Amantadine

151.25

151.25

212-201-2

BF4C9Z1J53

341865

DTXSID8022117

C61632

HEXAKISTETRAHEDRAL CRYSTALS BY SUBLIMATION

N04BB01|N - Nervous system

29213000

26

2.3

White to cream Powder

1.1±0.1 g/cm3

180 °C

225.7±8.0 °C at 760 mmHg

96.0±9.7 °C

1.558

soluble in organic solvents. Insoluble in water.1 M HCl: soluble 5%, clear to hazy, colorless to faint yellow or tan

Store in a cool, dry location. Keep containers tightly sealed.

0.13 mm Hg at 25 deg C (est)

LD50 oral in rat: 900mg/kg

Henry's Law constant = 8.3X10-6 atm-cu m/mol at 25 °C (est)

pKa = 10.45 (est)

ODORLESS; BITTER TASTE; DOES NOT MELT UP TO 300 °C, BUT SUBLIMES SLOWLY; PKA: 10.36 AT 30 °C; PH (1 IN 5 SOLN) BETWEEN 3.0 & 5.5. WHITE OR NEARLY WHITE CRYSTALLINE POWDER; 1 G IN 2.5 ML WATER, 5.1 ML ALCOHOL, 18 ML CHLOROFORM, 70 ML POLYETHYLENE GLYCOL 400 /AMANTADINE HYDROCHLORDIE/|Hydroxyl radical reaction rate constant = 4.0X10-11 cu cm/molecule-sec at 25 °C (est)

NONH for all modes of transport

3

22-36/37/38

26-36

YD1925000

Xn,Xi

Stable in light, heat & air /Amantadine hydrochloride/

P261-P305 + P351 + P338

H302-H315-H319-H335

SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for occupational exposure or environmental contamination. Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in soil or water; effects on animal, aquatic, and plant life; and conformance with environmental and public health regulations.

The Approved Drug Products with Therapeutic Equivalence Evaluations List identifies currently marketed prescription drug products, incl amantadine hydrochloride, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act. /Amantadine hydrochloride/

|Warning|H226 (64.23%): Flammable liquid and vapor [Warning Flammable liquids]|P210, P233, P240, P241, P242, P243, P261, P264, P270, P271, P273, P280, P301+P312, P302+P352, P303+P361+P353, P304+P340, P305+P351+P338, P312, P321, P330, P332+P313, P337+P313, P362, P370+P378, P403+P233, P403+P235, P405, and P501|Aggregated GHS information provided by 137 companies from 8 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Amantadine was identified, not quantified, in the effluent of municipal sewage treatment plants in Stuttgart, Germany in 1999(1).

Deaths have been reported from overdose with amantadine. The lowest reported acute lethal dose was 2 grams. 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 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, hallucination, 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.

Despite widespread use, there is little evidence that amantadine when given orally causes liver injury, either in the form of serum enzyme elevations or clinically apparent liver disease.

The anti-influenza A activities of amantadine and ribavirin were investigated seperately and in combination. In ferret tracheal ciliated epithelium, the combination of drugs synergistically delayed the virus-induced cytopathic effect.|Concurrent use /of alcohol/ with amantadine is not recommended since this may increase the potential for CNS effects such as dizziness, lightheadedness, orthostatic hypotension, or confusion.|Concurrent use /of anticholinergics, or other medications with anticholinergic activity; tricyclic antidepressants; other antidyskinetics; antihistamines; or phenothiazines/ with amantadine may potentiate the anticholinergic-like side effects, especially those of confusion, hallucinations, and nightmares; dosage adjustments of these medications or of amantadine may be necessary; also, patients should be advised to report occurrences of gastrointestinal problems promptly since paralytic ileus may occur with concurrent therapy.|Concurrent use /of opioid- and anticholinergic-containing antidiarrheals/ with amantadine may potentiate the anticholinergic-like side effects; although significant interaction is unlikely with usual doses of opioid- and anticholinergic-containing antidiarrheals, significant interaction may occur if these medications are abused.|For more Interactions (Complete) data for AMANTADINE (10 total), please visit the HSDB record page.

