NDC 0002-1407 Quinidine Gluconate

Quinidine Gluconate

NDC Product Code 0002-1407

NDC Product Information

Quinidine Gluconate with NDC 0002-1407 is a a human prescription drug product labeled by Eli Lilly And Company. The generic name of Quinidine Gluconate is quinidine gluconate. The product's dosage form is solution and is administered via intravenous form.

Labeler Name: Eli Lilly And Company

Dosage Form: Solution - A clear, homogeneous liquid1 dosage form that contains one or more chemical substances dissolved in a solvent or mixture of mutually miscible solvents.

Product Type: Human Prescription Drug What kind of product is this?
Indicates the type of product, such as Human Prescription Drug or Human Over the Counter Drug. This data element matches the “Document Type” field of the Structured Product Listing.

Quinidine Gluconate Active Ingredient(s)

What is the Active Ingredient(s) List?
This is the active ingredient list. Each ingredient name is the preferred term of the UNII code submitted.


Inactive Ingredient(s)

About the Inactive Ingredient(s)
The inactive ingredients are all the component of a medicinal product OTHER than the active ingredient(s). The acronym "UNII" stands for “Unique Ingredient Identifier” and is used to identify each inactive ingredient present in a product.

  • WATER (UNII: 059QF0KO0R)

Administration Route(s)

What are the Administration Route(s)?
The translation of the route code submitted by the firm, indicating route of administration.

  • Intravenous - Administration within or into a vein or veins.

Pharmacological Class(es)

What is a Pharmacological Class?
These are the reported pharmacological class categories corresponding to the SubstanceNames listed above.

  • Antiarrhythmic - [EPC] (Established Pharmacologic Class)
  • Cytochrome P450 2D6 Inhibitor - [EPC] (Established Pharmacologic Class)
  • Cytochrome P450 2D6 Inhibitors - [MoA] (Mechanism of Action)

Product Labeler Information

What is the Labeler Name?
Name of Company corresponding to the labeler code segment of the Product NDC.

Labeler Name: Eli Lilly And Company
Labeler Code: 0002
FDA Application Number: NDA007529 What is the FDA Application Number?
This corresponds to the NDA, ANDA, or BLA number reported by the labeler for products which have the corresponding Marketing Category designated. If the designated Marketing Category is OTC Monograph Final or OTC Monograph Not Final, then the Application number will be the CFR citation corresponding to the appropriate Monograph (e.g. “part 341”). For unapproved drugs, this field will be null.

Marketing Category: NDA - A product marketed under an approved New Drug Application. What is the Marketing Category?
Product types are broken down into several potential Marketing Categories, such as NDA/ANDA/BLA, OTC Monograph, or Unapproved Drug. One and only one Marketing Category may be chosen for a product, not all marketing categories are available to all product types. Currently, only final marketed product categories are included. The complete list of codes and translations can be found at www.fda.gov/edrls under Structured Product Labeling Resources.

Start Marketing Date: 07-12-1950 What is the Start Marketing Date?
This is the date that the labeler indicates was the start of its marketing of the drug product.

End Marketing Date: 10-09-2019 What is the End Marketing Date?
This is the date the product will no longer be available on the market. If a product is no longer being manufactured, in most cases, the FDA recommends firms use the expiration date of the last lot produced as the EndMarketingDate, to reflect the potential for drug product to remain available after manufacturing has ceased. Products that are the subject of ongoing manufacturing will not ordinarily have any EndMarketingDate. Products with a value in the EndMarketingDate will be removed from the NDC Directory when the EndMarketingDate is reached.

Exclude Flag: N What is the NDC Exclude Flag?
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Quinidine Gluconate Product Labeling Information

The product labeling information includes all published material associated to a drug. Product labeling documents include information like generic names, active ingredients, ingredient strength dosage, routes of administration, appearance, usage, warnings, inactive ingredients, etc.

Product Labeling Index


Quinidine is an antimalarial schizonticide and an antiarrhythmic agent with class
1a activity; it is the d–isomer of quinine and its molecular weight
is 324.43. Quinidine gluconate
is the gluconate salt of quinidine; its chemical name is cinchonan–9–ol, 6'–methoxy–,
mono–D–gluconate; its structural formula isits empirical formula is C20H24N2O2•C6H12O7,
and its molecular weight is 520.58, of which 62.3% is quinidine base.Each vial of Quinidine Gluconate Injection
contains 800 mg (1.5 mmol) of quinidine gluconate (500
mg of quinidine)
in 10 mL of Sterile Water for Injection, 0.005% of edetate disodium, 0.25%
phenol, and (as needed) D–gluconic acid δ–lactone to adjust
the pH.

