P: Antiparasitic products, insecticides and repellents

ATC group P for modelers: life cycle stages as separate targets, parasitemia decline as the endpoint, and wide patient-driven variability.
Modified

September 22, 2026

Drugs directed at eukaryotic parasites: protozoa, helminths and ectoparasites. Their targets resemble host cells far more closely than a bacterium does, so selective targets are harder to find [1,2], though the therapeutic window varies sharply across the group rather than being uniformly narrow.

A fourth-century recipe by Ge Hong said to wring qinghao out in cold water, so Tu Youyou switched to low-temperature ether extraction. Her extract 191, dated 4 October 1971, gave complete inhibition of rodent malaria, and artemisinin won her a share of the 2015 Nobel Prize [3].

Table 1: ATC P level 2 codes
Level 2 code Description In plain terms Example drug
P01 Antiprotozoals kill single-celled parasites: malaria, amoebiasis, giardiasis Artemether/lumefantrine (P01BF01) / metronidazole (P01AB01)
P02 Anthelmintics deworming drugs against parasitic worms Albendazole (P02CA03) / praziquantel (P02BA01)
P03 Ectoparasiticides, incl. scabicides, insecticides and repellents kill skin parasites: scabies mites, lice; repellents Permethrin (P03AC04) / diethyltoluamide, i.e. DEET (P03BX01)

Modeling notes

Life cycle stages are separate targets. A drug active against one stage may be inactive against the next [4,5], so the model must declare which stage the effect attaches to. Synchronized replication, sequestration of mature forms and dormant liver forms all produce behavior a direct-effect model on total burden will not reproduce [6,7].

Endpoint. Parasitemia decline for the blood-dwelling protozoa [8], estimated as a clearance slope from the whole profile rather than a single visit [9,10]. For helminths it is the faecal egg count, reported as cure rate and egg reduction rate [11,12].

Variability is wide, and mostly about the patient. Endemic populations skew pediatric, so weight-band dosing [13,14] and allometric scaling with maturation [15] are the starting point. For the lipophilic agents, fat-dependent absorption is the first thing to characterize: a normal meal roughly doubles lumefantrine bioavailability [16,17].

References

[1]
Chan JD et al. Polypharmacology of anthelmintics at host and parasite ion channels. PLoS Pathogens 2026. https://doi.org/10.1371/journal.ppat.1013977.
[2]
Horn D et al. Antiparasitic chemotherapy: From genomes to mechanisms. Annual Review of Pharmacology and Toxicology 2014. https://doi.org/10.1146/annurev-pharmtox-011613-135915.
[3]
Su X-Z, Miller LH. The discovery of artemisinin and the Nobel Prize in Physiology or Medicine. Science China Life Sciences 2015;58:1175–9. https://doi.org/10.1007/s11427-015-4948-7.
[4]
Delves M et al. The activities of current antimalarial drugs on the life cycle stages of plasmodium: A comparative study with human and rodent parasites. PLoS Medicine 2012. https://doi.org/10.1371/journal.pmed.1001169.
[5]
White NJ et al. Malaria. The Lancet 2014. https://doi.org/10.1016/S0140-6736(13)60024-0.
[6]
Saralamba S et al. Intrahost modeling of artemisinin resistance in plasmodium falciparum. Proceedings of the National Academy of Sciences of the United States of America 2011. https://doi.org/10.1073/pnas.1006113108.
[7]
Hodel EM et al. Incorporating stage-specific drug action into pharmacological modeling of antimalarial drug treatment. Antimicrobial Agents and Chemotherapy 2016. https://doi.org/10.1128/aac.01172-15.
[8]
Krause A et al. Pharmacokinetic/pharmacodynamic modelling of the antimalarial effect of Actelion-451840 in an induced blood stage malaria study in healthy subjects. British Journal of Clinical Pharmacology 2016. https://doi.org/10.1111/bcp.12962.
[9]
Flegg JA et al. Standardizing the measurement of parasite clearance in falciparum malaria: The parasite clearance estimator. Malaria Journal 2011. https://doi.org/10.1186/1475-2875-10-339.
[10]
Stepniewska K et al. In vivo parasitological measures of artemisinin susceptibility. The Journal of Infectious Diseases 2010. https://doi.org/10.1086/650301.
[11]
Moser W et al. One mean to rule them all? The arithmetic mean based egg reduction rate can be misleading when estimating anthelminthic drug efficacy in clinical trials. PLoS Neglected Tropical Diseases 2020. https://doi.org/10.1371/journal.pntd.0008185.
[12]
Brussee JM et al. Population pharmacokinetics and exposure-response analysis of tribendimidine to improve treatment for children with hookworm infection. Antimicrobial Agents and Chemotherapy 2021. https://doi.org/10.1128/aac.01778-20.
[13]
Waalewijn H et al. Simplifying medicine dosing for children by harmonising weight bands across therapeutic areas. The Lancet Child & Adolescent Health 2025;9:274–82. https://doi.org/10.1016/S2352-4642(25)00025-2.
[14]
Banda CG, Tarning J, Barnes KI. Use of population pharmacokinetic-pharmacodynamic modelling to inform antimalarial dose optimization in infants. British Journal of Clinical Pharmacology 2025;91:968–80. https://doi.org/10.1111/bcp.16132.
[15]
Germovsek E, Barker CI, Sharland M, Standing JF. Scaling clearance in paediatric pharmacokinetics: All models are wrong, which are useful? British Journal of Clinical Pharmacology 2017;83:777–90. https://doi.org/10.1111/bcp.13160.
[16]
Ezzet F, Vugt M van, Nosten F, Looareesuwan S, White NJ. Pharmacokinetics and pharmacodynamics of lumefantrine (benflumetol) in acute falciparum malaria. Antimicrobial Agents and Chemotherapy 2000;44:697–704. https://doi.org/10.1128/aac.44.3.697-704.2000.
[17]
Jain JP, Leong FJ, Chen L, Kalluri S, Koradia V, Stein DS, et al. Bioavailability of lumefantrine is significantly enhanced with a novel formulation approach, an outcome from a randomized, open-label pharmacokinetic study in healthy volunteers. Antimicrobial Agents and Chemotherapy 2017;61:e00868–17. https://doi.org/10.1128/aac.00868-17.