Veterinary Ivermectin: Animal Uses and Forms

Ivermectin was an animal medicine before it was a human one. It was introduced as a veterinary drug in 1981 [1], and its move from animal health into widespread use in people came afterward [2]. Veterinary products include injections, oral products and products applied to the skin for livestock, and monthly heartworm medicines for dogs [1].

This page reports what published research describes about ivermectin in animals: its forms; its uses in horses, cattle, sheep and goats; why dogs and cats with a faulty copy of the multidrug resistance 1 (MDR1) gene, also called ABCB1, are sensitive to it; resistance in livestock worms; and its effects on the insects that break down dung. It also reports what poison-center records and case reports describe in people who took products made for animals.

Table of Contents

  1. A Veterinary Drug First
  2. Forms Used in Animals
  3. Horses
  4. Cattle, Sheep and Goats
  5. Dogs, Cats and the MDR1 (ABCB1) Gene
  6. Resistance in Livestock Worms
  7. Ivermectin in the Environment
  8. People Taking Veterinary Ivermectin
  9. Acute Human Toxicity of Macrocyclic Lactones
  10. Key Research Papers
  11. Connections
  12. Featured Videos

A Veterinary Drug First

Ivermectin was discovered in the late 1970s. It is a chemically modified form of avermectin, made by a single microorganism isolated from Japanese soil at the Kitasato Institute in Tokyo. It was first introduced as a veterinary drug, killing a wide range of internal and external parasites in livestock and companion animals, before its widespread use in humans [2]. A 1990 review notes that it came to market in 1981 with approved claims covering both nematodes (roundworms) and arthropods (insects, mites and ticks), a claim structure it calls unique [1].

Ivermectin belongs to the macrocyclic lactones, a family of parasite- and insect-killing compounds, including the avermectins and the milbemycins, that soil-dwelling microorganisms produce by fermentation. Ivermectin was the first of them released for use in both animals and humans. Others, such as abamectin, emamectin and moxidectin, followed as insecticides and acaricides (mite and tick killers) for crop protection, or as parasite treatments for animals [3].

In invertebrates such as worms and insects, ivermectin is believed to open chloride channels in nerve and muscle cells that are controlled by the signal chemicals glutamate and gamma-aminobutyric acid (GABA), leaving the parasite paralyzed. A 2007 review says it transformed the control of parasitic worms in veterinary medicine, and of some worm infections in people, such as river blindness (onchocerciasis), lymphatic filariasis (a worm infection of the lymph vessels) in Africa and strongyloidiasis (a threadworm infection) [4]. It was a joint focus of the 2015 Nobel Prize in Physiology or Medicine, though a 2017 review notes that how it works is still not fully understood [5]. A 2025 review lists its approved human uses as head lice, river blindness, rosacea, scabies and gut worm infections [6].

Forms Used in Animals

In veterinary medicine, ivermectin comes in a range of formulations given by mouth, on the skin and by injection. For people, a 2025 review notes, it is approved only as a single dose by mouth and as a skin cream [6]. The 1990 review lists the veterinary products then available [1]:

The livestock products delivered 200 to 500 micrograms of ivermectin per kilogram of the animal’s body weight, and the dog heartworm products 6 micrograms per kilogram [1]. For horses, one of the oral forms is a paste: in a 1989 study, ponies were given ivermectin as an oral paste or by injection into a muscle or a vein [7]. A 2023 study in cattle compared the traditional 1% ivermectin injection with a long-acting 3.15% injection [8].

Why the base liquid matters

The liquid or base a drug is mixed into, called the vehicle, affects how quickly the drug is absorbed and how much of it reaches the bloodstream. In a 1999 study, two injectable products with the same kind of base were injected under the skin of 16 pigs and 16 calves. In the calves, ivermectin was detectable in the blood from 12 hours to 30 days, peaking at 40.5 to 46.4 ng/mL (nanograms, or billionths of a gram, per milliliter) at two days, and the two products were bioequivalent in both species, giving equivalent blood levels [9].

Horses

Ivermectin was the avermectin chosen for development as a parasite treatment for horses. A 1982 review found that, injected at 200 micrograms per kilogram, it was highly effective against the large strongyles, roundworms of the horse’s gut (Strongylus vulgaris, Strongylus edentatus and Triodontophorus species), and against adult and immature small strongyles (cyathostomes), including strains resistant to the benzimidazole dewormers, the class that includes fenbendazole. It also controlled the horse pinworm, the horse roundworm and several stomach worms, and was highly effective against stomach bots, the larvae of bot flies [10].

