Table 2.

Antimalarial formulation based on active drug targeting mechanism

S. no.	Drug	Formulation	Targeting organ	Receptor	Ligand	Comments	Reference
1.	Primaquine (PQ)	PEGylated galactosylated nanostructured lipid carriers (NLCs)	Liver	Asialoglycoprotein receptor (ASGP-R)	Galactose	Sustained drug release improved antiparasitic effect against chloroquine-resistant strain, selective accumulation of NLCs with contents in liver	[23]
2.	–	“PS specific peptide (PSP)”–conjugated liposomes (PSP-liposomes)	RBC	Phosphatidylserine (PS)	“PS specific peptide (PSP)”	Could deliver higher amount of drug to iRBCs, cause RBC eryptosis	[24]
3.	Chloroquine phosphate	Chitosan nanoparticles (CSN)	RBC	GLUT-1	Dehydroascorbic acid (DHA)	CSN better uptake with and preferential iRBCs targeting. At 1 nM could inhibit parasite proliferation	[22]
4.	Pyronaridine and atovaquone	Immunoliposome	RBC	Glycophorin A	Antibodies against glycophorin A	Immunoliposomal nanovector loaded with hydrophilic and lipophilic drugs exhibits significantly higher activity.	[25]
5.	Aminoquinoline and amino alcohol	ImmunoPEGliposomes	RBC	Glycophorin A	Mouse monoclonal IgG2b antihuman GPA (SM3141P) and rat monoclonal IgG2b antimouse TER-119 (AM31858PU-N)	Significant reduction in blood-stage parasitemia with significantly better effect than plain liposomes	[26]
6.	Artemisinin (ART)	TF-ART-NLCs	Brain (cerebral malaria)	Transferrin receptor	Transferrin (TF)	NLCs entrapped ART could express higher toxicity on the U-87 MG cell line.	[27]
7.	Artemether	Glyceryl-dilaurate nanolipid carriers (GDL-NLCs)	RBC	Parasitic mitochondria	GDL	GDL-NLCs lead to the mitochondrial membrane polarization, Ca (2+) ion accumulation, ROS release, and stage-specific lysis of the infected RBCs resulted in iRBCs fast clearance. It could disrupt TVN and restore the flexibility of the infected RBCs.	[28]
8.	Chloroquine (CQ)	Solid lipid nanoparticle (SLN)	RBC	GAG-like receptors	Heparin	Resulted in better antiparasitic value against chloroquine-resistant with IC50 value of 4.72 ± 0.14	[29]