Fatalities have been reported following overdosage of amantadine. The lowest reported acute lethal dose of the drug has been 1 g.

Approximately 67% bound to plasma proteins over a concentration range of 0.1 to 2.0 µg/mL.

Amantadine's production and use as an antiviral agent and a drug for the treatment of Parkinson disease(1) may result in its release to the environment through various waste streams(SRC).

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 385(SRC), determined from a structure estimation method(2), indicates that amantadine is expected to have moderate mobility in soil(SRC). The pKa of amantadine is estimated as 10.45(SRC), using a method based on perturbed molecular orbital theory and linear free energy (LFER) methods(3). This pKa value indicates that amantadine will exist primarily in its protonated form in the environment and cations tend to adsorb to soils stronger than neutral molecules(4). Amantadine will not volatilize from moist soil surfaces since cations do not volatilize. Amantadine is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 0.13 mm Hg(SRC), determined from a fragment constant method(5). Biodegradation data were not available(SRC, 2006).|AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 385(SRC), determined from a structure estimation method(2), indicates that amantadine is expected to adsorb to suspended solids and sediment(SRC). The pKa of amantadine is estimated as 10.45(SRC), using a method based on perturbed molecular orbital theory and linear free energy (LFER) methods(3). This pKa value indicates that amantadine will exist primarily in its protonated form in the environment and cations do not volatilize from water(4). According to a classification scheme(5), an estimated BCF of 15(SRC), from a log Kow of 2.44(6) and a regression-derived equation(7), suggests the potential for bioconcentration in aquatic organisms is low (SRC). Biodegradation data were not available(SRC, 2006).|ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), amantadine, which has an estimated vapor pressure of 0.13 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), is expected to exist solely as a vapor in the ambient atmosphere. Vapor-phase amantadine is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals(SRC); the half-life for this reaction in air is estimated to be 10 hours(SRC), calculated from its rate constant of 4.0X10-11 cu cm/molecule-sec at 25 °C(SRC) that was derived using a structure estimation method(3).

The rate constant for the vapor-phase reaction of amantadine with photochemically-produced hydroxyl radicals has been estimated as 4.0X10-11 cu cm/molecule-sec at 25 °C(SRC) using a structure estimation method(1). This corresponds to an atmospheric half-life of about 10 hours at an atmospheric concentration of 5X10+5 hydroxyl radicals per cu cm(1). Amantadine is not expected to undergo hydrolysis in the environment due to the lack of hydrolyzable functional groups(2) nor to directly photolyze due to the lack of absorption in the environmental UV spectrum (>290 nm).

An estimated BCF of 15 was calculated for amantadine(SRC), using a log Kow of 2.44(1) and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is low(SRC).

Using a structure estimation method based on molecular connectivity indices(1), the Koc for amantadine can be estimated to be 385(SRC). According to a classification scheme(2), this estimated Koc value suggests that amantadine is expected to have moderate mobility in soil(SRC). The pKa of amantadine is estimated as 10.45(SRC), using an estimation method based on perturbed molecular orbital theory and linear free energy (LFER) methods(3). This estimated pKa indicates that amantadine will exist primarily in the protonated form in the environment and cations generally adsorb more strongly to organic carbon and clay than their neutral counterparts(4).

An estimated pKa of 10.45(SRC), obtained using an estimation method based on perturbed molecular orbital theory and linear free energy (LFER) methods(1), indicates that amantadine will exist primarily in its protonated form in the environment. Volatilization from moist soil and water surfaces will not be an important fate process since cations do not volatilize(2). Amantadine is not expected to volatilize from dry soil surfaces(SRC) based on its estimated vapor pressure of 0.13 mm Hg(SRC), determined from a fragment constant method(3).

Amantadine is distributed into breast milk.

