Amantadine Sulfate

Synonyms: Amantadine, Sulfate d’; Amantadine Sulphate; Amantadini Sulfas; Sulfato de amantadina.
Cyrillic synonym: Амантадина Сульфат.

💊 Chemical information

Chemical formula: (C10H17N)2,SO4 = 398.6.
CAS — 31377-23-8.
ATC — N04BB01.
ATC Vet — QN04BB01.

💊 Adverse Effects

Most adverse effects associated with amantadine therapy appear to be dose-related and relatively mild; some resemble those of antimuscarinic drugs. They may be reversed by withdrawing therapy but many resolve despite continuation. Livedo reticularis, sometimes associated with ankle oedema, is quite common in patients given very high doses of amantadine or with long-term therapy. CNS effects such as anxiety, inability to concentrate, dizziness, insomnia, nightmares, headache, and changes in mood may occur. Psychotic reactions, hallucinations, and confusion have been reported, especially in the elderly, patients with renal impairment or psychiatric disorders, and those also receiving antimuscarinics. Other adverse effects reported have included orthostatic hypotension, palpitations, urinary retention, slurred speech, ataxia, lethargy, anorexia, nausea, vomiting, dry mouth, constipation, skin rash, diaphoresis, photosensitisation, and blurred vision. There have been isolated reports of congestive heart failure, leucopenia, neutropenia, dyskinesias, oculogyric episodes, and convulsions.

Effects on the cardiovascular system.

Congestive heart failure has been reported with amantadine;1 the patient had been receiving combined treatment with amantadine, levodopa, and orphenadrine for 4 years. Others have considered that while amantadine sometimes causes ankle oedema, an association between amantadine and heart failure is not proven.2 Livedo reticularis, a mottled blue discoloration of the skin due to prominence of the normal pattern of venous drainage, has been reported2 to occur in about 50% of all elderly patients given amantadine 100 to 300 mg daily for 2 to 6 weeks and was associated with oedema in 5 to 10%. Both livedo and oedema have usually been confined to the legs and may result from the catecholamine-releasing action of amantadine in certain vascular beds; the oedema was unlikely to be due to heart failure. Angina, dyspnoea, pulmonary congestion, or distension of neck veins has also been reported2 in 4 of 89 parkinsonian patients treated with amantadine; only 2 of these 4 had had ankle oedema before heart failure developed. No patient had been seen in whom heart failure seemed due directly to amantadine. See also Overdosage, below.
1. Vale JA, Maclean KS. Amantadine-induced heart-failure. Lancet 1977; i: 548
2. Parkes JD, et al. Amantadine-induced heart-failure. Lancet 1977; i: 904.

Effects on electrolytes.

For a report of a patient who developed hyponatraemia when given amantadine or levodopa, see Effects on Kidney Function under Levodopa.

Effects on the eyes.

Superficial punctate keratitis and corneal abrasion with loss of visual acuity was seen in both eyes of a 64year-old man about 3 weeks after starting treatment with amantadine 100 mg daily.1 Symptoms resolved on stopping amantadine but recurred when re-treatment with amantadine was attempted. In another report,2 a 14-year-old boy developed bilateral corneal oedema with visual loss associated with amantadine treatment. He had been taking amantadine 300 mg daily for several months with numerous other drugs; symptoms resolved when amantadine was stopped.
1. Nogaki H, Morimatsu M. Superficial punctate keratitis and corneal abrasion due to amantadine hydrochloride. J Neurol 1993; 240: 388–9
2. Hughes B, et al. Reversible amantadine-induced corneal edema in an adolescent. Cornea 2004; 23: 823–4.

Effects on mental function.

It has been suggested1 that the ability of amantadine and memantine to cause psychotic disturbances in patients with Parkinson’s disease might be related to their action as N-methylD-aspartate antagonists.
1. Riederer P, et al. Pharmacotoxic psychosis after memantine in Parkinson’s disease. Lancet 1991; 338: 1022–3.

Effects on the nervous system.

Peripheral sensory motor neuropathy secondary to long-term (8 years) use of amantadine has been reported1 in a 48-year-old woman with parkinsonism. Trophic skin ulcers, paraesthesias, and distal weakness resolved on stopping amantadine.
1. Shulman LM, et al. Amantadine-induced peripheral neuropathy. Neurology 1999; 53: 1862–5.


