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Anthelmintic effect of papain on Heligmosomoides bakeriAnthelmintics or antihelminthics are a group of antiparasitic drugs that expel parasitic worms (helminths) and other internal parasites from the body by either stunning or killing them and without causing significant damage to the host. They may also be called vermifuges (those that stun) or vermicides (those that kill). Anthelmintics are used to treat people who are infected by helminths, a condition called helminthiasis. These drugs are also used to treat infected animals, particularly small ruminants such as goats and sheep.[1]
Anthelmintic medication is also used in mass deworming campaigns of school-aged children in many developing countries.[2][3] Anthelmintics are also used for mass deworming of livestock. The drugs of choice for soil-transmitted helminths are mebendazole and albendazole;[4] for schistosomiasis and tapeworms it is praziquantel.[5]
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Many early treatments were herbal, such as the oil of herbs of the genus Chenopodium that were given as anthelmintic treatment for centuries. In it was found that the active constituent was ascaridole.[6] From the s to the s, halogenated hydrocarbons were used in a string of continually more efficacious anthelmintics, until their underlying host toxicity was revealed.[6] The modern broad-spectrum anthelmintics were developed by pharmaceutical companies that can afford the screening programs and testing systems that modern drug development involves.[6][7]
Historically, there have been three main classes of broad-spectrum anthelmintics.[8] These are benzimidazoles, imidazothiazoles/tetrahydropyrimidines, and macrocyclic lactones.
The benzimidazole nucleusAnthelmintic resistance
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Anthelmintic resistance occurs when a heritable genetic change occurs in the parasite's DNA, rendering it insensitive to a previously effective anthelmintic drug. This is a particularly serious problem in helminth parasites of small ruminant farm animals.[12] There are many factors that contribute to anthelmintic resistance, such as frequent, mass anthelmintic treatment, underdosing, treating repeatedly with only one anthelmintic, and resistance being transmitted during transfer of animals.[12] Anthelmintic resistance in parasites is widespread; drug resistance exists in all livestock hosts and to all anthelmintic drug classes.[13] This is a major threat to the sustainability of modern ruminant livestock production, resulting in reduced productivity, compromised animal health and welfare,[12] and increased greenhouse gas emissions through increased parasitism and farm inputs.[14] A database of published and unpublished European AR research on gastrointestinal nematodes was collated in . A total of 197 publications were available for analysis, representing 535 studies in 22 countries and spanning the period &#;. Results in sheep and goats since reveal an average prevalence of resistance to benzimidazoles of 86%, moxidectin 52%, and levamisole 48%. All major gastrointestinal nematode genera survived treatment in various studies. In cattle, prevalence of anthelminthic resistance varied between anthelmintic classes from 0&#;100% (benzimidazoles and macrocyclic lactones), 0&#;17% (levamisole) and 0&#;73% (moxidectin), and both Cooperia and Ostertagia survived treatment.[14] However, resistance is not seen as often in the parasitic helminths that affect cattle, compared to sheep. Reasons for this include the fact that cattle receive anthelminthic drugs less frequently than sheep, and the different nature of their faecal pats that could leave different numbers of resistant infective larvae on the pasture.[7] Unlike sheep, cattle can develop sufficient immunoprotection against such parasites.[15]
The ability of parasites to survive treatments that are generally effective at the recommended doses is a major threat to the future control of worm parasites in small ruminants and horses. This is especially true of nematodes, and has helped spur development of aminoacetonitrile derivatives for treatment against drug-resistant nematodes, as well as exploration of doxycycline to kill their endosymbiotic Wolbachia bacteria.[citation needed]
Both in vitro (egg hatch assay, larval development test, larval motility test, polymerase chain reaction and in vivo methods (fecal egg count reduction test) can be used to detect anthelmintic resistance.[11]
Treatment with an antihelminthic drug kills worms whose phenotype renders them susceptible to the drug, but resistant parasites survive and pass on their "resistance" genes. Resistant varieties accumulate, and treatment failure finally occurs.[16]
The ways in which anthelmintics are used have contributed to a major anthelmintic resistance issue worldwide. From the s to the s, new classes of effective and inexpensive anthelmintics were made available every decade, leading to excessive use throughout agriculture and disincentivizing alternative anti-nematodal strategies.[13] Developing new anthelmintics is time consuming and expensive therefore, it is important to use the ones that currently exist in a way that will minimize or prevent the development of anthelmintic resistance.[11] Some of these methods are ensuring animals are not being underdosed, rotating the anthelmintics that are being used, and rotation of grazing land to reduce the parasite population.[1] Other methods include using a combination of multiple different anthelmintics, and the use of refugia based strategies. Refugia refers to the portion of the parasite population not being exposed to anthelmintics. This population is therefore not undergoing selection for resistance. Use of refugia helps to slow down the speed of evolution of resistance to anthelmintic drugs.[17] Due to the problem of anthelmintic resistance, research into alternatives is continuing, including in the field of rational drug design.[18]
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References
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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. 5 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 . 6 , 7 Despite being approved since , the exact mechanism of action is yet to be elucidated. 7
Praziquantel is an anthelmintic medication used to treat parasitic worm infections such as schistosomiasis, clonorchiasis, and opisthorchiasis
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.9
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.9
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.10
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.1
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.10,1
Increased exposure of antigens on the worm surface was also observed, but little research has been done to elucidate on the mechanism of action.1
TargetActionsOrganismA
Schistosome calcium ion (Ca2+) channelsother/unknown
SchistosomaAfter 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.10
Following a single oral dose of 40 mg/kg of praziquantel in healthy volunteers, the volume of distribution was estimated to be ± L.4
Approximately 80% of praziquantel is bound exclusively to albumin.3
Praziquantel is rapidly metabolized by the cytochrome P450 enzyme system and undergoes a first-pass effect after oral administration.10
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Approximately 80% of an oral dose of praziquantel is excreted in the kidneys, almost exclusively (greater than 99%) in the form of praziquantel metabolites.10
Following oral administration, the elimination half-life of praziquantel in serum ranges between 0.8 to 1.5 hours.10
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.4
The acute toxicity of praziquantel is relatively low, as demonstrated by oral LD50 values ranging between 200 - mg/kg in various species.9
Published studies have not identified an association between praziquantel use during pregnancy and major birth defects, miscarriage, or adverse maternal or fetal outcomes. In animal reproduction studies conducted in pregnant rats and rabbits no adverse developmental outcomes were observed with oral administration of praziquantel during organogenesis at approximately 0.65 times (rats) or 1.3 times (rabbits) the highest recommended human daily dose of 75 mg/kg/day, based on body surface area.10
Mutagenicity studies of praziquantel published in the scientific literature are inconclusive. Long-term oral carcinogenicity studies in rats and golden hamsters did not reveal any carcinogenic effect at doses up to 250 mg/kg/day (about half of the human daily dose based on body surface area). Praziquantel had no effect on fertility and general reproductive performance of male and female rats when given at oral doses ranging from 30 to 300 mg/kg body weight (up to 0.65 times the human daily dose based on body surface area).10
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