プラジカンテル

2.5

2.43

3.81e-01 g/L

>46.9 [ug/mL] (The mean of the results at pH 7.4)

Breast Feeding; Lactation; Milk, Human; Anti-Infective Agents; Anthelmintics; Antiparasitic Agents

FDA approved drugs -> Active ingredient

FDA approved drugs -> Active ingredient

Antischistosomals and other antitrematode medicines

EMA approved medicines: Veterinary medicine

Active Ingredients (Praziquantel) -> FDA Greenbook

Pharmaceuticals -> UK Veterinary Medicines Directorate List

Pharmaceuticals -> Animal Drugs -> Approved in Taiwan

136-138 °C

136 °C

178.5 Ų [M+H]+ [CCS Type: DT; Buffer gas: N2; Ionization: APCI+; Dataset: TOXCAST; Source Identifier: DTXSID9021182]

162.35 Ų [M+H-H2O]+ [CCS Type: TW; Method: calibrated with polyalanine and drug standards]

176.5 Ų [M+H]+ [CCS Type: TW; Method: calibrated with polyalanine and drug standards]

This chemical does not meet GHS hazard criteria for 1.8% (2 of 113) of reports.

H412 (91.2%): Harmful to aquatic life with long lasting effects [Hazardous to the aquatic environment, long-term hazard]

P273, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 113 reports by companies from 7 notifications to the ECHA C&L Inventory.

Praziquantel therapy has been associated with elevations in serum aminotransferase levels in up to 27% of patients, but these abnormalities were self-limiting. Praziquantel has been rarely associated with clinically apparent liver injury, which generally accompanied hypersensitivity reactions such as rash and fever. In a large retrospective survey from China, 2 of 25,000 treated patients were reported to have developed jaundice after praziquantel therapy, but no specific information about the two cases was provided. There have been few studies of long term therapy with praziquantel, and most controlled trials of this agent have used one day courses without serum aminotransferase monitoring. However, millions of people have been treated with praziquantel as a part of large scale control strategies in China where schistosomiasis Japonica is endemic. The combination of praziquantel preventive therapy and snail control has resulted in marked decreases in the prevalence of infection in the population with no evidence of significant toxicity. Thus, mild acute liver injury can accompany systemic hypersensitivity reactions to praziquantel, but both the allergic reaction and the liver injury tend to be short-lived and resolve rapidly even without specific therapy.

Praziquantel is the drug of choice for the treatment of all forms of schistosomiasis. It has low toxicity and mild side effects; however, a major weakness is its relative inefficacy against recent infections, and this might occasionally result in low cure rates in hyperendemic areas.

Drug Induced Liver Injury Rank (DILIrank 2.0)

Praziquantel

Ambiguous-DILI-concern

3

Warnings & precautions

DOI:10.1016/j.drudis.2016.02.015

P - Antiparasitic products, insecticides and repellents

QP - Antiparasitic products, insecticides and repellents

P02BA01

In vitro studies on trematodes and cestodes have shown that praziquantel induces a rapid contraction of schistosomas by a specific effect on the permeability of the cell membrane. The drug further causes vacuolization and disintegration of the schistosome tegument. The effect is more marked on adult worms compared to young worms. An increased Ca2⁺-influx may play an important role. Secondary effects are inhibition of glucose uptake, lowering of glycogen levels and stimulation of lactate release. The action of praziquantel is specific to trematodes and cestodes; nematodes (including filariae) are not affected. Praziquantel is active against schistosoma (for example, Schistosoma mekongi, Schistosoma japonicum, Schistosoma mansoni and Schistosoma hematobium), and infections due to the liver flukes, Clonorchis sinensis/Opisthorchis viverrini. Published in vitro data have shown a potential lack of efficacy of praziquantel against migrating schistosomulae. An interesting quirk of praziquantel is that it is relatively ineffective against juvenile schistosomes. While initially effective, effectiveness against schistosomes decreases until it reaches a minimum at 3-4 weeks. Effectiveness then increases again until it is once again fully effective at 6-7 weeks.

Although the exact mechanism of action is unknown, praziquantel was hypothesized to target the β subunits of voltage-gated Ca₂₊ channels, particularly in Schistosoma mansoni and Schistosoma japonicum, due to the lack of two conserved serine residues in these subunits. This is supported by the finding that co-administration of calcium channel blockers like nicarpidine and nifedipine renders 50% of Schistosoma mansoni resistant to praziquantel. Increased exposure of antigens on the worm surface was also observed, but little research has been done to elucidate on the mechanism of action.

6490C9U457

PRAZIQUANTEL

Established Pharmacologic Class [EPC] - Anthelmintic

Praziquantel is an Anthelmintic.

PRAZIQUANTEL

Anthelmintic [EPC]

After oral administration of praziquantel, about 80% of the dose is absorbed. In subjects with normal hepatic function who received 40 mg/kg of praziquantel under fasting conditions, the mean ± SD Cmax and AUC were 0.83 ± 0.52 µg/mL and 3.02 ± 0.59 µg/mL x hr. The Tmax was 1.48 ± 0.74 hours.

Approximately 80% of an oral dose of praziquantel is excreted in the kidneys, almost exclusively (greater than 99%) in the form of praziquantel metabolites.

Following a single oral dose of 40 mg/kg of praziquantel in healthy volunteers, the volume of distribution was estimated to be 7695 ± 2716 L.

Following a single oral dose of 40 mg/kg of praziquantel in healthy volunteers, the clearance was estimated to be 11.4 ± 2.8 L/kg/h.

Animal Drugs -> FDA Approved Animal Drug Products (Green Book) -> Active Ingredients

Pharmaceuticals -> Animal Drugs -> Approved in Taiwan