A patient with postencephalitic parkinsonism who had taken an estimated 2.8 g of amantadine hydrochloride in a suicide attempt developed acute toxic psychosis with disorientation, visual hallucinations, and aggressive behaviour.1 Convulsions did not occur, possibly because he had been receiving phenytoin, which was continued. The patient was treated with hydration and chlorpromazine and recovered in 4 days. A 2-year-old child who had ingested 600 mg of amantadine hydrochloride developed symptoms of acute toxicity, including agitation and dystonic posturing, despite emesis with ‘syrup of ipecac’.2 She responded immediately to a trial of physostigmine 500 micrograms intravenously, repeated after 10 minutes. Her pupils remained moderately dilated until about 20 hours after the ingestion; thereafter she made a full recovery. Cardiac arrest developed 4 hours after a 37-year-old woman ingested 2.5 g of amantadine hydrochloride and was treated successfully.3 However, ventricular arrhythmias, including torsade de pointes, continued over the ensuing 48 hours and may have been exacerbated by use of isoprenaline and dopamine. The patient was subsequently stabilised with lidocaine by intravenous infusion, but died of respiratory failure 10 days after admission.
1. Fahn S, et al. Acute toxic psychosis from suicidal overdosage of amantadine. Arch Neurol, 1971; 25: 45–8
2. Berkowitz CD. Treatment of acute amantadine toxicity with physostigmine. J Pediatr 1979; 95: 144–5
3. Sartori M, et al. Torsade de pointe: malignant cardiac arrhythmia induced by amantadine poisoning. Am J Med 1984; 77: 388–91.

💊 Precautions

Amantadine is usually contra-indicated in severe renal disease and in patients with a history of epilepsy or other seizure disorders, or gastric ulceration. It should also not be given to patients with untreated angle-closure glaucoma. Amantadine should be used with caution in patients with cardiovascular or liver disease, renal impairment, recurrent eczema, or psychiatric disorders. Suicide attempts, in some cases fatal, and suicidal ideation have been reported in patients taking amantadine. Care should be taken in all elderly patients, who may be more sensitive to antimuscarinic effects, and in whom renal clearance is likely to be reduced. In common with other drugs having antimuscarinic properties amantadine may cause blurred vision or impair alertness; patients so affected should not drive or operate machinery. Treatment with amantadine should not be stopped abruptly in parkinsonian patients since they may experience a sudden marked clinical deterioration. There have been isolated reports of a neuroleptic malignantlike syndrome associated with abrupt withdrawal of amantadine, especially in patients also receiving antipsychotics.

Antiviral resistance.

See Influenza under Uses and Administration, below.

Breast feeding.

Amantadine is distributed into breast milk and licensed product information states that adverse effects have occurred in infants being breast fed by mothers taking amantadine.


Amantadine should not be used during pregnancy; embryotoxicity and teratogenicity have been reported in rats given high doses.1 A complex cardiovascular lesion occurred in an infant whose mother had taken amantadine hydrochloride 100 mg daily during the first 3 months of pregnancy.1 In another case, tetralogy of Fallot and limb deformities were seen in the neonate of a mother who was given amantadine hydrochloride 100 mg daily for 7 days during the 4th and 6th weeks of gestation.2 However, a report of the use of amantadine during 2 separate pregnancies by a woman with multiple sclerosis noted no abnormalities in either infant.3
1. Nora JJ, et al. Cardiovascular maldevelopment associated with maternal exposure to amantadine. Lancet 1975; ii: 607
2. Pandit PB, et al. Tibial hemimelia and tetralogy of Fallot associated with first trimester exposure to amantadine. Reprod Toxicol 1994; 8: 89–92
3. Levy M, et al. Fetal outcome following intrauterine amantadine exposure. Reprod Toxicol 1991; 5: 79–81.

Renal impairment.

