Nexterone

Amiodarone is a prescription medicine used in adults to treat life-threatening heartbeat problems called ventricular arrhythmias, for which other treatment did not work or was not tolerated. 

This medication may be prescribed for other uses. Ask your doctor or pharmacist for more information.

• Baxter Healthcare Corporation

Nexterone is part of the drug class:

• Antiarrhythmics, class III

This medication is intended for use only in patients with the indicated life-threatening arrhythmias because its use is accompanied by substantial toxicity.

Amiodarone has several potentially fatal toxicities, the most important of which is pulmonary toxicity (hypersensitivity pneumonitis or interstitial/alveolar pneumonitis) that has resulted in clinically manifest disease at rates as high as 10 to 17% in some series of patients with ventricular arrhythmias given doses around 400 mg/day, and as abnormal diffusion capacity without symptoms in a much higher percentage of patients. Pulmonary toxicity has been fatal about 10% of the time. Liver injury is common with this medication, but is usually mild and evidenced only by abnormal liver enzymes. Overt liver disease can occur, however, and has been fatal in a few cases. Like other antiarrhythmics, Amiodarone can exacerbate the arrhythmia, e.g., by making the arrhythmia less well tolerated or more difficult to reverse. This has occurred in 2 to 5% of patients in various series, and significant heart block or sinus bradycardia has been seen in 2 to 5%. All of these events should be manageable in the proper clinical setting in most cases. Although the frequency of such proarrhythmic events does not appear greater with amiodarone than with many other agents used in this population, the effects are prolonged when they occur.

Even in patients at high risk of arrhythmic death, in whom the toxicity of amiodarone is an acceptable risk, Amiodarone poses major management problems that could be life-threatening in a population at risk of sudden death, so that every effort should be made to utilize alternative agents first.

The difficulty of using amiodarone effectively and safely itself poses a significant risk to patients. Patients with the indicated arrhythmias must be hospitalized while the loading dose of amiodarone is given, and a response generally requires at least one week, usually two or more. Because absorption and elimination are variable, maintenance-dose selection is difficult, and it is not unusual to require dosage decrease or discontinuation of treatment. In a retrospective survey of 192 patients with ventricular tachyarrhythmias, 84 required dose reduction and 18 required at least temporary discontinuation because of adverse effects, and several series have reported 15 to 20% overall frequencies of discontinuation due to adverse reactions. The time at which a previously controlled life-threatening arrhythmia will recur after discontinuation or dose adjustment is unpredictable, ranging from weeks to months. The patient is obviously at great risk during this time and may need prolonged hospitalization. Attempts to substitute other antiarrhythmic agents when amiodarone must be stopped will be made difficult by the gradually, but unpredictably, changing amiodarone body burden. A similar problem exists when amiodarone is not effective; it still poses the risk of an interaction with whatever subsequent treatment is tried.

Nexterone is indicated for initiation of treatment and prophylaxis of frequently recurring ventricular fibrillation (VF) and hemodynamically unstable ventricular tachycardia (VT) in patients refractory to other therapy. Nexterone also can be used to treat patients with VT/VF for whom oral amiodarone is indicated, but who are unable to take oral medication. During or after treatment with Nexterone, patients may be transferred to oral amiodarone therapy [see Dosage and Administration (2)].

Use Nexterone for acute treatment until the patient's ventricular arrhythmias are stabilized. Most patients will require this therapy for 48 to 96 hours, but Nexterone may be safely administered for longer periods if necessary.

Nexterone should be administered only by physicians who are experienced in the treatment of life-threatening arrhythmias, who are thoroughly familiar with the risks and benefits of amiodarone therapy, and who have access to facilities adequate for monitoring the effectiveness and side effects of treatment.

Because of the long half-life of amiodarone and its metabolite desethylamiodarone, the potential for adverse reactions or interactions, as well as observed adverse effects, can persist following amiodarone withdrawal.

