Biltricide

Antitrematodal Agents

Take tablets orally with liquid during meals (food).
Do not chew or hold the tablets in the mouth (bitter taste may cause gagging or vomiting).
To prevent choking in pediatric patients younger than 6 years of age, tablets may be crushed or disintegrated and mixed with semi-solid food or liquid. Use crushed or disintegrated tablets within 1 hour of mixing.
Tablets are scored for cutting in half or one-fourth if dosage requires. Press the score with the thumbnails. If a quarter (one-fourth) of a tablet is required, this is best achieved by breaking the segment from the outer end.[28515]

ventricular fibrillation / Early / 0-1.0
arrhythmia exacerbation / Early / 0-1.0
bradycardia / Rapid / 0-1.0
AV block / Early / 0-1.0
seizures / Delayed / 0-1.0

eosinophilia / Delayed / 0-1.0
elevated hepatic enzymes / Delayed / Incidence not known

urticaria / Rapid / 0-1.0
drowsiness / Early / 0-1.0
abdominal pain / Early / 0-1.0
vertigo / Early / 0-1.0
anorexia / Delayed / 0-1.0
asthenia / Delayed / 0-1.0
pruritus / Rapid / 0-1.0
vomiting / Early / 0-1.0
diarrhea / Early / 0-1.0
myalgia / Early / 0-1.0
fatigue / Early / Incidence not known
dizziness / Early / Incidence not known
nausea / Early / Incidence not known
weakness / Early / Incidence not known
headache / Early / Incidence not known
rash / Early / Incidence not known
fever / Early / Incidence not known
malaise / Early / Incidence not known

Biltricide

Rx

Oral anthelmintic agent (trematodicide)
Used for schistosomiasis, clonorchiasis, and opisthorchiasis; also effective for certain cestode (tapeworm) infections
Alternative to albendazole for cysticercosis, but associated with higher incidence of side effects

20 mg/kg/dose PO 3 times daily for 1 day; separate doses by 4 to 6 hours.[28515]

20 mg/kg/dose PO 3 times daily for 1 day; separate doses by 4 to 6 hours.[28515]

20 mg/kg/dose PO 2 times daily for 1 day. The FDA-approved dose is 20 mg/kg/dose PO 3 times daily for 1 day; separate doses by 4 to 6 hours.[28515]

20 mg/kg/dose PO 2 times daily for 1 day. The FDA-approved dose is 20 mg/kg/dose PO 3 times daily for 1 day; separate doses by 4 to 6 hours.[28515]

25 mg/kg/dose PO 3 times daily for 1 day; separate doses by 4 to 6 hours.[28515]

25 mg/kg/dose PO 3 times daily for 1 day; separate doses by 4 to 6 hours.[28515]

50 mg/kg/day PO given in 3 divided doses for 2 to 4 weeks. Surgery is indicated for intraocular cysts; intraocular cysts should be removed before administration of antiparasitic treatment to avoid irreversible eye damage due to the inflammatory response.

50 mg/kg/day PO given in 3 divided doses for 2 to 4 weeks. Surgery is indicated for intraocular cysts; intraocular cysts should be removed before administration of antiparasitic treatment to avoid irreversible eye damage due to the inflammatory response.

50 mg/kg/day PO in 3 divided doses for 10 to 14 days combined with albendazole and corticosteroids.

50 mg/kg/day PO in 3 divided doses for 10 to 14 days combined with albendazole and corticosteroids.

50 mg/kg/day PO in 3 divided doses combined with albendazole and corticosteroids. Continue treatment for 2 to 12 months or until resolution of cystic lesions on neuroimaging studies.

50 mg/kg/day PO in 3 divided doses combined with albendazole and corticosteroids. Continue treatment for 2 to 12 months or until resolution of cystic lesions on neuroimaging studies.

5 to 10 mg/kg/dose PO as a single dose.

5 to 10 mg/kg/dose PO as a single dose.

40 mg/kg/dose PO once weekly, or alternately, 40 mg/kg/dose PO once daily in short-term treatment, although this dose was not always tolerated. Praziquantel may be useful preoperatively or in the case of spillage of cyst contents.

25 mg/kg/dose PO 3 times daily for 2 days.[63870]

25 mg/kg/dose PO 3 times daily for 2 days.

†Indicates off-label use

Monitor hepatosplenic patients with moderate to severe hepatic impairment (Child-Pugh class B and C) for adverse reactions when administering praziquantel; reduced metabolism can occur in these patients, resulting in considerably higher and longer lasting plasma concentrations of unmetabolized drug. Specific recommendations regarding dosage adjustment in hepatic impairment are not available.[28515]

Specific guidelines for dosage adjustments in renal impairment are not available; it appears that no dosage adjustments are needed.