Small strongyles and larval cyathostomiasis

Small strongyles can cause a disease of their own, larval cyathostomiasis, when large numbers of their larvae are suddenly released from the lining of the large intestine. A 2000 review lists diarrhea, swelling under the belly, fever, colic, weight loss and poor body condition as typical signs; the disease may appear in late winter and early spring, or after a deworming that removes the worms inside the gut. At the time, moxidectin and fenbendazole had been shown to work against the larvae encysted in the gut wall, and small strongyles were resistant to every class of drug then available except the macrocyclic lactones, ivermectin and moxidectin [11].

Bot-fly larvae in horses’ gums

In the 1989 pony study described below, the youngest larvae of the horse bot fly, Gasterophilus intestinalis, were found in the mouth and older ones in the stomach [7]. Another 1989 study described the damage the young larvae do, including under the microscope. First- and second-stage larvae burrowed through the top millimeter of the tongue and then embedded themselves in the gum between the teeth, removing virtually all tissue in their path, including its nerve and blood supply. Air shafts they dug in the tongue let bacteria into the tunnels, where the bacteria stuck to the larvae and started microabscesses (tiny pockets of pus). Invaded gums were engorged with blood and stripped of their surface layer; the gum receded and ulcerated into periodontal pockets, the gaps between gum and tooth seen in gum disease. Heavy invasion produced compound pockets, with the larvae’s mouth hooks tearing at engorged capillaries [12].

A 2006 report from clinics that routinely examine horses’ mouths with an endoscope (a camera on a rigid tube) found second-stage bot-fly larvae between the upper cheek teeth of 14 warmblood horses, aged 2 to 17 years, over 2002 to 2004. All had been brought in for chewing problems or trouble accepting the bit; in one, the gullet became blocked during the larvae’s migration [13].

The 1989 pony study gave every pony 500 first-stage Gasterophilus intestinalis larvae; the ponies were also naturally infected, including with a second species, Gasterophilus nasalis. Thirty-six ponies received ivermectin at 200 micrograms per kilogram of body weight: 12 by injection into a vein, 12 by injection into a muscle and 12 as an oral paste. Another 24 were left untreated or given only the vehicle (the drug-free base). At post-mortem examination 21 days later, every untreated or vehicle-treated pony had larvae in the mouth and the stomach, while no bots were found in any ivermectin-treated pony: ivermectin was 100% effective against the mouth and stomach stages. No adverse reactions were seen in the ponies given ivermectin into a muscle or by mouth. One pony given the vehicle alone into a vein, and one given ivermectin (in the vehicle) into a vein, had an anaphylactic reaction, a sudden and severe allergic-type reaction, and the ivermectin-treated pony died. The report speculated that the reaction was caused by histamines released in response to the vehicle’s components given into the vein [7].

A soil roundworm that can invade horses

Halicephalobus gingivalis, a roundworm found throughout the environment that lives on decaying matter, has been reported to infect people and horses. It can form granulomas (firm lumps of inflamed tissue) in the skin, or spread to organs, favoring the brain, spinal cord and kidneys; once signs of brain or spinal cord involvement develop, the disease is rapidly fatal [14].

Reports of ivermectin resistance in horse worms are summarized under Resistance in Livestock Worms.

Cattle, Sheep and Goats

Across livestock, the 1990 review describes ivermectin as effective against roundworms of the gut, the airways, the eye’s conjunctival sac (the moist lining around the eyeball) and the soft tissues. In cattle, its approved arthropod targets included the horn fly (Haematobia irritans), screw-worm fly larvae, warble-fly larvae (Hypoderma species), lice, mange mites and ticks; in sheep, the larvae of the sheep nasal bot fly (Oestrus ovis) and mange mites [1].

Mange mites in beef cattle

Psoroptic mange, a skin disease caused by the mite Psoroptes ovis, causes significant productivity losses in cattle, and macrocyclic lactones are among the main drugs used against it. A 2023 study on commercial grazing farms ran three trials in steers with active mange, comparing ivermectin with doramectin, a related macrocyclic lactone, and counting mites in skin scrapings 14, 21 and 28 days after treatment [8]:

The authors concluded that doramectin could offer some advantages in field situations where ivermectin fails to control mange, and that long-acting formulations can be useful depending on how susceptible the mite population is [8].

