DrugindexOnline^{2nd edition}

Generic Name: Amantadine hydrochloride
Dosage Form: Syrup, usp

Amantadine Description

Amantadine hydrochloride is designated chemically as 1-adamantanamine hydrochloride.

Amantadine hydrochloride is a stable white or nearly white crystalline powder, freely soluble in water and soluble in alcohol and in chloroform. The pH range is between 2.0 and 3.0.

Amantadine has pharmacological actions as both an anti-Parkinson and an antiviral drug.

Each 5 mL, for oral administration, contains 50 mg Amantadine hydrochloride and the following inactive ingredients: Artificial Raspberry Flavor; Citric Acid, USP; Methylparaben, NF; Propylene Glycol, USP; Propylparaben, NF; Purified Water, USP; Saccharin Sodium, USP; Sodium Citrate, USP and Sorbitol Solution, USP.

Amantadine - Clinical Pharmacology

Mechanism of Action

Parkinson's Disease

The mechanism of action of Amantadine in the treatment of Parkinson's disease and drug-induced extrapyramidal reactions is not known. It has been shown to cause an increase in dopamine release in the animal brain. The drug does not possess anticholinergic activity in dogs at doses of 31.5 mg/kg, equivalent to an approximate human dose of 15.8 mg/kg (based on body surface area conversions).

Antiviral

The mechanism by which Amantadine exerts its antiviral activity is not clearly understood. It appears to mainly prevent the release of infectious viral nucleic acid into the host cell by interfering with the function of the transmembrane domain of the viral M2 protein. In certain cases, Amantadine is also known to prevent virus assembly during virus replication. It does not appear to interfere with the immunogenicity of inactivated influenza A virus vaccine.

Antiviral Activity

Amantadine inhibits the replication of influenza A virus isolates from each of the subtypes, i.e., H1N1, H2N2 and H3N2. It has very little or no activity against influenza B virus isolates. A quantitative relationship between the in vitro susceptibility of influenza A virus to Amantadine and the clinical response to therapy has not been established in man. Sensitivity test results, expressed as the concentration of Amantadine required to inhibit by 50% the growth of virus (ED50) in tissue culture vary greatly (from 0.1 µg/mL to 25.0 µg/mL) depending upon the assay protocol used, size of virus inoculum, isolates of influenza A virus strains tested, and the cell type used. Host cells in tissue culture readily tolerated Amantadine up to a concentration of 100 µg/mL.

Drug Resistance

Influenza A variants with reduced in vitro sensitivity to Amantadine have been isolated from epidemic strains in areas where adamantane derivatives are being used. Influenza viruses with reduced in vitro sensitivity have been shown to be transmissible and to cause typical influenza illness. The quantitative relationship between the in vitro sensitivity of influenza A variants to Amantadine and the clinical response to therapy has not been established.

Pharmacokinetics

Amantadine is well absorbed orally. Maximum plasma concentrations are directly related to dose for doses up to 200 mg/day. Doses above 200 mg/day may result in a greater than proportional increase in maximum plasma concentrations. It is primarily excreted unchanged in the urine by glomerular filtration and tubular secretion. Eight metabolites of Amantadine have been identified in human urine. One metabolite, an N-acetylated compound, was quantified in human urine and accounted for 5–15% of the administered dose. Plasma acetylAmantadine accounted for up to 80% of the concurrent Amantadine plasma concentration in 5 of 12 healthy volunteers following the ingestion of a 200 mg dose of Amantadine. AcetylAmantadine was not detected in the plasma of the remaining seven volunteers. The contribution of this metabolite to efficacy or toxicity is not known.

There appears to be a relationship between plasma Amantadine concentrations and toxicity. As concentration increases toxicity seems to be more prevalent, however absolute values of Amantadine concentrations associated with adverse effects have not been fully defined.

After oral administration of a single dose of 100 mg Amantadine hydrochloride in a syrup formulation to five healthy volunteers, the mean ± SD maximum plasma concentration Cmax was 0.24 ± 0.04 µg/mL and ranged from 0.18 to 0.28 µg/mL. After 15 days of Amantadine 100 mg b.i.d., the Cmax was 0.47 ± 0.11 µg/mL in four of the five volunteers.

Plasma Amantadine clearance ranged from 0.2 to 0.3 L/hr/kg after the administration of 5 mg to 25 mg intravenous doses of Amantadine to 15 healthy volunteers.

