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| Clinical data | |
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| Trade names | Albenza, others |
| AHFS/Drugs.com | Monograph |
| MedlinePlus | a610019 |
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| Routes of administration | By mouth |
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| Pharmacokinetic data | |
| Bioavailability | <5%[2] |
| Protein binding | 70%[2] |
| Metabolism | Liver[2] |
| Eliminationhalf-life | 8–12 hours[2] |
| Excretion | Bile duct (humans) Kidney (ruminants) |
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| CompTox Dashboard(EPA) | |
| ECHA InfoCard | 100.053.995 |
| Chemical and physical data | |
| Formula | C12H15N3O2S |
| Molar mass | 265.33 g·mol−1 |
| 3D model (JSmol) | |
| Melting point | 208 to 210 °C (406 to 410 °F) |
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Albendazole is a broad-spectrumantihelmintic andantiprotozoal agent of thebenzimidazole type.[3] It is used for the treatment of a variety ofintestinal parasite infections, includingascariasis,pinworm infection,hookworm infection,trichuriasis,strongyloidiasis,taeniasis,clonorchiasis,opisthorchiasis,cutaneous larva migrans,giardiasis, andgnathostomiasis, among other diseases.[3]
Common side effects includenausea, abdominal pain, andheadache.[3] Rare but potentially serious side effects includebone marrow suppression which usually improves on discontinuing the medication.Liver inflammation has been reported and those with prior liver problems are at greater risk.[3] It ispregnancy category D in Australia, meaning it may cause harm if taken by pregnant women.[3][4]
Albendazole was developed in 1975.[5] It is on theWorld Health Organization's List of Essential Medicines.[6] Albendazole is available in afixed-dose combination withivermectin.[7]
Albendazole is an effective treatment for:
Though albendazole is effective in treating many diseases, it is only FDA-approved for treating hydatid disease caused by dog tapeworm larvae and neurocysticercosis caused by pork tapeworm larvae.[27]
When co-administered, ivermectin and albendazole act in synergy.[28] Ivermectin targets the parasite's nervous and muscular systems, causing paralysis, while albendazole disrupts the parasite's metabolism and energy production.[28] This dual approach immobilizes and kills the parasite and improves the treatment's effectiveness.[28]
In January 2025, theCommittee for Medicinal Products for Human Use (CHMP) of theEuropean Medicines Agency (EMA) adopted a positive scientific opinion for ivermectin/albendazole for the treatment of infections caused by several types of worm parasites including lymphatic filariasis, a neglected tropical disease.[28] Ivermectin/albendazole isindicated for use in people aged five years of age or older, for the treatment of soil-transmitted helminth infections, caused by different types of intestinal parasitic worms, which are spread through soil contaminated by human feces in areas with poor sanitation.[28] Among the worms responsible for these diseases are hookworms (Ancylostoma duodenale, Necator americanus), roundworms (Ascaris lumbricoides), whipworms (Trichuris trichiura) and a roundworm calledStrongyloides stercoralis.[28] Ivermectin/albendazole is also indicated for the treatment of microfilaraemia (the presence of worm larvae in the blood) in people with lymphatic filariasis.[28] Lymphatic filariasis is a neglected tropical disease commonly known as elephantiasis, which impairs the lymphatic system and can lead to the abnormal enlargement of body parts, causing pain, severe disability and social stigma.[28] Ivermectin/albendazole is indicated for the treatment of cases of lymphatic filariasis caused byWuchereria bancrofti, a parasite which is responsible for 90% of cases worldwide.[28]
Hypersensitivity to the benzimidazole class of compounds contraindicates its use.[19]
The most common side effects of albendazole are experienced by over 10% of people and includeheadache and abnormal liver function.[2] Elevation ofliver enzymes occurs in 16% of patients receiving treatment specifically for hydatid disease and goes away when treatment ends.[12][29] Liver enzymes usually increase to two to four times the normal levels (a mild to moderate increase).[30] An estimated 1–10% of people experienceabdominal pain,nausea orvomiting,dizziness orvertigo, increasedintracranial pressure, meningeal signs, temporaryhair loss, andfever. The headache, nausea, and vomiting are thought to be caused by the sudden destruction ofcysticerci (tapeworm larvae), which causes acute inflammation.[31] Fewer than 1% of people gethypersensitivity reactions such as rashes and hives,leukopenias (drop in white blood cell levels) such asagranulocytosis andgranulocytopenia,thrombocytopenia (reduced platelet count),pancytopenia (drop in white blood cells, red blood cells, and platelets),hepatitis, acuteliver failure,acute kidney injury, irreversiblebone marrow suppression, andaplastic anemia.[2][32]
