Absorption, Distribution and Excretion
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.

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Metabolism / Metabolites
Praziquantel is rapidly metabolized by the cytochrome P450 enzyme system and undergoes a first-pass effect after oral administration.

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Biological Half-Life
Following oral administration, the elimination half-life of praziquantel in serum ranges between 0.8 to 1.5 hours.

Hepatotoxicity
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.
Likelihood score: D (possible rare cause of clinically apparent liver injury usually as a part of a systemic hypersensitivity reaction).

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Effects During Pregnancy and Lactation
◉ Summary of Use during Lactation
Because of the minute levels of praziquantel in breastmilk, amounts ingested by the infant are small and would not be expected to cause any adverse effects in breastfed infants. Expert opinion holds that lactation should not be a contraindication to maternal treatment with praziquantel. To minimize infant exposure, a single dose can be taken just before the infant's longest sleep period or an alternate method of feeding (e.g., stored milk) can be used for 24 hours after a single dose or the last of a series of doses.
◉ Effects in Breastfed Infants
Relevant published information was not found as of the revision date.
◉ Effects on Lactation and Breastmilk
Relevant published information was not found as of the revision date.

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Protein Binding
Approximately 80% of praziquantel is bound exclusively to albumin.

Internal Med. 1983, 99:195-198.

2-[cyclohexyl(oxo)methyl]-3,6,7,11b-tetrahydro-1H-pyrazino[2,1-a]isoquinolin-4-one is a member of isoquinolines.
Praziquantel is a pyrazino-isoquinolein derivative from the thioxantonic group used as a broad anthelmintic spectrum. Specifically, it is known as a treatment of trematodes and cestodes infections such as schistosomiasis, taeniasis, and cysticercosis. The efficacy of praziquantel in treating parasitic flatworms infection with low cost (~US$0.20 drug cost to treat a child) makes it an integral to WHO's plan to eliminate schistosomiasis by 2030. Despite being approved since 1980, the exact mechanism of action is yet to be elucidated.
Praziquantel is an Anthelmintic.
Praziquantel is an anthelmintic agent with activity against a broad spectrum of trematodes and cestodes that is used predominantly in the therapy of schistosomiasis, liver flukes, and cysticercosis. Praziquantel therapy has been reported to cause serum aminotransferase elevations during therapy, but clinically apparent liver injury after its use is rare if it occurs at all.
Praziquantel is a pyrazinoisoquinoline derivative with anthelminthic property. Praziquantel increases the permeability of the tegument of susceptible worms, resulting in an influx and increase in intra-tegumental calcium leading to rapid contractions and paralysis of the worm's musculature through a subsequent increase in levels of calcium in the sarcoplasmic reticulum. In addition, vacuolization of the tegumental syncytium and blebbing results in tegument disintegration, leads to antigen exposure and elicit host defense responses to the worm. The result is the formation of granulomas and phagocytosis.
An anthelmintic used in most schistosome and many cestode infestations.
See also: Praziquantel; Pyrantel Pamoate (component of); Emodepside; Praziquantel (component of); Eprinomectin; Praziquantel (component of) ... View More ...

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Drug Indication
Praziquantel is indicated in patients aged 1 year and older for the treatment of the schistosomiasis due to all species of Schistosoma (for example, Schistosoma mekongi, Schistosoma japonicum, Schistosoma mansoni and Schistosoma hematobium) and clonorchiasis and opisthorchiasis due to the liver flukes, Clonorchis sinensis/Opisthorchis viverrini (approval of this indication was based on studies in which the two species were not differentiated).
FDA Label

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Mechanism of Action
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.

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Pharmacodynamics
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.

C19H24N2O2

312.41

312.183

C, 73.05; H, 7.74; N, 8.97; O, 10.24

55268-74-1

Praziquantel-d11;1246343-36-1

4891

Solid powder

1.2±0.1 g/cm3

544.1±50.0 °C at 760 mmHg

136-142ºC

254.6±22.5 °C

0.0±1.5 mmHg at 25°C

1.615

2.44

40.62

0

2

1

23

472

0

O=C1CN(C(C2CCCCC2)=O)CC3N1CCC4=C3C=CC=C4

FSVJFNAIGNNGKK-UHFFFAOYSA-N

InChI=1S/C19H24N2O2/c22-18-13-20(19(23)15-7-2-1-3-8-15)12-17-16-9-5-4-6-14(16)10-11-21(17)18/h4-6,9,15,17H,1-3,7-8,10-13H2

2-(cyclohexanecarbonyl)-3,6,7,11b-tetrahydro-1H-pyrazino[2,1-a]isoquinolin-4-one

Droncit Biltricide Praziquantel

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ~50 mg/mL (~160.05 mM)
H2O : ~0.1 mg/mL (~0.32 mM)

配方 1 中的溶解度: ≥ 2.5 mg/mL (8.00 mM) (饱和度未知) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将100 μL 25.0 mg/mL澄清DMSO储备液加入到400 μL PEG300中，混匀；然后向上述溶液中加入50 μL Tween-80，混匀；加入450 μL生理盐水定容至1 mL。
*生理盐水的制备：将 0.9 g 氯化钠溶解在 100 mL ddH₂O中，得到澄清溶液。

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配方 2 中的溶解度: ≥ 2.5 mg/mL (8.00 mM) (饱和度未知) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将 100 μL 25.0 mg/mL澄清DMSO储备液加入900 μL 20% SBE-β-CD生理盐水溶液中，混匀。
*20% SBE-β-CD 生理盐水溶液的制备（4°C，1 周）：将 2 g SBE-β-CD 溶解于 10 mL 生理盐水中，得到澄清溶液。

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配方 3 中的溶解度: ≥ 2.5 mg/mL (8.00 mM) (饱和度未知) in 10% DMSO + 90% Corn Oil (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将 100 μL 25.0 mg/mL 澄清 DMSO 储备液加入到 900 μL 玉米油中并混合均匀。

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配方 4 中的溶解度: 12.5 mg/mL (40.01 mM) in 50% PEG300 50% Saline (这些助溶剂从左到右依次添加，逐一添加), 悬浮液； 超声助溶 (<60°C).
*生理盐水的制备：将 0.9 g 氯化钠溶解在 100 mL ddH₂O中，得到澄清溶液。

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请根据您的实验动物和给药方式选择适当的溶解配方/方案：
1、请先配制澄清的储备液(如：用DMSO配置50 或 100 mg/mL母液(储备液));
2、取适量母液，按从左到右的顺序依次添加助溶剂，澄清后再加入下一助溶剂。以 下列配方为例说明 (注意此配方只用于说明，并不一定代表此产品 的实际溶解配方):
10% DMSO → 40% PEG300 → 5% Tween-80 → 45% ddH2O (或 saline);
假设最终工作液的体积为 1 mL, 浓度为5 mg/mL: 取 100 μL 50 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀/澄清；向上述体系中加入50 μL Tween-80，混合均匀/澄清；然后继续加入450 μL ddH2O (或 saline)定容至 1 mL；
3、溶剂前显示的百分比是指该溶剂在最终溶液/工作液中的体积所占比例;
4、 如产品在配制过程中出现沉淀/析出，可通过加热(≤50℃)或超声的方式助溶;
5、为保证最佳实验结果，工作液请现配现用！
6、如不确定怎么将母液配置成体内动物实验的工作液，请查看说明书或联系我们;
7、 以上所有助溶剂都可在 Invivochem.cn网站购买。