Albendazole: (Moderate) The serum concentration of albendazole may be increased if coadministered with praziquantel. Use albendazole cautiously in combination with praziquantel.
Apalutamide: (Contraindicated) The concomitant use of apalutamide with praziquantel is contraindicated due to the potential for decreased exposure and efficacy of praziquantel. If treatment with praziquantel is necessary, treatment with apalutamide should be discontinued 4 weeks before administration of praziquantel. Treatment with apalutamide can then be restarted 1 day after completion of praziquantel treatment. Apalutamide is a strong CYP3A4 inducer and praziquantel is a CYP3A4 substrate. In a crossover study with a 2-week washout period, administration of praziquantel followed by another strong CYP3A inducer resulted in undetectable plasma concentrations of praziquantel in 7 out of 10 subjects. When praziquantel was administered two weeks after discontinuation of the strong inducer, the mean praziquantel AUC and Cmax were 23% and 35% lower, respectively, than when praziquantel was given alone.
Armodafinil: (Major) In vitro and drug interactions studies suggest that the CYP3A4 isoenzyme is the major enzyme involved in praziquantel metabolism. Therefore, use of praziquantel with armodafinil, a CYP3A4 inducer, should be done with caution as concomitant use may produce therapeutically ineffective concentrations of praziquantel.
Belzutifan: (Moderate) Monitor for reduced response to praziquantel if coadministered with belzutifan. Concomitant use may produce therapeutically ineffective concentrations of praziquantel. In vitro and drug interactions studies suggest that the CYP3A isoenzyme is the major enzyme involved in praziquantel metabolism; belzutifan is a weak CYP3A inducer.
Bexarotene: (Major) In vitro and drug interactions studies suggest that the CYP3A4 isoenzyme is the major enzyme involved in praziquantel metabolism. Therefore, use of praziquantel with bexarotene, a CYP3A4 inducer, should be done with caution as concomitant use may produce therapeutically ineffective concentrations of praziquantel.
Bosentan: (Major) In vitro and drug interactions studies suggest that the CYP3A4 isoenzyme is the major enzyme involved in praziquantel metabolism. Therefore, use of praziquantel with bosentan, a CYP3A4 inducer, should be done with caution as concomitant use may produce therapeutically ineffective concentrations of praziquantel.
Brigatinib: (Moderate) Monitor for reduced response to praziquantel if coadministered with brigatinib. Concomitant use may produce therapeutically ineffective concentrations of praziquantel. In vitro and drug interactions studies suggest that the CYP3A4 isoenzyme is the major enzyme involved in praziquantel metabolism. Brigatinib is a weak CYP3A4 inducer.
Carbamazepine: (Contraindicated) The concomitant use of carbamazepine with praziquantel is contraindicated due to decreased exposure and efficacy of praziquantel. If treatment with praziquantel is necessary, treatment with carbamazepine should be discontinued 4 weeks before administration of praziquantel. Treatment with carbamazepine can then be restarted 1 day after completion of praziquantel treatment. Carbamazepine is a strong CYP3A4 inducer and praziquantel is a CYP3A4 substrate; coadministration may result in decreased plasma concentrations of praziquantel. In a crossover study with a 2-week washout period, administration of praziquantel followed by another strong CYP3A inducer resulted in undetectable plasma concentrations of praziquantel in 7 out of 10 subjects. When praziquantel was administered two weeks after discontinuation of the strong inducer, the mean praziquantel AUC and Cmax were 23% and 35% lower, respectively, than when praziquantel was given alone.
Cenobamate: (Moderate) Monitor for reduced response to praziquantel if coadministered with cenobamate. Concomitant use may produce therapeutically ineffective concentrations of praziquantel. In vitro and drug interactions studies suggest that the CYP3A4 isoenzyme is the major enzyme involved in praziquantel metabolism. Cenobamate is a moderate CYP3A4 inducer.
Chloroquine: (Minor) Concomitant administration of chloroquine and praziquantel can reduce praziquantel bioavailability and maximum serum concentrations. The mechanism of the interaction is not certain. Clinicians should be alert to the possibility of praziquantel failure if chloroquine is used.
Cimetidine: (Moderate) Drugs that inhibit hepatic metabolism via the microsomal CYP450 enzyme system, such as cimetidine, may increase the bioavailability of praziquantel.
Clobazam: (Moderate) Use of praziquantel with clobazam should be done with caution as concomitant use may produce therapeutically ineffective concentrations of praziquantel. Clobazam is a weak CYP3A4 inducer. In vitro and drug interactions studies suggest that the CYP3A4 isoenzyme is the major enzyme involved in praziquantel metabolism.
Dabrafenib: (Major) In vitro and drug interactions studies suggest that the CYP3A4 isoenzyme is the major enzyme involved in praziquantel metabolism. Therefore, use of praziquantel with dabrafenib, a CYP3A4 inducer, should be done with caution as concomitant use may produce therapeutically ineffective concentrations of praziquantel.
Deferasirox: (Major) In vitro and drug interactions studies suggest that the CYP3A4 isoenzyme is the major enzyme involved in praziquantel metabolism. Therefore, use of praziquantel with deferasirox, a CYP3A4 inducer, should be done with caution as concomitant use may produce therapeutically ineffective concentrations of praziquantel.
