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Clinical data
Trade names Albenza, Valbazen, others
AHFS/ Monograph
MedlinePlus a610019
  • AU: D
  • US: C (Risk not ruled out)
Routes of
By mouth
ATC code
Legal status
Legal status
  • AU: S4 (Prescription only)
  • CA: ℞-only
  • UK: POM (Prescription only)
  • US: ℞-only (for humans; veterinary suspension and paste are both OTC)[1]
Pharmacokinetic data
Bioavailability <5%[2]
Protein binding 70%[2]
Metabolism Hepatic[2]
Biological half-life 8-12 hours[2]
Excretion Bile (humans)
Urine (ruminants)
CAS Number
PubChem CID
ECHA InfoCard 100.053.995
Chemical and physical data
Formula C12H15N3O2S
Molar mass 265.333 g/mol
3D model (JSmol)
Melting point 208 to 210 °C (406 to 410 °F)

Albendazole, also known as albendazolum,[1] is a medication used for the treatment of a variety of parasitic worm infestations.[3] It is useful for giardiasis, trichuriasis, filariasis, neurocysticercosis, hydatid disease, pinworm disease, and ascariasis, among others.[3] It is taken by mouth.[3]

Common side effects include nausea, abdominal pains, and headaches.[3] Potentially serious side effects include bone marrow suppression which usually improves on stopping the medication.[3] Liver inflammation has been reported and those with prior liver problems are at greater risk.[3] It is pregnancy category C in the United States and category D in Australia, meaning it may cause harm if taken by pregnant women.[3][4] Albendazole is a broad-spectrum antihelminthic agent of the benzimidazole type.[3]

Albendazole was developed in 1975.[5] It is on the World Health Organization's List of Essential Medicines, the most effective and safe medicines needed in a health system.[6] The wholesale cost in the developing world is between 0.01 and 0.06 USD per dose.[7] In the United States, however, it is very expensive as of 2015 at about 201 USD per dose.[8]

Medical uses[edit]

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.[21]


Albendazole is a pregnancy class D drug in Australia and pregnancy class C in the United States. 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 be teratogenic,[22][23] albendazole has been found to be safe in humans during the second and third trimesters.[24][25] It can, however, possibly cause infantile eczema when given during pregnancy.[26]

In pregnant dogs, albendazole use has led to puppies with reduced weight and with cleft palates. Birds have lower rates of laying eggs and hatching when given albendazole.[27]

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.[22][28]


Hypersensitivity to the benzimidazole class of compounds contraindicates its use.[15]

Side effects[edit]

Close-up of a pork tapeworm cyst. Destruction of these cysts can cause inflammation.

The most common side effects by albendazole are, experienced by over 10% of people, headache and abnormal liver function.[2] Elevation of liver enzymes occur in 16% of patients receiving treatment specifically for hydatid disease and goes away when treatment ends.[11][29] The liver enzymes normally increase to two to four times the normal levels (a mild to moderate increase).[30] An estimated 1–10% of people experience abdominal pain, nausea or vomiting, dizziness or vertigo, increased intracranial pressure, meningeal signs, temporary hair loss, and fever. The headache, nausea, and vomiting are thought to be caused by the sudden destruction of cysticerci (tapeworm larvae), which causes acute inflammation.[31] Fewer than 1% of people get hypersensitivity reactions (such as rashes and hives), leukopenias (drop in white blood cell levels) such as agranulocytosis and granulocytopenia, thrombocytopenia (reduced platelet count), pancytopenia (drop in white blood cells, red blood cells, and platelets), hepatitis, acute liver failure, and acute renal failure, irreversible bone marrow suppression, and aplastic 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; 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 as seizures, increased intracranial pressure, and focal 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 face retinal damage if they are not first checked for ocular cysticeri; since changes to existing lesions in the eye by albendazole can cause permanent blindness.[11]