In six healthy volunteers, the ratio of Amantadine renal clearance to apparent oral plasma clearance was 0.79 ± 0.17 (mean ± SD).

The volume of distribution determined after the intravenous administration of Amantadine to 15 healthy subjects was 3 to 8 L/kg, suggesting tissue binding. Amantadine, after single oral 200 mg doses to 6 healthy young subjects and to 6 healthy elderly subjects has been found in nasal mucus at mean ± SD concentration of 0.15 ± 0.16, 0.28 ± 0.26 and 0.39 ± 0.34 µg/g at 1, 4 and 8 hours after dosing, respectively. These concentrations represented 31 ± 33%, 59 ± 61% and 95 ± 86% of the corresponding plasma Amantadine concentrations. Amantadine is approximately 67% bound to plasma proteins over a concentration range of 0.1 to 2.0 µg/mL. Following the administration of Amantadine 100 mg as a single dose, the mean ± SD red blood cell to plasma ratio ranged from 2.7 ± 0.5 in 6 healthy subjects to 1.4 ± 0.2 in 8 patients with renal insufficiency.

The apparent oral plasma clearance of Amantadine is reduced and the plasma half-life and plasma concentrations are increased in healthy, elderly individuals age 60 and older. After single dose administration of 25 to 75 mg to 7 healthy, elderly male volunteers, the apparent plasma clearance of Amantadine was 0.10 ± 0.04 L/hr/kg (range 0.06 to 0.17 L/hr/kg) and the half-life was 29 ± 7 hours (range 20 to 41 hours). Whether these changes are due to decline in renal function or other age related factors is not known.

Compared with otherwise healthy adult individuals, the clearance of Amantadine is significantly reduced in adult patients with renal insufficiency. The elimination half-life increases two to three fold or greater when creatinine clearance is less than 40 mL/min/1.73 m2 and averages eight days in patients on chronic maintenance hemodialysis. Amantadine is removed in negligible amounts by hemodialysis.

The pH of the urine has been reported to influence the excretion rate of Amantadine. Since the excretion rate of Amantadine increases rapidly when the urine is acidic, the administration of urine acidifying drugs may increase the elimination of the drug from the body.

Indications and Usage for Amantadine

Amantadine hydrochloride syrup is indicated for the prophylaxis and treatment of signs and symptoms of infection caused by various strains of influenza A virus. Amantadine hydrochloride is also indicated in the treatment of parkinsonism and drug-induced extrapyramidal reactions.

Influenza A Prophylaxis

Amantadine hydrochloride is indicated for chemoprophylaxis against signs and symptoms of influenza A virus infection when early vaccination is not feasible or when the vaccine is contraindicated or not available. In the prophylaxis of influenza, early vaccination on an annual basis as recommended by the Centers for Disease Control's Immunization Practices Advisory Committee is the method of choice. Because Amantadine does not completely prevent the host immune response to influenza A infection, individuals who take this drug may still develop immune responses to natural disease or vaccination and may be protected when later exposed to antigenically related viruses. Following vaccination during an influenza A outbreak, Amantadine prophylaxis should be considered for the 2 to 4 week time period required to develop an antibody response.

Influenza A Treatment

Amantadine hydrochloride is also indicated in the treatment of uncomplicated respiratory tract illness caused by influenza A virus strains especially when administered early in the course of illness. There are no well-controlled clinical studies demonstrating that treatment with Amantadine will avoid the development of influenza A virus pneumonitis or other complications in high risk patients.

There is no clinical evidence indicating that Amantadine is effective in the prophylaxis or treatment of viral respiratory tract illnesses other than those caused by influenza A virus strains.

Parkinson's Disease/Syndrome

Amantadine is indicated in the treatment of idiopathic Parkinson's disease (Paralysis Agitans), postencephalitic parkinsonism, and symptomatic parkinsonism which may follow injury to the nervous system by carbon monoxide intoxication. It is indicated in those elderly patients believed to develop parkinsonism in association with cerebral arteriosclerosis. In the treatment of Parkinson's disease Amantadine is less effective than levodopa, (-)-3-(3,4-dihydroxyphenyl)-L-alanine, and its efficacy in comparison with the anticholinergic antiparkinson drugs has not yet been established.

Drug-Induced Extrapyramidal Reactions

Amantadine hydrochloride is indicated in the treatment of drug-induced extrapyramidal reactions. Although anticholinergic-type side effects have been noted with Amantadine when used in patients with drug-induced extrapyramidal reactions, there is a lower incidence of these side effects than that observed with the anticholinergic antiparkinson drugs.

