Metronidazole phosphate is a water-soluble prodrug of metronidazole.

Menoctone is a potent liver-stage antimalarial with corresponding erythrocytic stage efficacy. This drug is an effective treatment against Theileria parva, a parasitic protozoan that causes East Coast fever in cattle. Menoctone most likely targets the mitochondrial respiration chain of Plasmodium.

Clioxanide is a derivative of diiodobenzanilide, developed by Parke, Davis & Co in the 1960s. It was used as an antihelmintic against Fasciola hepatica and Haemonchus contortus. In sheep, the compound was demonstrated high efficiency (greater than 90%) when administered at 20-40 mg/kg. Later it was found that clioxanide is an inhibitor of Type III Secretion in Yersinia bacteria.

Parbendazole is a potent inhibitor of microtubule assembly that was studied as an anthelmintic agent. Information about the current use of this drug is not available.

Dimetridazole is an anti-fungal and anti-protozoal drug traditionally used in veterinary for the prevention and treatment of histomoniasis in turkeys, genital trichomoniasis in cattle and hemorrhagic enteritis in pigs. Results from the in vitro and in vivo tests suggested, that dimetridazole was not genotoxic compound, but its use is legally limited, although this compound is still can be found in eggs.

Halofantrine is a blood schizonticidal antimalarial agent with no apparent action on the sporozoite, gametocyte or hepatic stages of the infection. It is used only to treat but not to prevent malaria. Has been marketed by GlaxoSmithKline as HALFAN (halofantrine hydrochloride) in 250 mg tablets indicated for the treatment of adults who can tolerate oral medication and who have mild to moderate malaria (equal to or less than 100,000 parasites/mm3) caused by Plasmodium falciparum or Plasmodium vivax. Among side effects is cardiac arrhythmia. It belongs to the phenanthrene class of compounds that includes quinine and lumefantrine. It was reported that halofantrine binds to hematin in vitro (crystal structure of the complex) and to to plasmpesin, a haemoglobin degrading enzyme unique to the malarial parasites.

Niclosamide is an antihelminth used against tapeworm infections. It may act by the uncoupling of the electron transport chain to ATP synthase. The disturbance of this crucial metabolic pathway prevents creation of adenosine tri-phosphate (ATP), an essential molecule that supplies energy for metabolism. Niclosamide works by killing tapeworms on contact. Adult worms (but not ova) are rapidly killed, presumably due to uncoupling of oxidative phosphorylation or stimulation of ATPase activity. The killed worms are then passed in the stool or sometimes destroyed in the intestine. Niclosamide may work as a molluscicide by binding to and damaging DNA. Niclosamide is used for the treatment of tapeworm and intestinal fluke infections: Taenia saginata (Beef Tapeworm), Taenia solium (Pork Tapeworm), Diphyllobothrium latum (Fish Tapeworm), Fasciolopsis buski (large intestinal fluke). Niclosamide is also used as a molluscicide in the control of schistosomiasis. Niclosamide was marketed under the trade name Niclocide, now discontinued.

Oxamniquine is an anthelmintic with schistosomicidal activity against Schistosoma mansoni, but not against other Schistosoma spp. Oxamniquine is a potent single-dose agent for treatment of S. mansoni infection in man, and it causes worms to shift from the mesenteric veins to the liver, where the male worms are retained; the female worms return to the mesentery, but can no longer release eggs. Oxamniquine is a semisynthetic tetrahydroquinoline and possibly acts by DNA binding, resulting in contraction and paralysis of the worms and eventual detachment from terminal venules in the mesentry, and death. Its biochemical mechanisms are hypothesized to be related to an anticholinergic effect, which increases the parasite’s motility, as well as to synthesis inhibition of nucleic acids. Oxamniquine acts mainly on male worms, but also induces small changes on a small proportion of females. Like praziquantel, it promotes more severe damage of the dorsal tegument than of the ventral surface. The drug causes the male worms to shift from the mesenteric circulation to the liver, where the cellular host response causes its final elimination. The changes caused in the females are reversible and are due primarily to the discontinued male stimulation rather than the direct effect of oxamniquine