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Praziquantel is a synthetic anthelmintic agent that is structurally unrelated to other currently available anthelmintic agents.

Praziquantel Uses

Trematode (Fluke) Infections

Schistosomiasis

Praziquantel is used for the treatment of schistosomiasis (bilharziasis) caused by all Schistosoma species pathogenic to humans. The drug has been used effectively for the treatment of individual patients and in mass-treatment and control programs.

Praziquantel is effective against all stages of Schistosoma infection including the acute phase and the chronic phase which may be associated with hepatosplenic involvement. The drug appears to be effective in the treatment of severe schistosomiasis (e.g., neuroschistosomiasis); however, to prevent substantial morbidity and long-term sequelae (e.g., paraplegia, persistent impotence) associated with this condition, therapy with praziquantel must be initiated promptly. Drug therapy may be initiated in patients with suspected neuroschistosomiasis pending the results of confirmative tests. Adult schistosomes do not multiply within the human host; therefore, the worm load depends on the intensity and frequency of infection and the life-span of the worm. Mature schistosomes constantly produce eggs, most of which are retained in host tissues eliciting an immunologic granulomatous response and tissue injury and scarring. The severity of disease is related to the intensity of infection. Efficacy of antischistosomal drugs results from markedly reducing the worm load and thus preventing production of eggs.

Praziquantel has produced cure rates of 75-95% and/or egg reduction percentages of 80-98% in patients with schistosomiasis and is considered the drug of choice in the treatment of infections caused by S. haematobium, S. japonicum, S. mansoni, or S. mekongi; the drug is the only currently available anthelmintic shown to be effective in the treatment of infections caused by S. intercalatum or S. mekongi. Oxamniquine (no longer commercially available in the US) is considered an alternative to praziquantel in the treatment of infections caused by S. mansoni. Use of niridazole or antimony salts for the treatment of S. japonicum infections has been replaced by praziquantel because of decreased toxicity and increased efficacy. The efficacy of praziquantel in the treatment of schistosomiasis may vary as a function of patient age and the degree of infection. Cure rates are generally lower in children and in patients with massive infections.

Travelers

Travelers to endemic areas of the Caribbean, South America, Africa, and Asia are at risk for schistosomiasis. Because there is no practical way for travelers to distinguish between infested and noninfested water, fresh-water swimming in rural areas of endemic countries should be avoided. Outbreaks of schistosomiasis have occurred among adventure travelers participating in river trips in Africa as well as resident expatriates and Peace Corps volunteers in high-risk areas. Those at greatest risk are travelers who engage in wading, swimming, or bathing in fresh water in areas where poor sanitation and appropriate snail hosts are present. To minimize the risk of morbidity associated with delayed recognition of schistosomal infections, the US Centers for Disease Control and Prevention (CDC) recommends that travelers and expatriates with a history of fresh-water exposure (e.g., recreational) returning from Schistosoma-endemic areas undergo serologic screening for the infection. Following thorough clinical evaluation, seropositive individuals should receive praziquantel therapy. The possibility of neuroschistosomiasis should be suspected in any individual with CNS abnormalities who has returned from endemic areas. Such infections can occur several months after exposure to infested water, and eggs may be undetectable or difficult to identify in urine and stool. Presumptive praziquantel therapy should be initiated promptly whenever a strong suspicion of infection exists and should not be delayed pending confirmatory tests.

Clonorchiasis and Opisthorchiasis

Praziquantel is used for the treatment of clonorchiasis caused by Clonorchis sinensis (Chinese liver fluke) and opisthorchiasis caused by Opisthorchis viverrini (Southeast Asian liver fluke). Praziquantel has produced a cure rate of 86-98% in patients with clonorchiasis or opisthorchiasis and currently is considered the drug of choice for the treatment of these infections.

Other Trematode Infections

Praziquantel has been used effectively for the treatment of other trematode (fluke) infections caused by Paragonimus westermani (lung fluke), Metagonimus yokogawai (intestinal fluke), Nanophyetus salmincola (formerly Troglotrema salmincola) (intestinal fluke), Heterophyes heterophyes (intestinal fluke), Fasciolopsis buski (intestinal fluke) and Metorchis conjunctus (North American liver fluke) and is currently considered the drug of choice in these infections. Praziquantel has been used in a limited number of patients for infections caused by Fasciola hepatica (sheep liver fluke), but the drug was inactive against the trematode in vitro in one study and treatment failures have been reported; therefore, other agents (e.g., bithionol or triclabendazole [drugs not commercially available in the US]) are preferred for the treatment of these infections. Praziquantel also has been effective in a limited number of patients with infections caused by P. kellicotti (American lung fluke), P. heterotrema (lung fluke), and P. uterobilateralis (African lung fluke).

