Mechanism of action Like chloroquine,<unk>  is thought to function by accumulating in the parasite digestive vacuole and interfering with the detoxification of heme into hemozoin. Resistance Parasites that survive<unk>  treatment have been increasingly reported since 2010, particularly in Southeast Asia. The epicenter of<unk>  resistance appears to be western Cambodia where in 2014 over 40% of dihydroartemisinin-piperaquine treatments failed to eliminate parasites from the patient's blood. Characterizing<unk> -resistant parasites has been technically challenging, as parasites that survive<unk>  treatment in patients appear to remain sensitive to<unk>  in vitro; i.e.<unk>  appears to have the same IC50 in sensitive parasites and resistant parasites. The mechanism by which parasites become resistant to<unk>  remains unclear. Amplification of the parasite proteases plasmepsin 2 and plasmepsin 3, both involved in degrading host hemoglobin, is associated with resistance to<unk> . Similarly, mutations in a gene related to chloroquine resistance, PfCRT, have been associated with<unk>  resistance; however, parasites that are resistant to chloroquine remain sensitive to<unk> . In contrast, amplification of the gene for the parasite transporter PfMDR1, a mechanism of parasite resistance to mefloquine, is inversely correlated with<unk>  resistance. Pharmacokinetics<unk>  is a lipophilic drug and therefore is rapidly absorbed and distributed across much of the body. The drug reaches its maximal concentrations approximately 2 hours after administration.
Piperaquine
Primaquine
Tafenoquine
Artemether
Amodiaquine
Chloroquine
Mefloquine
Delamanid