Contraindications

Amantadine hydrochloride is contraindicated in patients with known hypersensitivity to the drug.

Warnings

Deaths

Deaths have been reported from overdose with Amantadine. The lowest reported acute lethal dose was 2 grams. Acute toxicity may be attributable to the anticholinergic effects of Amantadine. Drug overdose has resulted in cardiac, respiratory, renal or central nervous system toxicity. Cardiac dysfunction included arrhythmia, tachycardia and hypertension (see OVERDOSAGE).

Suicide Attempts

Suicide attempts, some of which have been fatal, have been reported in patients treated with Amantadine, many of whom received short courses for influenza treatment or prophylaxis. The incidence of suicide attempts is not known and the pathophysiologic mechanism is not understood. Suicide attempts and suicidal ideation have been reported in patients with and without prior history of psychiatric illness. Amantadine can exacerbate mental problems in patients with a history of psychiatric disorders or substance abuse. Patients who attempt suicide may exhibit abnormal mental states which include disorientation, confusion, depression, personality changes, agitation, aggressive behavior, hallucinations, paranoia, other psychotic reactions and somnolence or insomnia. Because of the possibility of serious adverse effects, caution should be observed when prescribing Amantadine to patients being treated with drugs having CNS effects, or for whom the potential risks outweigh the benefit of treatment. Because some patients have attempted suicide by overdosing with Amantadine, prescriptions should be written for the smallest quantity consistent with good patient management.

CNS Effects

Patients with a history of epilepsy or other "seizures" should be observed closely for possible increased seizure activity.

Patients receiving Amantadine who note central nervous system effects or blurring of vision should be cautioned against driving or working in situations where alertness and adequate motor coordination are important.

Other

Patients with a history of congestive heart failure or peripheral edema should be followed closely as there are patients who developed congestive heart failure while receiving Amantadine.

Patients with Parkinson's disease improving on Amantadine should resume normal activities gradually and cautiously, consistent with other medical considerations, such as the presence of osteoporosis or phlebothrombosis.

Precautions

Amantadine should not be discontinued abruptly in patients with Parkinson's disease since a few patients have experienced a parkinsonian crisis, i.e., a sudden marked clinical deterioration, when this medication was suddenly stopped. The dose of anticholinergic drugs or of Amantadine should be reduced if atropine-like effects appear when these drugs are used concurrently.

Neuroleptic Malignant Syndrome (NMS)

Sporadic cases of possible Neuroleptic Malignant Syndrome (NMS) have been reported in association with dose reduction or withdrawal of Amantadine therapy.

NMS is an uncommon but life-threatening syndrome characterized by fever or hyperthermia; neurologic findings including muscle rigidity, involuntary movements, altered consciousness; other disturbances such as autonomic dysfunction, tachycardia, tachypnea, hyper- or hypotension; laboratory findings such as creatine phosphokinase elevation, leukocytosis and increased serum myoglobin.

The early diagnosis of this condition is important for the appropriate management of these patients. Considering NMS as a possible diagnosis and ruling out other acute illnesses (e.g., pneumonia, systemic infection, etc.) is essential. This may be especially complex if the clinical presentation includes both serious medical illness and untreated or inadequately treated extrapyramidal signs and symptoms (EPS). Other important considerations in the differential diagnosis include central anticholinergic toxicity, heat stroke, drug fever and primary central nervous system (CNS) pathology.

The management of NMS should include: 1) intensive symptomatic treatment and medical monitoring, and 2) treatment of any concomitant serious medical problems for which specific treatments are available. Dopamine agonists, such as bromocriptine, and muscle relaxants, such as dantrolene are often used in the treatment of NMS, however, their effectiveness has not been demonstrated in controlled studies.

Other

Because Amantadine is mainly excreted in the urine, it accumulates in the plasma and in the body when renal function declines. Thus, the dose of Amantadine should be reduced in patients with renal impairment and in individuals who are 65 years of age or older. The dose of Amantadine may need careful adjustment in patients with congestive heart failure, peripheral edema, or orthostatic hypotension.

Care should be exercised when administering Amantadine to patients with liver disease, a history of recurrent eczematoid rash, or to patients with psychosis or severe psychoneurosis not controlled by chemotherapeutic agents. Rare instances of reversible elevation of liver enzymes have been reported in patients receiving Amantadine, though a specific relationship between the drug and such changes has not been established.

