
  • In the absence of a functioning artificial pacemaker, quinidine is also contraindicated in any patient whose cardiac rhythm is dependent upon a junctional or idioventricular pacemaker, including patients in complete atrioventricular block.
  • Quinidine is also contraindicated in patients who, like those with myasthenia gravis, might be adversely affected by an anticholinergic agent.
  • Mortality
  • Heart Block
  • In patients without implanted pacemakers who are at high risk of complete atrioventricular block(those with digitalis intoxication, second-degree atrioventricular block, or severe intraventricular conduction defects), quinidine should be used only with caution.
  • Drug Interactions
  • Arrayn- Altered pharmacokinetics of quinidine
  • u00a0n- carbonic-anhydrase inhibitors, sodium bicarbonate,thiazide diuretics
  • By pharmacokinetic mechanisms that are not well understood, quinidine levels are increased by coadministration of or Very rarely, and again by mechanisms not understood, quinidine levels are decreased by coadministration of n
  • Hepatic elimination of quinidine may be accelerated by coadministration of drugs () that induce production of cytochrome P450.
  • Perhaps because of competition for the P450 metabolic pathway, quinidine levels rise when is coadministered.
  • Coadministration of usually does not affect quinidine pharmacokinetics, but in some studies the u03b2-blocker appeared to cause increases in the peak serum levels of quinidine, decreases in quinidineu2019s volume of distribution, and decreases in total quinidine clearance. The effects (if any) of coadministration of u03b2on quinidine pharmacokinetics have not been adequately studied.
  • Diltiazem significantly decreases the clearance and increases the tof quinidine, but quinidine does not alter the kinetics of diltiazem. Hepatic clearance of quinidine is significantly reduced during coadministration of , with corresponding increases in serum levels and half-life.
  • u00a0
  • Arrayn- Altered pharmacokinetics of other drugs
  • u00a0n- digoxin n- digoxin
  • By a mechanism that is not understood, quinidine potentiates the anticoagulatory action of , and the anticoagulant dosage may need to be reduced. Cytochrome P450 is an enzyme critical to the metabolism of many drugs, notably including , some , and most . Constitutional deficiency of cytochrome P450IID6 is found in less than 1% of Orientals, in about 2% of American blacks, and in about 8% of American whites. Testing with debrisoquine is sometimes used to distinguish the P450-deficient u201cpoor metabolizersu201d from the majority-pheno-type u201cextensive metabolizersu201d.
  • When drugs whose metabolism is P450IID6-dependent are given to poor metabolizers, the serum levels achieved are higher, sometimes much higher, than the serum levels achieved when identical doses are given to extensive metabolizers. To obtain similar clinical benefit without toxicity, doses given to poor metabolizers may need to be greatly reduced. In the cases of prodrugs whose actions are actually mediated by P450-produced metabolites (for example, and , whose analgesic and antitussive effects appear to be mediated by morphine and hydromorphone, respectively), it may not be possible to achieve the desired clinical benefits in poor metabolizers.
  • Quinidine is not metabolized by cytochrome P450, but therapeutic serum levels of quinidine inhibit the action of cytochrome P450, effectively converting extensive metabolizers into poor metabolizers. Caution must be exercised whenever quinidine is prescribed together with drugs metabolized by cytochrome P450.
  • Perhaps by competing for pathways of renal clearance, coadministration of quinidine causes an increase in serum levels of .
  • Serum levels of are increased when quinidine is coadministered.
  • Presumably because both drugs are metabolized by cytochrome P450, coadministration of quinidine causes variable slowing of the metabolism of . Interactions with other dihydropyridine calcium-channel blockers have not been reported, but these agents (including , , and ) are all dependent upon P450 for metabolism, so similar interactions with quinidine should be anticipated.
  • Arrayn- Altered pharmacodynamics of other drugs
  • u00a0n- verapamil
  • Quinidine potentiates the actions of depolarizing (succinylcholine, decamethonium) and nondepolarizing (-tubocurarine, pancuronium) . These phenomena are not well understood, but they are observed in animal models as well as in humans. In addition, addition of quinidine to the serum of pregnant women reduces the activity of pseudocholinesterase, an enzyme that is essential to the metabolism of succinylcholine.
  • Arrayn- Non-interactions of quinidine with other drugs
  • u00a0n- diltiazem,flecainide, mephenytoin,metoprolol, propafenone, propranolol,quinine, timolol, n- tocainide
  • Conversely, the pharmacokinetics of quinidine are not significantly affected by or Quinidineu2019s pharmacokinetics are also unaffected by cigarette smoking.
