**1. Introduction**

Avermectins are a complex of 16-membered macrocyclic lactones produced from soil fermentation of the actinomycete *S. avermitilis* [1, 2]. There exist eight avermectin compounds (A1a, A1b, A2a, A2b, B1a, B1b, B2a, and B2b), of which ivermectin is the most commonly employed due to its semi-synthetic mixture (80% B1a and 20% B1b), and its potent antiparasitic activity as well as its safety [3]. The family of compounds from which Ivermectin is derived was discovered by Nobel laureates Satoshi Omura and William Campbell in the 1970s. The chemical is effective against a wide number of parasites and arthropods - pinworms, mites, lice, heartworms and fleas in dogs, parasitic worms in pasture animals by disrupting the fluid exchange through the insect's cell membrane, and in the past 40 years, ivermectin has been used extensively for agriculture and veterinary purposes [4–7].

The success of ivermectin treatment as antiparasitic is due to its high affinity for the glutamate-gated chloride channels (Glu-Cl) present in parasite cells but absent in vertebrates. The ivermectin-channel-interaction prevents channel closure, leading to plasma membrane hyperpolarization, paralyzing the target parasite's pharyngeal and somatic muscles, triggering its death [2]. In addition to activating the Glu-Cl parasites channels, ivermectin acts as a dose-dependent positive allosteric regulator of several vertebrate ligand-gated channels, including the γ-aminobutyric acid type-A receptor (GABA receptor), glycine receptor, neuronal α7-nicotinic receptor, and purinergic P2X4 receptor. The effects of ivermectin over these receptors include the potentiation of agonist-induced currents at low concentrations and channel opening at higher concentrations [8]. However, GABA-sensitive neurons are protected by the blood–brain barrier within the central nervous system, protecting vertebrates against the potentially harmful effects of Ivermectin [3, 6].
