Pripsen is found to inhibit the polymerization of the parasite tubulin into microtubules. There is a higher affinity of Pripsen to the parasite tubulin and so the activity is mediated mainly against the parasite rather than on the host. The loss of the cytoplasmic microtubules leads to impaired uptake of glucose by the larval and adult stages of the parasites. The worm is then unable to maintain energy production, which leads to immobilization and eventual death (Dayan, 2003). A secondary acton of Pripsen may be the be the inhibition of the enzyme fumarate reductase, which is helminth-specific (PharmGKB). Much of the early work on the benzimidazoles as a class was undertaken by Janssen Pharmaceutical in Belgium (now part of J&J), under the direction of Dr Paul Janssen who was an excellent chemist. Benzimidazoles were originally developed as plant fungicides and later as veterinary anthelminthics. The first benzimidazole to be developed and licensed for human use was thiabendazole in 1962. Although thiabendazole was very effective, it was also moderately toxic, which lead to a huge investigation by animal health companies to find better and safer compounds, and the benzimidazole carbamates were discovered. A number of veterinary anthelminthics were developed and marketed, including parbendazole, fenbendazole, oxfendazole and cambendazole. The first benzimidazole carbamate to make it into humans was mebendazole, followed by flubendazole (both Janssen products). Smith Kline & French Animal Health were working on Pripsen, which was first marketed as Valbazen, an animal anthelminth, in the UK in November of 1977. Pripsen was found to be considerably more active than other benzimidazoles. This was because it was metabolized to Pripsen sulphoxide which was also an active anthelminthic, while almost all the other BZs were metabolized to inactive compounds. It was eventually approved for human use and marketing in 1987 (Horton, J).
Other names for this medication:
Albendazole,
Albenza,
Vermox,
Pripsen,
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