Hypotension

Hypotension is the most common adverse reaction seen with intravenous amiodarone. In clinical trials, treatment-emergent, drug-related hypotension was reported as an adverse effect in 288 (16%) of 1836 patients treated with intravenous amiodarone. Clinically significant hypotension during infusions was seen most often in the first several hours of treatment and was not dose related, but appeared to be related to the rate of infusion. Hypotension necessitating alterations in intravenous amiodarone therapy was reported in 3% of patients, with permanent discontinuation required in less than 2% of patients.

Treat hypotension initially by slowing the infusion; additional standard therapy may be needed, including the following: vasopressor drugs, positive inotropic agents, and volume expansion. Monitor the initial rate of infusion closely and do not exceed the recommended rate [see Dosage and Administration (2)].

In some cases, hypotension may be refractory and result in a fatal outcome [see Adverse Reactions (6.2)].

Bradycardia and Atrio-ventricular Block

In 90 (4.9%) of 1836 patients in clinical trials, drug-related bradycardia that was not dose-related occurred while they were receiving intravenous amiodarone for life-threatening VT/VF. Treat bradycardia by slowing the infusion rate or discontinuing Nexterone. In some patients, inserting a pacemaker is required. Despite such measures, bradycardia was progressive and terminal in 1 patient during the controlled trials. Treat patients with a known predisposition to bradycardia or AV block with Nexterone in a setting where a temporary pacemaker is available.

Hepatic Injury

Elevations of blood hepatic enzyme values [alanine aminotransferase (ALT), aspartate aminotransferase (AST), and gamma-glutamyl transferase (GGT)] are commonly seen in patients with immediately life-threatening VT/VF. Interpreting elevated AST activity can be difficult because the values may be elevated in patients who have had recent myocardial infarction, congestive heart failure, or multiple electrical defibrillations. Approximately 54% of patients receiving intravenous amiodarone in clinical studies had baseline liver enzyme elevations, and 13% had clinically significant elevations. In 81% of patients with both baseline and on-therapy data available, the liver enzyme elevations either improved during therapy or remained at baseline levels. Baseline abnormalities in hepatic enzymes are not a contraindication to treatment. Elevated bilirubin levels have been reported in patients administered intravenous amiodarone.

Acute, centrolobular confluent hepatocellular necrosis leading to hepatic coma, acute renal failure, and death has been associated with the administration of intravenous amiodarone [see Dosage and Administration (2)].

In patients with life-threatening arrhythmias, the potential risk of hepatic injury should be weighed against the potential benefit of Nexterone therapy. Carefully monitor patients receiving Nexterone for evidence of progressive hepatic injury. In such cases, consider reducing the rate of administration or withdrawing Nexterone.

Proarrhythmia

Like all antiarrhythmic agents, Nexterone may cause a worsening of existing arrhythmias or precipitate a new arrhythmia, sometimes leading to fatal outcomes [see Adverse Reactions (6.2)]. Proarrhythmia, primarily torsade de pointes (TdP), has been associated with prolongation, by intravenous amiodarone, of the QTc interval to 500 ms or greater. Although QTc prolongation occurred frequently in patients receiving intravenous amiodarone, TdP or new-onset VF occurred infrequently (less than 2%). Monitor patients for QTc prolongation during infusion with Nexterone. Reserve the combination of amiodarone with other antiarrhythmic therapies that prolong the QTc to patients with life-threatening ventricular arrhythmias who are incompletely responsive to a single agent.

Correct hypokalemia, hypomagnesemia or hypocalcemia whenever possible before initiating treatment with Nexterone, as these disorders can exaggerate the degree of QTc prolongation and increase the potential for TdP. Give special attention to electrolyte and acid-base balance in patients experiencing severe or prolonged diarrhea or in patients receiving concomitant diuretics and laxatives.

Amiodarone causes thyroid dysfunction in some patients, which may lead to potentially fatal breakthrough or exacerbated arrhythmias.

Pulmonary Injury

There have been postmarketing reports of acute-onset (days to weeks) pulmonary injury in patients treated with intravenous amiodarone. Findings have included pulmonary infiltrates and masses on X-ray, bronchospasm, wheezing, fever, dyspnea, cough, hemoptysis, and hypoxia. Some cases have progressed to respiratory failure or death.