Clinical Studies

Clinical Effects


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

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.

infusion rate — Overly
rapid infusion of quinidine (see Dosage and Administration) may cause peripheral
vascular collapse and severe hypotension.

effects — Like many other
drugs (including all other class 1a antiarrhythmics), quinidine prolongs
the QTc interval, and this can lead to torsades de pointes, a life–threatening
ventricular arrhythmia (see Overdosage). The risk of torsades is increased by any
of bradycardia, hypokalemia, hypomagnesemia, and high serum levels of quinidine,
but it may appear in the absence of any of these risk factors. The best predictor
of this arrhythmia appears to be the length of the QTc interval,
and quinidine should
be used with extreme care in patients who have preexisting long–QT syndromes,
who have histories of torsades
de pointes of any cause, or who have previously responded to quinidine (or
other drugs that prolong ventricular repolarization) with marked lengthening
of the QTc interval. Estimation of the incidence of torsades in patients
with therapeutic levels of quinidine is not possible from the available data.Other ventricular arrhythmias that have been reported with quinidine include
frequent extrasystoles, ventricular tachycardia, ventricular flutter, and
ventricular fibrillation.

increase in ventricular rate in atrial flutter/fibrillation — When quinidine is
administered to patients with atrial flutter/fibrillation, the desired pharmacologic
reversion to sinus rhythm may (rarely) be preceded by a slowing of the atrial
rate with a consequent increase in the rate of beats conducted to the ventricles.
The resulting ventricular rate may be very high (greater than 200 beats per
minute) and poorly tolerated. This hazard may be decreased if partial atrioventricular
block is achieved prior to initiation of quinidine therapy,
using conduction–reducing drugs such as digitalis, verapamil, diltiazem, or a ß–receptor blocking

bradycardia in sick sinus syndrome — In
patients with the sick sinus syndrome, quinidine has
been associated with marked sinus node depression and bradycardia.

Vagolysis — Because quinidine opposes
the atrial and A–V nodal effects of vagal stimulation, physical or pharmacological
vagal maneuvers undertaken to terminate paroxysmal supraventricular tachycardia
may be ineffective in patients receiving quinidine.

By pharmacokinetic mechanisms that are not well understood, quinidine levels
are increased by coadministration of amiodarone or cimetidine. Very rarely, and again by mechanisms
not understood, quinidine levels
are decreased by coadministration of nifedipine.

Hepatic elimination of quinidine may be accelerated by coadministration of drugs (phenobarbital, phenytoin, rifampin) that induce production of cytochrome

Perhaps because of competition of the P450IIIA4 metabolic pathway, quinidine levels
rise when ketaconazole is

Coadministration of propranolol usually
does not affect quinidine pharmacokinetics,
but in some studies, the ß–blocker appeared to cause increases
in the peak serum levels of quinidine, decreases in quinidine's
volume of distribution and decreases in total quinidine clearance.
The effects (if any) of coadministration of other ß–blockers on quinidine pharmacokinetics
have not been adequately studied.

Hepatic clearance of quinidine is significantly reduced during coadministration of verapamil, with corresponding
increases in serum levels and half–life.

Altered pharmacokinetics of other drugs: Quinidine slows
the elimination of digoxin and
simultaneously reduces digoxin's apparent volume of distribution. As a result,
serum digoxin levels may be as much as doubled. When quinidine and
digoxin are coadministered, digoxin doses usually need to be reduced. Serum
levels of digitoxin are
also raised when quinidine is
coadministered, although the effect appears to be smaller.

By a mechanism that is not understood, quinidine potentiates
the anticoagulatory action of warfarin, and the anticoagulant dosage may need
to be reduced.

Cytochrome P450IID6 is an enzyme critical to the metabolism of many
drugs, notably including mexiletine,
some phenothiazines,
and most polycyclic
antidepressants. 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 P450IID6–deficient "poor metabolizers" from the majority–phenotype
"extensive metabolizers."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 P450IID6–produced metabolites
(for example, codeine and hydrocodone, 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 P450IID6, but therapeutic serum levels of quinidine inhibit
the action of cytochrome P450IID6, effectively converting extensive metabolizers
into poor metabolizers. Caution must be exercised whenever quinidine is
prescribed together with drugs metabolized by cytochrome P450IID6.

Perhaps by competing for pathways of renal clearance, coadministration
of quinidine causes
an increase in serum levels of procainamide.

Serum levels of haloperidol are
increased when quinidine is

Presumably because both drugs are metabolized by cyctochrome P450IIIA4,
coadministration of quinidine causes
variable slowing of the metabolism of nifedipine. Interactions with other dihydropyridine
calcium–channel blockers have not been reported, but these agents (including felodipine, nicardipine, and nimodipine) are all
dependent upon P450IIIA4 for metabolism, so similar interactions with quinidine should
be anticipated.