Because of its low solubility, albendazole often cannot be absorbed in high enough quantities to be toxic.[31] The oral LD50 of albendazole in rats was found to be 2,500 mg/kg.[23] It takes 20 times the normal dose to kill a sheep, and 30 times the normal dose to kill cattle.[1] Overdose effects the liver, testicles, and GI tract the most. It can manifest with lethargy, loss of appetite, vomiting, diarrhea, intestinal cramps, dizziness, convulsions, and sleepiness. There is no specified antidote.[27]


The antiepileptics carbamazepine, phenytoin, and phenobarbital lower the plasma concentration and the half life of albendazole sulfoxide's R(+) enantiomer.[33]

Antiepileptics and pharmacokinetics
of albendazole sulfoxide[18]
Drug Change in AUC Change in Cmax
Carbamazepine 49% decrease 50–63% decrease
Phenobarbitol 61% decrease 50–63% decrease
Phenytoin 66% decrease 50–63% decrease

The antacid cimetidine heightens serum albendazole concentrations, increases the half life of albendazole, and doubles albendazole sulfoxide levels in bile.[34][29] It was originally thought to work by increasing albendazole bioavailability directly; however, it is now known that cimetidine inhibits the breakdown of albendazole sulfoxide by interfering with CYP3A4.[14] The half-life of albendazole sulfoxide thus increases from 7.4 hours to 19 hours.[35] This might be a helpful interaction on more severe cases, because it boosts the potency of albendazole.[36] Paradoxically, cimetidine also inhibits the absorption of albendazole by reducing gastric acidity.[35]

Several other interactions exist. Corticosteroids increase the steady-state plasma concentration of albendazole sulfoxide;[11] dexamethasone, for example, can increase the concentration by 56% by inhibiting the elimination of albendazole sulfoxide.[29][31] The anti-parasitic praziquantel increases the maximum plasma concentration of albendazole sulfoxide by 50%,[29] and the anti-parasitic levamisole increases the AUC (total drug exposure) by 75%.[18] Grapefruit inhibits the metabolism of albendazole within the intestinal mucosa. Finally, long-term administration of the antiretroviral ritonavir, which works as a CYP3A4 inhibitor, decreases the maximum concentration of albendazole in the plasma as well as the AUC.[35]


A microtubule is composed of polymers of α- and β-tubulin.

Mechanism of action[edit]

As a vermicidal, albendazole causes degenerative alterations in the intestinal cells of the worm by binding to the colchicine-sensitive site of β-tubulin, thus inhibiting its polymerization or assembly into microtubules (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 their glycogen stores. Albendazole also prevents the formation of spindle fibers needed for cell division, which in turn blocks egg production and development; existing eggs are prevented from hatching.[14][37] Cell motility, maintenance of cell shape, and intracellular transport are also disrupted.[38] At higher concentrations, it disrupts the helminths' metabolic pathways by inhibiting metabolic enzymes such as malate dehydrogenase and fumarate reductase, with inhibition of the latter leading to less energy produced by the Krebs cycle.[1][27][39] Due to diminished ATP production, the parasite is immobilized and eventually dies.

Some parasites have evolved to have some resistance to albendazole by having a different set of acids comprising β-tubulin, decreasing the binding affinity of albendazole.[29]


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.[40]

The absorption also largely depends on gastric pH. People have varying gastric pHs on empty stomachs, and thus absorption from one person to another can vary wildly when taken without food.[17] 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.[18] Food stimulates gastric acid secretion, lowering the pH and making albendazole more soluble and thus more easily absorbed.[35] Oral absorption is especially increased with a fatty meal, as albendazole dissolves better in lipids, allowing it to cross the lipid barrier created by the mucus surface of the GI tract.[38][40] To target intestinal parasites, albendazole is taken on an empty stomach in order to stay within the gut.[41]

Absorption is also affected by how much of the albendazole is degraded within the small intestine by metabolic enzymes in the vili.[17]

General metabolism of albendazole and its sulfoxides.

