There's more in the article, but this is all I had access to. The references were not available (dammit)

ABSTRACT Although the broad-spectrum anti-parasitic effects of the avermectin derivative ivermectin are well documented, its anti-inflammatory activity has only recently been demonstrated. For over 25 years, ivermectin has been used to treat parasitic infections in mammals, with a good safety profile that may be attributed to its high affinity to invertebrate neuronal ion channels and its inability to cross the blood–brain barrier in humans and other mammals. Numerous studies report low rates of adverse events, as an oral treatment for parasitic infections, scabies and head lice. Ivermectin has been used off-label to treat diseases associated with Demodex mites, such as blepharitis and demodicidosis. New evidence has linked Demodex mites to rosacea, a chronic inflammatory disease. Ivermectin has recently received FDA and EU approval for the treatment of adult patients with inflammatory lesions of rosacea, a disease in which this agent has been shown to be well tolerated. After more than 25 years of use, ivermectin continues to provide a high margin of safety for a growing number of indications based on its anti-parasitic and anti-inflammatory activities.

INTRODUCTION The recent approval of ivermectin for the treatment of the inflammatory lesions of rosacea is the latest in a series of indications spanning the past 25 years. The aim of this publication is to provide an overview of the history and safety of ivermectin during its clinical use, with particular focus on its anti-inflammatory action, in addition to examining the safety data for the recent indication for the treatment of the inflammatory lesions of rosacea. Since its development in the 1970s, ivermectin has been used to treat parasitic infections in billions of animals and people worldwide. Ivermectin is a semi-synthetic derivative of the avermectin series of compounds (22, 23-dihydroavermectin B1, Figure 1), which are naturally-occurring fermentation products of the soil organism Streptomyces avermitilis. Avermectin demonstrated profound anti-parasitic bioactivity in vitro, and ivermectin was selected for further study development following demonstration of a good safety profile and potent anti-parasitic efficacy in vivo.

The potency of ivermectin as an anti-parasitic drug stems from its unique mode of action; it interacts with invertebrate-specific cell membrane ion channels in a broadspectrum of parasites causing paralysis and death. Ivermectin binds selectively and with high affinity to glutamate-gated ion channels, which are unique to invertebrates, on muscle and nerve cell membranes and, by keeping these channels open, it increases membrane permeability to chloride ions and causes hyperpolarization. Avermectin derivatives, however, have a considerably lower affinity for the ligand-gated channels expressed in mammals. In addition to glutamate-gated ion channels, ivermectin also acts as an agonist to the neurotransmitter-gated gamma-aminobutyric acid (GABA). 9 In mammals, GABA-gated channels are found exclusively in the central nervous system, and because ivermectin does not readily cross the blood–brain barrier in mammals, it has a good safety profile in humans and the vast majority of animals, including cattle, sheep, swine, and horses.

Avermectins are macrolide lactone derivatives, which, in contrast to macrolide antibiotics, lack significant antibacterial or antifungal activity. 6 Although ivermectin is an avermectin derivative (Figure 1), as a macrolide lactone, it has the potential to modulate host immune responses and suppress inflammatory responses, via inhibition of liposaccharide (LPS)-induced cytokine production. 12 LPS is recognized by the toll-like receptors (TLRs) on the cell surface of macrophages, triggering a signaling cascade that results in expression and secretion of cytokines such as tumor necrosis factor-α (TNF-α), interleukin (IL)-β6 and IL-6. 12 Ivermectin has been shown to significantly reduce levels of these pro-inflammatory cytokines in vivo. An increased expression of TLR-2 on keratinocytes, 14 enhancing production of KLK5 and subsequent protease activity as well

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