Pour-on products and licking

Pour-on products are used worldwide in cattle. A 2001 study in 12 Holstein cattle tested how natural licking changes what happens to pour-on ivermectin. When licking was prevented, the drug left the blood more slowly (its half-life, the time for the blood level to fall by half, was 363 hours, against 154 hours in cattle that licked) and less of it reached the bloodstream (19% against 33%). In the cattle that licked, nearly 70% of the dose came out unchanged in the dung, against only 6.6% when licking was prevented, consistent with the drug being taken in by mouth rather than through the skin. The authors raised concerns about the drug’s known toxicity in the environment, unexpected residues in the edible tissues of untreated animals that lick treated ones, and low drug levels, a factor in drug resistance [17].

In a 2011 study, four heifers treated with pour-on ivermectin were kept with six untreated heifers, all infected with the stomach worm Ostertagia ostertagi and the intestinal worm Cooperia oncophora. Ivermectin was found in the blood and dung of all six untreated animals, at peak levels two to three times lower than the lowest levels in the treated ones, and its effect on their worm egg counts ranged from none to full, with values between 30% and 80% in between. The authors described blood levels of 0.1 to 1 ng/mL, a range of partial effect, as a potential selection window for resistance [18].

Sheep and goats

For sheep, the 1990 review lists injectable and oral products [1]. A 2019 review describes worm resistance to the macrocyclic lactones as commonplace worldwide in sheep and goats [19]; the studies are summarized under Resistance in Livestock Worms below.

Dogs, Cats and the MDR1 (ABCB1) Gene

In dogs, the 1990 review describes ivermectin given in small monthly doses to prevent heartworm disease [1]. Some dogs, and a small number of cats, are far more sensitive to the drug than others, because of a fault in one gene.

The drug pump that guards the brain

The MDR1 gene carries the instructions for P-glycoprotein, a pump in cell membranes that actively pushes many drugs back out of cells. It is found in the intestine, the kidney tubules, the cells lining the brain’s capillaries and the bile channels of the liver, among other tissues. There it limits how much of a drug is absorbed from the gut and how much enters the brain [20]. At the blood-brain barrier, it restricts the entry of drugs that can harm nerve cells, such as ivermectin [21].

Herding-breed dogs

A variant of the MDR1 gene in herding-breed dogs, including collies and Australian shepherds, has been shown to cause their sensitivity to ivermectin. The variant is a deletion of 4 base pairs (letters of DNA), and evidence suggests it also makes the dogs more susceptible to the toxicity of several other drugs [20]. In dogs, the mutation is linked to a dramatic increase in the amount of ivermectin that builds up in the brain, and to life-threatening toxicity to the nervous system [22].

Cats

In cats as in dogs, deletion mutations in this gene have been associated with increased nerve toxicity after ivermectin treatment [21]. A 2021 report described two Maine Coon cats that developed nerve toxicity after standard doses of ivermectin injected under the skin. Both carried two copies of a 2-base-pair deletion in the cat gene, a mutation previously linked to drug sensitivity in cats. The researchers built a new genetic test and used it on more than 50 relatives: about half carried one copy of the mutation, and none of the relatives that had been treated with ivermectin before had a history of drug sensitivity [22].

A 2026 study of 800 cats from Germany found the mutation in 0.625% of the gene copies examined. In cell experiments, the mutant dog and cat pumps showed a complete loss of function, and ivermectin and other antiparasitic drugs, such as eprinomectin, moxidectin and selamectin, blocked the normal pumps of both species [21].

Resistance in Livestock Worms

In veterinary medicine, resistance to ivermectin is now widespread, and the 2017 review notes that its mechanisms are unresolved [5]. The 2007 review called it a serious problem for parasite control in livestock, with concern that resistance could also develop and spread in worms that infect people [4]. A 2019 review describes resistance to the macrocyclic lactones as commonplace worldwide in the worms of sheep and goats, of increasing concern in horses, cattle, dogs and other animals, and suspected in Onchocerca volvulus, the worm behind river blindness. In most animals, resistance arose first to the avermectins, such as ivermectin, and later to moxidectin, which is usually the more effective of the two where worms are resistant. The review relates this to moxidectin being stored in fat tissue, less likely to be removed by pump proteins and long-lasting in the body [19].