Cestode (Tapeworm) Infections

Praziquantel has been used for the treatment of cestodiasis (tapeworm infections) caused by certain cestodes pathogenic to humans including Diphyllobothrium latum (fish tapeworm), Dipylidium caninum (dog and cat tapeworm), Taenia saginata (beef tapeworm), and T. solium (pork tapeworm).

Praziquantel or niclosamide (no longer commercially available in the US) is currently considered the drug of choice in infections caused by these cestodes. Praziquantel has also been used for the treatment of infections caused by Hymenolepis nana (dwarf tapeworm) and is currently considered the drug of choice for these infections. Praziquantel is effective against the adult, juvenile, and larval stages of all of these cestodes. Although niclosamide and paromomycin are effective for the treatment of cestodiasis caused by T. solium, some clinicians consider praziquantel the drug of choice for this infection because niclosamide and paromomycin cause disintegration of worm segments and release of viable eggs, which may be associated with a theoretical risk for the development of cysticercosis; niclosamide is not effective against cysticerci.

Praziquantel also has been used effectively for the treatment of cysticercosis caused by Cysticercus cellulosae (larval or tissue stage of T. solium) and praziquantel or albendazole is currently considered the drug of choice in this infection. Although praziquantel has been effective in the treatment of adult Echinococcus infections in dogs, studies in rodents and sheep have failed to demonstrate any efficacy of the drug in the treatment of larval Echinococcus infections (hydatid cysts), and it is unlikely that these infections in humans will respond to the drug; surgical resection of the cysts or, when surgery is contraindicated or the cysts rupture spontaneously during surgery, mebendazole or albendazole is currently considered the therapy of choice.

Because praziquantel can kill Echinococcus (e.g., protoscoleces), the drug may be useful for perioperative prophylaxis or in case of spilling of cyst contents during surgery. Praziquantel has been used effectively, preferably in conjunction with corticosteroids, for the treatment of neurocysticercosis caused by T. solium. In a limited number of patients with neurocysticercosis caused by T. solium, praziquantel therapy has been shown to cause a long-term decrease in the frequency of seizures and the frequency and severity of episodes of increased intracranial pressure and has produced radiographic evidence of a reduction in the number and size of cysts. Because adverse nervous system effects (CSF reaction syndrome) occur frequently during praziquantel therapy for neurocysticercosis, further study is needed to fully determine the benefit-to-risk of therapy with the drug in this condition. Occasionally, surgical ventricular shunting for hydrocephalus and, rarely, surgical removal of cysts (e.g., in the ventricles and/or basal cisterns) may be necessary. Most clinicians recommend that corticosteroids be used concomitantly with praziquantel in patients with neurocysticercosis to reduce the frequency and severity of praziquantel-induced adverse nervous system effects. (See Cautions: Nervous System Effects.)

Patients undergoing praziquantel therapy for neurocysticercosis usually should be hospitalized for the duration of treatment.Because praziquantel-induced CSF reaction syndrome may be more hazardous in patients with spinal cysticercosis than in other forms of neurocysticercosis, some clinicians have recommended that the drug not be used for the management of this condition. Spinal cysticercosis generally requires surgery to relieve spinal cord dysfunction caused by compression or an intramedullary mass. The drug has been ineffective in a limited number of patients with intraocular cysticercosis, and the manufacturer and some clinicians state that praziquantel should not be used in the treatment of this condition because of the risk of irreversible intraocular lesions secondary to killing of the cysts.

Dosage and Administration

Administration

Praziquantel is administered orally. The tablets should not be chewed but can be halved or quartered to allow administration of individualized doses. Patients should be instructed to immediately swallow the praziquantel tablets, halves, and/or quarters with a sufficient amount of liquid during meals, since retention of the tablets or tablet segments in the mouth may cause gagging or vomiting as a result of the drug's bitter taste. Some clinicians state that regurgitation during administration of the tablets may theoretically predispose the patient to the development of cysticercosis during therapy for T. solium infections.

