<unk>  <unk>  bound to a C. elegans GluClR.<unk>  molecules interact with a binding pocket formed by the transmembrane domains of adjacent GluClR subunits, "locking" the receptor in an activated (open) conformation that allows unrestricted passage of chloride (Cl−) ions into the cell. (The plasma membrane is represented as a blue–pink gradient.) From . Mechanism of action<unk>  and its related drugs act by interfering with the nerve and muscle functions of helminths and insects. The drug binds to glutamate-gated chloride channels common to invertebrate nerve and muscle cells. The binding pushes the channels open, which increases the flow of chloride ions and hyper-polarizes the cell membranes, paralyzing and killing the invertebrate.<unk>  is safe for mammals (at the normal therapeutic doses used to cure parasite infections) because mammalian glutamate-gated chloride channels only occur in the brain and spinal cord: the causative<unk> s usually do not cross the blood–brain barrier, and are unlikely to bind to other mammalian ligand-gated channels. Pharmacokinetics<unk>  can be given by mouth, topically, or via injection. It does not readily cross the blood–brain barrier of mammals due to the presence of P-glycoprotein (the MDR1 gene mutation affects the function of this protein). Crossing may still become significant if<unk>  is given at high doses, in which case brain levels peak 2–5 hours after administration. In contrast to mammals,<unk>  can cross the blood–brain barrier in tortoises, often with fatal consequences.
Ivermectin
Avermectin
Praziquantel
Mebendazole
Albendazole
Flubendazole
Pyrantel
Artemether