In sheep and goats

A 2021 survey of 24 dairy goat herds in the Czech Republic, using laboratory tests on worm eggs and larvae, found ivermectin-resistant worms in 13 herds (54%), eight of them (62%) highly resistant. Resistance to the benzimidazole dewormers was confirmed on 18 farms (75%), and 11 herds (46%) were resistant to both drug classes. The main resistant worms were Teladorsagia/Trichostrongylus and Haemonchus. A high stocking rate, meaning many animals kept per area of pasture, was significantly associated with ivermectin resistance [23].

In horses

In 2000, the review of larval cyathostomiasis described small strongyles as resistant to every class of horse dewormer except the macrocyclic lactones [11]. Two recent field studies have reported ivermectin resistance in horse worms, using the fecal egg count reduction test, which compares the number of worm eggs in dung before and after treatment:

How worms resist

The 2007 review describes several mechanisms. Ivermectin is readily carried by ATP-binding cassette (ABC) transporters, pump proteins that include the worms’ own P-glycoproteins: the drug favors worms that make different amounts of these pumps, and altered pump levels contribute to resistance. There is also growing evidence that ivermectin selects for changes in beta-tubulin, a structural protein, in some worms, while the evidence that changes in the drug’s ion-channel targets are the most important cause of resistance is far from clear [4]. In dogs, P-glycoprotein is the pump that keeps ivermectin out of the brain [20]. Low drug levels in the animal are another suspected factor, such as the levels reached in cattle that lick treated herd-mates, described above [17][18].

Ivermectin in the Environment

When livestock are treated, most of the ivermectin leaves the body unchanged in the dung within 5 days [26]. In pour-on-treated cattle that licked, nearly 70% of the dose came out unchanged in the dung [17]. That dung feeds the dung fauna, the beetles, flies and other small animals that break dung down on pastures.

Dung beetles

A 2002 review found most macrocyclic lactones, including abamectin, ivermectin, eprinomectin and doramectin, highly toxic to dung beetles, with moxidectin the least toxic of them, while dung residues of the benzimidazole and levamisole/morantel dewormers are relatively harmless to dung fauna. It noted that the harm to these non-target organisms has been considered acceptable because of the economic importance of the parasites to commercial livestock production [27].

A 2020 meta-analysis pooled 22 studies of dung residues from endectocides (drugs active against both internal and external parasites) and aphodiine dung beetles, a group of small dung beetles. Adult beetles tended to be attracted to dung containing residues, but larvae were less likely to occur in it, and the numbers of both adults and larvae were significantly reduced; the authors judged it more likely that larvae hatching in such dung die early in development than that the adults lay no eggs there. Of the individual drugs, only ivermectin showed a significantly negative effect on the numbers of both adults and larvae, possibly because fewer studies covered the others, and in field research only pour-on applications were shown to reduce larval numbers [28].

A tropical field test

Most of this research comes from temperate climates. In a 2025 field experiment in tropical Tanzania, termites colonized dung pats from ivermectin-treated cattle more readily than untreated pats, yet the treated pats lost wet weight significantly more slowly in the first two weeks, and after the first month they held more organic matter and fewer larvae. The work was prompted by ivermectin’s ability to kill mosquitoes that take a blood meal from a treated host, which makes mass treatment of people and livestock a candidate method for reducing malaria transmission. The authors called for these environmental effects to be investigated further and weighed against the potential benefits for malaria control [26].

People Taking Veterinary Ivermectin

During the coronavirus disease 2019 (COVID-19) pandemic, some people took ivermectin, including products made for animals, to prevent or treat the infection. In August 2021 the US Centers for Disease Control and Prevention (CDC) issued a health alert after a rapid increase in ivermectin prescriptions and in reports of severe illness linked to ivermectin products used for COVID-19, and the US Food and Drug Administration (FDA) and the CDC discouraged its use for COVID-19 outside clinical trials [29]. The debate over whether ivermectin works against COVID-19 is covered on Ivermectin and COVID-19; this section reports what poison-center and toxicology records describe.

