The original antimalarial agent, quinine took its name from the Peruvian Indian word "kina" meaning "bark of the tree" referring to the cinchona tree. From this tree, quinine was first obtained. The Peruvian Indians called it "the fever tree."

Quinine, a large and complex molecule, is the most important alkaloid found in cinchona bark. Until World War I, it was the only effective treatment for malaria. In fact, quinine was the first chemical compound to be successfully used to treat an infectious disease.

Quinine was isolated in crystalline form in 1820 by J.B. Caventou and P.J. Pelletier. In one of the classical achievements of synthetic organic chemistry, R.B. Woodward and W. Doering first made synthetic quinine in 1944.

Quinine acts by interfering with the growth and reproduction of the Plasmodium, the malarial parasite that lives within the victim's red blood cells. Quinine causes the parasites to disappear from the blood and the symptoms of the disease are thereby alleviated. However, when quinine treatment ends, many patients relapse. They suffer another attack of malaria due to the failure of quinine to kill the malarial parasites in cells of the body other than the red blood cells. These parasites persist and, after a time, they reinvade the red blood cells and precipitate the relapse.

Since quinine does not permanently cure malaria, better drugs were sought. A number were discovered that replaced quinine during and after World War II. Some of these drugs (such as chloroquine and chloroguanide) are more effective than quinine in suppressing the growth of the blood forms of the malarial parasite. Others (such as primaquine and pyrimethamine) act upon both the blood and tissue phases of the parasite, producing a complete cure and preventing a relapse.

Quinine has been used outside of malaria as a remedy for fever and pain and to treat and prevent leg cramps. Prolonged administration of quinine may produce toxic symptoms such as deafness, disturbances in vision, skin rashes, and digestive upsets.