Two percent (2%) of patients were reported to have adult respiratory distress syndrome (ARDS) during clinical studies involving 48 hours of therapy.

There have been reports of early development of pulmonary fibrosis (within 1 to 3 months) following initiation of amiodarone treatment. Only 1 of more than 1000 patients treated with intravenous amiodarone in clinical studies developed pulmonary fibrosis. In that patient, the condition was diagnosed 3 months after treatment with intravenous amiodarone, during which time the patient received oral amiodarone. Pulmonary toxicity is a well-recognized complication of long-term amiodarone use (see package insert for oral amiodarone).

Loss of Vision

Cases of optic neuropathy and optic neuritis, usually resulting in visual impairment, have been reported in patients treated with oral amiodarone or intravenous amiodarone. In some cases, visual impairment has progressed to permanent blindness. Optic neuropathy and neuritis may occur at any time following initiation of therapy. A causal relationship to the drug has not been clearly established. Perform an ophthalmic examination if symptoms of visual impairment appear, such as changes in visual acuity and decreases in peripheral vision. Re-evaluate the necessity of amiodarone therapy if optic neuropathy or neuritis is suspected. Perform regular ophthalmic examination, including fundoscopy and slit-lamp examination, during administration of Nexterone.

Thyroid Abnormalities

Amiodarone inhibits peripheral conversion of thyroxine (T4) to triiodothyronine (T3) and may cause increased T4 levels, decreased T3 levels, and increased levels of inactive reverse T3 (rT3) in clinically euthyroid patients. Amiodarone is also a potential source of large amounts of inorganic iodine and can cause either hypothyroidism or hyperthyroidism. Evaluate thyroid function prior to treatment and periodically thereafter, particularly in elderly patients, and in any patient with a history of thyroid nodules, goiter, or other thyroid dysfunction. Because of the slow elimination of amiodarone and its metabolites, high plasma iodide levels, altered thyroid function, and abnormal thyroid-function tests may persist for several weeks or even months following Nexterone withdrawal.

There have been postmarketing reports of thyroid nodules/thyroid cancer in patients treated with amiodarone. In some instances hyperthyroidism was also present.

Amiodarone causes hyperthyroidism in about 2% of patients. Thyrotoxicosis and arrhythmia with fatal outcome has been reported in the presence of pre-existing hyperthyroidism even following a single intravenous amiodarone dose. Consider the possibility of hyperthyroidism if any new signs of arrhythmia appear.

Hyperthyroidism may result from iodine load (type 1 amiodarone-induced thyrotoxicosis [type 1 AIT]; in particular in patients with underlying autonomous thyroid nodules or latent Grave’s disease). Hyperthyroidism may also result from direct amiodarone-induced destructive thyroiditis that occurs in individuals with no underlying thyroid disease (type 2 AIT), resulting in the release of preformed thyroid hormone into the bloodstream from damaged thyroid follicular epithelium. Mixed forms of hyperthyroidism as a result of both pathogenic mechanisms (excessive thyroid hormone production and thyroid destruction) can also occur. The risk of hyperthyroidism may be higher among patients with prior inadequate dietary iodine intake.

Identify hyperthyroidism by relevant clinical signs and symptoms, subnormal serum levels of thyroid stimulating hormone (TSH), abnormally elevated serum free T4, and elevated or normal serum T3. Since arrhythmia breakthroughs may accompany amiodarone-induced hyperthyroidism, aggressive medical treatment is indicated, including, if possible, dose reduction or withdrawal of amiodarone. Amiodarone hyperthyroidism may be followed by a transient period of hypothyroidism.

The institution of antithyroid drugs, β-adrenergic blockers or temporary corticosteroid therapy may be necessary. The action of antithyroid drugs may be especially delayed in amiodarone-induced thyrotoxicosis because of substantial quantities of preformed thyroid hormones stored in the gland. Radioactive iodine therapy is not recommended because of the low radioiodine uptake associated with amiodarone-induced hyperthyroidism.

When aggressive treatment of amiodarone-induced thyrotoxicosis has failed or amiodarone cannot be discontinued because it is the only drug effective against the resistant arrhythmia, surgical management may be an option. Experience with thyroidectomy as a treatment for amiodarone-induced thyrotoxicosis is limited, and this form of therapy could induce thyroid storm. Therefore, surgical and anesthetic management require careful planning.

