Side effects in humans may include poor coordination, abdominal pain, vomiting, headache, and allergic reactions.[5] While it may be used during pregnancy, it is not recommended for use during breastfeeding.[5] Praziquantel is in the anthelmintic class of medications.[4] It works partly by affecting the function of the worm's sucker.[4]
The majority of side effects develop due to the release of the contents of the parasites as they are killed and the consequent host immune reaction. The heavier the parasite burden, the heavier and more frequent the side effects normally are.[25]
Central nervous system (CNS): Frequently occurring side effects are dizziness, headache, and malaise. Drowsiness, somnolence, fatigue, and vertigo have also been seen. Almost all patients with cerebral cysticercosis experience CNS side effects related to the cell-death of the parasites (headache, worsening of pre-existing neurological problems, seizures, arachnoiditis, and meningism). These side effects may be life-threatening and can be reduced by coadministration of corticosteroids. All patients with cerebral cysticercosis are strongly recommended to be hospitalized during treatment.
Gastrointestinal tract: About 90% of all patients have abdominal pain or cramps with or without nausea and vomiting. Diarrhea may develop and may be severe with colic. Sweating, fever, and sometimes bloody stools may occur together with diarrhea. Praziquantel also has a bitter taste that can result in gagging or vomiting.[26]
Liver: Asymptomatic and transient increases of liver enzymes (AST and ALT) are noted frequently (up to 27%). No case of symptomatic liver damage has been seen so far.
Other locations/body as a whole: Lower back pain, myalgia, arthralgia, fever, sweating, various cardiac arrhythmias, and hypotension
Pregnancy
The WHO states praziquantel is safe during pregnancy (although does not recommend use during the first trimester).[27][28] Animal studies have failed to reveal evidence of fetal harm. Praziquantel is effective in reducing schistosomiasis during pregnancy.[29] Another trial found that treatment with praziquantel did not increase the rates of low birthweight, fetal death, or congenital anomalies.[30]
Experimental evidence indicates praziquantel increases the permeability of the membranes of schistosome cells towards calcium ions. The drug thereby induces contraction of the parasites' muscle, resulting in paralysis in the contracted state. Another early effect of praziquantel on schistosomes is morphological disruption of the tegumental surface of the worm, exposing parasite antigens to the host immune system, and likely rendering the parasite more susceptible to host immune attack.[36] The dying parasites are dislodged from their site of action in the host organism and may enter systemic circulation or may be destroyed by host immune reaction (phagocytosis). Additional mechanisms including focal disintegrations and disturbances of oviposition (laying of eggs) are seen in other types of sensitive parasites.[37]
Praziquantel is administered as a racemate; the (R)-enantiomer has greater antiparasitic activity than the (S)-enantiomer, both in vitro and in vivo; the enantiomers may be separated using a resolution of an amine obtained from praziquantel, as well as by other methods.[38]
Praziquantel is not effective against juvenile (3-4 week post-infection) mammalian-stage schistosomes, a property that has implications for efficacy and timing of drug treatment.[39]
The primary molecular target of the drug appears to be TRPMPZQ, a Ca2+-permeable transient receptor potential (TRP) ion channel that is found in schistosomes and other praziquantel-sensitive platyhelminths.[40] TRPMPZQ is a voltage-independent channel that is a member of the TRPM family of the TRP ion channel superfamily.[41][42] The active (R)-enantiomer of praziquantel activates Schistosoma mansoni TRPMPZQ with an EC50 of 597 nM (154 nM at 37°C); the EC50 for the less biologically active (S)-enantiomer is 27.9 μM. TRPMPZQ is also found in the praziquantel-insensitive liver fluke, Fasciola hepatica, but exhibits a critical amino acid change in the praziquantel binding pocket from asparagine to threonine, resulting in insensitivity to activation of the channel by praziquantel. Schistosomes selected for diminished sensitivity to praziquantel exhibit reduced levels of TRPMPZQ expression.[40] The physiological role of TRPMPZQ in the parasite is currently unknown.[40]
Interestingly, the inactive (S)-enantiomer of praziquantel activates a human TRPM8 channel, and it has been suggested that this interaction may enhance a praziquantel-induced elimination of schistosomes by increasing vascular contraction in host mesenteric vessels, where parasites may reside (the interaction with TRPM8 may as well be responsible for the unpleasant taste of the drug).[43]