Side effects can be different when treating for hydatid disease versus neurocysticercosis: for example, those being treated for the former are more likely to experience elevated liver enzymes and abdominal pain, while those being treated for the latter are more likely to experience headache.[29] Treating hydatid disease can also unmask undiagnosed neurocysticercosis.[29] People receiving albendazole for the treatment of neurocysticercosis can have neurological side effects such asseizures, increased intracranial pressure, andfocal signs caused by the inflammatory reaction that occurs when parasites in the brain are killed. Steroids and anticonvulsants are often given with albendazole when treating neurocysticercosis to avoid these effects.[29] Those being treated for retinal neurocysticercosis can faceretinal damage if they are not first checked for ocular cysticeri, since changes to existing lesions in the eye by albendazole can cause permanent blindness.[12]
Albendazole is apregnancy class D drug in Australia. It is contraindicated in the first trimester of pregnancy, and should be avoided up to one month before conception. While studies in pregnant rats and rabbits have shown albendazole to beteratogenic,[33][34] albendazole has been found to be safe in humans during the second and third trimesters.[35][36] It can, however, possibly cause infantileeczema when given during pregnancy.[37]
In pregnant dogs, albendazole use has led to puppies with reduced weight and withcleft palates. Birds have lower rates of laying eggs and hatching when given albendazole.[38]
Albendazole sulfoxide is secreted into breast milk at around 1.5% of the maternal dose, though oral absorption is poor enough that it is unlikely to affect nursing infants.[33][39]
Because of its low solubility, albendazole often cannot be absorbed in high enough quantities to be toxic.[31] The oralLD50 of albendazole in rats was found to be 2,500 mg/kg.[34] It takes 20 times the normal dose to kill a sheep, and 30 times the normal dose to kill cattle.[1] Overdose affects the liver, testicles, andgastrointestinal tract (GI tract) the most. It can manifest with lethargy, loss of appetite, vomiting, diarrhea, intestinal cramps, dizziness, convulsions, and sleepiness.[medical citation needed] There is no specified antidote.[38]
The antiepilepticscarbamazepine,phenytoin, andphenobarbital lower the plasma concentration andhalf-life of albendazole sulfoxide's R(+) enantiomer.[40]
| Drug | Change inAUC | Change inCmax |
|---|---|---|
| Carbamazepine | 49% decrease | 50–63% decrease |
| Phenobarbitol | 61% decrease | 50–63% decrease |
| Phenytoin | 66% decrease | 50–63% decrease |
The antacidcimetidine heightensserum albendazole concentrations, increases the half-life of albendazole, and doubles albendazole sulfoxide levels in bile.[41][29] It was originally thought to work by increasing albendazolebioavailability directly; however, it is now known that cimetidine inhibits the breakdown of albendazole sulfoxide by interfering withCYP3A4.[15] The half-life of albendazole sulfoxide thus increases from 7.4 hours to 19 hours.[42] This might be a helpful interaction on more severe cases, because it boosts thepotency of albendazole.[43] Paradoxically, cimetidine also inhibits the absorption of albendazole by reducing gastric acidity.[42]
Several other interactions exist.Corticosteroids increase thesteady-state plasma concentration of albendazole sulfoxide;[12]dexamethasone, for example, can increase the concentration by 56% by inhibiting the elimination of albendazole sulfoxide.[29][31] The anti-parasiticpraziquantel increases the maximum plasma concentration of albendazole sulfoxide by 50%,[29] and the anti-parasiticlevamisole increases theAUC (total drug exposure) by 75%.[24]Grapefruit inhibits the metabolism of albendazole within the intestinal mucosa. Finally, long-term administration of theantiretroviralritonavir, which works as a CYP3A4 inhibitor, decreases themaximum concentration of albendazole in the plasma as well as the AUC.[42]
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As avermicide, albendazole causes degenerative alterations in the intestinal cells of the worm by binding to thecolchicine-sensitive site ofβ-tubulin, thus inhibiting its polymerization or assembly intomicrotubules (it binds much better to the β-tubulin of parasites than that of mammals).[3][29] Albendazole leads to impaired uptake of glucose by the larval and adult stages of the susceptible parasites, and depletes theirglycogen stores. Albendazole also prevents the formation ofspindle fibers needed for cell division, which in turn blocks egg production and development; existing eggs are prevented from hatching.[15][44] Cell motility, maintenance of cell shape, and intracellular transport are also disrupted.[45] At higher concentrations, it disrupts the helminths' metabolic pathways by inhibiting metabolic enzymes such asmalate dehydrogenase andfumarate reductase, with inhibition of the latter leading to less energy produced by theKrebs cycle.[1][38][46] Due to diminished ATP production, the parasite is immobilized and eventually dies.