Altered pharmacodynamics of other drugs: Quinidine's
anticholinergic, vasodilating, and negative inotropic actions may be additive
to those of other drugs with these effects, and antagonistic to those of drugs
with cholinergic, vasoconstricting, and positive inotropic effects. For example,
when quinidine and verapamil are coadministered
in doses that are each well tolerated as monotherapy, hypotension attributable
to additive peripheral α–blockade is sometimes reported.

Quinidine potentiates
the actions of depolarizing (succinylcholine, decamethonium) and nondepolarizing
pancuronium) neuromuscular blocking agents. These phenomena are not well understood,
but they are observed in animal models as well as in humans. In addition, in vitro addition
of quinidine to
the serum of pregnant women reduces the activity of pseudocholinesterase,
an enzyme that is essential to the metabolism of succinylcholine.

Diltiazem significantly decreases the clearance and increases the t½ of quinidine,
but quinidine does
not alter the kinetics of diltiazem. Non–interactions of quinidine with
other drugs: Quinidine has
no clinically significant effect on the pharmacokinetics of diltiazem, flecainide, mephenytoin, metoprolol, propafenone, propranolol, quinine, timolol, or tocainide.

Conversely, the pharmacokinetics of quinidine are
not significantly affected by caffeine, ciprofloxacin,
digoxin, felodipine, omeprazole, or quinine. Quinidine's
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 heart–burn/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 Warnings.Adverse Experiences in a 245–Patient PVC
(%)diarrhea85 (35)"upper gastrointestinal distress"55 (22)lightheadedness37 (15)headache18 (7)fatigue17 (7)palpitations16 (7)angina–like pain14 (6)weakness13 (5)rash11 (5)visual problems8 (3)change in sleep habits7 (3)tremor6 (2)nervousness5 (2)discoordination3 (1)Intramuscular injections of quinidine gluconate are
typically followed by moderate to severe local pain. Some patients will develop
tender nodules at the site of injection that persist for several weeks.Vomiting and diarrhea can occur as isolated
reactions to therapeutic levels of quinidine,
but they may also be the first signs of cinchonism, 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 hepatotoxicity, 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 associated with quinidine therapy
have included fever, urticaria, flushing, exfoliative rash, bronchospasm,
pneumonitis, psoriasiform rash, pruritus and lymphadenopathy, hemolytic anemia,
vasculitis, thrombocytopenic purpura, uveitis, angioedema, agranulocytosis,
the sicca syndrome, arthralgia, myalgia, elevation in serum levels of skeletal–muscle
enzymes, and a disorder resembling systemic lupus erythematosus.Convulsions, apprehension, and ataxia have been
reported, but it was 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, photo–sensitivity, and
abnormalities of pigmentation.

are only scattered reports of overdosage with intravenous quinidine,
but overdoses with oral 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 QTc interval
is a better predictor of quinidine–induced ventricular arrhythmias.The
necessary treatment of hemodynamically unstable polymorphic ventricular tachycardia
(including torsades
de pointes) 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 QTc interval.Quinidine–associated
ventricular tachyarrhythmias with normal underlying QTc 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 α–blocking
properties of bretylium might be additive to those of quinidine,
resulting in problematic hypotension.If
the post–cardioversion QTc interval is prolonged,
then the pre–cardioversion polymorphic ventricular tachyarrhythmia was
(by definition) torsades
de pointes. 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 QTc prolongation
(especially hypokalemia and hypomagnesemia) should be sought out and (if possible)
aggressively corrected. Prevention of recurrent torsades may require sustained overdrive pacing
or the cautious administration of isoproterenol (30–150 ng/kg/min).Hypotension — Quinidine–induced
hypotension that is not due to an arrhythmia is likely to be a consequence
of quinidine–related α–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 α–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 Physicians' Desk Reference (PDR). 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 2–6 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 usefully removed from the circulation by dialysis.Following quinidine overdose, drugs that delay elimination
of quinidine (cimetidine, carbonic–anhydrase inhibitors, diltiazem, thiazide diuretics) should
be withdrawn unless absolutely required.