Oregon Poison Center, 2021 to 2022

The Oregon Poison Center reviewed the ivermectin exposures for COVID-19 prevention or treatment that led to a healthcare visit over 24 weeks, from 14 August 2021 to 31 January 2022. It identified 37 cases of ivermectin toxicity. The median age was 64 years, and most patients were male. Twenty-one were hospitalized, 13 were treated in an emergency department and 3 as outpatients; one patient died. Seventeen had taken veterinary formulations and fifteen prescription tablets; 23 had taken ivermectin as treatment for COVID-19 and 14 as prevention. The clinical effects were neurotoxicity (effects on the brain and nerves) in 30 patients, gastrointestinal symptoms in 14 and musculoskeletal (muscle, bone and joint) complaints in 7 [30].

Fifteen US medical centers, 2020 to 2021

A toxicology surveillance project at 15 major academic medical centers in 12 US states recorded 40 patients with adverse events from ivermectin used against COVID-19 over 15 months, October 2020 to December 2021; 18 of the 40 had medicated themselves with veterinary formulations. Thirty-three went to emergency departments and 19 were admitted to hospital. Patients reported using ivermectin for prevention (24/40), for treatment of symptoms (19/40) and for treatment of documented COVID-19 (8/40). Neurological toxicity was the most frequent finding; 15 patients had minor symptoms and 25 developed severe toxicity. The authors wrote that the potential adverse effects were primarily neurological, especially when patients were treating themselves and using formulations intended for non-human use [29].

South Africa’s Western Cape, 2015 to 2021

In South Africa, ivermectin tablets and injectable formulations were not registered for human use by the national regulator. The Poisons Information Helpline of the Western Cape compared ivermectin calls from 1 June 2015 to 30 June 2020 with calls from 1 July 2020 to 31 July 2021, the dividing line being the first publication reporting ivermectin activity against the COVID-19 virus in the laboratory. Of 65 cases analyzed, 19 came in the first period and 46 in the second. Of those 46, 25 (54.3%) were related to COVID-19 use; 24 (52.2%) involved veterinary preparations, 3 (6.5%) human preparations and 19 (41.3%) unknown preparations. Symptoms were reported in 14 cases (73.7%) in the first period and 30 (65.2%) in the second. Across all 65 cases, the organ systems most often involved were the central nervous system (26 cases; 40.0%), the gastrointestinal system (18; 27.7%), the eyes (9; 13.8%) and the skin (5; 7.7%) [31].

Veterinary ivermectin injected into a vein

A 2022 case report described a patient with confirmed COVID-19 who developed severe neurotoxicity after an intravenous (into a vein) dose of veterinary ivermectin, and who needed care in an intensive care unit. The ivermectin level in the blood serum was 187.74 ng/mL. The authors noted that ivermectin for human use is available only as an oral formulation, and that injection under the skin is used only in veterinary medicine; they described the case as unprecedented [32].

Acute Human Toxicity of Macrocyclic Lactones

A 2012 review of acute human toxicity across the macrocyclic lactone family describes ivermectin treatment as generally well tolerated: adverse effects are usually transient and mild to moderate, and severe ones are rare and can generally be controlled by treating the symptoms. Exposures outside treatment, to ivermectin or to other members of the family, can also cause toxic effects, but significant toxicity probably develops only after a large amount is swallowed. In large doses these drugs may pass the blood-brain barrier and mimic GABA, the brain’s main calming signal, although the exact mechanisms remain unclear. Severely poisoned patients usually present with coma, low blood pressure (hypotension), respiratory failure and even death. There is no specific treatment, but the review describes the outlook as likely to be favorable unless severe hypotension or respiratory failure complicates the poisoning [3].

A 2022 mini-review in a clinical toxicology journal explains why ivermectin toxicity is rarely reported in mammals. The drug binds to ion-channel receptors for glutamate, GABA and glycine, paralyzing and killing parasites, and vertebrate species express these receptors differently. Ivermectin is also carried by P-glycoprotein, which limits its toxicity to the nervous system in people. Genetic variants of P-glycoprotein, or taking drugs that block the pump at the same time, may increase ivermectin’s neurotoxicity. Other toxic effects reported after oral treatment at therapeutic doses include swelling (edema), rash, headache and eye complaints, most of them mild and short-lived [33].

Variants of the MDR1 gene also occur in people. Some change how drugs are handled in the body, and some have been linked to susceptibility to conditions such as Parkinson’s disease, inflammatory bowel disease and hard-to-control seizures [20]. How ivermectin acts in the body, and its safety in approved human use, are covered on How Ivermectin Works.