Hypothyroidism has been reported in 2 to 10% of patients receiving amiodarone and may be primary or subsequent to resolution of preceding amiodarone-induced hyperthyroidism. This condition may be identified by clinical symptoms and elevated serum TSH levels. Cases of severe hypothyroidism and myxedema coma, sometimes fatal, have been reported in association with amiodarone therapy. In some clinically hypothyroid amiodarone-treated patients, free thyroxine index values may be normal. Manage hypothyroidism by reducing the dose of or discontinuing Nexterone and considering the need for thyroid hormone supplement.

Neonatal Injury

Amiodarone can cause fetal harm when administered to a pregnant woman. Fetal exposure may increase the potential for adverse experiences including cardiac, thyroid, neurodevelopmental, neurological and growth effects in neonate. Inform the patient of the potential hazard to the fetus if Nexterone is administered during pregnancy or if the patient becomes pregnant while taking Nexterone [See Pregnancy (8.1)].

Exaggerated Effects of Perisurgical Therapy

Perform close perioperative monitoring in patients undergoing general anesthesia who are on amiodarone therapy as they may be more sensitive to the myocardial depressant and conduction defects of halogenated inhalational anesthetics.

Interference with Corneal Refractive Laser Surgery

Advise patients that most manufacturers of corneal refractive laser surgery devices contraindicate corneal refractive laser surgery in patients taking amiodarone.

Hypersensitivity Reactions

Anaphylactic/anaphylactoid reactions have been reported with intravenous amiodarone including shock (sometimes fatal), cardiac arrest, and the following manifestations: hypotension, tachycardia, hypoxia, cyanosis, rash, flushing, hyperhidrosis and cold sweat. Since Nexterone contains dextrose, patients with allergy to corn or corn products are at risk for allergic reaction.

Pharmacodynamic Interactions

Drugs prolonging the QT interval: Co-administration of drugs prolonging the QT interval (such as class I and III antiarrhythmics, lithium, certain phenothiazines, tricyclic antidepressants, certain fluoroquinolone and macrolide antibiotics, azole antifungals, halogenated inhalation anesthetic agents) increases the risk of Torsade de Pointes. In general, avoid concomitant use of drugs that prolong the QT interval [see Warnings and Precautions (5.4)].

Drugs that slow heart rate: Concomitant use of drugs with depressant effects on the sinus and AV node (e.g., digoxin, beta blockers, verapamil, diltiazem, ivabradine, clonidine) can potentiate the electrophysiologic and hemodynamic effects of amiodarone, resulting in bradycardia, sinus arrest, and AV block. Monitor heart rate in patients on amiodarone and concomitant drugs that slow heart rate.

Pharmacokinetic Interactions

Effect of other drugs on amiodarone

Amiodarone is metabolized to the active metabolite desethylamiodarone (DEA) by the cytochrome P450 (CYP450) enzyme group, specifically CYP3A and CYP2C8. Amiodarone has the potential for interactions with drugs or substances that may be substrates, inhibitors or inducers of CYP450 enzymes (e.g., inhibitors such as protease inhibitors, grapefruit juice, certain fluoroquinolone and macrolide antibiotics, azole antifungals and inducers such as St. John’s Wort) or P-glycoprotein. In view of the long and variable half-life of amiodarone, potential for drug interactions exists not only with concomitant medication but also with drugs administered after discontinuation of amiodarone [see Clinical Pharmacology (12.3)].

Patients should avoid grapefruit juice beverages while taking amiodarone because exposure to amiodarone is significantly increased [see Clinical Pharmacology (12.3)].

Effect of amiodarone on other drugs

Amiodarone and DEA are inhibitors of P-glycoprotein and certain CYP450 enzymes, including CYP1A2, CYP2C9, CYP2D6 and CYP3A [see Clinical Pharmacology (12.3)].