Some parasites have evolved some resistance to albendazole by having a different set of amino acids constitute β-tubulin, decreasing thebinding affinity of albendazole.[29] Some parasites (especially filarial nematodes) live insymbiosis withWolbachia, a type ofintracellular parasitebacteria. In such cases theWolbachia are necessary to the survival of the parasitic worms.[47] Elimination ofWolbachia from these filarial nematodes generally results in either death or sterility of the host nematode.[48]
To target intestinal parasites, which is the most common indication for prescription, albendazole is taken on an empty stomach to stay within the gut.[49]
Oral absorption of albendazole varies among species, with 1–5% of the drug being successfully absorbed in humans, 20–30% in rats, and 50% in cattle.[50]
The absorption also largely depends ongastric pH. People have varying levels of gastric pHs on empty stomachs, and thus absorption from one person to another can vary wildly when taken without food.[23] Generally, the absorption in the GI tract is poor due to albendazole's low solubility in water.[3] It is, however, better absorbed than other benzimidazole carbamates.[24] Food stimulates gastric acid secretion, lowering the pH and making albendazole more soluble and thus more easily absorbed.[42] Oral absorption is especially increased with a fatty meal, as albendazole dissolves better in lipids, allowing it to cross the lipid barrier created by themucus surface of the GI tract.[45][50]
Absorption is also affected by how much of the albendazole is degraded within the small intestine by metabolic enzymes in the villi.[23]
The pharmacokinetics of albendazole differ slightly between men and women: women have a lower oralclearance andvolume of distribution, while men have a lower serum peak concentration.[42]
Albendazole undergoes very fastfirst-pass metabolism in all species, such that the unchanged drug is undetectable in plasma.[50] Most of it is oxidized into albendazole sulfoxide (also known asricobendazole andalbendazole oxide[34][51]) in the liver bycytochrome P450 oxidases (CYPs) and aflavin-containing monooxygenase (FMO),[52] which was discovered later.[53] In humans, the cytochrome P450 oxidases are thought to includeCYP3A4[54] andCYP1A1,[50] while those in the rats are thought to be CYP2C6 and CYP2A1.[55]
Oxidation to albendazole sulfoxide by FMO produces R(+)enantiomers, while oxidation the cytochromes and by some enzymes in the gut epithelium produce S(−). Different species produce the R(+) and S(−) enantiomers in different quantities; humans, dogs, and most other species[55] produce the R(+) enantiomer more (with the human AUC ratio being 80:20).[31][42][50] Compared to the S(−) enantiomer, the R(+) has greater pharmacological activity, lasts longer in the bloodstream, is found in higher concentrations in the infected host tissues, and is found in higher concentrations within the parasites themselves.[55][45] Some albendazole is also converted to hydroxyalbendazole, mainly byCYP2J2.[37][56]
For systemic parasites, albendazole acts as aprodrug, while albendazole sulfoxide reaches systemic circulation and acts as the real antihelminthic.[15] Albendazole sulfoxide is able to cross theblood–brain barrier and enter thecerebrospinal fluid at 43% of plasma concentrations; its ability to enter the central nervous system allows it to treat neurocysticercosis.[42]
Albendazole sulfoxide is converted to the inactive albendazole sulfone by cytochrome P450 oxidases, thought to include CYP3A4[42] orCYP2C.[15] Other inactive metabolites include: 2-aminosulfone, ω-hydroxysulfone, and β-hydroxysulfone.[52][31] The major final metabolites that are excreted by humans are:[15]
There are also some minor hydroxylated sulfated or glucuronidated derivatives.[15] No unchanged albendazole is excreted, as it is metabolized too quickly.[2]
In humans, the metabolites are excreted mostly in bile, with only a small amount being excreted in urine (less than 1%) and feces.[2][15] In ruminants, 60–70% of the metabolites are excreted in urine.[38]
