Fenben lab fenbendazol is an antiparasitic agent that has long been used for treatment of helminth parasites in livestock. It has been shown to be effective against Ascaris, hookworms (mainly Necator americanus), and nematodes including Giardia lamblia, Trichomonas vaginalis, and Schistosoma japonicum. In addition it is effective in dogs for the control of intestinal helminths such as Toxacara canis, Toxascaris leonina, Ancylostoma tubaeforme, and Crenosoma procyonis. It has also been used to control pulmonary helminths including Strongyloides leonina and Heterobilharzia americana.
Recently, during a facility treatment for Aspiculuris pinworms using a fenbendazole diet at our institution, human lymphoma xenografts failed to grow in C.B-17/Icr-Prkdcscid/Crl (SCID) mice in an established xenograft model. This failure occurred despite the use of a sterilizable fenbendazole-treated diet that was supplemented with additional vitamins to compensate for losses during sterilization. This suggested that the lack of tumor growth was due to a reduction in the concentration of vitamins in the diet.
The exact mechanism of fenbendazole action is not known, but it is thought that it works by binding to b-tubulin, an important component of microtubules, and preventing them from functioning properly. Consequently, cell division is halted and the parasite is killed. The effect on the host is not permanent, however, because b-tubulin quickly replenishes itself after fenbendazole exposure.
In the present study, SCID mice were assigned to 4 different groups: control, fenbendazole, vitamin alone, and both fenbendazole and vitamins together. Initial and terminal white blood counts did not differ significantly among the groups, but the fenbendazole group had significantly lower total white and neutrophil responses at study termination than did the vitamin only or control groups.
These findings are similar to those obtained by Mukhopadhyay and co-workers in 2002 when they reported that mebendazole, a related compound to fenbendazole, induces expression of CYP1A, which is necessary for metabolizing the benzimidazole compounds. The ability of fenbendazole to induce CYP1A indicates that it is a more potent inhibitor of parasite metabolism than mebendazole, which probably explains its superior efficacy in reducing parasite levels. The fenbendazole/mebendazole combination was more potent than either drug alone and was comparable to the level of inhibition observed in mice treated with praziquantel. fenben lab fenbendazol