Antiarrhythmics: The metabolism of quinidine, procainamide, flecainide can be inhibited by amiodarone. In general, initiate any added antiarrhythmic drug at a lower than usual dose and monitor the patient carefully. During transfer to oral amiodarone, reduce the dose levels of previously administered agents by 30 to 50% several days after the addition of oral amiodarone. Review the continued need for the other antiarrhythmic agent after the effects of amiodarone have been established, and attempt discontinuation [see Clinical Pharmacology (12.3)].

Digoxin: In patients receiving digoxin therapy, administration of oral amiodarone results in an increase in serum digoxin concentration. Reduce dose of digoxin by half or discontinue digoxin. If digitalis treatment is continued, monitor serum levels closely and observe patients for clinical evidence of toxicity [see Clinical Pharmacology (12.3)].

HMG-CoA Reductase Inhibitors: Limit the dose of simvastatin in patients on amiodarone to 20 mg daily. Limit the daily dose of lovastatin to 40 mg. Lower starting and maintenance doses of other CYP3A4 substrates (e.g., atorvastatin) may be required as amiodarone may increase the plasma concentration of these drugs.

Anticoagulants: Potentiation of warfarin-type (CYP2C9 and CYP3A substrate) anticoagulant response is almost always seen in patients receiving amiodarone and can result in serious or fatal bleeding. Since the concomitant administration of warfarin with amiodarone increases the INR by 100% after 3 to 4 days, reduce the dose of the anticoagulant by one-third to one-half, and monitor INR closely.

Cyclosporine (CYP3A substrate) administered in combination with oral amiodarone has been reported to produce persistently elevated plasma concentrations of cyclosporine resulting in elevated creatinine, despite reduction in dose of cyclosporine. Monitor cyclosporine drug levels and renal function in patients taking both drugs.

Increased steady-state levels of phenytoin during concomitant therapy with amiodarone have been reported. Monitor phenytoin levels in patients taking both drugs.

Serious Symptomatic Bradycardia When Co-administered with Ledipasvir/Sofosbuvir or with Sofosbuvir with Simeprevir

Postmarketing cases of symptomatic bradycardia, some requiring pacemaker insertion and at least one fatal, have been reported when ledipasvir/sofosbuvir or sofosbuvir with simeprevir were initiated in patients on amiodarone. Bradycardia generally occurred within hours to days, but in some cases up to 2 weeks after initiating antiviral treatment. Bradycardia generally resolved after discontinuation of antiviral treatment. The mechanism for this effect is unknown. Monitor heart rate in patients taking or recently discontinuing amiodarone when starting antiviral treatment.

Apart from studies in patients with VT or VF, described below, there are two other studies of amiodarone showing an antiarrhythmic effect before significant levels of DEA could have accumulated. A placebo-controlled study of intravenous amiodarone (300 mg over 2 hours followed by 1200 mg/day) in post-coronary artery bypass graft patients with supraventricular and 2- to 3-consecutive-beat ventricular arrhythmias showed a reduction in arrhythmias from 12 hours on. A baseline-controlled study using a similar IV regimen in patients with recurrent, refractory VT/VF also showed rapid onset of antiarrhythmic activity; amiodarone therapy reduced episodes of VT by 85% compared to baseline.

The acute effectiveness of intravenous amiodarone in suppressing recurrent VF or hemodynamically unstable VT is supported by two randomized, parallel, dose-response studies of approximately 300 patients each. In these studies, patients with at least two episodes of VF or hemodynamically unstable VT in the preceding 24 hours were randomly assigned to receive doses of approximately 125 or 1000 mg over the first 24 hours, an 8-fold difference. In one study, a middle dose of approximately 500 mg was evaluated. The dose regimen consisted of an initial rapid loading infusion, followed by a slower 6-hour loading infusion, and then an 18-hour maintenance infusion. The maintenance infusion was continued up to hour 48. Additional 10-minute infusions of 150 mg intravenous amiodarone were given for "breakthrough" VT/VF more frequently to the 125 mg dose group, thereby considerably reducing the planned 8-fold differences in total dose to 1.8- and 2.6-fold, respectively, in the two studies.