Dexamethasone: (Moderate) Monitor for reduced response to praziquantel if coadministered with dexamethasone. Concomitant use may produce therapeutically ineffective concentrations of praziquantel. In vitro and drug interactions studies suggest that the CYP3A isoenzyme is the major enzyme involved in praziquantel metabolism; dexamethasone is a weak CYP3A inducer.
Efavirenz: (Major) In vitro and drug interactions studies suggest that the CYP3A4 isoenzyme is the major enzyme involved in praziquantel metabolism. Therefore, use of praziquantel with efavirenz, a CYP3A4 inducer, should be done with caution as concomitant use may produce therapeutically ineffective concentrations of praziquantel.
Efavirenz; Emtricitabine; Tenofovir Disoproxil Fumarate: (Major) In vitro and drug interactions studies suggest that the CYP3A4 isoenzyme is the major enzyme involved in praziquantel metabolism. Therefore, use of praziquantel with efavirenz, a CYP3A4 inducer, should be done with caution as concomitant use may produce therapeutically ineffective concentrations of praziquantel.
Efavirenz; Lamivudine; Tenofovir Disoproxil Fumarate: (Major) In vitro and drug interactions studies suggest that the CYP3A4 isoenzyme is the major enzyme involved in praziquantel metabolism. Therefore, use of praziquantel with efavirenz, a CYP3A4 inducer, should be done with caution as concomitant use may produce therapeutically ineffective concentrations of praziquantel.
Elagolix: (Moderate) Monitor for reduced response to praziquantel if coadministered with elagolix. Concomitant use may produce therapeutically ineffective concentrations of praziquantel. In vitro and drug interactions studies suggest that the CYP3A4 isoenzyme is the major enzyme involved in praziquantel metabolism. Elagolix is a weak to moderate CYP3A4 inducer.
Elagolix; Estradiol; Norethindrone acetate: (Moderate) Monitor for reduced response to praziquantel if coadministered with elagolix. Concomitant use may produce therapeutically ineffective concentrations of praziquantel. In vitro and drug interactions studies suggest that the CYP3A4 isoenzyme is the major enzyme involved in praziquantel metabolism. Elagolix is a weak to moderate CYP3A4 inducer.
Enzalutamide: (Contraindicated) The concomitant use of enzalutamide with praziquantel is contraindicated due to the potential for decreased exposure and efficacy of praziquantel. If treatment with praziquantel is necessary, treatment with enzalutamide should be discontinued 4 weeks before administration of praziquantel. Treatment with enzalutamide can then be restarted 1 day after completion of praziquantel treatment. Enzalutamide is a strong CYP3A4 inducer and praziquantel is a CYP3A4 substrate. In a crossover study with a 2-week washout period, administration of praziquantel followed by another strong CYP3A inducer resulted in undetectable plasma concentrations of praziquantel in 7 out of 10 subjects. When praziquantel was administered two weeks after discontinuation of the strong inducer, the mean praziquantel AUC and Cmax were 23% and 35% lower, respectively, than when praziquantel was given alone.
Erythromycin: (Moderate) Erythromycin is a significant CYP3A4 inhibitor and may reduce metabolism of praziquantel. This interaction may be beneficial. The combination may prolong the exposure of the parasites to praziquantel and may not result in an increased risk of side effects.
Eslicarbazepine: (Moderate) In vitro and drug interactions studies suggest that the CYP3A4 isoenzyme is the major enzyme involved in praziquantel metabolism. Therefore, use of praziquantel with eslicarbazepine, a CYP3A4 inducer, should be done with caution as concomitant use may produce therapeutically ineffective concentrations of praziquantel.
Etravirine: (Major) In vitro and drug interactions studies suggest that the CYP3A4 isoenzyme is the major enzyme involved in praziquantel metabolism. Therefore, use of praziquantel with etravirine, a CYP3A4 inducer, should be done with caution as concomitant use may produce therapeutically ineffective concentrations of praziquantel.
Felbamate: (Major) In vitro and drug interactions studies suggest that the CYP3A4 isoenzyme is the major enzyme involved in praziquantel metabolism. Therefore, use of praziquantel with felbamate, a CYP3A4 inducer, should be done with caution as concomitant use may produce therapeutically ineffective concentrations of praziquantel.
Flutamide: (Major) In vitro and drug interactions studies suggest that the CYP3A4 isoenzyme is the major enzyme involved in praziquantel metabolism. Therefore, use of praziquantel with flutamide, a CYP3A4 inducer, should be done with caution as concomitant use may produce therapeutically ineffective concentrations of praziquantel.
Fosamprenavir: (Major) In vitro and drug interactions studies suggest that the CYP3A4 isoenzyme is the major enzyme involved in praziquantel metabolism. Therefore, use of praziquantel with fosamprenavir, which is metabolized to a CYP3A4 inducer (amprenavir), should be done with caution as concomitant use may produce therapeutically ineffective concentrations of praziquantel.