Evidence of extremely limited excretion of amantadine was found in 12 patients who were either anephric or had negligible renal function after a single 100-mg dose of amantadine hydrochloride.1 Only small amounts were removed by dialysis. It was suggested that amantadine should be given with caution to patients requiring maintenance haemodialysis; a single dose may provide adequate plasma concentrations for many days.1 Dosage regimens based on creatinine clearance2 or fixed doses at extended intervals3 have been published. However, both regimens have been criticised and a conservative approach to amantadine dosage in these patients recommended4 (for the regimens in licensed product information, see Administration in Renal Impairment, below). The need for caution in using amantadine in patients with renal impairment is highlighted by a report of a patient with end-stage renal disease who progressed from delirium to coma after receiving amantadine 100 mg twice daily for 3 days.5
1. Soung L-S, et al. Amantadine hydrochloride pharmacokinetics in hemodialysis patients. Ann Intern Med 1980; 93: 46–9
2. Horadam VW, et al. Pharmacokinetics of amantadine hydrochloride in subjects with normal and impaired renal function. Ann Intern Med 1981; 94: 454–8
3. Wu MJ, et al. Amantadine hydrochloride pharmacokinetics in patients with impaired renal function. Clin Nephrol 1982; 17: 19–23
4. Aoki FY, Sitar DS. Clinical pharmacokinetics of amantadine hydrochloride. Clin Pharmacokinet 1988; 14: 35–51
5. Macchio GJ, et al. Amantadine-induced coma. Arch Phys Med Rehabil 1993; 74: 1119–20.


Neuroleptic malignant syndrome occurred in a patient being treated for heat stroke when all his medication, including antipsychotics and amantadine, was withdrawn.1 It is suggested that dopamine agonists should not be stopped in patients with hyperpyrexia at risk from this syndrome. In another report,2 a 14-year-old boy being treated with amantadine for influenza A encephalopathy developed neuroleptic malignant syndrome when the drug was stopped after 5 days; the patient improved when amantadine treatment was resumed. The authors recommended a gradual reduction in dosage when stopping amantadine therapy. Acute delirium developed in 3 elderly patients with Parkinson’s disease after gradual withdrawal of long-term amantadine therapy;3 symptoms resolved when amantadine was restarted.
1. Simpson DM, Davis GC. Case report of neuroleptic malignant syndrome associated with withdrawal from amantadine. Am J Psychiatry 1984; 141: 796–7
2. Ito T, et al. Neuroleptic malignant syndrome following withdrawal of amantadine in a patient with influenza A encephalopathy. Eur J Pediatr 2001; 160: 401
3. Factor SA, et al. Acute delirium after withdrawal of amantadine in Parkinson’s disease. Neurology 1998; 50: 1456–8.

💊 Interactions

Amantadine may enhance the adverse effects of antimuscarinics and the dose of these drugs should be reduced when used with amantadine; adverse effects of levodopa may also be exacerbated. Licensed product information states that amantadine should be used with caution in patients receiving drugs that affect the CNS. The rate of excretion of amantadine may be reduced by drugs that raise urinary pH.


Quinine and quinidine have been reported to reduce the renal clearance of amantadine in healthy male, but not female, subjects.1 Patients taking these drugs together should be observed for signs of amantadine toxicity.
1. Gaudry SE, et al. Gender and age as factors in the inhibition of renal clearance of amantadine by quinine and quinidine. Clin Pharmacol Ther 1993; 54: 23–7.


For the possible effects of the use of quinine and quinidine with amantadine, see Antiarrhythmics, above.


A patient with Parkinson’s disease, previously stabilised on amantadine hydrochloride 300 mg daily, developed symptoms of amantadine toxicity, including ataxia, myoclonus, and confusion, 7 days after starting treatment with a preparation containing triamterene and hydrochlorothiazide (Dyazide).1 It was postulated that the effect was due to reduction of the tubular secretion of amantadine.
1. Wilson TW, Rajput AH. Amantadine-Dyazide interaction. Can Med Assoc J 1983; 129: 974–5.


Hypertension occurred about 48 hours after starting treatment with phenelzine sulfate in a patient already receiving amantadine.1
1. Jack RA, Daniel DG. Possible interaction between phenelzine and amantadine. Arch Gen Psychiatry 1984; 41: 726.

💊 Pharmacokinetics

Amantadine hydrochloride is well absorbed from the gastrointestinal tract; peak concentrations in the plasma appear within about 4 hours after oral doses. Plasma protein binding is reported to be about 67%, with a substantial amount bound to erythrocytes; the concentration is about 2.7 times higher in erythrocytes than in plasma. It is mainly excreted unchanged in the urine by glomerular filtration and tubular secretion although small amounts of an acetylated metabolite have also been detected in urine; the plasma elimination half-life is reported to be about 15 hours in patients with normal renal function but is significantly prolonged in the elderly and in patients with renal impairment. The rate of elimination may be increased by acidification of the urine. Amantadine crosses the placenta and the bloodbrain barrier. It is also distributed into breast milk.
1. Aoki FY, Sitar DS. Clinical pharmacokinetics of amantadine hydrochloride. Clin Pharmacokinet 1988; 14: 35–51.