Dosage

Trematode (Fluke) Infections Schistosomiasis

For the treatment of schistosomiasis caused by all species of Schistosoma pathogenic to humans, the usual dose of praziquantel recommended by the manufacturer in adults and children 4 years of age and older is 60 mg/kg given in 3 equally divided doses on the same day. Some clinicians recommend lower dosages (40 mg/kg given as a single dose or in 2 equally divided doses), which have been effective in the treatment of schistosomiasis in some patients. Some clinicians recommend that adult or pediatric patients with schistosomiasis caused by Schistosoma haematobium or S. mansoni receive praziquantel in a dosage of 40 mg/kg given in 2 equally divided doses on the same day and that those with infections caused by S. japonicum or S. mekongi receive a dosage of 60 mg/kg given in 3 equally divided doses on the same day.

Clonorchiasis and Opisthorchiasis

Praziquantel

For the treatment of infections caused by Clonorchis sinensis or Opisthorchis viverrini, the usual dosage of praziquantel in adults and children is 75 mg/kg given in 3 equally divided doses on the same day. Lower dosages (40-50 mg/kg given as a single dose) have been effective in the treatment of C. sinensis or O. viverrini infections in some patients; however, these dosages may be associated with lower cure rates. Other Trematode Infections For the treatment of trematodiasis caused by Fasciolopsis buski, Heterophyes heterophyes, or Metagonimus yokogawai, the usual dosage of praziquantel in adults and children is 75 mg/kg given in 3 equally divided doses on the same day.

Nanophyetus salmincola

For the treatment of trematode infections caused by Nanophyetus salmincola, the usual dosage of praziquantel in adults and children is 60 mg/kg given in 3 equally divided doses on the same day. For the treatment of trematodiasis caused by Fasciola hepatica, a dosage of 25 mg/kg 3 times daily for 5-8 days has been used in a limited number of adults and children, but treatment failures have occurred. (See Other Trematode Infections under Uses: Trematode [Fluke] Infections.)

Paragonimus westermani

For the treatment of trematode infections caused by Paragonimus westermani, the usual dosage in adults and children is 25 mg/kg 3 times daily for 2 days. For the treatment of trematodiasis caused by P. uterobilateralis, a dosage of 25 mg/kg 3 times daily for 2 days has been effective.

Cestode (Tapeworm) Infections Adult or Intestinal Stage

For the treatment of cestodiasis caused by Diphyllobothrium latum, Dipylidium caninum, Taenia saginata, or T. solium, the usual dose of praziquantel in adults and children is 5-10 mg/kg, given as a single dose. For the treatment of cestodiasis caused by Hymenolepis nana, the usual dose in adults and children is 25 mg/kg, given as a single dose. Larval or Tissue Stage For the treatment of cysticercosis caused by Cysticercus cellulosae, the usual dosage of praziquantel in adults and children is 50-100 mg/kg given in 3 divided doses daily for 30 days. A praziquantel dosage of 50 mg/kg given in 3 equally divided doses daily for 14 or 15 days has usually been used for the treatment of neurocysticercosis; this dosage has also been used for 21 days in a few patients. Because of the risk of praziquantel-induced adverse nervous system effects, most clinicians recommend that corticosteroids (e.g., dexamethasone 6-24 mg daily, prednisone 30-60 mg daily) be administered concomitantly with praziquantel in patients with neurocysticercosis. Although the potential benefit of additional courses of praziquantel therapy in adults with neurocysticercosis has not been determined, some clinicians suggest that repeated courses of therapy may be useful in patients who show only partial resolution of cysts 3 months after a course or whose condition deteriorates.

Praziquantel

Cautions

At recommended dosage, praziquantel generally is well tolerated. Adverse effects associated with praziquantel therapy occur frequently but are usually transient and mild to moderate in severity and usually do not require treatment. Some adverse effects associated with praziquantel therapy may be secondary to the parasitic infection being treated and/or to dead and dying parasites rather than to the drug itself, and such effects may be more frequent and/or severe in patients with a heavy worm burden.

Nervous System Effects

Adverse nervous system effects occur frequently with praziquantel; however, most of these effects are mild and transient. The most frequent adverse nervous system effects of praziquantel are dizziness, headache, and malaise. Other adverse nervous system effects of praziquantel include drowsiness, and lassitude (fatigue). Giddiness has been reported rarely.

