CURAFLUKE

Indications

• Intestinal nematodes
• Cestodes
• Helminth infections in veterinary practice

Dosage

Children: Refer to the BNF for Children for appropriate dosing recommendations for paediatric patients.

Adults: Refer to the BNF for specific dosing guidelines, as adult doses may vary depending on the type of infection being treated.

Mechanism of action

Fenbendazole exerts its antiparasitic effects by binding to beta-tubulin in parasites, leading to microtubule destabilization and inhibiting tubulin polymerization. This process disrupts cellular functions, including glucose uptake and energy management, particularly in the anterior intestine, where it is most effective due to its poor absorption following oral administration.

Pharmacodynamics

The primary pharmacodynamic action of fenbendazole involves its ability to alter the structure and function of microtubules in parasitic cells. By inhibiting the polymerization of tubulin, fenbendazole interferes with various cellular processes, including mitosis and the transport of secretory vesicles. This ultimately results in the death of the parasites, as they are unable to maintain essential cellular functions.

Pharmacokinetics

Fenbendazole has low oral bioavailability due to poor absorption from the gastrointestinal tract. It undergoes hepatic metabolism and is excreted primarily in the faeces. The duration of action is affected by the persistence of the drug in the intestinal lumen, where it maintains its anthelmintic effects.

Pregnancy

Fenbendazole is not recommended during pregnancy due to potential risks to the developing fetus.

Breast-feeding

It is not known whether fenbendazole is excreted in human milk. Caution is advised when administering to nursing mothers.

Storage

Store at room temperature, away from moisture and heat. Keep out of reach of children.

Formulations

• {'formulation': 'Powder for oral suspension', 'strength': 'Various strengths available'}
• {'formulation': 'Tablets', 'strength': 'Various strengths available'}

Indications

• Fasciolosis
• Liver fluke infections
• Parasitic infections in livestock

Dosage

Children: Refer to the BNF for Children for specific dosing information.

Adults: Refer to the BNF for specific dosing information.

Mechanism of action

Rafoxanide functions by inhibiting the succinate dehydrogenase enzyme in the parasite's mitochondria, which disrupts the energy production process. This ultimately leads to a depletion of ATP in the parasite, resulting in its death. The drug has a high affinity for the parasite's mitochondrial membranes, making it effective against trematodes and some nematodes.

Pharmacodynamics

Rafoxanide exhibits a rapid onset of action against susceptible parasites. The drug’s effectiveness is influenced by its lipophilicity, which aids in its absorption and distribution within the host. It demonstrates a high level of activity against adult and juvenile stages of flukes, providing a therapeutic benefit in the management of trematodiasis.

Pharmacokinetics

Rafoxanide is well absorbed after administration and achieves peak plasma concentrations relatively quickly. The drug is extensively metabolized in the liver, with metabolites being primarily excreted via the bile. Its elimination half-life allows for dosing at intervals that effectively manage parasitic infections. The pharmacokinetics may vary based on the animal species and health status.

Pregnancy

There is limited data on the use of rafoxanide in pregnancy. Caution is advised.

Breast-feeding

It is not known if rafoxanide is excreted in human milk. Caution is advised.

Storage

Store in a cool, dry place away from direct sunlight.

Mechanism of action

Due to its poor absorption by oral administration, fenbendazole is particularly effective for targeting intestinal parasites. It exerts its antiparasitic effects primarily in the anterior intestine by depolymerizing microtubules, inhibiting intestinal secretory vesicle transport. When fenbendazole binds to beta-tubulin in parasites, it causes microtubule destabilization and hinders tubulin polymerization. This destabilization disrupts cellular function, such as glucose uptake, and thus affects the energy management of parasites.