Occupational exposure to amantadine may occur through inhalation and dermal contact with this compound at workplaces where it is produced or used. Amantadine is a prescription drug used as an antiviral agent and for the treatment of Parkinson's disease(1); therefore, patients taking this medication will be directly exposed through ingestion(SRC).

For the chemoprophylaxis, prophylaxis, and treatment of signs and symptoms of infection caused by various strains of influenza A virus. Also for the treatment of parkinsonism and drug-induced extrapyramidal reactions.|FDA Label

Amantadine is a primary amine that has both antiviral and dopaminergic activity and is used in the therapy of influenza A and management of Parkinson disease. Amantadine has not been associated with clinically apparent liver injury.

Antiviral Agents; Antiparkinson Agents

Antiparkinson Agents; Antiviral Agents; Dopamine Agents|Amantadine is used in the management of certain aspects of fatigue associated with multiple sclerosis, including lowered energy level, deceased sense of well-being, decreased perceived attention and memory, and diminished problem solving ability. /NOT included in US or Canadian product labeling/|Amantadine is indicated in the treatment of idiopathic parkinsonism (paralysis agitans; shaking palsy), post-encephalitic parkinsonism, drug-induced extrapyramidal reactions, symptomatic parkinsonism following injury to the nervous system caused by carbon monoxide intoxication, and parkinsonism associated with cerebral arteriosclerosis in the elderly. /Included in US product labeling/|Amantadine is indicated as a primary agent in the prophylaxis and treatment of respiratory tract infections caused by influenza A virus strains in high-risk patients (including those with pulmonary or cardiovascular disease, the elderly, and residents of nursing homes and other chronic care facilities who have chronic medical conditions), hospital ward contacts of high-risk patients, immunocompromised patients, those in critical public service positions (eg, police, firefighters, medical personnel), in high-risk patients for whom the influenza vaccine is contraindicated, and patients with severe influenza A viral infections. It is effective against all strains of influenza A virus that have been tested to date, including Russian, Brazilian, Texan, London, and others. It may be given as chemoprophylaxis concurrently with inactivated influenza A virus vaccine until protective antibodies develop. However, it should be emphasized that vaccination of high-risk persons each year is the single most important measure for reducing the impact of influenza. No well-controlled studies have examined whether amantadine prevents complication of influenza A in high-risk persons. Resistant strains of influenza A have been reported in patients receiving rimantadine; these resistant strains were also apparently transmitted household contacts. Rimantadine has a similar chemical structure, spectrum of activity, and mechanism of action to amantadine, and drug-resistant strains of virus have cross-resistance to amantadine and rimantadine. /Included in US product labeling/|For more Therapeutic Uses (Complete) data for AMANTADINE (6 total), please visit the HSDB record page.

Swine influenza (H1N1) viruses contain a unique combination of gene segments that have not been reported previously among swine or human influenza viruses in the US or elsewhere. The H1N1 viruses are resistant to amantadine and rimantadine but not to oseltamivir or zanamivir.|Suicide attempts (resulting in death in some patients) have been reported rarely in patients receiving amantadine, many of whom received short courses of the drug for influenza prophylaxis or treatment. The manufacturer states that the incidence and pathophysiology of these suicide attempts are not known. Suicide ideation or attempts have been reported in patients with or without a prior history of psychiatric disorders. Amantadine can exacerbate mental status in patients with a history of psychiatric disorders or substance abuse. Patients with suicidal tendencies may exhibit abnormal mental states including disorientation, confusion, depression, personality changes, agitation, aggressive behavior, hallucinations, paranoia, other psychotic reactions, somnolence, or insomnia.|Possible neuroleptic malignant syndrome (NMS) has been reported in patients receiving amantadine and was associated with dosage reduction or withdrawal of the drug. NMS is potentially fatal and requires immediate initiation of intensive symptomatic and supportive care. Patients should be observed closely when the dosage of amantadine is reduced or the drug is discontinued; this precaution is especially important in patients receiving concomitant therapy with an antipsychotic agent.|Nausea is one of the most frequent adverse effects of amantadine and has been reported in 5-10% of patients receiving the usual dosage of the drug. Anorexia, constipation, diarrhea, and dry mouth have been reported in 1-5% and vomiting has been reported in up to 1% of patients receiving amantadine. Abdominal discomfort or dysphagia also has been reported. The incidence of adverse GI effects is comparable for amantadine and rimantadine.|For more Drug Warnings (Complete) data for AMANTADINE (19 total), please visit the HSDB record page.