Fosphenytoin: (Contraindicated) The concomitant use of fosphenytoin with praziquantel is contraindicated due to decreased exposure and efficacy of praziquantel. If treatment with praziquantel is necessary, treatment with fosphenytoin should be discontinued 4 weeks before administration of praziquantel. Treatment with fosphenytoin can then be restarted 1 day after completion of praziquantel treatment. Fosphenytoin is a strong CYP3A4 inducer and praziquantel is a CYP3A4 substrate; coadministration may result in decreased plasma concentrations of praziquantel. In a crossover study with a 2-week washout period, administration of praziquantel followed by another strong CYP3A inducer, rifampin, resulted in undetectable plasma concentrations of praziquantel in 7 out of 10 subjects. When praziquantel was administered two weeks after discontinuation of the strong inducer, the mean praziquantel AUC and Cmax were 23% and 35% lower, respectively, than when praziquantel was given alone.
Glycerol Phenylbutyrate: (Moderate) Monitor for reduced response to praziquantel if coadministered with glycerol phenylbutyrate. Concomitant use may produce therapeutically ineffective concentrations of praziquantel. In vitro and drug interactions studies suggest that the CYP3A isoenzyme is the major enzyme involved in praziquantel metabolism; glycerol phenylbutyrate is a weak CYP3A inducer.
Grapefruit juice: (Moderate) Coadministration of grapefruit juice with praziquantel has been reported to increase blood levels and AUC of praziquantel, which may be advantageous in the treatment of various parasitic infections. However, more study is needed to determine if this interaction is beneficial or harmful.
Hydroxychloroquine: (Minor) Hydroxychloroquine may reduce praziquantel bioavailability and maximum serum concentrations as was observed with the structurally similar chloroquine. The mechanism of the interaction is not certain. Clinicians should be alert to the possibility of praziquantel failure if hydroxychloroquine is used.
Isoniazid, INH; Pyrazinamide, PZA; Rifampin: (Contraindicated) The concomitant use of rifampin with praziquantel is contraindicated due to decreased exposure and efficacy of praziquantel. If treatment with praziquantel is necessary, treatment with rifampin should be discontinued 4 weeks before administration of praziquantel. Treatment with rifampin can then be restarted 1 day after completion of praziquantel treatment. Rifampin is a strong CYP3A4 inducer and praziquantel is a CYP3A4 substrate. In a crossover study with a 2-week washout period, administration of praziquantel followed by rifampin resulted in undetectable plasma concentrations of praziquantel in 7 out of 10 subjects. When praziquantel was administered two weeks after discontinuation of rifampin, the mean praziquantel AUC and Cmax were 23% and 35% lower, respectively, than when praziquantel was given alone.
Isoniazid, INH; Rifampin: (Contraindicated) The concomitant use of rifampin with praziquantel is contraindicated due to decreased exposure and efficacy of praziquantel. If treatment with praziquantel is necessary, treatment with rifampin should be discontinued 4 weeks before administration of praziquantel. Treatment with rifampin can then be restarted 1 day after completion of praziquantel treatment. Rifampin is a strong CYP3A4 inducer and praziquantel is a CYP3A4 substrate. In a crossover study with a 2-week washout period, administration of praziquantel followed by rifampin resulted in undetectable plasma concentrations of praziquantel in 7 out of 10 subjects. When praziquantel was administered two weeks after discontinuation of rifampin, the mean praziquantel AUC and Cmax were 23% and 35% lower, respectively, than when praziquantel was given alone.
Itraconazole: (Moderate) Itraconazole inhibits CYP3A4 and may reduce metabolism of praziquantel. This interaction may be beneficial. The combination may prolong the exposure of the parasites to praziquantel and may not result in an increased risk of side effects.
Ketoconazole: (Moderate) Ketoconazole inhibits CYP3A4 and may reduce metabolism of praziquantel. This interaction may be beneficial. The combination may prolong the exposure of the parasites to praziquantel and may not result in an increased risk of side effects.
Lesinurad: (Moderate) Lesinurad may decrease the systemic exposure and therapeutic efficacy of praziquantel; monitor for potential reduction in efficacy. In vitro and drug interaction studies suggest praziquantel may be a CYP3A substrate, and lesinurad is a weak CYP3A inducer.
Lesinurad; Allopurinol: (Moderate) Lesinurad may decrease the systemic exposure and therapeutic efficacy of praziquantel; monitor for potential reduction in efficacy. In vitro and drug interaction studies suggest praziquantel may be a CYP3A substrate, and lesinurad is a weak CYP3A inducer.
Levoketoconazole: (Moderate) Ketoconazole inhibits CYP3A4 and may reduce metabolism of praziquantel. This interaction may be beneficial. The combination may prolong the exposure of the parasites to praziquantel and may not result in an increased risk of side effects.
Lopinavir; Ritonavir: (Moderate) Monitor for increased side effects of praziquantel if administered with ritonavir. Concurrent administration may result in elevated praziquantel plasma concentrations. Praziquantel is metabolized by the hepatic isoenzyme CYP3A4; ritonavir is an inhibitor of this enzyme.
Lorlatinib: (Moderate) Monitor for reduced response to praziquantel if coadministered with lorlatinib. Concomitant use may produce therapeutically ineffective concentrations of praziquantel. In vitro and drug interactions studies suggest that the CYP3A4 isoenzyme is the major enzyme involved in praziquantel metabolism. Lorlatinib is a moderate CYP3A4 inducer.