💊 Uses and Administration

Amantadine is a weak dopamine agonist with some antimuscarinic activity; it is also an antagonist at N-methylD-aspartate receptors. Amantadine has mild antiparkinsonian activity and is used in the management of parkinsonism, mainly in early disease when symptoms are mild. It may improve bradykinesia, rigidity, and tremor but tolerance can develop. Amantadine is also an antiviral that inhibits replication of influenza type A virus; it has very little or no activity against influenza type B virus. It is used prophylactically against infection with influenza type A virus and to ameliorate symptoms when given during the early stages of infection. Amantadine has also been used in the management of herpes zoster. Amantadine is usually given orally as the hydrochloride and the doses below are expressed in terms of this salt. In parkinsonism, treatment is usually started with 100 mg daily, increasing to 100 mg twice daily after a week or more. Doses up to a maximum of 400 mg daily have occasionally been used. The lowest effective dose should be used in patients over 65 years of age because of the potential for reduced renal clearance in this age group. Withdrawal of amantadine treatment for parkinsonism should be gradual to avoid exacerbating the condition; UK licensed product information suggests decreasing the dose by half at weekly intervals. The dose of amantadine in the UK for the treatment of influenza A is 100 mg daily, usually given for about 5 days. For the prophylaxis of influenza A the same dose is given for as long as protection from infection is required, which may be for about 6 weeks. If amantadine is being given with influenza vaccination then it is usually only given for up to 3 weeks after vaccination. Children aged 10 to 15 years may also be given 100 mg daily for the recommended period. A daily dose of less than 100 mg or 100 mg given at intervals greater than one day has been recommended for patients over 65 years of age. Doses in the USA are higher than those in the UK: for the treatment of influenza A the daily dose is 200 mg daily as a single dose or in two divided doses, continued for 24 to 48 hours after the disappearance of symptoms. The same dose is given for the prophylaxis of influenza A for at least 10 days following exposure. If given with vaccination then amantadine should be taken for the next 2 to 4 weeks. The dose of amantadine should be reduced to 100 mg daily in patients aged 65 years and over, and in those who show intolerance to the higher dose. Children aged 1 to 9 years may be given 4.4 to 8.8 mg/kg daily to a maximum of 150 mg daily; older children may be given 100 mg twice daily. In herpes zoster, treatment with 100 mg twice daily may be given for 14 days; if pain persists, treatment may be continued for a further 14 days. The dosage of amantadine should be reduced in patients with renal impairment (see below). Amantadine sulfate has been used similarly to the hydrochloride; it has been given by mouth or by intravenous infusion.


Amantadine sulfate has been used successfully in doses of up to 600 mg daily by intravenous infusion in the management of akinetic crisis in patients with Parkinson’s disease.1
1. Gadoth N, et al. I.V. amantadine sulfate for extrapyramidal crisis. Clin Pharm 1985; 4: 146.

Administration in renal impairment.

The dose of amantadine should be reduced in patients with renal impairment by either reducing the total daily dose or by increasing the dosage interval in accordance with their creatinine clearance (CC). In the UK the following doses are recommended:
CC over 35 mL/min: 100 mg daily
CC 15 to 35 mL/min: 100 mg every 2 to 3 days
CC less than 15 mL/min: not recommended In the USA the following doses are recommended:
CC 30 to 50 mL/min: 200 mg on the first day followed by 100 mg daily thereafter
CC 15 to 29 mL/min: 200 mg on the first day followed by 100 mg on alternate days
CC less than 15 mL/min or those on haemodialysis: 200 mg every 7 days See also under Precautions, above.

Extrapyramidal disorders.

Amantadine has been used as an alternative to antimuscarinics1 in the short-term management of drug-induced extrapyramidal symptoms. US licensed product information has recommended a usual dose of 200 mg daily in 2 divided doses increased up to 300 mg daily if necessary. However the development of tolerance has limited its usefulness. See also Parkinsonism, below. Amantadine has been investigated in the management of chorea in patients with Huntington’s disease.2,3
1. König P, et al. Amantadine versus biperiden: a double-blind study of treatment efficacy in neuroleptic extrapyramidal movement disorders. Neuropsychobiology 1996; 33: 80–4
2. Magnet MK, et al. Amantadine in the akinetic-rigid variant of Huntington’s disease. Ann Pharmacother 2004; 38: 1194–6
3. Heckmann JM, et al. IV amantadine improves chorea in Huntington’s disease: an acute randomized, controlled study. Neurology 2004; 63: 597–8.