Patients are sometimes dramatically improved, but usual response is moderate to mediocre. Even when response is excellent, usually after 6 to 8 weeks of continuous treatment efficacy gradually wanes, and control may be lost between second and 18th month. Such tolerance is minimal if drug is used for periods of only 2 to 3 weeks, seperated by intervals of several weeks. /amantadine hydrochloride/

Amantadine is an antiviral drug which also acts as an antiparkinson agent, for which it is usually combined with L-DOPA when L-DOPA responses decline (probably due to tolerance). It is a derivate of adamantane, like a similar drug rimantadine. 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, and does not possess anticholinergic activity.

A subclass of analgesic agents that typically do not bind to OPIOID RECEPTORS and are not addictive. Many non-narcotic analgesics are offered as NONPRESCRIPTION DRUGS. (See all compounds classified as Analgesics, Non-Narcotic.)|Any drugs that are used for their effects on dopamine receptors, on the life cycle of dopamine, or on the survival of dopaminergic neurons. (See all compounds classified as Dopamine Agents.)|Agents used in the prophylaxis or therapy of VIRUS DISEASES. Some of the ways they may act include preventing viral replication by inhibiting viral DNA polymerase; binding to specific cell-surface receptors and inhibiting viral penetration or uncoating; inhibiting viral protein synthesis; or blocking late stages of virus assembly. (See all compounds classified as Antiviral Agents.)|Agents used in the treatment of Parkinson's disease. The most commonly used drugs act on the dopaminergic system in the striatum and basal ganglia or are centrally acting muscarinic antagonists. (See all compounds classified as Antiparkinson Agents.)

Amantadine is well absorbed orally from the gastrointestinal tract.|It is primarily excreted unchanged in the urine by glomerular filtration and tubular secretion.|3 to 8 L/kg [healthy subjects]|0.2 - 0.3 L/hr/kg|Rapidly and almost completely absorbed from gastrointestinal tract.|Amantadine is distributed into breast milk.|Elimination: Renal; >90% excreted unchanged in urine by glomerular filtration and renal tubular secretion. Rate of excretion rapidly increased in acid urine. In dialysis: Only small amounts (approximately 4%) removed from the blood by hemodialysis.|Distributed into saliva, tear film, and nasal secretions; in animals, tissue (especially lung) concentrations are higher than serum concentrations. Crosses the placenta and blood-brain barrier; distributed into breast milk. Cerebral spinal fluid concentrations were 52% of corresponding plasma concentrations in one patient. VolD - 4.4 + or - 0.2 L/kg (normal renal function); 5.1 + or - 0.2 L/kg (renal failure).|For more Absorption, Distribution and Excretion (Complete) data for AMANTADINE (7 total), please visit the HSDB record page.

No appreciable metabolism, although negligible amounts of an acetyl metabolite have been identified.|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..

Mean half-lives ranged from 10 to 14 hours, however renal function impairment causes a severe increase in half life to 7 to 10 days.|Amantadine pharmacokinetics were determined in 24 normal adult male volunteers after the oral administration of a single amantadine hydrochloride 100 mg soft gel capsule. ... The half-life was 17 + or - 4 hours (range: 10 to 25 hours). Across other studies, amantadine plasma half-life has averaged 16 + or - 6 hours (range: 9 to 31 hours) in 19 healthy volunteers.|Normal renal function: 11 to 15 hours. Elderly patients: 24 to 29 hours. Renal function impairment, severe: 7 to 10 days. Hemodialysis: 24 hours.|The elimination half-life increases two to three fold or greater when creatinine clearance is less than 40 mL/min/1.73 sqm and averages eight days in patients on chronic maintenance hemodialysis.