Lumacaftor; Ivacaftor: (Contraindicated) The concomitant use of lumacaftor; ivacaftor with praziquantel is contraindicated due to decreased exposure and efficacy of praziquantel. If treatment with praziquantel is necessary, treatment with lumacaftor; ivacaftor should be discontinued 4 weeks before administration of praziquantel. Treatment with lumacaftor; ivacaftor can then be restarted 1 day after completion of praziquantel treatment. Lumacaftor is a strong CYP3A4 inducer and praziquantel is a CYP3A4 substrate; coadministration may result in decreased plasma concentrations of praziquantel. In a crossover study with a 2-week washout period, administration of praziquantel followed by another strong CYP3A inducer resulted in undetectable plasma concentrations of praziquantel in 7 out of 10 subjects. When praziquantel was administered two weeks after discontinuation of the strong inducer, the mean praziquantel AUC and Cmax were 23% and 35% lower, respectively, than when praziquantel was given alone.
Lumacaftor; Ivacaftor: (Contraindicated) The concomitant use of lumacaftor; ivacaftor with praziquantel is contraindicated due to decreased exposure and efficacy of praziquantel. If treatment with praziquantel is necessary, treatment with lumacaftor; ivacaftor should be discontinued 4 weeks before administration of praziquantel. Treatment with lumacaftor; ivacaftor can then be restarted 1 day after completion of praziquantel treatment. Lumacaftor is a strong CYP3A4 inducer and praziquantel is a CYP3A4 substrate; coadministration may result in decreased plasma concentrations of praziquantel. In a crossover study with a 2-week washout period, administration of praziquantel followed by another strong CYP3A inducer resulted in undetectable plasma concentrations of praziquantel in 7 out of 10 subjects. When praziquantel was administered two weeks after discontinuation of the strong inducer, the mean praziquantel AUC and Cmax were 23% and 35% lower, respectively, than when praziquantel was given alone.
Mavacamten: (Moderate) Monitor for reduced response to praziquantel if coadministered with mavacamten. Concomitant use may produce therapeutically ineffective concentrations of praziquantel. In vitro and drug interactions studies suggest that the CYP3A isoenzyme is the major enzyme involved in praziquantel metabolism; mavacamten is a moderate CYP3A inducer.
Mitapivat: (Moderate) Monitor for reduced response to praziquantel if coadministered with mitapivat. Concomitant use may produce therapeutically ineffective concentrations of praziquantel. In vitro and drug interactions studies suggest that the CYP3A isoenzyme is the major enzyme involved in praziquantel metabolism; mitapivat is a weak CYP3A inducer.
Mitotane: (Contraindicated) The concomitant use of mitotane with praziquantel is contraindicated due to decreased exposure and efficacy of praziquantel. If treatment with praziquantel is necessary, treatment with mitotane should be discontinued 4 weeks before administration of praziquantel. Treatment with mitotane can then be restarted 1 day after completion of praziquantel treatment. Mitotane is a strong CYP3A4 inducer and praziquantel is a CYP3A4 substrate; coadministration may result in decreased plasma concentrations of praziquantel. In a crossover study with a 2-week washout period, administration of praziquantel followed by another strong CYP3A inducer resulted in undetectable plasma concentrations of praziquantel in 7 out of 10 subjects. When praziquantel was administered two weeks after discontinuation of the strong inducer, the mean praziquantel AUC and Cmax were 23% and 35% lower, respectively, than when praziquantel was given alone.
Mobocertinib: (Moderate) Monitor for reduced response to praziquantel if coadministered with mobocertinib. Concomitant use may produce therapeutically ineffective concentrations of praziquantel. In vitro and drug interactions studies suggest that the CYP3A isoenzyme is the major enzyme involved in praziquantel metabolism; mobocertinib is a weak CYP3A inducer.
Modafinil: (Major) In vitro and drug interactions studies suggest that the CYP3A4 isoenzyme is the major enzyme involved in praziquantel metabolism. Therefore, use of praziquantel with modafinil, a CYP3A4 inducer, should be done with caution as concomitant use may produce therapeutically ineffective concentrations of praziquantel.
Nafcillin: (Major) In vitro and drug interactions studies suggest that the CYP3A4 isoenzyme is the major enzyme involved in praziquantel metabolism. Therefore, use of praziquantel with nafcillin, a CYP3A4 inducer in vitro, should be done with caution as concomitant use may produce therapeutically ineffective concentrations of praziquantel.
Nevirapine: (Moderate) Monitor for reduced response to praziquantel if coadministered with nevirapine. Concomitant use may produce therapeutically ineffective concentrations of praziquantel. In vitro and drug interactions studies suggest that the CYP3A4 isoenzyme is the major enzyme involved in praziquantel metabolism; nevirapine is a weak CYP3A4 inducer.
Nirmatrelvir; Ritonavir: (Moderate) Monitor for increased side effects of praziquantel if administered with ritonavir. Concurrent administration may result in elevated praziquantel plasma concentrations. Praziquantel is metabolized by the hepatic isoenzyme CYP3A4; ritonavir is an inhibitor of this enzyme.