Like all benzimidazoles, albendazole has no residual effect, and thus protects poorly against reinfestations.[34]
Albendazole, patented in 1975, was invented by Robert J. Gyurik and Vassilios J. Theodorides and assigned to SmithKline Corporation.[57][58] It was introduced in 1977 as an antihelminthic for sheep in Australia, and was registered for human use in 1982.[12][15]
The pharmaceutical companyAmedra increased the price after purchasing the rights to the drug, instead of lowering it as generics are predicted to do, drawing criticism from patients' rights advocates.[59]
In 2013,GlaxoSmithKline donated 763 million albendazole tablets for the treatment and prevention of parasitic infections in developing countries, bringing the total to over 4 billion tablets donated since 1998.[60]
Brand names include: Albenza,[29] Alworm, Andazol, Eskazole, Noworm, Zentel, Alben-G, ABZ, Cidazole, Wormnil etc.
Albendazole and related compounds or metabolites like albendazole sulfone (ALB-SO2) exhibit antibacterial effects via an unknown, possiblyFtsZ-related, mechanism. It inhibits division ofWolbachia andMycobacterium tuberculosis, turning them into a long "filament" shape as they grow and fail todivide. SinceBrugia malayi relies on symbioticWolbachia, this would mean that albendazole is targeting both the worm and its essential symbioant.[61]
Albendazole is mainly used in cattle and sheep, but has found some use in cats and dogs as well;[35] it is also used inratite birds for flagellate parasites and tapeworms. It is also used off-label to treat endoparasites in goats and pigs.[1]
| Cattle | Sheep | Others | |
|---|---|---|---|
| Platyhelminthes (flatworms) | |||
| Trematodes | |||
| Dicrocoelium (liver flukes) | D. dendriticum (lancet liver fluke)[65] | D. dendriticum[66] | |
| Fasciola (liver flukes) | F. hepatica | F. hepatica | ForF. hepatica andF. gigantica in people[3] |
| Fascioloides (liver flukes) | F. magna[65] | F. magna | Also forF. magna in South Americancamelids (ex. llama and alpaca)[66] |
| Paragonimus (lung flukes) | — | — | ForP. kellicotti in cats and dogs[66] |
| Platynosomum | — | — | ForPlatynosomum infections in cats |
| Opisthorchiidae | — | — | ForOpisthorchiidae infections in cats |
| Cestodes (tapeworms) | |||
| Echinococcus | – | — | ForEchinococcus cysts in horses and humans[66][3] |
| Moniezia | M. expansa M. benedini | M. expansa | |
| Taenia | T. saginata larvae | — | ForT. saginata,T. solium, andT. crassiceps in humans[10][11] andTaenia infections in dogs[67] |
| Thysanosoma | — | T. actinoides | |
| Nematodes (roundworms) | |||
| Ancylostoma | — | – | ForAncylostoma infections in dogs, cats, and humans[66][3] |
| Bunostomum | B. phlebotomum | – | |
| Capillaria | — | — | For causative agents of various forms of capillariasis in cats and dogs (includingC. philippinensis,C. hepatica,C. aerophila, andC. plica) and intestinal capillariasis (C. philippinensis) in humans. |
| Chabertia | — | C. ovina | |
| Cooperia | C. oncophora C. punctata | C. oncophora | |
| Dictyocaulus (lungworm) | D. viviparus | D. filaria | ForD. amfieldi infections in horses |
| Filaroides (lungworm) | — | — | ForF. hirthi andF. osleri in dogs |
| Haemonchus | H. contortus H. placei | H. contortus | |
| Marshallagia | — | M. marshalli | |
| Metastrongylus | — | — | ForM. apri in swine |
| Nematodirus | N. spathiger N. helvetianus | N. spathiger N. filicollis | |
| Parascaris | — | — | ForP. equorum in horses[63] |
| Ostertagia | O. ostertagi | O. circumcincta | ForO. bifurcum in humans |
| Oesophagostomum | O. radiatum | O. columbianum | |
| Strongyloides | — | — | ForS. stercoralis in dogs and humans[3][66] |
| Strongylus | — | — | ForS. equinus in horses[66] |
| Toxocara | — | — | ForT. canis infections in dogs[66] and toxocariasis in humans (caused byT. canis andT. cati) |
| Trichostrongylus | T. axei T. colubriformis | T. axei T. colubriformis | For anyTrichostrongylus infection in humans |
