Albendazole

Albendazole
Clinical data
Trade names	Albenza, others
AHFS/Drugs.com	Monograph
MedlinePlus	a610019
License data	US DailyMed: Albendazole;
Pregnancy; category	AU: D;
Routes of; administration	By mouth
ATC code	P02CA03 (WHO) QP52AC11 (WHO);
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);
Pharmacokinetic data
Bioavailability	<5%
Protein binding	70%
Metabolism	Liver
Elimination half-life	8–12 hours
Excretion	Bile duct (humans); Kidney (ruminants)
Identifiers
CAS Number	54965-21-8 ;
PubChem CID	2082;
DrugBank	DB00518 ;
ChemSpider	1998 ;
UNII	F4216019LN;
KEGG	D00134 ;
ChEBI	CHEBI:16664 ;
ChEMBL	ChEMBL1483 ;
NIAID ChemDB	007895;
CompTox Dashboard (EPA)	DTXSID0022563 ;
ECHA InfoCard	100.053.995
Chemical and physical data
Formula	C12H15N3O2S
Molar mass	265.33 g·mol−1
3D model (JSmol)	Interactive image;
Melting point	208 to 210 °C (406 to 410 °F)
	SMILES CCCSc2ccc1nc(NC(=O)OC)[nH]c1c2;
	InChI InChI=1S/C12H15N3O2S/c1-3-6-18-8-4-5-9-10(7-8)14-11(13-9)15-12(16)17-2/h4-5,7H,3,6H2,1-2H3,(H2,13,14,15,16) ; Key:HXHWSAZORRCQMX-UHFFFAOYSA-N ;
	(verify)

Albendazole is a broad-spectrum antihelmintic and antiprotozoal agent of the benzimidazole type.^[3] It is used for the treatment of a variety of intestinal parasite infections, including ascariasis, pinworm infection, hookworm infection, trichuriasis, strongyloidiasis, taeniasis, clonorchiasis, opisthorchiasis, cutaneous larva migrans, giardiasis, and gnathostomiasis, among other diseases.^[3]

Quick Facts Clinical data, Trade names ...

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Common side effects include nausea, abdominal pain, and headache.^[3] Rare but potentially serious side effects include bone 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 is pregnancy 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 the World Health Organization's List of Essential Medicines.^[6]

Albendazole is an effective treatment for:

Flatworms
- Clonorchiasis^[7]
- Fasciolosis^[3]
- Opisthorchiasis^[8]
- Cestodes (tapeworms), as an alternative to praziquantel or niclosamide for adult beef tapeworms and as an alternative to praziquantel for pork tapeworms.^[9] It is also given for infections by T. crassiceps.^[10] Though praziquantel is often better at treating tapeworm infections, albendazole is used more often in endemic countries due to being cheaper and having a broader spectrum.^[11]
  - Cysticercosis^[12] (especially neurocysticercosis), which is caused by the larval form of the pork tapeworm^[3] (i.e. albendazole is the drug of choice for larval pork tapeworms, but not adult pork tapeworms).^[9] Old cysts are not affected.^[11]
  - Echinococcosis^[12]^[13] of the liver, lung, and peritoneum (caused by the larval form of the dog tapeworm, or of the alveoli (caused by E. multilocularis) when surgical excision is not possible.^[3] Alveolar and cystic echinococcosis may require lifelong treatment with albendazole, which only prevents the parasites from growing and reproducing rather than killing them.^[14]
Nematodes
- Anatrichosomiasis^[15]
- Angiostrongyliasis^[16]
- Anisakiasis^[17]
- Ascariasis, which can be cured with a single dose of albendazole.^[18]^[19]
- Baylisascariasis, caused by the raccoon roundworm. Albendazole can achieve good results (95–100% efficacy after a 10-day course of treatment) if treatment is initiated within 72 hours of ingestion of the egg-containing raccoon feces.^[20]^{[unreliable medical source?]} Corticosteroids are sometimes added in cases of eye and CNS infections.^[3]
- Pinworm infection^[18]
- Filariasis; since albendazole's disintegration of the microfilariae ("pre-larva") can cause an allergic reaction, antihistamines or corticosteroids are sometimes added to treatment. In cases of lymphatic filariasis (elephantiasis) caused by Wuchereria bancrofti or Brugia malayi, albendazole is sometimes given as an adjunct to ivermectin or diethylcarbamazine in order to suppress microfilaremia. It can also be given for Loa loa filariasis as an adjunct or replacement to diethylcarbamazine.^[3]^[11] Albendazole has an embryotoxic effect on Loa loa adults and thus slowly reduces microfilaremia.^[19]
- Gnathostomiasis when caused by Gnathostoma spinigerum.^[3] Albendazole has a similar effectiveness to ivermectin in these cases, though it needs to be given for 21 days rather than the 2 days needed for ivermectin.^[14]
- Gongylonemiasis^[3]
- Hepatic capillariasis caused by Capillaria hepatica^[21]
- Hookworm infections,^[18] including cutaneous larva migrans caused by hookworms of genus Ancylostoma. A single dose of albendazole is sufficient to treat intestinal infestations by A. duodenale or Necator americanus.^[3]^[19]
- Intestinal capillariasis,^[18] as an alternative to mebendazole^[3]
- Mansonelliasis when caused by Mansonella perstans. Albendazole is effective against adult worms but not against the immature microfilariae.^[14]
- Oesophagostomumiasis, when caused by Oesophagostomum bifurcum^[3]
- Strongyloidiasis,^[18] as an alternative to ivermectin or thiabendazole.^[3]^[22] Albendazole can be given with diethylcarbamazine to lower microfilaremia levels.^[19]
- Toxocariasis, also called "visceral larva migrans", when caused by the dog roundworm Toxocara canis or cat roundworm T. catis. Corticosteroids can be added in severe cases, and surgery might be required to repair secondary damage.^[3]
- Trichinosis, when caused by Trichinella spiralis^[9] or T. pseudospiralis. Albendazole has a similar efficacy to thiabendazole, but fewer side effects.^[14] It works best when given early, acting on the adult worms in the intestine before they generate larva that can penetrate the muscle and cause a more widespread infection. Corticosteroids are sometimes added on to prevent inflammation caused by dying larva.^[11]
- Trichostrongyliasis, as an alternative to pyrantel pamoate.^[3]^[18] A single dose is sufficient for treatment.^[11]
- Trichuriasis (whipworm infection),^[18] sometimes considered as an alternative to mebendazole^[3]^[9] and sometimes considered to be the drug of choice. Only a single dose of albendazole is needed.^[19] It can also be given with ivermectin.^[23]
Giardiasis, as an alternative or adjunct to metronidazole, especially in children^[3]^[24]
Microsporidiosis, including ocular microsporidiosis caused by Encephalitozoon hellem or E. cuniculi, when combined with topical fumagillin^[3]^[24]
Granulomatous amoebic encephalitis, when caused by the amoeba Balamuthia mandrillaris, in combination with miltefosine and fluconazole^[10]
Arthropods
- Crusted scabies, when combined with topical crotamiton and salicylic acid^[10]
- Head lice infestation, though ivermectin is much better^[10]
- Intestinal myiasis^[25]