Drug Interactions

Careful observation is required when Amantadine is administered concurrently with central nervous system stimulants.

Coadministration of thioridazine has been reported to worsen the tremor in elderly patients with Parkinson's disease, however, it is not known if other phenothiazines produce a similar response.

Coadministration of triamterene/hydrochlorothiazide capsules resulted in a higher plasma Amantadine concentration in a 61 year old man receiving Amantadine 100 mg TID for Parkinson's disease.1 It is not known which of the components of triamterene/hydrochlorothiazide capsules contributed to the observation or if related drugs produce a similar response.

Carcinogenesis, Mutagenesis, Impairment of Fertility

Long-term in vivo animal studies designed to evaluate the carcinogenic potential of Amantadine have not been performed. In several in vitro assays for gene mutation, Amantadine did not increase the number of spontaneously observed mutations in four strains of Salmonella typhimurium (Ames Test) or in a mammalian cell line (Chinese Hamster Ovary cells) when incubations were performed either with or without a liver metabolic activation extract. Further, there was no evidence of chromosome damage observed in an in vitro test using freshly derived and stimulated human peripheral blood lymphocytes (with and without metabolic activation) or in an in vivo mouse bone marrow micronucleus test (140–550 mg/kg; estimated human equivalent doses of 11.7–45.8 mg/kg based on body surface area conversion).

In a three litter reproduction study in rats, Amantadine at a dose of 32 mg/kg/day (estimated human equivalent dose of 4.5 mg/kg/day, based on body surface area conversions) administered to both males and females slightly impaired fertility. There were no effects on fertility at a dose level of 10 mg/kg/day (estimated human equivalent dose of 1.4 mg/kg/day); intermediate doses were not tested.

Pregnancy

Teratogenic Effects

Pregnancy Category C. Amantadine has been shown to be embryotoxic and teratogenic in rats at 50 mg/kg/day (estimated human equivalent dose of 7.1 mg/kg/day based on body surface area conversion), while a dose of 37 mg/kg/day (estimated human equivalent dose of 5.3 mg/kg/day) was without effect. Embryotoxic and teratogenic effects were not seen in rabbits that received 32 mg/kg/day (estimated human equivalent dose of 9.6 mg/kg/day, based on body surface area conversion). There are no adequate and well-controlled studies in pregnant women. Amantadine should be used during pregnancy only if the potential benefit justifies the potential risk to the embryo or fetus.

Nursing Mothers

Amantadine is excreted in human milk. Use is not recommended in nursing mothers.

Pediatric Use

The safety and efficacy of Amantadine hydrochloride in newborn infants and infants below the age of 1 year have not been established.

Usage in the Elderly

Because Amantadine hydrochloride is primarily excreted in the urine, it accumulates in the plasma and in the body when renal function declines. Thus, the dose of Amantadine should be reduced in patients with renal impairment and in individuals who are 65 years of age or older. The dose of Amantadine may need reduction in patients with congestive heart failure, peripheral edema, or orthostatic hypotension (see DOSAGE AND ADMINISTRATION).

Adverse Reactions

The adverse reactions reported most frequently at the recommended dose of Amantadine (5–10%) are: nausea, dizziness (lightheadedness), and insomnia.

Less frequently (1–5%) reported adverse reactions are: depression, anxiety and irritability, hallucinations, confusion, anorexia, dry mouth, constipation, ataxia, livedo reticularis, peripheral edema, orthostatic hypotension, headache, somnolence, nervousness, dream abnormality, agitation, dry nose, diarrhea and fatigue.

Infrequently (0.1–1%) occurring adverse reactions are: congestive heart failure, psychosis, urinary retention, dyspnea, fatigue, skin rash, vomiting, weakness, slurred speech, euphoria, confusion, thinking abnormality, amnesia, hyperkinesia, hypertension, decreased libido, and visual disturbance including punctuate subepithelial or other corneal opacity, corneal edema, decreased visual acuity, sensitivity to light, and optic nerve palsy.

Rare (less than 0.1%) occurring adverse reactions are: instances of convulsion, leukopenia, neutropenia, eczematoid dermatitis, oculogyric episodes, suicidal attempt, suicide, and suicidal ideation (see WARNINGS).