Adverse nervous system effects (CSF reaction syndrome), including headache, exacerbation of neurologic signs and symptoms such as seizures, increased CSF protein concentrations and anticysticercal IgG levels, arachnoiditis, meningism, hyperthermia, and intracranial hypertension occur in almost all patients during praziquantel therapy for neurocysticercosis and may rarely be life-threatening. The CSF reaction syndrome is thought to result from an intense inflammatory response to dead and dying larvae in the CNS52, 53, 72, 73, 74, 76, 114, 115, 116, 121, 123 and may be similar to the Jarisch-Herxheimer reaction that occurs during penicillin therapy for syphilis; the risk of serious reactions probably is related to the number, size, and location of viable cysts in the CNS. Concomitant use of corticosteroids during praziquantel therapy for neurocysticercosis reportedly substantially reduces the frequency and severity of these adverse nervous system effects.

GI Effects

Adverse GI effects of praziquantel occur frequently. Abdominal pain or discomfort with or without nausea occurs in about 90% of patients receiving the drug. Vomiting, epigastric pain, anorexia, urge to defecate, and diarrhea have also been reported. GI reactions, principally colicky, crampy abdominal pain, occasionally may be severe, occurring suddenly within 1 hour after administration of the drug; such reactions may be accompanied by fever, sweating, and bloody stools.

Hepatic Effects

Mild to moderate, transient increases in serum AST (SGOT) and/or ALT (SGPT) concentrations have occurred in about 3-27% of patients receiving praziquantel; however, there has been no evidence of serious drug-induced adverse hepatic effects, even in patients with schistosomal infection associated with severe hepatosplenic involvement.

Other Adverse Effects

Urticaria, rash (e.g., maculopapular), pruritus, low back pain, myalgia or arthralgia, fever or hot sensation, sweating, palpitation, and hypotension have been reported in some patients receiving praziquantel. Minimal increases in eosinophil count have occurred in a few patients with schistosomiasis treated with the drug; however, eosinophilia is also associated with schistosomiasis and may also be a consequence of a host-mediated immunologic response to antigen release during drug-induced killing of the worms. Similarly, urticaria may result from an immunologic response to antigen release from the worms. Although praziquantel has been shown to induce a positive inotropic effect on rat atria in vitro, this effect has not been reported to date in humans receiving the drug and the clinical importance of this finding has not been determined.

Precautions and Contraindications

Patients should be warned that praziquantel may impair their ability to perform activities requiring mental alertness or physical coordination (e.g., operating machinery, driving a motor vehicle), and, therefore, the manufacturer recommends that patients not perform such activities on the day of, and the day following, praziquantel therapy. Some clinicians state that praziquantel should be used with caution in patients with a history of seizures. Praziquantel is contraindicated in patients who are hypersensitive to the drug. The manufacturer and some clinicians state that the drug also is contraindicated in patients with intraocular cysticercosis. In addition, some clinicians recommend that praziquantel not be used in patients with spinal cysticercosis. (See Uses: Cestode [Tapeworm] Infections.)

Pediatric Precautions

Safety of praziquantel in children younger than 4 years of age has not been established.

Mutagenicity and Carcinogenicity

It is not known whether praziquantel is mutagenic or carcinogenic in humans. Although praziquantel has been reported by one laboratory to be mutagenic in bacteria, these results have not been reproducible, and other studies have not shown the drug to be mutagenic in bacteria or mammalian cells. The drug has been shown to act as a comutagen, increasing the mutagenicity of several mutagenic and/or carcinogenic chemicals in vitro in bacteria and animal cells. No evidence of carcinogenesis was seen in animals receiving oral praziquantel dosages up to 250 mg/kg once weekly for 2 years.

Pregnancy, Fertitlity and Lactation

Reproduction studies in rats and rabbits using praziquantel dosages up to 40 times the usual human dosage have not revealed evidence of harm to the fetus. An increase in the rate of spontaneous abortion occurred in rats following administration of praziquantel dosages 3 times the usual human dosage. There are no adequate and controlled studies to date using praziquantel in pregnant women, and the drug should be used during pregnancy only when clearly needed. It is not known whether praziquantel affects fertility in humans. Reproduction studies in rats and rabbits using praziquantel dosages up to 40 times the usual human dosage have not revealed evidence of impaired fertility. Since praziquantel is distributed into milk, women should temporarily discontinue nursing on the day of praziquantel therapy and for 72 hours after administration of the last dose of the drug.

