[9] Approved for human use in 1987,[10] it is used to treat infestations including head lice, scabies, river blindness (onchocerciasis), strongyloidiasis, trichuriasis, ascariasis and lymphatic filariasis.

[15] It is on the World Health Organization's List of Essential Medicines,[16][17] and is approved by the U.S. Food and Drug Administration (FDA) as an antiparasitic agent.

[34][35] The U.S. Centers for Disease Control and Prevention (CDC) recommends ivermectin, albendazole, or mebendazole as treatments for ascariasis.

Scabies – infestation with the mite Sarcoptes scabiei – is most commonly treated with topical permethrin or oral ivermectin.

[citation needed] For most scabies cases, ivermectin is used in a two-dose regimen: the first dose kills the active mites, but not their eggs.

[43] For severe "crusted scabies", where the parasite burden is orders of magnitude higher than usual, the CDC recommends up to seven doses of ivermectin over the course of a month, along with a topical antiparasitic.

[51] However, the American Academy of Pediatrics cautions against use of ivermectin in such patients, as the blood–brain barrier is less developed, and thus there may be an increased risk of particular CNS side effects such as encephalopathy, ataxia, coma, or death.

[52] The American Academy of Family Physicians also recommends against use in these patients, given a lack of sufficient data to prove drug safety.

[60] One concern is neurotoxicity after large overdoses, which in most mammalian species may manifest as central nervous system depression,[59] ataxia, coma, and death,[61][27] as might be expected from potentiation of inhibitory chloride channels.

These drugs include statins, HIV protease inhibitors, many calcium channel blockers, lidocaine, benzodiazepines, and glucocorticoids such as dexamethasone.

[68] The binding pushes the channels open, which increases the flow of chloride ions and hyper-polarizes the cell membranes,[59] paralyzing and killing the invertebrate.

[69] Ivermectin 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).

[70] Crossing may still become significant if ivermectin is given at high doses, in which case brain levels peak 2–5 hours after administration.

[6] Fermentation of Streptomyces avermitilis yields eight closely related avermectin homologues, of which B1a and B1b form the bulk of the products isolated.

[7] In 1970, Ōmura isolated a strain of Streptomyces avermitilis from woodland soil near a golf course along the southeast coast of Honshu, Japan.

[7] Ōmura sent the bacteria to William Campbell, who showed that the bacterial culture could cure mice infected with the roundworm Heligmosomoides polygyrus.

[7] They synthesized modified forms of avermectin B1 to improve its pharmaceutical properties, eventually choosing a mixture of at least 80% 22,23-dihydroavermectin B1a and up to 20% 22,23-dihydroavermectin B1b, a combination they called "ivermectin".

[7] Following its blockbuster success as a veterinary antiparasitic, another Merck scientist, Mohamed Aziz, collaborated with the World Health Organization to test the safety and efficacy of ivermectin against onchocerciasis in humans.

[10] They found it to be highly safe and effective,[78] triggering Merck to register ivermectin for human use as "Mectizan" in France in 1987.

[7] Half of the 2015 Nobel Prize in Physiology or Medicine was awarded jointly to Campbell and Ōmura for discovering ivermectin, "the derivatives of which have radically lowered the incidence of river blindness and lymphatic filariasis, as well as showing efficacy against an expanding number of other parasitic diseases".

While scientists and physicians largely remained skeptical, some nations adopted ivermectin as part of their pandemic-control efforts.

[103][58] Mass drug administration of a population with ivermectin to treat and prevent nematode infestation is effective for eliminating malaria-bearing mosquitos and thereby potentially reducing infection with residual malaria parasites.

[104] Whilst effective in killing malaria-bearing mosquitos, a 2021 Cochrane review found that, to date, the evidence shows no significant impact on reducing incidence of malaria transmission from the community administration of ivermectin.

[110] In 2013, ivermectin was demonstrated as a novel ligand of the farnesoid X receptor,[111][112] a therapeutic target for nonalcoholic fatty liver disease (NAFLD).

[116][117] Additionally, the use of Ivermectin for livestock has a profound impact on dung beetles, such as T. lusitanicus, as it can lead to acute toxicity within these insects.