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.^[26]

Pregnancy

Albendazole is a pregnancy 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 be teratogenic,^[27]^[28] albendazole has been found to be safe in humans during the second and third trimesters.^[29]^[30] It can, however, possibly cause infantile eczema when given during pregnancy.^[31]

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.^[32]

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.^[27]^[33]

Hypersensitivity to the benzimidazole class of compounds contraindicates its use.^[18]

The most common side effects of albendazole are experienced by over 10% of people and include headache and abnormal liver function.^[2] Elevation of liver enzymes occurs in 16% of patients receiving treatment specifically for hydatid disease and goes away when treatment ends.^[11]^[34] Liver enzymes usually increase to two to four times the normal levels (a mild to moderate increase).^[35] 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.^[36] 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, acute kidney injury, irreversible bone marrow suppression, and aplastic anemia.^[2]^[37]

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.^[34] Treating hydatid disease can also unmask undiagnosed neurocysticercosis.^[34] 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.^[34] 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.^[36] The oral LD₅₀ of albendazole in rats was found to be 2,500 mg/kg.^[28] 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, and gastrointestinal 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.^[32]

The antiepileptics carbamazepine, phenytoin, and phenobarbital lower the plasma concentration and half-life of albendazole sulfoxide's R(+) enantiomer.^[38]

More information Drug, Change in AUC ...

Antiepileptics and pharmacokinetics
of albendazole sulfoxide^[23]
Drug	Change in AUC	Change in C_max
Carbamazepine	49% decrease	50–63% decrease
Phenobarbitol	61% decrease	50–63% decrease
Phenytoin	66% decrease	50–63% decrease

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The antacid cimetidine heightens serum albendazole concentrations, increases the half-life of albendazole, and doubles albendazole sulfoxide levels in bile.^[39]^[34] 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.^[40] This might be a helpful interaction on more severe cases, because it boosts the potency of albendazole.^[41] Paradoxically, cimetidine also inhibits the absorption of albendazole by reducing gastric acidity.^[40]

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.^[34]^[36] The anti-parasitic praziquantel increases the maximum plasma concentration of albendazole sulfoxide by 50%,^[34] and the anti-parasitic levamisole increases the AUC (total drug exposure) by 75%.^[23] 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.^[40]

Mechanism of action

As a vermicide, 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]^[34] 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]^[42] Cell motility, maintenance of cell shape, and intracellular transport are also disrupted.^[43] 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]^[32]^[44] 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 the binding affinity of albendazole.^[34] Some parasites (especially filarial nematodes) live in symbiosis with Wolbachia, a type of intracellular parasite bacteria. In such cases the Wolbachia are necessary to the survival of the parasitic worms.^[45] Elimination of Wolbachia from these filarial nematodes generally results in either death or sterility of the host nematode.^[46]