Drug Interactions

Oxamniquine Although the clinical importance is unclear, limited evidence from one study in mice indicates that the antischistosomal activity of praziquantel and oxamniquine (no longer commercially available in the US) may be synergistic against Schistosoma mansoni when the two drugs are administered concomitantly.

Acute Toxcicity

Limited information is available on the acute toxicity of praziquantel.

Pathogenesis

The acute lethal dose of praziquantel in humans has not been determined. Toxicologic studies in animals have shown that the oral LD50 of praziquantel is about 2.5 g/kg in mice, about 2.8 g/kg in rats, 1.05 g/kg in rabbits, and greater than 200 mg/kg in dogs; however, an actual acute oral lethal dose could not be established in dogs because of the emetic effect of the drug in this species.

Pathogenesis

Although there has been no experience to date with acute praziquantel overdosage in humans, the manufacturer states that a fast-acting laxative should be given following acute ingestion of an overdose of the drug.

Mechanism of Action

Activity Against Trematodes

The exact mechanism of praziquantel's activity against trematodes (flukes), including its antischistosomal activity, has not been fully elucidated. Praziquantel appears to directly kill susceptible adult schistosomes in vivo. In addition, the drug causes the dead or dying worms to be dislodged from their usual sites of residence in the mesenteric or pelvic (e.g., vesical plexus) veins to the liver where they are retained and subsequently elicit host tissue reactions (e.g., phagocytosis).

The dislodgment of worms appears to result principally from contraction and paralysis of their musculature and subsequent immobilization of their suckers, which causes the worms to detach from the blood vessel wall, thereby allowing passive dislodgment by normal blood flow. The drug-induced contraction and subsequent paralysis in the contracted state appear to result from an increased permeability of the cell membrane of susceptible worms to calcium and consequent influx of calcium ions. Evidence from studies in animals with schistosomal infections indicates that praziquantel is readily taken up by schistosomes and that the drug-induced dislodgment of schistosomes to the liver is rapid, occurring within 1 hour after administration of a single oral dose; contraction and paralysis of the worms occur almost immediately but may be reversible at subtherapeutic plasma praziquantel concentrations (less than 0.3 mcg/mL).

Following administration of praziquantel, intense, focal vacuolization and subsequent disintegration at distinct sites of the schistosomal integument occur. Vacuolization and disintegration of the integument result in formation of a defect in the surface of the worms and cause most schistosomes to lose their normal copulatory position, thus substantially reducing oviposition (laying of eggs). Evidence from animal studies indicates that praziquantel-induced vacuolization of schistosomal integument begins within 15 minutes following administration of the drug and that after 1 day the integument is largely destroyed where vacuolization has occurred; eosinophilic granulocytes from the definitive host attach to the vacuolized regions and subsequently infiltrate the interior of the schistosomes resulting in a progressive internal lysis. Male Schistosoma mansoni worms appear to be more susceptible than females; however, evidence from studies in animals with schistosomal infections caused by S. mansoni indicates that all worms were dead 7 days following treatment with the drug. The number of worms affected and the degree of integumental injury appear to be dose related; in addition, the degree of injury increases with time posttreatment.

Limited evidence in animals suggests that female S. haematobium worms may be more susceptible than males. Studies in animals with experimentally induced schistosomal infections indicate that praziquantel is active against all developmental stages of schistosomes including the miracidia and cercariae (the free-swimming larvae that emerge from the intermediate snail host). The exact mechanism of praziquantel's activity against other trematodes also has not been fully characterized; however, the drug has been shown to cause focal vacuolization and subsequent disintegration at distinct sites of these worms similar to the effects induced by the drug in schistosomes. In addition, studies using Opisthorchis viverrini indicate that praziquantel increases permeability of the liver fluke tegument to calcium, presumably by interfering with the mechanism that regulates calcium binding or transport across the tegumental membrane.