| Trichuris (whipworm) | Most species, but those usually found in cattle are:[68] T. discolor T. globulosa T. ovis | Most species, but those usually found in sheep are:[68] T. discolor T. globulosa T. ovis | Albendazole is also used forTrichuris infections in humans (usuallyT. trichiura, causative agent of trichuriasis), dogs (usuallyT. vulpis andT. campanula), cats (usuallyT. serrata andT. campanula), pigs (usuallyT. suis), and other ruminants (same species as those found in cattle and sheep).[68] |
| Other | |||
| Encephalitozoon | — | — | ForE. cuniculi infections (microsporidiosis) in humans and rabbits |
| Giardia | G. lamblia (causative agent ofgiardiasis) | — | Also treats giardiasis in humans, dogs, and small mammals |
| Leishmania | — | — | Treatsleishmaniasis, caused by various species ofLeishmania, in dogs |
Albendazole has been used as an antihelminthic and for control of flukes in a variety of animal species, including cattle, sheep, goats, swine, camels, dogs, cats, elephants, poultry, and others.[38][69] Side effects include anorexia in dogs and lethargy, depression, and anorexia in cats,[1] with more than 10% of dogs and cats having anorexia.[39] Of dogs and cats, 1–10% experience elevated liver enzymes, nausea, vomiting, and diarrhea. Less than 1% experience neutropenia or aplastic anemia, though these require a use of at least 5 days.[39] While it is also associated with bone marrow suppression and toxicity in cats and dogs at high doses, albendazole has a higher margin of safety in other species.[35][62] Thus, it is usually only prescribed in cats and dogs when an infection is present that is resistant to the commonly prescribedmetronidazole andfenbendazole.[70]
It is extensively used for ruminant livestock inLatin America.[34] It is marketed for this purpose by Zoetis (formerly Pfizer Animal Health) in numerous countries (including the United States and Canada) as Valbazen in oral suspension and paste formulations;[1][35] by Interchemie in the Netherlands and elsewhere as Albenol-100; by Channelle Animal Health Ltd. in the United Kingdom as Albex; and by Ravensdown in New Zealand (as Albendazole). Although most formulations are administered orally, Ricomax (ricobendazole, or albendazole sulfoxide) is administered by subcutaneous injection.[citation needed]
Albendazole has greater bioavailability in ruminants: some albendazole sulfoxide, when released back into the rumen, is reduced to albendazole by the resident microbiota, with a preference of the (+) enantiomer being the substrate.[55][45] Cats and dogs, having no rumen reservoir, sometimes need higher or more frequent doses as compared to ruminants. In dogs, albendazole sulfoxide is detectable in the plasma for less than 12 hours, but in sheep and goats, it remains at measurable levels for around three days.[38]
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The limitations in early pregnancy are due to a limited period during which teratogenic effects may occur. Summarized research data relating to the durations of these preslaughter and early pregnancy periods when albendazole should not be administered are found in US FDA NADA 110-048 (cattle) and 140-934 (sheep). Some data and inferences regarding goats are found in US FDA Supplemental NADA 110-048 (approved 24 January 2008).
Maximum residue limits (MRLs) for albendazole in food, adopted by the FAO/WHOCodex Alimentarius in 1993, are 5000, 5000, 100, and 100 micrograms per kilogram of body weight (μg/kg) for kidney, liver, fat, and muscle, respectively, and 100 μg/L for milk. For analysis purposes, MRLs of various nations may pertain to concentration of a marker substance which has been correlated with concentrations of the administered substance and its metabolized products. For example, in Canada, the marker substance specified by Health Canada is albendazole-2-aminosulfone, for which the MRL in liver of cattle is 200 μg/kg.
There is a 27-day cattlewithdrawal time for meat.[35]
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