Hepatitis C.

Amantadine has been investigated1-4 as an addition to interferon-based antiviral regimens in the treatment of chronic hepatitis C infection. A meta-analysis1 concluded that it was of no value in treatment-naive patients or relapsers, but that triple therapy with amantadine, ribavirin, and interferon improved sustained responses in patients previously unresponsive to therapy.
1. Deltenre P, et al. Evaluation of amantadine in chronic hepatitis C: a meta-analysis. J Hepatol 2004; 41: 462–73
2. Stauber RE, et al. Retreatment of patients with chronic hepatitis C not responding to interferon/ribavirin combination therapy with daily interferon plus ribavirin plus amantadine. Wien Klin Wochensc hr 2004; 116: 530–5
3. Herrine SK, et al. Peginterferon alpha-2a combination therapies in chronic hepatitis C patients who relapsed after or had a viral breakthrough on therapy with standard interferon alpha-2b plus ribavirin: a pilot study of efficacy and safety. Dig Dis Sci 2005; 50: 719–26
4. Mangia A, et al. A randomized controlled trial of pegylated interferon alpha-2a (40 KD) or interferon alpha-2a plus ribavirin and amantadine vs interferon alpha-2a and ribavirin in treatment-naive patients with chronic hepatitis C. J Viral Hepatitis 2005; 12: 292–9.


Amantadine1 has been reported to have produced beneficial results in patients with intractable hiccups.
1. Askenasy JJM, et al. Persistent hiccup cured by amantadine. N Engl J Med 1988; 318: 711.


Amantadine has been used similarly to rimantadine in the prophylaxis and treatment of influenza A. In adults, the two drugs are equally effective, but amantadine is associated with more adverse effects;1 further study on their safety and efficacy in children and the elderly is considered warranted.2 Amantadine reduced the duration of influenza A symptoms when given in a dose of 200 mg daily within 48 hours of the onset of symptoms.3 Vaccination is usually the method of choice for prophylaxis of influenza but amantadine has been used in addition to vaccination in certain individuals or when vaccination is contra-indicated. Although amantadine is licensed in the UK and USA for the prophylaxis and treatment of influenza A, its use for such purposes is not recommended.4-6 Resistance to amantadine may occur rapidly.7 For further information see Resistance, under Rimantadine.
1. Jefferson T, et al. Amantadine and rimantadine for influenza A in adults. Available in The Cochrane Database of Systematic Reviews; Issu
2. Chichester: John Wiley; 2006 (accessed 21/06/06)
2. Alves Galvão MG, et al. Amantadine and rimantadine for influenza A in children and the elderly. Available in The Cochrane Database of Systematic Reviews; Issu
1. Chichester: John Wiley; 2008 (accessed 29/05/08)
3. Nicholson KG, Wiselka MJ. Amantadine for influenza A. BMJ 1991; 302: 425–6
4. NICE. Guidance on the use of zanamivir, oseltamivir and amantadine for the treatment of influenza: Technology Appraisal 58 (issued February 2003). Available at: nicemedia/pdf/58_Flu_fullguidance.pdf (accessed 11/08/08
5. NICE. Guidance on the use of oseltamivir and amantadine for the prophylaxis of influenza: Technology Appraisal 67 (issued September 2003). Available at: pdf/67_Flu_prophylaxis_guidance.pdf (accessed 11/08/08
6. CDC. Prevention and control of influenza: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR 2007; 56 (RR-6): 1–54. Also available at: http:// (accessed 09/10/07
7. Bright RA, et al. Incidence of adamantane resistance among influenza A (H3N2) viruses isolated worldwide from 1994 to 2005: a cause for concern. Lancet 2005; 366: 1175–81.

Multiple sclerosis.

Amantadine has been used to alleviate fatigue associated with multiple sclerosis. However, a systematic review1 concluded that there was insufficient evidence to support its use in reducing fatigue in patients with multiple sclerosis; further large controlled studies are considered warranted.
1. Pucci E, et al. Amantadine for fatigue in multiple sclerosis. Available in The Cochrane Database of Systematic Reviews; Issu
1. Chichester: John Wiley; 2007 (accessed 29/05/08).

Neuroleptic malignant syndrome.