Activity Against Cestodes

Although the exact mechanism of praziquantel's activity against cestodes (tapeworms) has not been determined, the drug generally does not kill susceptible adult cestodes in vivo, but causes the worms to be dislodged from their usual sites of residence in the intestine. The dislodgment of the worms appears to result from drug-induced impairment of the function of the worms' suckers. The effects of praziquantel against cestodes is concentration dependent in vitro. At low concentrations (1-10 ng/mL) in vitro, the drug stimulates cestode motility and impairs the function of their suckers. As the in vitro concentration of the drug increases (10-100 ng/mL), contraction of the strobila (chain of proglottids) occurs and, at high concentrations (greater than 1000 ng/mL), instantaneous, irreversible contraction of the strobila occurs. Praziquantel also causes irreversible focal vacuolization and subsequent disintegration at specific sites of the cestodal integument. The characteristic integumental lesions are restricted to the growth zone of the neck region; the proglottids of the central and posterior portions of the strobila are not affected. Spectrum Praziquantel has a broad spectrum of anthelmintic activity. The drug has activity against many trematodes, including schistosomes, and also has activity against many cestodes.

Trematodes

Praziquantel is active against all Schistosoma species pathogenic to humans, including S. mansoni, S. haematobium, S. japonicum, S. mekongi, and S. intercalatum. In vitro, susceptible schistosomes are rapidly killed by praziquantel concentrations of 0.3 mcg/mL and greater. Praziquantel has also been shown to be active against other trematodes, including the liver flukes Clonorchis sinensis, Opisthorchis viverrini, and Fasciola hepatica; the lung flukes Paragonimus westermani, P. uterobilateralis, and P. kellicotti; and the intestinal flukes Metagonimus yokogawai, Nanophyetus salmincola (formerly Troglotrema salmincola), Fasciolopsis buski, and Heterophyes heterophyes.

Cestodes

Praziquantel has been shown to be active against adult, juvenile, and larval stages of certain cestodes (tapeworms) pathogenic to humans including Diphyllobothrium latum (fish tapeworm), Dipylidium caninum (dog and cat tapeworm), Hymenolepis nana (dwarf tapeworm), Taenia saginata (beef tapeworm), T. solium (pork tapeworm), and Cysticercus cellulosae (larval or tissue stage of T. solium).

Pharmacokinetics

Absorption

Praziquantel is well absorbed following oral administration. Approximately 80% of an oral dose of the drug is absorbed from the GI tract; however, because of extensive first-pass metabolism, only a small portion reaches systemic circulation as unchanged praziquantel. Peak serum concentrations of praziquantel occur approximately 1-3 hours after oral administration of usual doses of the drug. Following oral administration of a single 50-mg/kg dose in healthy adults in one study, peak serum drug concentrations of about 1 mcg/mL occurred at 1-2 hours.

Distribution

Distribution of praziquantel into human body tissues and fluids has not been fully characterized. In studies in rats, concentrations of free (unbound) praziquantel in CSF were similar to those in serum. The concentration of the drug in CSF is reported to be 14-20% of the concurrent total (free plus protein-bound) plasma concentration. Praziquantel is distributed into milk in concentrations about 25% of maternal serum concentrations.

Abdominal pain

Elimination

Praziquantel has a serum half-life of about 0.8-1.5 hours in adults with normal renal and hepatic function; however, the serum half-life of metabolites of the drug is about 4-5 hours. Although the exact metabolic fate of praziquantel is not clearly established, the drug is rapidly and extensively metabolized, principally in the liver via hydroxylation to monohydroxylated and polyhydroxylated metabolites. It is not known if these metabolites possess anthelmintic activity. Praziquantel and its metabolites are excreted mainly in urine. Following a single oral dose of the drug, approximately 70-80% of the dose is excreted in urine within 24 hours, principally as metabolites; less than 0.1% of an oral dose is excreted in urine unchanged.

Chemistry and Stability

Chemistry

Praziquantel, a pyrazinoisoquinoline derivative, is a synthetic heterocyclic anthelmintic agent. The drug is structurally unrelated to other currently available anthelmintic agents. Praziquantel occurs as a white to nearly white, hygroscopic, crystalline powder with a bitter taste and is very slightly soluble in water and soluble in alcohol.

Stability

Praziquantel tablets should be stored in tight containers at a temperature less than 30°C.

Preparations

Praziquantel Oral Tablets, film- 600 mg Biltricide®, (with povidone; coated scored) Bayer

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