The pharmacokinetics of albendazole differ slightly between men and women: women have a lower oral clearance and volume of distribution, while men have a lower serum peak concentration.[35]

Albendazole undergoes very fast 1st-pass metabolism in all species, such that the unchanged drug is undetectable in plasma.[40] Most of it is oxidized into albendazole sulfoxide (also known as ricobendazole and albendazole oxide[23][42]) in the liver by cytochrome P450 oxidases (CYPs) and a flavin-containing monooxygenase (FMO),[43] which was discovered later.[44] In humans, the cytochrome P450 oxidases are thought to include CYP3A4[45] and CYP1A1,[40] while those in the rats are thought to be CYP2C6 and CYP2A1.[46]

While 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[46] produce the R(+) enantiomer more (with the human AUC ratio being 80:20).[31][35][40] 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.[46][38] Some albendazole is also converted to hydroxyalbendazole, mainly by CYP2J2.[26][47]

For systemic parasites, albendazole acts as a prodrug, while albendazole sulfoxide reaches systemic circulation and acts as the real antihelminthic.[14] Albendazole sulfoxide is able to cross the blood-brain barrier and enter the cerebrospinal fluid at 43% of plasma concentrations; its ability to enter the central nervous system is what allows it to treat neurocystocercosis.[35]

Albendazole sulfoxide is converted to the inactive albendazole sulfone by cytochrome P450 oxidases, thought to include CYP3A4[35] and/or CYP2C.[14] Other inactive metabolites include: 2-aminosulfone, ω-hydroxysulfone, and β-hydroxysulfone.[43][31] The major final metabolites that are excreted by humans are:[14]

  • methyl [5-(propylsulfonyl-1H-benzimidazol-2-yl)] carbamate,
  • methyl [6-hydroxy 5-(n-propylsulfonyl)-1H-benzimidazole-2-yl)] carbamate,
  • methyl [5-(n-propylsulfinyl)-1H-benzimidazole-2-yl)] carbamate,
  • 5-(n-propylsulfonyl)-1H-benzimidazole-2-yl amine, and
  • 5-(n-propysulfinyl)-1H-benzimidazole-2-yl amine.

There are also some minor hydroxylated sulfated or glucuronidated derivatives.[14] No unchanged albendazole is excreted, as it is metabolized too quickly.[2]

In humans, the metabolites mostly excreted in the bile, with only a small amount being excreted in the urine (less than 1%) and feces.[2][14] In ruminants, however, 60–70% of the metabolites are excreted in the urine.[27]

Like all benzimidazoles, albendazole has no residual effect, and thus does not protect well against reinfestations.[23]


Albendazole, patented in 1975, was invented by Robert J. Gyurik and Vassilios J. Theodorides and assigned to SmithKline Corporation.[48][49] It was introduced in 1977 as an antihelminthic for sheep in Australia, and was registered for human use in 1982.[11][14]

Society and culture[edit]

Discarded bottles of albendazole distributed in Africa

Brand names[edit]

Brand names include: Albenza,[29] Alworm, Andazol, Eskazole, Noworm, Zentel, Alben-G, ABZ, Cidazole, Wormnil etc.


In many areas of the world it costs between US$0.01 and US$0.06 per dose.[7] In the United States, however, it costs about 50 USD per dose, as of 2014.[3][50]

In Raleigh, North Carolina, the brand-name prescription cost was around US$800, and US$540 for the generic. The pharmaceutical company Amedra increased the price after purchasing the rights to the drug, drawing criticism from patients' rights advocates and US Democratic Party politicians.[51]

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.[52]

Veterinary use[edit]

Albendazole is mainly used in cattle and sheep, but has found some use in cats and dogs as well;[24] it is also used in ratite birds for flagellate parasites and tapeworms. It is also used off-label to treat endoparasites in goats and pigs.[1]

