Final answer:
Antimalarial drugs like artemisinin produce reactive oxygen species to damage parasites, while repurposed drugs such as doxycycline inhibit protein synthesis or folate synthesis in the parasite. Combination therapies like ACT use both rapid-acting and long-acting drugs to combat resistance.
Step-by-step explanation:
Antimalarial drugs work by targeting different stages of the Plasmodium parasite's life cycle within the human host, thereby preventing or treating malaria. For instance, artemisinin and its derivatives, some of the most effective antimalarial drugs, likely act as prodrugs that produce reactive oxygen species (ROS) when metabolized, leading to the damage of target cells. These reactive oxygen species are believed to interfere with the parasite's life cycle, thus helping to clear the infection. Another approach involves repurposed drugs like doxycycline, a synthetic tetracycline, which has shown prophylactic efficacy against malaria. Doxycycline is thought to work by inhibiting the protein synthesis of the parasite. Additionally, antibiotics such as clindamycin and sulfonamide disrupt folate synthesis, a crucial process for the parasite's nucleic acid production. These drugs not only treat malaria but also serve as preventive measures. Due to the rise in drug-resistant strains of malaria, there is a push for combination therapies; for example, the use of artemisinin-based combination therapy (ACT) merges the rapid but short-lived efficacy of artemisinins with longer-acting drugs like quinolines. This approach not only hastens recovery but also mitigates the risk of the parasite developing resistance to the medications.