Malaria is one of the most common diseases in developing countries and
poses a great challenge to world health. Resistance of malaria parasites
to available antimalarial drugs remains the main challenge to the
effective control of the disease. The physiological conditions
prevailing with in the acidic digestive vacuoles of the malaria
parasites provide a suitable physiochemical environment for conversion
of heam to beta-hematin/hemozoin. Though the both protein as well as
lipids mediated beta-hematin formation remain valid hypothesis but later
seems to be more relevant, when mechanism of hemozoin synthesis is
considered as a simple physiochemical reaction. Some repeats earlier
heme show loss of beta-hematin formation activity of the parasite lysate
by protenase K and heat treatment. The digestion of this cytosol, which
consists essentially of hemoglobin results in the formation of
potentially toxic ferriprotoporphyrin IX (FP). Several antimalarial
drugs are thought to exert their effect by complexing with FP, thus
inhibiting its detoxification through polymerization to hemozoin. Our
aim shows that inhibition of heam polymerization by Arteether.