Albendazole use in animals[1][24][53][54][55]
Cattle Sheep Others
Platyhelminthes (flatworms)
Dicrocoelium (liver flukes) D. dendriticum (lancet liver fluke)[56] D. dendriticum[57]
Fasciola (liver flukes) F. hepatica F. hepatica For F. hepatica and F. gigantica in people[3]
Fascioloides (liver flukes) F. magna[56] F. magna Also for F. magna in South American camelids (ex. llama and alpaca)[57]
Paragonimus (lung flukes) For P. kellicotti in cats and dogs[57]
Platynosomum For Platynosomum infections in cats
Opisthorchiidae For Opisthorchiidae infections in cats
Cestodes (tapeworms)
Echinococcus For Echinococcus cysts in horses and humans[57][3]
Moniezia M. expansa
M. benedini
M. expansa
Taenia T. saginata larvae For T. saginata, T. solium, and T. crassiceps in humans[9][10] and Taenia infections in dogs[58]
Thysanosoma T. actinoides
Nematodes (roundworms)
Ancylostoma For Ancylostoma infections in dogs, cats, and humans[57][3]
Bunostomum B. phlebotomum
Capillaria For causative agents of various forms of capillariasis in cats and dogs (including C. philippinensis, C. hepatica, C. aerophila, and C. plica) and intestinal capillariasis (C. philippinensis) in humans.
Chabertia C. ovina
Cooperia C. oncophora
C. punctata
C. oncophora
Dictyocaulus (lungworm) D. viviparus D. filaria For D. amfieldi infections in horses
Filaroides (lungworm) For F. hirthi and F. osleri in dogs
Haemonchus H. contortus
H. placei
H. contortus
Marshallagia M. marshalli
Metastrongylus For M. apri in swine
Nematodirus N. spathiger
N. helvetianus
N. spathiger
N. filicollis
Parascaris For P. equorum in horses[54]
Ostertagia O. ostertagi O. circumcincta For O. bifurcum in humans
Oesophagostomum O. radiatum O. columbianum
Strongyloides For S. stercoralis in dogs and humans[3][57]
Strongylus For S. equinus in horses[57]
Toxocara For T. canis infections in dogs[57] and toxocariasis in humans (caused by T. canis and T. cati)
Trichostrongylus T. axei
T. colubriformis
T. axei
T. colubriformis
For any Trichostrongylus infection in humans
Trichuris (whipworm) Most species, but those usually found in cattle are:[59]
T. discolor
T. globulosa
T. ovis
Most species, but those usually found in sheep are:[59]
T. discolor
T. globulosa
T. ovis
Albendazole is also used for Trichuris infections in humans (usually T. trichiura, causative agent of trichuriasis), dogs (usually T. vulpis and T. campanula), cats (usually T. serrata and T. campanula), pigs (usually T. suis), and other ruminants (same species as those found in cattle and sheep).[59]
Encephalitozoon For E. cuniculi infections (microsporidiosis) in humans and rabbits
Giardia G. lamblia (causative agent of giardiasis) Also treats giardiasis in humans, dogs, and small mammals
Leishmania Treats leishmaniasis, caused by various species of Leishmania, in dogs

Albendazole has been used as an anthelminthic and for control of flukes in a variety of animal species, including cattle, sheep, goats, swine, camels, dogs, cats, elephants, poultry, and others.[27][60] Side effects include anorexia in dogs and lethargy, depression, and anorexia in cats,[1] with more than 10% of dogs and cats having anorexia.[28] 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.[28] 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.[24][53] Thus, it is usually only prescribed in cats and dogs when an infection is present that is resistant to the commonly prescribed metronidazole and fenbendazole.[61]

It is extensively used for ruminant livestock in Latin America.[23] 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][24] 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.[46][38] 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.[27]


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 January 24, 2008).

Maximum residue limits (MRLs) for albendazole in food, adopted by the FAO/WHO Codex 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 days cattle withdrawal time for meat.[24]

See also[edit]


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