Odevixibat: (Moderate) Monitor for reduced response to praziquantel if coadministered with odevixibat. Concomitant use may produce therapeutically ineffective concentrations of praziquantel. In vitro and drug interactions studies suggest that the CYP3A isoenzyme is the major enzyme involved in praziquantel metabolism; odevixibat is a weak CYP3A inducer.
Olutasidenib: (Moderate) Monitor for reduced response to praziquantel if coadministered with olutasidenib. Concomitant use may produce therapeutically ineffective concentrations of praziquantel. In vitro and drug interactions studies suggest that the CYP3A isoenzyme is the major enzyme involved in praziquantel metabolism; olutasidenib is a weak CYP3A inducer.
Omaveloxolone: (Moderate) Monitor for reduced response to praziquantel if coadministered with omaveloxolone. Concomitant use may produce therapeutically ineffective concentrations of praziquantel. In vitro and drug interactions studies suggest that the CYP3A isoenzyme is the major enzyme involved in praziquantel metabolism; omaveloxolone is a weak CYP3A inducer.
Omeprazole; Amoxicillin; Rifabutin: (Major) In vitro and drug interactions studies suggest that the CYP3A4 isoenzyme is the major enzyme involved in praziquantel metabolism. Therefore, use of praziquantel with rifabutin, a CYP3A4 inducer, should be done with caution as concomitant use may produce therapeutically ineffective concentrations of praziquantel.
Oritavancin: (Major) Praziquantel is metabolized by CYP3A4; oritavancin is a weak CYP3A4 inducer. Plasma concentrations and efficacy of praziquantel may be reduced if these drugs are administered concurrently.
Oxcarbazepine: (Major) In vitro and drug interactions studies suggest that the CYP3A4 isoenzyme is the major enzyme involved in praziquantel metabolism. Therefore, use of praziquantel with oxcarbazepine, a CYP3A4 inducer, should be done with caution as concomitant use may produce therapeutically ineffective concentrations of praziquantel.
Perampanel: (Major) In vitro and drug interactions studies suggest that the CYP3A4 isoenzyme is the major enzyme involved in praziquantel metabolism. Therefore, use of praziquantel with perampanel, a weak CYP3A4 inducer in vitro, should be done with caution as concomitant use may produce therapeutically ineffective concentrations of praziquantel.
Phenobarbital: (Contraindicated) The concomitant use of phenobarbital with praziquantel is contraindicated due to decreased exposure and efficacy of praziquantel. If treatment with praziquantel is necessary, treatment with phenobarbital should be discontinued 4 weeks before administration of praziquantel. Treatment with phenobarbital can then be restarted 1 day after completion of praziquantel treatment. Phenobarbital is a strong CYP3A4 inducer and praziquantel is a CYP3A4 substrate. In a crossover study with a 2-week washout period, administration of praziquantel followed by another strong CYP3A inducer resulted in undetectable plasma concentrations of praziquantel in 7 out of 10 subjects. When praziquantel was administered two weeks after discontinuation of the strong inducer, the mean praziquantel AUC and Cmax were 23% and 35% lower, respectively, than when praziquantel was given alone.
Phenobarbital; Hyoscyamine; Atropine; Scopolamine: (Contraindicated) The concomitant use of phenobarbital with praziquantel is contraindicated due to decreased exposure and efficacy of praziquantel. If treatment with praziquantel is necessary, treatment with phenobarbital should be discontinued 4 weeks before administration of praziquantel. Treatment with phenobarbital can then be restarted 1 day after completion of praziquantel treatment. Phenobarbital is a strong CYP3A4 inducer and praziquantel is a CYP3A4 substrate. In a crossover study with a 2-week washout period, administration of praziquantel followed by another strong CYP3A inducer resulted in undetectable plasma concentrations of praziquantel in 7 out of 10 subjects. When praziquantel was administered two weeks after discontinuation of the strong inducer, the mean praziquantel AUC and Cmax were 23% and 35% lower, respectively, than when praziquantel was given alone.
Phenytoin: (Contraindicated) The concomitant use of phenytoin with praziquantel is contraindicated due to decreased exposure and efficacy of praziquantel. If treatment with praziquantel is necessary, treatment with phenytoin should be discontinued 4 weeks before administration of praziquantel. Treatment with phenytoin can then be restarted 1 day after completion of praziquantel treatment. Phenytoin is a strong CYP3A4 inducer and praziquantel is a CYP3A4 substrate; coadministration may result in decreased plasma concentrations of praziquantel. In a crossover study with a 2-week washout period, administration of praziquantel followed by another strong CYP3A inducer resulted in undetectable plasma concentrations of praziquantel in 7 out of 10 subjects. When praziquantel was administered two weeks after discontinuation of the strong inducer, the mean praziquantel AUC and Cmax were 23% and 35% lower, respectively, than when praziquantel was given alone.