Because the kinetics of absorption may vary with the patient's
peripheral perfusion, intramuscular injection of quinidine gluconate is
not recommended.

of P. falciparum malaria — Two
regimens have each been shown to be effective, with or without concomitant
exchange transfusion. There are no data indicating that either should be preferred
to the other.In Regimen
A, each patient received a loading dose of 15 mg/kg of quinidine base
(that is, 24 mg/kg of quinidine gluconate)
in 250 mL of normal saline infused over 4 hours. Thereafter, each patient received a maintenance
regimen of 7.5 mg/kg of base (12 mg/kg of quinidine gluconate) infused over 4 hours every 8 hours, starting 8 hours after the beginning of the loading dose. This regimen was continued for 7 days, except that in patients
able to swallow, the maintenance infusions were discontinued, and approximately
the same daily doses of quinidine were supplied orally, using 300–mg tablets of quinidine sulfate.In Regimen
B, each patient received a loading dose of 6.25 mg/kg of quinidine base
(that is, 10 mg/kg of quinidine gluconate) in approximately 5 mL/kg of normal saline over 1–2 hours. Thereafter, each patient received a maintenance infusion of 12.5 μg/kg/min of base (that is, 20 μg/kg/min
of quinidine gluconate). In patients able to swallow, the maintenance infusion was discontinued, and eight–hourly oral quinine sulfate was administered to provide approximately as much daily quinine base as the patient had been receiving quinidine base (for example, each adult patient received 650 mg of quinine sulfate every eight hours). Quinidine/quinine therapy was continued for 72 hours or until parasitemia had decreased to 1% or less, whichever came first. After completion of quinidine/quinine
therapy, adults able to swallow received a single 1500–mg/75–mg dose of sulfadoxine/pyrimethamine (FANSIDAR®, Roche Laboratories) or a seven–day course of tetracycline (250 mg four
times daily), while those unable to swallow received seven–day courses
of intravenous doxycycline hyclate (VIBRAMYCIN®,
Roerig), 100 mg twice daily. Most of the patients described as having been
treated with this regimen also underwent exchange transfusion. Small children
have received this regimen without dose adjustment and with apparent good
results, notwithstanding the known differences in quinidine pharmacokinetics
between pediatric patients and adults (see Clinical
Pharmacology).Even in patients without preexisting cardiac disease, antimalarial
use of quinidine has
occasionally been associated with hypotension, QTc prolongation,
and cinchonism; see Warnings.

of symptomatic atrial fibrillation/flutter — A
patient receiving an intravenous infusion of quinidine must
be carefully monitored, with frequent or continuous electrocardiography and
blood–pressure measurement. The infusion should be discontinued as soon
as sinus rhythm is restored: the QRS complex widens to 130% of
its pre–treatment duration; the QTc 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.To prepare quinidine for infusion, the contents of the supplied vial (80 mg/mL) should be diluted
to 50 mL (16 mg/mL) with 5% dextrose. The resulting solution may be stored
for up to 24 hours at room temperature or up to 48 hours at 4°C (40°F).Because quinidine may be absorbed to PVC tubing, tubing length should be minimized. In one
study (Am J Health
Syst Pharm. 1996; 53:655–8), use of 112 inches of tubing
resulted in 30% loss of quinidine, but drug loss was less than 3% when only 12 inches of tubing was used.An infusion of quinidine must be delivered slowly, preferable under control of a volumetric pump,
no faster than 0.25 mg/kg/min (that is, no faster than 1 mL/kg/hour). During
the first few minutes of the infusion, the patient should be monitored especially
closely for possible hypersensitive or idiosyncratic reactions.Most arrhythmias that will respond to intravenous quinidine will
respond to a total dose of less than 5 mg/kg, but some patients may require
as much as 10 mg/kg. If conversion to sinus rhythm has not been achieved after
infusion of 10 mg/kg, then the infusion should be discontinued, and other
means of conversion (eg, direct–current cardioversion) should be considered.

of life–threatening ventricular arrhythmias — Dosing
regimens for the use of intravenous quinidine gluconate in
controlling life–threatening ventricular arrhythmias have not been adequately
studied. Described regimens have generally been similar to the regimen described
just above for the treatment of symptomatic atrial fibrillation/flutter.

The 80 mg/mL, 10 mL Multiple–Dose Vial is available
as:            1NDC 0002–1407–01 (VL530)

Literature revised February 24, 2012Marketed by: Lilly USA, LLC, Indianapolis, IN 46285, USAPV 3851 AMP


considerations — Renal
or hepatic dysfunction causes the elimination of quinidine to
be slowed, while congestive heart failure causes a reduction in quinidine’s
apparent volume of distribution. Any of these conditions can lead to quinidine toxicity
if dosage is not appropriately reduced. In addition, interactions with coadministered
drugs can alter the serum concentration and activity of quinidine,
leading either to toxicity or to lack of efficacy if the dose of quinidine is
not appropriately modified (see Precautions/Drug Interactions).

Storage And Handling

Store at 25°C (77°F); excursions permitted to 15–30°C
(59–86°F). [see USP Controlled Room Temperature].

Package Carton – Quinidine 80 Mg Carton 1Ct

NDC 0002-1407-01
10 mL
VIAL No. 530
80 mg per mL
Multiple Dose
Rx only

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