The prospectively defined primary efficacy end point was the rate of VT/VF episodes per hour. For both studies, the median rate was 0.02 episodes per hour in patients receiving the high dose and 0.07 episodes per hour in patients receiving the low dose, or approximately 0.5 versus 1.7 episodes per day (p=0.07, 2-sided, in both studies). In one study, the time to first episode of VT/VF was significantly prolonged (approximately 10 hours in patients receiving the low dose and 14 hours in patients receiving the high dose). In both studies, significantly fewer supplemental infusions were given to patients in the high-dose group. At the end of double-blind therapy or after 48 hours, all patients were given open access to whatever treatment (including intravenous amiodarone) was deemed necessary. Mortality was not affected in these studies.

Amiodarone has the potential to cause serious side effects that limit its use to life-threatening and hemodynamically unstable cardiac arrhythmias. Advise female patients to discontinue nursing while being treated with amiodarone, as breast-feeding could expose the nursing infant to a significant dose of the drug. Recommend that patients avoid grapefruit juice, over-the-counter cough medicine (that commonly contain dextromethorphan), and St. John's Wort. Inform patients that most manufacturers of corneal refractive laser surgery devices contraindicate corneal refractive laser surgery in patients taking amiodarone. Discuss the symptoms of hypo- and hyper-thyroidism, particularly if patients will be transitioned to oral amiodarone.

Baxter, Galaxy and Nexterone are trademarks of Baxter International Inc.

Baxter Healthcare Corporation
Deerfield, IL 60015

07-19-77-918

Container Label

Container Label

NDC 43066-360-20
For Intravenous Use

Nexterone
(amiodarone HCl)
Premixed Injection

360 mg/200 mL
(1.8 mg/mL)

GALAXY
200mL Single-Dose Container
Discard unused portion

Iso-osmotic solution in Dextrose
Code 2G3450
Sterile, Nonpyrogenic

Each mL contains: 1.8 mg amiodarone HCl, USP; 18 mg Betadex Sulfobutyl Ether Sodium, NF;
0.362 mg citric acid anhydrous, 0.183 mg sodium citrate dihydrate, and 41.4 mg dextrose anhydrous in water for injection. Sodium hydroxide or hydrochloric acid may have been
added to adjust pH.

CAUTIONS: Check for minute leaks by squeezing bag firmly. If leaks are found, discard bag
as sterility may be impaired. Do not use unless solution is clear.

Do not add supplemental medication. Must not be used in series connections.

Store at 20º to 25º C (68º to 77º F); excursions permitted to 15º to 30º C (59º to 86º F).
See USP Controlled Room Temperature. Protect from freezing. Avoid excessive heat.

USE CARTON TO PROTECT CONTENTS FROM LIGHT UNTIL USE.

Rx Only

Baxter, Galaxy and Nexterone are trademarks of Baxter International Inc.

Baxter Logo
Baxter Healthcare Corporation, Deerfield, IL 60015 USA
Made in the USA

PL2501 Plastic
07-34-72-795

Carton Label

Carton Label

For Intravenous Use
NDC 43066-360-20
Code 2G3450

Nexterone
(amiodarone HCl)
Premixed Injection

360 mg/200 mL
(1.8 mg/mL)

Rx Only

USE CARTON TO PROTECT
CONTENTS FROM LIGHT UNTIL USE

1 GALAXY Single-Dose Container
Discard unused portion

Baxter Logo
Baxter Healthcare Corporation, Deerfield, IL 60015 USA

For Intravenous Use

Nexterone
(amiodarone HCl)
Premixed Injection

360 mg/200 mL
(1.8 mg/mL)

For Intravenous Use
Iso-osmotic solution in Dextrose
Sterile, Nonpyrogenic

Nexterone
(amiodarone HCl)
Premixed Injection

360 mg/200 mL
(1.8 mg/mL)

UNVARNISHED AREA FOR ON-LINE
PRINTING OF LOT & EXP

*UPC-A
Bar Code Placement
343066360207

Each mL contains: 1.8 mg amiodarone HCl, USP; 18 mg Betadex Sulfobutyl Ether
Sodium, NF; 0.362 mg citric acid anhydrous, 0.183 mg sodium citrate dihydrate,
and 41.4 mg dextrose anhydrous in water for injection. Sodium hydroxide or
hydrochloric acid may have been added to adjust pH.