  • Quinidine preparations have been used for many years, but there are only sparse data from which to estimate the incidence of various adverse reactions. The adverse reactions most frequently reported have consistently been gastrointestinal, including diarrhea, nausea, vomiting, and heartburn/esophagitis. In one study of 245 adult outpatients who received quinidine to suppress premature ventricular contractions, the incidences of reported adverse experiences were as shown in the table below. The most serious quinidine-associated adverse reactions are described above under n
  • Vomiting and diarrhea can occur as isolated reactions to therapeutic levels of quinidine, but they may also be the first signs of a syndrome that may also include tinnitus, reversible high-frequency hearing loss, deafness, vertigo, blurred vision, diplopia, photophobia, headache, confusion, and delirium.
  • Cinchonism is most often a sign of chronic quinidine toxicity, but it may appear in sensitive patients after a single moderate dose.
  • A few cases of , including granulomatous hepatitis, have been reported in patients receiving quinidine. All of these have appeared during the first few weeks of therapy, and most (not all) have remitted once quinidine was withdrawn.
  • Autoimmune and inflammatory syndromes
  • Convulsions, apprehension, and ataxia have been reported, but it is not clear that these were not simply the results of hypotension and consequent cerebral hypoperfusion. There are many reports of syncope. Acute psychotic reactions have been reported to follow the first dose of quinidine, but these reactions appear to be extremely rare.
  • Other adverse reactions occasionally reported include depression, mydriasis, disturbed color perception, night blindness, scotomata, optic neuritis, visual field loss, photosensitivity, and abnormalities of pigmentation.
  • Overdoses with various oral formulations of quinidine have been well described. Death has been described after a 5-gram ingestion by a toddler, while an adolescent was reported to survive after ingesting 8 grams of quinidine.
  • The most important ill effects of acute quinidine overdoses are ventricular arrhythmias and hypotension. Other signs and symptoms of overdose may include vomiting, diarrhea, tinnitus, high-frequency hearing loss, vertigo, blurred vision, diplopia, photophobia, headache, confusion, and delirium.
  • Arrhythmias
  • Serum quinidine levels can be conveniently assayed and monitored, but the electrocardiographic QT interval is a better predictor of quinidine-induced ventricular arrhythmias.
  • The necessary treatment of hemodynamically unstable polymorphic ventricular tachycardia (including ) is withdrawal of treatment with quinidine and either immediate cardioversion or, if a cardiac pacemaker is in place or immediately available, immediate overdrive pacing. After pacing or cardioversion, further management must be guided by the length of the QT interval.
  • Quinidine-associated ventricular tachyarrhythmias with normal underlying QT intervals have not been adequately studied. Because of the theoretical possibility of QT-prolonging effects that might be additive to those of quinidine, other antiarrhythmics with Class I (disopyramide, procainamide) or Class III activities should (if possible) be avoided.
  • Similarly, although the use of bretylium in quinidine overdose has not been reported, it is reasonable to expect that the u03b1-blocking properties of bretylium might be additive to those of quinidine, resulting in problematic hypotension.
  • If the post-cardioversion QT interval is prolonged, then the pre-cardioversion polymorphic ventricular tachyarrhythmia was (by definition) . In this case, lidocaine and bretylium are unlikely to be of value, and other Class I antiarrhythmics (disopyramide, procainamide) are likely to exacerbate the situation. Factors contributing to QT prolongation (especially hypokalemia, hypomagnesemia, and hypocalcemia) should be sought out and (if possible) aggressively corrected.
  • Prevention of recurrent may require sustained overdrive pacing or the cautious administration of isoproterenol (30 to 150 ng/kg/min).
  • Hypotension
  • Quinidine-induced hypotension that is not due to an arrhythmia is likely to be a consequence of quinidine-related u03b1-blockade and vasorelaxation. Simple repletion of central volume Trendelenburg positioning, saline infusion) may be sufficient therapy; other interventions reported to have been beneficial in this setting are those that increase peripheral vascular resistance, including u03b1-agonist catecholamines (norepinephrine, metaraminol) and the Military Anti-Shock Trousers.
  • Treatment
  • To obtain up-to-date information about the treatment of overdose, a good resource is your certified Regional Poison-Control Center. Telephone numbers of certified poison-control centers are listed in the . In managing overdose, consider the possibilities of multiple-drug overdoses, drug-drug interactions, and unusual drug kinetics in your patient.
  • Accelerated removal
  • Adequate studies of orally-administered activated charcoal in human overdoses of quinidine have not been reported, but there are animal data showing significant enhancement of systemic elimination following this intervention, and there is at least one human case report in which the elimination half-life of quinidine in the serum was apparently shortened by repeated gastric lavage.
  • Activated charcoal should be avoided if an ileus is present; the conventional dose is 1 gram/kg, administered every 2 to 6 hours as a slurry with 8 mL/kg of tap water.