Although TRPMPZQ appears to be the primary target of praziquantel, it is clear that praziquantel also interacts with other targets. These include a platyhelminth-specific voltage-gated calcium channel β subunit that, when paired with an α1 subunit, results in activation of the expressed channel by 100 nM praziquantel.[44] Praziquantel is also an inhibitor of, and a likely substrate for, a schistosome P-glycoprotein-like multidrug resistance transporter. Increased expression of this or another schistosome multidrug resistance transporter correlates with reduced sensitivity to praziquantel, while inhibition or knockdown of expression of these proteins increases worm responsiveness to praziquantel.[45][46] Another hypothesis for praziquantel mode of action is that it interferes with adenosine uptake in schistosomes.[47] This effect may have therapeutic relevance given that schistosomes, as well as Taenia and the Echinococcus (other praziquantel-sensitive parasites), are unable to synthesize purines, such as adenosine, de novo.[48]
Bayer's Animal Health Division website states, "Praziquantel is active against cestodes (tapeworms). Praziquantel is absorbed, metabolized in the liver, and excreted in the bile. Upon entering the digestive tract from the bile, cestocidal activity is exhibited. Following exposure to praziquantel, the tapeworm loses its ability to resist digestion by the mammalian host. Because of this, whole tapeworms, including the scolices (plural of "scolex"), are very rarely passed after administration of praziquantel. In many instances, only disintegrated and partially digested pieces of tapeworms will be seen in the stool. The majority of tapeworms are digested and are not found in the feces."[49][50]
Pharmacokinetics
Praziquantel is well absorbed (about 80%) from the gastrointestinal tract. However, due to extensive first-pass metabolism, only a relatively small amount enters systemic circulation. Praziquantel has a serumhalf-life of 0.8 to 1.5 hours in adults with normal renal and liver function. Metabolites have a half-life of 4 to 5 hours. In patients with significantly impaired liver function (Child-Pugh score B and C), the serum half-life is increased to 3 to 8 hours. Praziquantel and its metabolites are mainly excreted renally; within 24 h after a single oral dose, 70 to 80% is found in urine, but less than 0.1% as the unchanged drug. Praziquantel is metabolized through the cytochrome P450 pathway via CYP3A4. Agents that induce or inhibit CYP3A4 such as phenytoin, rifampin, and azole antifungals will affect the metabolism of praziquantel.[32][51]
Praziquantel has a particularly dramatic effect on patients with schistosomiasis. Studies of those treated have shown that within six months of receiving a dose of praziquantel, up to 90% of the damage done to internal organs due to schistosomiasis infection can be reversed.[16]
History
Praziquantel was developed in the laboratories for parasitological research of Bayer AG and Merck KGaA in Germany (Elberfeld and Darmstadt) in the mid-1970s.[52]
Interceptor Plus chewable tablets (combination with milbemycin) (Elanco) for veterinary use. Note regular Interceptor only has milbemycin and does not contain praziquantel.
Praziquantel is on the World Health Organization's List of Essential Medicines.[6]
Praziquantel is not licensed for use in humans in the UK, but it can be imported when necessary on a named-patient basis.[54] It is available in the UK as a veterinary anthelmintic.
Praziquantel is approved in the US for the treatment of schistosomiasis and liver flukes, although it is effective in other infections.[55]
In March 2025, the Committee for Veterinary Medicinal Products of the European Medicines Agency adopted a positive opinion, recommending the granting of a marketing authorization for the veterinary medicinal product 'Prazivetin premix for medicated feeding stuff' intended for sea bream.[2] The applicant for this veterinary medicinal product is Vethellas S.A.[2] The main benefit of Prazivetin is its efficacy against infestations of the gills caused by the monogeneanSparicotyle chrysophrii.[2] Praziquantel was authorized for veterinary use in the European Union in April 2025.[2][3]
123456"Prazivetin EPAR". European Medicines Agency (EMA). 13 March 2025. Retrieved 19 March 2025. Text was copied from this source which is copyright European Medicines Agency. Reproduction is authorized provided the source is acknowledged.
123"Prazivetin PI". Union Register of medicinal products. 28 April 2025. Retrieved 3 May 2025.
123456"Praziquantel". The American Society of Health-System Pharmacists. Archived from the original on 20 December 2016. Retrieved 8 December 2016.