Pharmacokinetics

To target intestinal parasites, which is the most common indication for prescription, albendazole is taken on an empty stomach to stay within the gut.^[47]

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.^[48]

The absorption also largely depends on gastric 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.^[22] 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.^[23] Food stimulates gastric acid secretion, lowering the pH and making albendazole more soluble and thus more easily absorbed.^[40] 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.^[43]^[48]

Absorption is also affected by how much of the albendazole is degraded within the small intestine by metabolic enzymes in the villi.^[22]

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.^[40]

Albendazole undergoes very fast first-pass metabolism in all species, such that the unchanged drug is undetectable in plasma.^[48] Most of it is oxidized into albendazole sulfoxide (also known as ricobendazole and albendazole oxide^[28]^[49]) in the liver by cytochrome P450 oxidases (CYPs) and a flavin-containing monooxygenase (FMO),^[50] which was discovered later.^[51] In humans, the cytochrome P450 oxidases are thought to include CYP3A4^[52] and CYP1A1,^[48] while those in the rats are thought to be CYP2C6 and CYP2A1.^[53]

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^[53] produce the R(+) enantiomer more (with the human AUC ratio being 80:20).^[36]^[40]^[48] 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.^[53]^[43] Some albendazole is also converted to hydroxyalbendazole, mainly by CYP2J2.^[31]^[54]

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 allows it to treat neurocysticercosis.^[40]

Albendazole sulfoxide is converted to the inactive albendazole sulfone by cytochrome P450 oxidases, thought to include CYP3A4^[40] or CYP2C.^[14] Other inactive metabolites include: 2-aminosulfone, ω-hydroxysulfone, and β-hydroxysulfone.^[50]^[36] 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 are excreted mostly in bile, with only a small amount being excreted in urine (less than 1%) and feces.^[2]^[14] In ruminants, 60–70% of the metabolites are excreted in urine.^[32]

Like all benzimidazoles, albendazole has no residual effect, and thus protects poorly against reinfestations.^[28]

Albendazole, patented in 1975, was invented by Robert J. Gyurik and Vassilios J. Theodorides and assigned to SmithKline Corporation.^[55]^[56] It was introduced in 1977 as an antihelminthic for sheep in Australia, and was registered for human use in 1982.^[11]^[14]

Economics

The pharmaceutical company Amedra 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.^[57]

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.^[58]

Brand names

Brand names include: Albenza,^[34] 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, possibly FtsZ-related, mechanism. It inhibits division of Wolbachia and Mycobacterium tuberculosis, turning them into a long "filament" shape as they grow and fail to divide. Since Brugia malayi relies on symbiotic Wolbachia, this would mean that albendazole is targeting both the worm and its essential symbioant.^[59]

Albendazole is mainly used in cattle and sheep, but has found some use in cats and dogs as well;^[29] 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]

More information Cattle, Sheep ...

Albendazole use in animals^[1]^[29]^[60]^[61]^[62]
	Cattle	Sheep	Others
Platyhelminthes (flatworms)
Trematodes
Dicrocoelium (liver flukes)	D. dendriticum (lancet liver fluke)^[63]	D. dendriticum^[64]
Fasciola (liver flukes)	F. hepatica	F. hepatica	For F. hepatica and F. gigantica in people^[3]
Fascioloides (liver flukes)	F. magna^[63]	F. magna	Also for F. magna in South American camelids (ex. llama and alpaca)^[64]
Paragonimus (lung flukes)	—	—	For P. kellicotti in cats and dogs^[64]
Platynosomum	—	—	For Platynosomum infections in cats
Opisthorchiidae	—	—	For Opisthorchiidae infections in cats
Cestodes (tapeworms)
Echinococcus	–	—	For Echinococcus cysts in horses and humans^[64]^[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^[65]
Thysanosoma	—	T. actinoides
Nematodes (roundworms)
Ancylostoma	—	–	For Ancylostoma infections in dogs, cats, and humans^[64]^[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^[61]
Ostertagia	O. ostertagi	O. circumcincta	For O. bifurcum in humans
Oesophagostomum	O. radiatum	O. columbianum
Strongyloides	—	—	For S. stercoralis in dogs and humans^[3]^[64]
Strongylus	—	—	For S. equinus in horses^[64]
Toxocara	—	—	For T. canis infections in dogs^[64] 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:^[66] T. discolor T. globulosa T. ovis	Most species, but those usually found in sheep are:^[66] 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).^[66]
Other
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

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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.^[32]^[67] Side effects include anorexia in dogs and lethargy, depression, and anorexia in cats,^[1] with more than 10% of dogs and cats having anorexia.^[33] 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.^[33] 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.^[29]^[60] 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.^[68]

It is extensively used for ruminant livestock in Latin America.^[28] 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]^[29] 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.^[53]^[43] 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.^[32]

Meat

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-day cattle withdrawal time for meat.^[29]

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