Primidone: (Contraindicated) The concomitant use of primidone with praziquantel is contraindicated due to decreased exposure and efficacy of praziquantel. If treatment with praziquantel is necessary, treatment with primidone should be discontinued 4 weeks before administration of praziquantel. Treatment with primidone can then be restarted 1 day after completion of praziquantel treatment. Primidone is a strong CYP3A4 inducer and praziquantel is a CYP3A4 substrate. In a crossover study with a 2-week washout period, administration of praziquantel followed by another strong CYP3A inducer resulted in undetectable plasma concentrations of praziquantel in 7 out of 10 subjects. When praziquantel was administered two weeks after discontinuation of the strong inducer, the mean praziquantel AUC and Cmax were 23% and 35% lower, respectively, than when praziquantel was given alone.
Quinine: (Major) In vitro and drug interactions studies suggest that the CYP3A4 isoenzyme is the major enzyme involved in praziquantel metabolism. Therefore, use of praziquantel with quinine, a CYP3A4 inducer and inhibitor, should be done with caution as concomitant use may produce therapeutically ineffective concentrations of praziquantel.
Rifabutin: (Major) In vitro and drug interactions studies suggest that the CYP3A4 isoenzyme is the major enzyme involved in praziquantel metabolism. Therefore, use of praziquantel with rifabutin, a CYP3A4 inducer, should be done with caution as concomitant use may produce therapeutically ineffective concentrations of praziquantel.
Rifampin: (Contraindicated) The concomitant use of rifampin with praziquantel is contraindicated due to decreased exposure and efficacy of praziquantel. If treatment with praziquantel is necessary, treatment with rifampin should be discontinued 4 weeks before administration of praziquantel. Treatment with rifampin can then be restarted 1 day after completion of praziquantel treatment. Rifampin is a strong CYP3A4 inducer and praziquantel is a CYP3A4 substrate. In a crossover study with a 2-week washout period, administration of praziquantel followed by rifampin resulted in undetectable plasma concentrations of praziquantel in 7 out of 10 subjects. When praziquantel was administered two weeks after discontinuation of rifampin, the mean praziquantel AUC and Cmax were 23% and 35% lower, respectively, than when praziquantel was given alone.
Rifapentine: (Contraindicated) Coadministration of praziquantel with rifapentine is contraindicated due to the potential for decreased exposure and efficacy of praziquantel. Praziquantel is a CYP3A4 substrate and rifapentine is a strong CYP3A4 inducer. In a crossover study with a 2-week washout period, administration of praziquantel followed by another strong CYP3A inducer resulted in undetectable plasma concentrations of praziquantel in 7 out of 10 subjects. When praziquantel was administered two weeks after discontinuation of the strong inducer, the mean praziquantel AUC and Cmax were 23% and 35% lower, respectively, than when praziquantel was given alone.
Ritonavir: (Moderate) Monitor for increased side effects of praziquantel if administered with ritonavir. Concurrent administration may result in elevated praziquantel plasma concentrations. Praziquantel is metabolized by the hepatic isoenzyme CYP3A4; ritonavir is an inhibitor of this enzyme.
Sodium Phenylbutyrate; Taurursodiol: (Moderate) Monitor for reduced response to praziquantel if coadministered with taurursodiol. Concomitant use may produce therapeutically ineffective concentrations of praziquantel. In vitro and drug interactions studies suggest that the CYP3A isoenzyme is the major enzyme involved in praziquantel metabolism; taurursodiol is a weak CYP3A inducer.
Sotorasib: (Moderate) Monitor for reduced response to praziquantel if coadministered with sotorasib. Concomitant use may produce therapeutically ineffective concentrations of praziquantel. In vitro and drug interactions studies suggest that the CYP3A4 isoenzyme is the major enzyme involved in praziquantel metabolism; sotorasib is a moderate CYP3A4 inducer.
St. John's Wort, Hypericum perforatum: (Contraindicated) The concomitant use of St. John's Wort with praziquantel is contraindicated due to decreased exposure and efficacy of praziquantel. If treatment with praziquantel is necessary, treatment with St. John's Wort should be discontinued 4 weeks before administration of praziquantel. Treatment with St. John's Wort can then be restarted 1 day after completion of praziquantel treatment. St. John's Wort is a strong CYP3A4 inducer and praziquantel is a CYP3A4 substrate; coadministration may result in decreased plasma concentrations of praziquantel. In a crossover study with a 2-week washout period, administration of praziquantel followed by another strong CYP3A inducer resulted in undetectable plasma concentrations of praziquantel in 7 out of 10 subjects. When praziquantel was administered two weeks after discontinuation of the strong inducer, the mean praziquantel AUC and Cmax were 23% and 35% lower, respectively, than when praziquantel was given alone.
Telotristat Ethyl: (Moderate) Monitor for reduced response to praziquantel if coadministered with telotristat. Concomitant use may produce therapeutically ineffective concentrations of praziquantel. In vitro and drug interactions studies suggest that the CYP3A4 isoenzyme is the major enzyme involved in praziquantel metabolism. Telotristat is a weak CYP3A4 inducer.
Vemurafenib: (Moderate) Vemurafenib is an inducer of CYP3A4 and decreased plasma concentrations of drugs metabolized by this enzyme, such as praziquantel, could be expected with concurrent use. Use caution, and monitor therapeutic effects of praziquantel when coadministered with vemurafenib.