12World Health Organization (2023). The selection and use of essential medicines 2023: web annex A: World Health Organization model list of essential medicines: 23rd list (2023). Geneva: World Health Organization. hdl:10665/371090. WHO/MHP/HPS/EML/2023.02.
↑Mas-Coma S, Bargues MD, Valero MA (October 2005). "Fascioliasis and other plant-borne trematode zoonoses". International Journal for Parasitology. 35 (11–12): 1255–1278. doi:10.1016/j.ijpara.2005.07.010. PMID16150452.
↑Rim HJ, Chu DS, Lee JS, Joo KH, Won CY (December 1978). "[Anthelmintic Effects Of Various Drugs Against Metagonimiasis]". Kisaengch'unghak Chapchi. The Korean Journal of Parasitology. 16 (2): 117–122. doi:10.3347/kjp.1978.16.2.117. PMID12902772.
↑Taraschewski H, Mehlhorn H, Bunnag D, Andrews P, Thomas H (November 1986). "Effects of praziquantel on human intestinal flukes (Fasciolopsis buski and Heterophyes heterophyes)". Zentralblatt für Bakteriologie, Mikrobiologie, und Hygiene. Series A, Medical Microbiology, Infectious Diseases, Virology, Parasitology. 262 (4): 542–550. doi:10.1016/s0176-6724(86)80148-1. PMID3799097.
↑Olliaro P, Delgado-Romero P, Keiser J (April 2014). "The little we know about the pharmacokinetics and pharmacodynamics of praziquantel (racemate and R-enantiomer)". The Journal of Antimicrobial Chemotherapy. 69 (4): 863–870. doi:10.1093/jac/dkt491. PMID24390933.
↑"WHO } Guideline". World Health Organisation: Schistosomiasis. Archived from the original on 17 June 2007. Retrieved 4 March 2020.
↑"WHO } Strategy"(PDF). WHO (2022) "WHO Guideline on control and elimination of human schistosomiasis" ISBN 978-92-4-004160-8. Retrieved 2 October 2024.
↑Metwally A, Bennett JL, Botros S, Ebeid F (April 1995). "Effect of cimetidine, bicarbonate and glucose on the bioavailability of different formulations of praziquantel". Arzneimittel-Forschung. 45 (4): 516–518. PMID7779153.
↑Masimirembwa CM, Naik YS, Hasler JA (January 1994). "The effect of chloroquine on the pharmacokinetics and metabolism of praziquantel in rats and in humans". Biopharmaceutics & Drug Disposition. 15 (1): 33–43. doi:10.1002/bdd.2510150103. PMID8161714. S2CID45098166.
↑Greenberg RM, Doenhoff MJ (2017). "Chemotherapy and Drug Resistance in Schistosomiasis and Other Trematode and Cestode Infections". In Mayers DL, Sobel JD, Ouellette M, Kaye KS (eds.). Antimicrobial Drug Resistance: Mechanisms of Drug Resistance. Vol.1. Cham: Springer International Publishing. pp.705–734. doi:10.1007/978-3-319-46718-4_47. ISBN978-3-319-46718-4.
↑Park SK, Sprague DJ, Marchant JS (2026). "The Molecular Drug Target of Praziquantel". In Spangenberg T (ed.). Praziquantel: Discovery and Development of an Anthelmintic Drug. Cham: Springer Nature Switzerland. pp.85–105. doi:10.1007/978-3-031-97397-0_5. ISBN978-3-031-97397-0.
↑Angelucci F, Basso A, Bellelli A, Brunori M, Pica Mattoccia L, Valle C (August 2007). "The anti-schistosomal drug praziquantel is an adenosine antagonist". Parasitology. 134 (Pt 9): 1215–1221. doi:10.1017/S0031182007002600. PMID17428352. S2CID22482704.
↑Brunton L, Chabner B, Knollman B (10 January 2011). Goodman and Gilman's The Pharmacological Basis of Therapeutics, Twelfth Edition (12ed.). New York: McGraw-Hill Education / Medical. ISBN978-0-07-162442-8.[pageneeded]
↑Schmahl G, Taraschewski H (1987). "Treatment of fish parasites. 2. Effects of praziquantel, niclosamide, levamisole-HCl, and metrifonate on monogenea (Gyrodactylus aculeati, Diplozoon paradoxum)". Parasitology Research. 73 (4): 341–351. doi:10.1007/bf00531089. PMID3615395. S2CID12241452.
External links
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