Key Research Papers

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  12. Cogley TP. Effects of migrating Gasterophilus intestinalis larvae (Diptera: Gasterophilidae) on the mouth of the horse. Vet Parasitol. 1989;31(3-4):317-31. PubMed PMID: 2763450
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  14. Pearce SG, Bouré LP, Taylor JA, Peregrine AS. Treatment of a granuloma caused by Halicephalobus gingivalis in a horse. J Am Vet Med Assoc. 2001;219(12):1735-8, 1708. PubMed PMID: 11767925
  15. Ferguson R, van Dreumel T, Keystone JS, Manning A, Malatestinic A, Caswell JL, et al. Unsuccessful treatment of a horse with mandibular granulomatous osteomyelitis due to Halicephalobus gingivalis. Can Vet J. 2008;49(11):1099-103. PubMed PMID: 19183732
  16. Fonderie P, Bert W, Hendrickx F, Houthoofd W, Moens T. Anthelmintic tolerance in free-living and facultative parasitic isolates of Halicephalobus (Panagrolaimidae). Parasitology. 2012;139(10):1301-8. PubMed PMID: 22716944
  17. Laffont CM, Alvinerie M, Bousquet-Mélou A, Toutain PL. Licking behaviour and environmental contamination arising from pour-on ivermectin for cattle. Int J Parasitol. 2001;31(14):1687-92. PubMed PMID: 11730797
  18. Bousquet-Mélou A, Jacquiet P, Hoste H, Clément J, Bergeaud JP, Alvinerie M, et al. Licking behaviour induces partial anthelmintic efficacy of ivermectin pour-on formulation in untreated cattle. Int J Parasitol. 2011;41(5):563-9. PubMed PMID: 21232538
  19. Prichard RK, Geary TG. Perspectives on the utility of moxidectin for the control of parasitic nematodes in the face of developing anthelmintic resistance. Int J Parasitol Drugs Drug Resist. 2019;10:69-83. PubMed PMID: 31229910
  20. Mealey KL. Therapeutic implications of the MDR-1 gene. J Vet Pharmacol Ther. 2004;27(5):257-64. PubMed PMID: 15500562
  21. Siegl L, Bethäuser M, Nürnberger D, Oswald S, Moritz A, Hamann M, et al. Functional Characterization of the Cat and Dog Wild-Type and Mutant MDR1 Carrier Proteins and Frequency of the MDR1 Gene Mutation in 800 Cats From Germany. J Vet Pharmacol Ther. 2026;49(3):237-256. PubMed PMID: 41474640
  22. Nürnberger D, Wagner L, Müller SF, Leiting S, Leidolf R, Alber J, et al. Detection of the ABCB11930_1931del TC Mutation in Two Suspected Ivermectin-Sensitive Cats and Their Relatives by a Novel TaqMan Allelic Discrimination Assay. Front Vet Sci. 2021;8:808392. PubMed PMID: 35265692
  23. Vadlejch J, Kyriánová IA, Várady M, Charlier J. Resistance of strongylid nematodes to anthelmintic drugs and driving factors at Czech goat farms. BMC Vet Res. 2021;17(1):106. PubMed PMID: 33663490
  24. Cooper LG, Benard BP, Nielsen MK, Caffe G, Arroyo F, Anziani OS. First report of ivermectin resistance in cyathostomins (small strongyles) of horses in Argentina. Vet Parasitol Reg Stud Reports. 2024;52:101046. PubMed PMID: 38880577
  25. Flota-Burgos GJ, Rosado-Aguilar JA, Rojas-Becerril R, Rodríguez-Vivas RI, Trinidad-Martínez I. Evidence of resistance to ivermectin in the gastrointestinal nematodes of horses from Mexican southeast. Vet Parasitol Reg Stud Reports. 2023;44:100907. PubMed PMID: 37652626
  26. Ruhinda M, Xia K, Rist C, Shija G, Lyimo IN, Meza F, et al. Treatment of cattle with ivermectin and its effect on dung degradation and larval abundance in a tropical savanna setting. One Health. 2025;20:100950. PubMed PMID: 39760016
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PubMed Topic Searches

  1. PubMed: Veterinary ivermectin formulations
  2. PubMed: Ivermectin sensitivity and the MDR1 gene
  3. PubMed: Ivermectin resistance in livestock worms
  4. PubMed: Human toxicity from veterinary ivermectin

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