Biltricide/Praziquantel Oral Tab: 600mg

75 mg/kg/day PO.

75 mg/kg/day PO.

75 mg/kg/day PO.

75 mg/kg/day PO.

Safety and efficacy have not been established.

Safety and efficacy have not been established.

Praziquantel works by increasing the cell membrane permeability in susceptible worms. This induces a rapid contraction of the schistosomes. Praziquantel further causes vacuolization and disintegration of the schistosome tegument.[28515]

Praziquantel is administered orally. It is metabolized by the liver. Approximately 80% of an administered dose is excreted via the kidney almost exclusively (more than 99%) as metabolites. The serum half-life is 0.8 to 1.5 hours.[28515]
 
Affected cytochrome P450 isoenzymes and drug transporters: CYP3A4
In general, drugs that inhibit hepatic metabolism via the microsomal CYP450 enzyme system increase the bioavailability of praziquantel and potent CYP450 enzyme inducers may decrease praziquantel serum concentrations.[28515] In vitro and drug interaction studies suggest that praziquantel may be a substrate of CYP3A4. Concomitant strong CYP3A4 inducers are contraindicated, while other CYP3A4 inducers may decrease effectiveness of praziquantel. CYP3A4 inhibitors may not have any clinical implications due to the dosing of praziquantel and the limited side effect profile.[27480] [28515] [34457] [34458] [34459]

Praziquantel is rapidly absorbed and undergoes first-pass metabolism. Bioavailability is approximately 80%. Maximal praziquantel serum concentrations occur within 1 to 3 hours after dosing.[28515]

Published studies, including 2 randomized, controlled studies, have not identified a risk of major birth defects, miscarriage, or adverse maternal or fetal outcomes with praziquantel use during human pregnancy.[28515] For mass prevention campaigns, the benefit of praziquantel use outweighs the risk at any stage of pregnancy. For individual patients in a clinical setting, weigh the risk of treatment in pregnancy with the risk of disease progression in the absence of treatment. Guidelines suggest deferring treatment for neurocysticercosis until after pregnancy unless intracranial pressure is elevated.[63735]

Praziquantel is excreted in human breast milk. In a study of 10 women, 5 receiving single-dose therapy and 5 receiving 3-dose therapy, the concentration in breast milk is about one-fourth (25%) that of maternal serum concentration or 0.0008% of the given dose. Breast milk concentrations were undetectable 24 to 32 hours after exposure.[28515] [48701] There are no data available on the effects of praziquantel on the breastfed infant or milk production.[28515] A consultation group to the World Health Organization (WHO) states that single dose-therapy may be administered to breast-feeding women. Alternatively, to reduce exposure in the breast-feeding infant, an alternate feeding method (e.g., stored milk) may be used for 24 to 36 hours after therapy.[48698] [48700] [48702] For mass prevention campaigns, praziquantel use is encouraged during breast-feeding. For individual patients in a clinical setting, weigh the risk of treatment with the risk to the infant and the risk of disease progression in the mother in the absence of treatment.