The effectiveness of Ivermectin stems from its precise mechanism of action, which targets specific pathways in parasites and other organisms. Understanding how this drug works is key to appreciating its broad therapeutic impact and ongoing research potential.

Ivermectin belongs to the avermectin class of compounds, which are potent endectocides. Its primary mode of action involves the potentiation of inhibitory neurotransmission in invertebrates. Specifically, Ivermectin binds to glutamate-gated chloride channels (GluCls) and, to a lesser extent, GABA receptors. These channels are crucial for nerve and muscle function in parasites and insects. By binding to these channels, Ivermectin increases the influx of chloride ions into the cells, leading to hyperpolarization of the neuronal membrane. This process causes flaccid paralysis and ultimately the death of the target organism.

Crucially, mammals possess different types of chloride channels, and the glutamate-gated chloride channels targeted by Ivermectin are largely absent or inaccessible in the mammalian central nervous system. This selectivity is the primary reason for Ivermectin's remarkable safety profile in humans and animals at therapeutic doses, as it generally does not cross the blood-brain barrier to a significant extent.

Beyond its direct antiparasitic effects, ongoing research suggests Ivermectin may exert its other therapeutic effects through various mechanisms. For instance, its potential antiviral activity is thought to involve the inhibition of host cellular processes like nuclear transport. Its antibacterial and anti-cancer properties are also being investigated, revealing complex interactions with cellular pathways that warrant further exploration. Delving into the ivermectin mechanism of action provides insight into its broad utility and the scientific basis for its continued investigation.