Quinine is one of several alkaloids derived from the bark of the cinchona tree. The mechanism by which it exerts its antimalarial activity is not known. It does not bind to DNA at antimalarial dosages. It may poison the parasite's feeding mechanism, and it has been termed a general protoplasmic poison, since many organisms are affected by it.

Quinine is rapidly absorbed following oral ingestion, with peak blood levels achieved in 1 to 4 hours. About 70 to 93% of the drug is bound to plasma proteins, depending on the severity of the infection. Quinine is extensively metabolized, with only about 20% of the parent compound eliminated in the urine.

The primary present-day indication for quinine and its isomer, quinidine, is in the intravenous treatment of severe manifestations and complications of chloro-quine-resistant malaria caused by P. falciparum.

Aside from its use as an antimalarial compound, quinine is used for the prevention and treatment of nocturnal leg muscle cramps, especially those resulting from arthritis, diabetes, thrombophlebitis, arteriosclerosis, and varicose veins.

Cinchonism describes the toxic state induced by excessive plasma levels of free quinine. Symptoms include sweating, ringing in the ears, impaired hearing, blurred vision, nausea, vomiting, and diarrhea. Quinine is a potent stimulus to insulin secretion and irritates the gastrointestinal mucosa. Also, a variety of relatively rare hematological changes occur, including leukopenia and agranulocytosis. Quinine is potentially neurotoxic in high dosages, and severe hypotension may follow its rapid intravenous administration.

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