Does not contain polysorbate 80 or benzul alcohol.

DOSAGE: See package insert for complete information on dosage and administration.

STORAGE: Store at 20º to 25º C (68º to 77º F); excursions permitted to 15º to 30º C
(59º to 86º F).
See USP Controlled Room Temperature. Protect from freezing. Avoid excessive heat.
USE CARTON TO PROTECT CONTENTS FROM LIGHT UNTIL USE.

Baxter, Galaxy and Nexterone are trademarks of Baxter International Inc.

Baxter Healthcare Corporation
Deerfield, IL 60015 USA

07-01-72-797

NDC 43066-150-10
For Intravenous Use

Nexterone
(amiodarone HCl)
Premixed Injection

150 mg/100 mL
(1.5 mg/mL)

GALAXY
100mL Single-Dose Container
Discard unused portion

Iso-osmotic solution in Dextrose
Code 2G3451
Sterile, Nonpyrogenic

Each mL contains: 1.5 mg amiodarone HCl, USP; 15 mg Betadex Sulfobutyl Ether Sodium, NF;
0.362 mg citric acid anhydrous, 0.183 mg sodium citrate dihydrate, and 42.1 mg dextrose
anhydrous in water for injection. Sodium hydroxide or hydrochloric acid may have been
added to adjust pH.

CAUTIONS: Check for minute leaks by squeezing bag firmly. If leaks are found, discard bag
as sterility may be impaired. Do not use unless solution is clear.

Do not add supplemental medication. Must not be used in series connections.

Store at 20º to 25º C (68º to 77º F); excursions permitted to 15º to 30º C (59º to 86º F).

See USP Controlled Room Temperature. Protect from freezing. Avoid excessive heat.

USE CARTON TO PROTECT CONTENTS FROM LIGHT UNTIL USE.

Rx Only

Baxter, Galaxy and Nexterone are trademarks of Baxter International Inc.

Baxter Logo
Baxter Healthcare Corporation, Deerfield, IL 60015 USA
Made in the USA

PL2501 Plastic
07-34-72-794

For Intravenous Use
NDC 43066-150-10
Code 2G3451

Nexterone
(amiodarone HCl)
Premixed Injection

150 mg/100 mL
(1.5 mg/mL)

Rx Only

USE CARTON TO PROTECT
CONTENTS FROM LIGHT UNTIL USE

1 GALAXY Single-Dose Container
Discard unused portion

Baxter Logo
Baxter Healthcare Corporation, Deerfield, IL 60015 USA

For Intravenous Use

Nexterone
(amiodarone HCl)
Premixed Injection

150 mg/100 mL
(1.5 mg/mL)

For Intravenous Use
Iso-osmotic solution in Dextrose
Sterile, Nonpyrogenic

Nexterone
(amiodarone HCl)
Premixed Injection

150 mg/100 mL
(1.5 mg/mL)

UNVARNISHED AREA FOR ON-LINE
PRINTING OF LOT & EXP

*UPC-A
Bar Code Placement
343066150105

Each mL contains: 1.5 mg amiodarone HCl, USP; 15 mg Betadex Sulfobutyl Ether
Sodium, NF; 0.362 mg citric acid anhydrous, 0.183 mg sodium citrate dihydrate,
and 42.1 mg dextrose anhydrous in water for injection. Sodium hydroxide or
hydrochloric acid may have been added to adjust pH.

Does not contain polysorbate 80 or benzyl alcohol.

DOSAGE: See package insert for complete information on dosage and administration.

STORAGE: Store at 20º to 25º C (68º to 77º F); excursions permitted to 15º to 30º C
(59º to 86º F).
See USP Controlled Room Temperature. Protect from freezing. Avoid excessive heat.
USE CARTON TO PROTECT CONTENTS FROM LIGHT UNTIL USE.

Baxter, Galaxy and Nexterone are trademarks of Baxter International Inc.

Baxter Healthcare Corporation
Deerfield, IL 60015 USA

07-01-72-796