  • Although renal elimination of quinidine might theoretically be accelerated by maneuvers to acidify the urine, such maneuvers are potentially hazardous and of no demonstrated benefit.
  • Quinidine is not usually removed from the circulation by dialysis.
  • Following quinidine overdose, drugs that delay elimination of quinidine (cimetidine, carbonicanhydrase inhibitors, thiazide diuretics) should be withdrawn unless absolutely required.
  • Treatment of P. malaria
  • Quinidine sulfate tablets are used in one of the approved regimens for the treatment of life-threatening malaria. The central component of the regimen is Quinidine Gluconate Injection, and the regimen is described in the package insert of Quinidine Gluconate Injection.
  • Conversion of atrial fibrillation/flutter to sinus rhythm
  • Especially in patients with known structural heart disease or other risk factors for toxicity, initiation or dose-adjustment of treatment with quinidine sulfate should generally be performed in a setting where facilities and personnel for monitoring and resuscitation are continuously available. Patients with symptomatic atrial fibrillation/ flutter should be treated with quinidine sulfate only after ventricular rate control (with digitalis or u03b2-blockers) has failed to provide satisfactory control of symptoms.
  • Adequate trials have not identified an optimal regimen of quinidine sulfate for conversion of atrial fibrillation/flutter to sinus rhythm. In one reported regimen, the patient first receives two tablets (400 mg; 332 mg of quinidine base) of quinidine sulfate every six hours. If this regimen has not resulted in conversion after 4 or 5 doses, then the dose is cautiously increased. If, at any point during administration, the QRS complex widens to 130% of its pre-treatment duration; the QT interval widens to 130% of its pre-treatment duration and is then longer than 500 ms; P waves disappear; or the patient develops significant tachycardia, symptomatic bradycardia, or hypotension, then quinidine sulfate is discontinued, and other means of conversion (direct-current cardioversion) are considered.
  • Reduction of frequency orelease into atrial fibrillation/flutter
  • In a patient with a history of frequent symptomatic episodes of atrial fibrillation/flutter, the goal of therapy with quinidine sulfate should be an increase in the average time between episodes. In most patients, the tachyarrhythmia during therapy with quinidine sulfate, and a single recurrence should not be interpreted as therapeutic failure.
  • Especially in patients with known structural heart disease or other risk factors for toxicity, initiation or dose-adjustment of treatment with quinidine sulfate should generally be performed in a setting where facilities and personnel for monitoring and resuscitation are continuously available. Monitoring should be continued for two or three days after initiation of the regimen on which the patient will be discharged.
  • Therapy with quinidine sulfate should be begun with 200 mg (equivalent to 166 mg of quinidine base) every six hours. If this regimen is well tolerated, if the serum quinidine level is still well within the laboratoryu2019s therapeutic range, and if the average time between arrhythmic episodes has not been satisfactorily increased, then the dose may be cautiously raised. The total daily dosage should be reduced if the QRS complex widens to 130% of its pretreatment duration; the QTC interval widens to 130% of its pretreatment duration and is then longer than 500 ms; P waves disappear; or the patient develops significant tachycardia, symptomatic bradycardia, or hypotension.
  • Suppression of ventricular arrhythmias
  • Dosing regimens for the use of quinidine sulfate in suppressing life-threatening ventricular arrhythmias have not been adequately studied. Described regimens have generally been similar to the regimen described just above for the prophylaxis of symptomatic atrial fibrillation/flutter. Where possible, therapy should be guided by the results of programmed electrical stimulation and/or Holter monitoring with exercise.
  • Quinidine Sulfate Tablets are supplied as follows:
  • 200 mg - White tablet scored imprinted n
  • 300 mg - White tablet scored imprinted n
  • Both are supplied in bottles of 100 and 1000
  • Store at 20u00b0-25u00b0C (68u00b0-77u00b0F) [see USP Controlled Room Temperature]. Dispense in a well-closed, light-resistant container.
  • To report SUSPECTEDADVERSE REACTIONS, contact Sandoz Inc. at 1-800-525-8747or FDA at 1-800-FDA-108 8or www.fda.gov/medwatch
  • Manufactured for
  • Sandoz Inc.
  • Princeton, NJ 08540
  • Manufactured by
  • Epic Pharma, LLC
  • Laurelton, NY 11413
  • Rev. 11/08
  • MF1047REV11/08
  • OS7281
  • MG #16904
  • NDC
  • Quinidine Sulfate Tablets, USP
  • 200 mg
  • Rx only
  • 100 Tablets
  • Sandoz
  • NDC
  • Quinidine Sulfate Tablets, USP
  • 300 mg
  • Rx only
  • 100 Tablets
  • Sandoz

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