Overdosage

Deaths have been reported from overdose with Amantadine. The lowest reported acute lethal dose was 2 grams. Acute toxicity may be attributable to the anticholinergic effects of Amantadine. Drug overdose has resulted in cardiac, respiratory, renal or central nervous system toxicity. Cardiac dysfunction includes arrhythmia, tachycardia and hypertension. Pulmonary edema and respiratory distress (including adult respiratory distress syndrome — ARDS) have been reported; renal dysfunction, including increased BUN, decreased creatinine clearance and renal insufficiency can occur. Central nervous system effects that have been reported include insomnia, anxiety, aggressive behavior, hypertonia, hyperkinesia, tremor, confusion, disorientation, depersonalization, fear, delirium, hallucinations, psychotic reactions, lethargy, somnolence and coma. Seizures may be exacerbated in patients with prior history of seizure disorders. Hyperthermia has also been observed in cases where a drug overdose has occurred.

There is no specific antidote for an overdose of Amantadine. However, slowly administered intravenous physostigmine in 1 and 2 mg doses in an adult2 at 1 to 2 hour intervals and 0.5 mg doses in a child3 at 5 to 10 minute intervals up to a maximum of 2 mg/hour have been reported to be effective in the control of central nervous system toxicity caused by Amantadine hydrochloride. For acute overdosing, general supportive measures should be employed along with immediate gastric lavage or induction of emesis. Fluids should be forced, and if necessary, given intravenously. Hemodialysis does not remove significant amounts of Amantadine: in patients with renal failure, a four hour hemodialysis removed 7 to 15 mg after a single 300 mg oral dose.4 The pH of the urine has been reported to influence the excretion rate of Amantadine. Since the excretion rate of Amantadine increases rapidly when urine is acidic, the administration of urine acidifying drugs may increase the elimination of the drug from the body. The blood pressure, pulse, respiration and temperature should be monitored. The patient should be observed for hyperactivity and convulsions: if required, sedation, and anticonvulsant therapy should be administered. The patient should be observed for the possible development of arrhythmias and hypotension: if required, appropriate antiarrhythmic and antihypotensive therapy should be given. The blood electrolytes, urine pH and urinary output should be monitored. If there is no record of recent voiding, catheterization should be done.

Amantadine Dosage and Administration

The dose of Amantadine hydrochloride may need reduction in patients with congestive heart failure, peripheral edema, orthostatic hypotension, or impaired renal function (see Dosage for Impaired Renal Function).

Dosage for Prophylaxis and Treatment of Uncomplicated Influenza A Virus Illness

Adult

The adult daily dosage of Amantadine hydrochloride is 200 mg (four teaspoonfuls of syrup) as a single daily dose. The daily dosage may be split into two teaspoonfuls of syrup twice a day. If central nervous system effects develop in once-a-day dosage, a split dosage schedule may reduce such complaints. In persons 65 years of age or older, the daily dosage of Amantadine hydrochloride is 100 mg.

A 100 mg daily dose has also been shown in experimental challenge studies to be effective as prophylaxis in healthy adults who are not at high risk for influenza-related complications. However, it has not been demonstrated that a 100 mg daily dose is as effective as a 200 mg daily dose for prophylaxis, nor has the 100 mg daily dose been studied in the treatment of acute influenza illness. In recent clinical trials, the incidence of central nervous system (CNS) side effects associated with the 100 mg daily dose was at or near the level of placebo. The 100 mg dose is recommended for persons who have demonstrated intolerance to 200 mg of Amantadine hydrochloride daily because of CNS or other toxicities.

Children

1 yr.–9 yrs. of age

The total daily dose should be calculated on the basis of 2 to 4 mg/lb/day (4.4 to 8.8 mg/kg/day), but not to exceed 150 mg per day.

9 yrs.–12 yrs. of age

The total daily dose is 200 mg given as two teaspoonfuls of syrup twice daily. The 100 mg daily dose has not been studied in children. Therefore, there are no data which demonstrate that this dose is as effective as or is safer than the 200 mg daily dose in this patient population.

Prophylactic dosing should be started in anticipation of an influenza A outbreak and before or after contact with individuals with influenza A virus respiratory tract illness.

Amantadine should be continued daily for at least 10 days following a known exposure. If Amantadine is used chemoprophylactically in conjunction with inactivated influenza A virus vaccine until protective antibody responses develop, then it should be administered for 2 to 4 weeks after the vaccine has been given. When inactivated influenza A virus vaccine is unavailable or contraindicated, Amantadine should be administered for the duration of known influenza A in the community because of repeated and unknown exposure.

Treatment of influenza A virus illness should be started as soon as possible, preferably within 24 to 48 hours after onset of signs and symptoms, and should be continued for 24 to 48 hours after the disappearance of signs and symptoms.

