**7. Current drugs are available in the market for malaria**

Utmost of the antimalarial drugs aim at the asexual erythrocytic stages of the parasite, therefore named blood schizonticidal drugs. Tissue schizonticidal drugs mark the hypnozoites (dormant stage of the parasite) in the liver, while gametocytocidal drugs destroy sexual erythrocytic formulae of the parasite in the bloodstream and thus inhibit transmission of malaria to mosquito. Sporontocides stop or inhibit the formation of malarial oocysts and sporozoites in an infected mosquito. Chloroquine, quinine, and mefloquine are typically fast-acting schizonticidal drugs. Pyrimethamine, sulphonamides, and sulphone also possess schizonticidal activities, nevertheless, their action is dawdling (**Table 2**). Primaquine, Tafenoquine, and other novel kinase inhibitors have gametocidal activities. The main sporontocidal drugs are primaquine and praguanil. These antimalarial drugs were considered based on major metabolic differences of the malaria parasite with its host. Nucleic acid metabolism, heme toxification, oxidative stress, and fatty acid biosynthesis are some of the major pathways that were targeted mostly for antimalarial drug design. However, in the chemotherapy of malaria, the emergence of resistance to the available drugs is the major obstacle.

Furthermost of the existing antimalarial drugs have been used for decades and now their use is restricted by the emergence of drug resistance. According to various literature, there are no existing anti-malarial drugs that were developed in a fully rational manner, with a focused attempt to inhibit a known drug target [35, 36, 47]. Instead, in all cases, anti-malarial potency has been identified in animal or *in vitro* model studies. Consequently, the target of action for most existing agents inside the malaria parasite remains indeterminate.