The mechanism of its antiparkinsonic effect is not fully understood, but it appears to be releasing dopamine from the nerve endings of the brain cells, together with stimulation of norepinephrine response. It also has NMDA receptor antagonistic effects. The antiviral mechanism seems to be unrelated. The drug interferes with a viral protein, M2 (an ion channel), which is needed for the viral particle to become "uncoated" once it is taken inside the cell by endocytosis.|Amantadine, like rimantadine, inhibits viral replication by interfering with the influenza A virus M2 protein, an integral membrane protein. The M2 protein of influenza A functions as a ion channel and is important in at least 2 aspects of virus replication, disassembly of the infecting virus particle and regulation of the ionic environment of the transport pathway. By interfering with the ion channel function of the M2 protein, amantadine inhibits 2 stages in the replicative cycle of influenza A. Early in the virus replicative cycle, amantadine inhibits uncoating of the virus particle, presumably by inhibiting the acid-mediated dissociation of the virion nucleic acid and proteins, which prevents nuclear transport of viral genome material. Amantadine also prevents viral maturation in some strains of influenza A (e.g., H7 strains) by promoting pH-induced conformational changes in influenza A hemagglutinin during its intracellular transport late in the replicative cycle. Adsorption of the virus to and penetration into cells do not appear to be affected by amantadine. In addition, amantadine does not interfere with the synthesis of viral components (e.g., RNA-directed RNA polymerase activity).|The mechanism of action of amantadine in the treatment of Parkinson's disease and drug-induced extrapyramidal reactions is not known. Data from earlier animal studies suggest that symmetrel may have direct and indirect effects on dopamine neurons. More recent studies have demonstrated that amantadine is a weak, non-competitive NMDA receptor antagonist (Ki = 10 uM). Although amantadine has not been shown to possess direct anticholinergic activity in animal studies, clinically, it exhibits anticholinergic-like side effects such as dry mouth, urinary retention, and constipation.|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.|In isolated ventricular muscle preparations (frog, rabbit, cat, dog, and calf) amantadine increased the action potential duration, decreased the amplitude and max diastolic potential, and induced phase 4 depolarization. These changes may be due to the effect of amantadine on potassium ion conductance.

There is no specific antidote for an overdose of /amantadine/. ... 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. 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. 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 e given. Electrocardiographic monitoring may be required after ingestion, since malignant tachyarrhythmias can appear after overdose.