Dosage for Parkinsonism

Adult

The usual dose of Amantadine hydrochloride is 100 mg twice a day when used alone. Amantadine has an onset of action usually within 48 hours.

The initial dose of Amantadine hydrochloride is 100 mg daily for patients with serious associated medical illnesses or who are receiving high doses of other antiparkinson drugs. After one to several weeks at 100 mg once daily, the dose may be increased to 100 mg twice daily, if necessary.

Occasionally, patients whose responses are not optimal with Amantadine hydrochloride at 200 mg daily may benefit from an increase up to 400 mg daily in divided doses. However, such patients should be supervised closely by their physicians.

Patients initially deriving benefit from Amantadine not uncommonly experience a fall-off of effectiveness after a few months. Benefit may be regained by increasing the dose to 300 mg daily. Alternatively, temporary discontinuation of Amantadine for several weeks followed by reinitiation of the drug, may result in regaining benefit in some patients. A decision to use other antiparkinson drugs may be necessary.

Dosage for Concomitant Therapy

Some patients who do not respond to anticholinergic antiparkinson drugs may respond to Amantadine. When Amantadine or anticholinergic antiparkinson drugs are each used with marginal benefit, concomitant use may produce additional benefit.

When Amantadine and levodopa are initiated concurrently, the patient can exhibit rapid therapeutic benefits. Amantadine should be held constant at 100 mg daily or twice daily while the daily dose of levodopa is gradually increased to optimal benefit.

When Amantadine is added to optimally well-tolerated doses of levodopa, additional benefit may result, including smoothing out the fluctuations in improvement which sometimes occur in patients on levodopa alone. Patients who require a reduction in their usual dose of levodopa because of development of side effects may possibly regain lost benefit with the addition of Amantadine.

Dosage for Drug-Induced Extrapyramidal Reactions

Adult

The usual dose of Amantadine hydrochloride is 100 mg twice a day. Occasionally, patients whose responses are not optimal with Amantadine hydrochloride at 200 mg daily may benefit from an increase up to 300 mg daily in divided doses.

Dosage for Impaired Renal Function

Depending upon creatinine clearance, the following dosage adjustments are recommended:

CREATININE CLEARANCE (mL/min/1.73m2)	Amantadine HYDROCHLORIDE DOSAGE
30–50	200 mg first day and 100 mg each day thereafter
15–29	200 mg first day followed by 100 mg on alternate days
<15	200 mg every 7 days

The recommended dosage for patients on hemodialysis is 200 mg every 7 days.

How is Amantadine Supplied

Amantadine Hydrochloride Syrup, USP 50 mg/5 mL is a colorless to pale yellow, raspberry-flavored syrup available in:
    1 Pint (473 mL) Bottles

Store at controlled room temperature, 15 °–30 °C (59 °–86 °F).

KEEP TIGHTLY CLOSED

Dispense in a tight container as defined in the USP.

Rx Only

REFERENCES

1W.W. Wilson and A.H. Rajput, Amantadine-Dyazide Interaction, Can. Med. Assoc. J.129:974–975, 1983.

2D.F. Casey, N. Engl. J. Med. 298:516, 1978.

3C.D. Berkowitz, J. Pediatr. 95:144, 1979.

4V.W. Horadam, et al, Ann. Intern. Med. 94:454, 1981.

Product No.: 8093

Manufactured By:
Morton Grove Pharmaceuticals, Inc.
Morton Grove, IL 60053

28093 ISS. 1-99

Amantadine Hydrochloride (Amantadine Hydrochloride)

PRODUCT INFO Product Code 60432-093 Dosage Form SYRUP Route Of Administration ORAL DEA Schedule

INGREDIENTS Name (Active Moiety) Type Strength Amantadine Hydrochloride (Amantadine) Active 50 MILLIGRAM  In 5 MILLILITER Raspberry Flavor Inactive   Citric Acid Inactive   Methylparaben Inactive   Propylene Glycol Inactive   Propylparaben Inactive   Purified Water Inactive   Saccharin Sodium Inactive   Sodium Citrate Inactive   Sorbitol Solution Inactive

IMPRINT INFORMATION Characteristic Appearance Characteristic Appearance Color Score Shape Symbol Imprint Code Coating Size

PACKAGING # NDC Package Description Multilevel Packaging 1 60432-093-16 473 MILLILITER In 1 BOTTLE None

Revised: 02/2006