Ipcaquin is a 4-aminoquinoline antimalarial with a similar mode of action to chloroquine.

Amodiaquine is an antimalarial with schizonticidal activity. It is effective against the erythrocytic stages of all 4 species of plasmodium. It is as effective as chloroquine against chloroquine-sensitive strains of Plasmodium falciparum and is also effective against some chloroquine-resistant strains.

Amodiaquine accumulates in the lysosomes and brings about loss of function. The parasite is unable to digest haemoglobin on which it depends for its energy.In general, 4-aminoquinolines derivatives appear to bind to nucleoproteins and inhibit DNA and RNA polymerase. High drug concentrations are found in the malaria parasite's digestive vacuoles.

Amodiaquine hydrochloride is readily absorbed from gastrointestinal tract. Amodiaquine is rapidly converted in the liver to the active metabolite desethylamodiaquine. Only a negligible amount of amodiaquine is being excreted unchanged in the urine. The plasma elimination half-life of desethylamodiaquine has varied from 1 to 10 days or more. About 5% of the total administered dose is recovered in urine while the rest is metabolised in the body. Amodiaquine and desethylamodiaquine have been detected in the urine several months after administration.

It is indicated in the treatment of acute attacks (febrile stage) of malaria caused by Plasmodium falciparum (either chloroquine sensitive or chloroquine resistant strains). It has also been employed successfully in the treatment of vivax and malariae infections. Since it acts on the erythrocytic forms of malaria parasites only and not on the asexual forms or the tissue forms of the parasite, a tissue schizonticidal drug should also be used later for eradication of malaria. However, it rapidly controls the clinical manifestations of the disease- fever and headache are generally brought under control within 24-48 hrs. after administration of the drug.

Because of its toxic side effects, it is not recommended for chemoprophylaxis of malaria.

Amodiaquine tablets are contraindicated in patients with known hypersensitivity to amodiaquine or 4-aminoquinolines. Because of resistance and risk of major toxicity, amodiaquine is not recommended for the prophylaxis of malaria. Amodiaquine is also contraindicated in patients with hepatic disorders.

Amodiaquine is no longer recommended for chemoprophylaxis of falciparum malaria because its use is associated with hepatic toxicity and agranulocytosis.

Severe neutropenia can occur. Large doses of amodiaquine have been reported to produce syncope, spasticity, convulsions and involuntary movements.

Amodiaquine may cause blood dyscrasias, hepatitis, peripheral neuropathy and haemolytic anaemia. If long term therapy is given, regular ophthalmic examination is recommended.

Because amodiaquine may concentrate in the liver, the drug should be used with caution in patients with hepatic disease or alcoholism and in patients receiving hepatotoxic drugs.

Since hemolysis and acute renal failure has been reported to occur in a few patients with glucose 6-phosphate dehydrogenase deficiency receiving chloroquine, this should also be considered when using amodiaquine.

Since chloroquine, a 4-aminoquinoline, has been reported to provoke seizures, amodiaquine should be used with care in patients with a history of epilepsy. Caution is also required in patients with psoriasis, since chloroquine has caused exacerbation of psoriasis.

Agranulocytosis and other blood dyscrasias, hepatitis and peripheral neuropathy have been reported occasionally after amodiaquine usage alone. Administration of quinoline type drugs has been associated with hemolytic anaemia.

In therapeutic doses used for malaria. amodiaquine may occasionally cause nausea, vomiting, diarrhoea, vertigo and lethargy. Abdominal pain, headache and photosensitivity have been reported with amodiaquine. When given for long periods, it sometimes causes corneal deposits, visual disturbances and bluish - grey pigmentation of the finger nails, skin and hard palate. These reactions clear somewhat slowly, on stopping treatment. However, because of the occasional development of irreversible retinopathy, regular ophthalmic examinations should be carried out if the drug is used over a long period. The drug can also cause irregular heart beats and tremors.

Prophylactic use of amodiaquine is associated with an unacceptably high incidence of serious toxicity. Approximately 1 in 2000 patients develop agranulocytosis. Serious hepatotoxicity has also been reported. Minor adverse effects are similar to those of chloroquine, although pruritus is less of a problem.

Amodiaquine is administered over 3 days at total doses ranging between 25 mg and 35 mg of amodiaquine base per kg in dosage regimens similar to those for chloroquine. At present there is no evidence that the higher doses are associated with either improved efficacy or increased toxicity. A regimen of 10 mg of amodiaquine base per day for 3 days (total dose 30 mg/kg) is recommended as it may offer the advantage of simplicity.

Suggested guidelines for different strengths as per age group and weight are as follows:

Intoxication with amodiaquine is far less frequent than chloroquine poisoning. However, large doses of amodiaquine have been reported to produce syncope, spasticity, convulsions and involuntary movements.

The usual signs and symptoms of an overdose are headache, vertigo and vomiting; the more severe manifestations including cardiac arrhythmias, convulsions and coma. The most dramatic feature is visual disturbance, including sudden loss of vision, which is usually transitory. Other symptoms include itching, cardiovascular abnormalities, dyskinesia, neuromuscular and haematological disorders and hearing loss.

Nausea, vomiting, diarrhoea, headache, drowsiness, blurred vision, blindness, convulsions, coma, hypotension, cardiac arrhythmias, cardiac arrest, and impaired respiration are the characteristic features of amodiaquine poisoning. ECG may show inverted or flattened T waves, widening of QRS, ventricular tachycardia and fibrillation. Hypokalemia may be present.

Treatment of overdosage is supportive and must be prompt since acute toxicity can progress rapidly, possibly leading to vascular collapse and respiratory and cardiac arrest.

Early endotracheal intubation and mechanical ventilation may be necessary. Early gastric lavage followed by administration of activated charcoal may provide some benefit in reducing absorption of the drug. These should be preceded by measures to correct cardiac and severe cardiovascular disturbances, if present and by respiratory support. Diazepam IV may control seizures and other manifestations of CNS stimulation. Seizures caused by anoxia should be corrected by oxygen and other respiratory support. Defibrillators and cardiac pacemakers may be required.

Keep in a cool place away from light.

50 strips of 3 tablets each