/SIGNS AND SYMPTOMS/ Acute overdosage of amantadine has resulted in cardiac dysfunction (e.g., arrhythmia, tachycardia, hypertension); pulmonary edema and respiratory distress (including adult respiratory distress syndrome [ARDS]); renal dysfunction (e.g., increased BUN, decreased creatinine clearance, renal insufficiency); or CNS toxicity (e.g., insomnia, anxiety, aggressive behavior, hypertonia, hyperkinesia, tremor, confusion, disorientation, depersonalization, fear, delirium, hallucinations, psychotic reactions, lethargy, somnolence, coma). Hyperthermia also has occurred with amantadine overdosage. In addition, seizures may be exacerbated in patients with a history of a seizure disorder.|/CASE REPORTS/ Amantadine, primarily an antiviral agent has several therapeutic indications. Human data regarding any teratogenicity following its advertent or inadvertent maternal use during pregnancy is scarce. This is limited to 2 prospective reports of 4 normal fetal outcomes in 2 women and a single retrospective report of an infant born with complex congenital heart disease, following prenatal exposure. /Investigators/ reported an infant with tetralogy of Fallot and tibial hemimelia with normal karyotype, born to a 37 years old primigravida woman of Austrian origin, after first trimester exposure to amantadine. Parents were nonconsanguineous with unremarkable family history and physical examination. The mother was treated with amantadine hydrochloride 100 mg orally for 7 days during the 6th and 7th week of gestation for an upper respiratory tract infection due to parainfluenza virus. Apart from that the pregnancy was uneventful. An appropriate for gestational age female infant was born by spontaneous vaginal delivery after preterm labor at 29 weeks gestation. Physical examination at birth revealed severe fixed equinovarus deformity and a short big toe in the right foot with shortened tibia and absent talus in the affected limb on skeletal survey. Investigation of a cardiac systolic murmur detected on the second day of life revealed tetralogy of Fallot along with a small patent ductus arteriosus and aorto-pulmonary collaterals on echocardiogram. The infant has remained acyanotic and hemodynamically stable. Although these malformations may not be related to amantadine use, its avoidance during pregnancy for non life-threatening conditions would be prudent.|/CASE REPORTS/ Amantadine hydrochloride is a commonly prescribed drug with a narrow therapeutic to toxic range. Toxicity is related to the anticholinergic properties of the drug and primarily affects the cardiovascular, central nervous, and respiratory systems. It was reported the case of an adolescent who ingested 1.3 g of amantadine and developed complex ventricular arrhythmias and altered mental status. The arrhythmias were completely suppressed with intravenous lidocaine. This case supports the hypothesis that lidocaine is effective for treatment of ventricular arrhythmias secondary to amantadine toxicity.|/CASE REPORTS/ In a patient who ingested 2.8 g of amantadine hydrochloride, manifestations of amantadine overdosage included slightly dilated pupils that contracted minimally to light; urinary retention; mild, mixed acid-base disturbances; and an acute toxic psychosis manifested as disorientation, visual hallucinations, and aggressive behavior.|For more Human Toxicity Excerpts (Complete) data for AMANTADINE (8 total), please visit the HSDB record page.

1 Aminoadamantane

Oral: Capsules, liquid-filled Tablets: 100 mg (available by nonpropriety name), 100 mg, Symmetrel, (Endo); Solution: 50 mg/5 mL, Symmetrel Syrup ( with parabens), (Endo).|Trade Names.Hydrochloride: Amazolon (Sawai), Mantadine (Du Pont), Mantadix (Du Pont, Rhône-Poulenc), Symmetrel (Ciba-Geigy), Virofral (Ferrosan). Sulfate: Contenton (SKD), PK-Merz (Merz).|administered PO, intranasal, SC, IP, or aerosol routes.

Tricyclo[3.3.1.13,7]decan-1-amine: ACTIVE|Available commercially as the free base or the hydrochloride, sulfate, or fumarate salts.

Analyte: amantadine; matrix: chemical identification; procedure: infrared absorption spectrophotometry with comparison to standards /amantadine hydrochloride/|Analyte: amantadine; matrix: chemical purity; procedure: dissolution in glacial acetic acid and mercuric acetate; potentiometric titration with perchloric acid using a suitable electrode system|Analyte: amantadine; matrix: pharmaceutical preparation (capsule); procedure: infrared absorption spectrophotometry with comparison to standards (chemical identification) /amantadine hydrochloride/|Analyte: amantadine; matrix: pharmaceutical preparation (capsule); procedure: gas chromatography with flame ionization detection with comparison to standards (chemical purity) /amantadine hydrochloride/

A sensitive, specific, and accurate capillary GC method with electron capture detection using pentfluorobenzoyl chloride is described for the determination of amantadine in human plasma. The method was used to determine amantadine plasma concentrations in subjects after a single oral dose of 100 mg of amantadine hydrochloride from 2 formulations as part of a bioequivalency study.

Human Drugs -> FDA Approved Drug Products with Therapeutic Equivalence Evaluations (Orange Book) -> Active Ingredients|Pharmaceuticals