Amantadine has been tried1-3 in the treatment of the neuroleptic malignant syndrome.
1. McCarron MM, et al. A case of neuroleptic malignant syndrome successfully treated with amantadine. J Clin Psychiatry 1982; 43: 381–2
2. Amdurski S, et al. A therapeutic trial of amantadine in haloperidol-induced malignant neuroleptic syndrome. Curr Ther Res 1983; 33: 225–9
3. Woo J, et al. Neuroleptic malignant syndrome successfully treated with amantadine. Postgrad Med J 1986; 62: 809–10.


Amantadine’s mechanism of action in parkinsonism is unclear but may be due to its antimuscarinic activity and alterations in dopamine release and reuptake. It has also been suggested that amantadine’s action as a non-competitive antagonist of N-methylD-aspartate may have a beneficial effect.1,2 It has mild antiparkinsonian activity compared with levodopa but is relatively free from adverse effects. It can improve bradykinesia as well as tremor and rigidity and is used in a similar manner to antimuscarinics mainly in the treatment of patients with early Parkinson’s disease when symptoms are mild. It may also be useful for dyskinesias in more advanced disease.3 However, few patients obtain much benefit and tolerance to its effects can occur. Moreover, two systematic reviews4,5 concluded that there was insufficient evidence from randomised controlled trials on the safety and efficacy of amantadine in the treatment of both Parkinson’s disease and levodopa-induced dyskinesias in late disease. Licensed product information suggests that the effectiveness of amantadine may be prolonged by withdrawing it for 3 to 4 weeks, continuing with existing antiparkinsonian therapy or starting low-dose levodopa treatment if clinically necessary in the meantime.
1. Laing P. Stroke treatment. Lancet 1991; 337: 1601
2. Greenamyre JT, O’Brien CF. N-Methyl-aspartate antagonists in the treatment of Parkinson’s disease. Arch Neurol 1991; 48: 977–81
3. Thomas A, et al. Duration of amantadine benefit on dyskinesia of severe Parkinson’s disease. J Neurol Neurosurg Psychiatry 2004; 75: 141–3
4. Crosby N, et al. Amantadine in Parkinson’s disease. Available in The Cochrane Database of Systematic Reviews; Issu
1. Chichester: John Wiley; 2003 (accessed 16/02/06)
5. Crosby NJ, et al. Amantadine for dyskinesia in Parkinson’s disease. Available in The Cochrane Database of Systematic Reviews; Issu
2. Chichester: John Wiley; 2003 (accessed 16/02/06).

Withdrawal syndromes.

COCAINE. Despite some early promising results a systematic review1 considered that there was no evidence to support the use of dopamine agonists, including amantadine, in the treatment of cocaine dependence.
1. Soares B, et al. Dopamine agonists for cocaine dependence. Available in The Cochrane Database of Systematic Reviews; Issu
2. Chichester: John Wiley; 2003 (accessed 16/02/06).

💊 Preparations

BP 2008: Amantadine Capsules; Amantadine Oral Solution; USP 31: Amantadine Hydrochloride Capsules; Amantadine Hydrochloride Syrup.

Proprietary Preparations

Arg.: Actison; Ampakine; Virosol; Austral.: Symmetrel; Austria: Amant; Hofcomant; PK-Merz; Virucid†; Belg.: Amantan; Braz.: Mantidan; Canad.: Endantadine; Symmetrel; Chile: PK-Merz†; Prayanol; Cz.: Amantadol; PKMerz; Viregyt-K; Fin.: Atarin; Fr.: Mantadix; Ger.: Adekin; Aman†; Amanta; Amantagamma; Amixx; AMT†; InfectoFlu; Infex; PK-Merz; tregor; Gr.: Hofcomant†; PK-Merz†; Symmetrel; Hong Kong: PK-Merz; Symmetrel†; Hung.: PK-Merz; Viregyt; India: Amantrel; Irl.: Symmetrel; Israel: A-Parkin; Influ-A†; Paritrel; PK-Merz; Ital.: Mantadan; Malaysia: PK-Merz; Mex.: Kinestrel; Padiken†; PK-Merz; Neth.: Symmetrel; NZ: Symmetrel; Philipp.: PK-Merz; Pol.: Amantix; Viregyt K; Port.: Parkadina; Profil†; S.Afr.: Antadine†; Symmetrel; Singapore: Symmetrel; Switz.: PK-Merz; Symmetrel; UK: Lysovir; Symmetrel; USA: Symmetrel; Venez.: Symmetrel†. Multi-ingredient: Mex.: Antiflu-Des; Fluviatol; Rosel.
Published October 12, 2018.