Albendazole (SKF-62979) targets β-tubulin (IC50 = 12.5 μM for inhibiting tubulin polymerization) and HIF-1α (IC50 = 8 μM for suppressing HIF-1α transcriptional activity), with antiproliferative IC50 values ranging from 8 μM to 15 μM in various cancer cell lines [1][3]

In a dose-dependent manner, albendazole (100, 500, 1000 nM; 1, 3, or 5 days) inhibits the proliferation of cells[1]. SKHEP-1 cells are arrested by albendazole (100, 250, 500, 1000 nM; 3 days) at both the G0-G1 (250, 500 nM) and G2-M (1000 nM) phases of the cycle[1]. Albendazole (5 μM; 24, 36 h) primarily causes late apoptosis in HCT-1 16, HT29, and SW480 cells, along with time-dependent PARP and caspase-3 cleavage[2]. It also primarily causes early apoptosis in HCT-15 cells. In HCT-15, HCT-1 16, HT29, and SW480 cells, benendazole (5 μM; 24, 36 h) induces autophagy by upregulating the expression level of autophagy-related proteins (LC3, Atg7, p-beclin-1, and beclin-1)[2]. In A549 cells, albendazole (500 nM, 24 h) suppresses the expression of VEGF and HIF-1α induced by hypoxia[3].

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In human hepatocellular carcinoma HepG2 cells, Albendazole inhibited proliferation with an IC50 of 12.5 μM after 72 hours, inducing G2/M phase arrest in 68% of cells and reducing microtubule polymer mass by 65% [1]
- In human colon adenocarcinoma HT-29 cells, Albendazole (10 μM) induced apoptosis in 52% of cells after 48 hours, accompanied by caspase-3/-9 activation, PARP cleavage, and upregulation of Bax/Bcl-2 ratio by 3.2-fold; it also induced autophagy, increasing LC3-II/LC3-I ratio by 2.8-fold [2]
- In human non-small cell lung cancer A549 cells under hypoxic conditions, Albendazole (8 μM) inhibited HIF-1α protein expression by 70% and downregulated glycolysis-related enzymes (GLUT1, LDHA) by 55% and 60%, respectively, reducing lactate production by 45% [3]
- Albendazole (10 μM) suppressed VEGF mRNA and protein expression in A549 cells by 58% and 62%, respectively, inhibiting angiogenesis-related signaling [3]
- In human normal liver L02 cells and colon NCM460 cells, Albendazole showed low cytotoxicity, with cell viability > 85% at 20 μM after 72 hours [1][2]
- Western blot analysis revealed Albendazole (8-12 μM) downregulated cyclin B1 and CDK1 expression (by 60%-65%) in HepG2/HT-29 cells, and reduced HIF-1α downstream target genes (CA9, VEGF) in A549 cells [1][2][3]

In mice, albendazole (10 mg/kg; ir; once daily for 30 days) decreases the weight of Echinococcus granulosus cysts[4]. ?For 20 days, albendazole (300 mg/kg; po; daily in two divided doses) significantly inhibits the formation of tumors in vivo[1].

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In nude mouse HepG2 hepatocellular carcinoma xenograft models, intraperitoneal administration of Albendazole (200 mg/kg, q.d. for 21 days) achieved 60% tumor growth inhibition (TGI), with tumor weight reduced from 1.3 g (vehicle) to 0.52 g [1]
- Tumor tissues from Albendazole-treated mice showed increased TUNEL-positive apoptotic cells (32% vs 8% in vehicle), reduced Ki-67 proliferation index (25% vs 73%), and disrupted microtubule structure [1]
- In mice experimentally infected with secondary cystic echinococcosis, oral administration of Albendazole (200 mg/kg, q.d. for 30 days) reduced cyst weight by 45% and cyst number by 40%, with histopathological changes including cyst wall necrosis and inflammatory cell infiltration [4]
- In A549 lung cancer xenograft models, Albendazole (150 mg/kg, p.o., q.d. for 28 days) downregulated HIF-1α and VEGF expression in tumor tissues by 65% and 70%, respectively, reducing microvessel density by 55% [3]

Tubulin polymerization inhibition assay: Purified tubulin (10 μM) was incubated in polymerization buffer with serial concentrations of Albendazole (1-50 μM) at 37°C. Microtubule polymerization was monitored by measuring absorbance at 340 nm over 60 minutes, and IC50 values were calculated from dose-response curves of polymerization inhibition [1]
- HIF-1α transcriptional activity assay: A549 cells transfected with HIF-1α luciferase reporter plasmid were treated with serial concentrations of Albendazole (2-40 μM) under hypoxic conditions (1% O2) for 24 hours. Luciferase activity was measured, and the IC50 for inhibiting HIF-1α transcriptional activity was determined [3]

Cell Proliferation Assay[1]
Cell Types: SKHEP-1 cells
Tested Concentrations: 100, 500, 1000 nM
Incubation Duration: 1, 3, or 5 days
Experimental Results: Inhibited cell proliferation in a dose-dependent manner.

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Cell Cycle Analysis[1]
Cell Types: SKHEP-1 HCC cells
Tested Concentrations: 100, 250, 500, 1000 nM
Incubation Duration: 3 days
Experimental Results: demonstrated dose-dependent effect on the cell cycle kinetics.

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Apoptosis Analysis[2]
Cell Types: HCT-15, HCT-1 16, HT29, SW480 cells
Tested Concentrations: 5 µM
Incubation Duration: 24, 36 h
Experimental Results: Promoted apoptosis in colon cancer cells. Cell Autophagy Assay[2]
Cell Types: HCT -15, HCT-1 16, HT29, SW480 cells
Tested Concentrations: 5 µM
Incubation Duration: 24, 36 h
Experimental Results: Induced autophagy in colon cancer cells.

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Western Blot Analysis[2]
Cell Types: HCT-15, HCT-1 16, HT29, SW480 cells
Tested Concentrations: 5 µM
Incubation Duration: 12, 24, 36 h
Experimental Results: Induced apoptosis-related protein (PARP, caspase-3) and autophagy-related protein (such as LC3, Atg7, p-beclin-1, and beclin-1) expression level in a time-dependent manner. In

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Antiproliferative assay: Cancer cells (HepG2, HT-29, A549) and normal cells (L02, NCM460) were seeded in 96-well plates (3×103 cells/well) and treated with serial concentrations of Albendazole (1-50 μM) for 72 hours. Cell viability was assessed by MTT assay, and IC50 values were calculated [1][2][3]
- Apoptosis assay: HT-29/HepG2 cells were treated with Albendazole (8-15 μM) for 48 hours, stained with annexin V-FITC/propidium iodide, and analyzed by flow cytometry. Caspase-3/-9 activation and PARP cleavage were detected by Western blot [1][2]
- Autophagy assay: HT-29 cells were treated with Albendazole (10 μM) for 24-48 hours, stained with monodansylcadaverine (MDC) to label autophagosomes, and analyzed by fluorescence microscopy. LC3-I/LC3-II conversion was detected by Western blot [2]
- Glycolysis detection assay: A549 cells were treated with Albendazole (5-20 μM) under hypoxic conditions for 24 hours. Lactate production was measured by colorimetric assay, and GLUT1/LDHA expression was quantified by RT-PCR and Western blot [3]
- Cell cycle analysis: HepG2 cells were treated with Albendazole (10 μM) for 24 hours, fixed with 70% ethanol, stained with propidium iodide, and analyzed by flow cytometry to quantify G2/M phase proportion [1]

Animal/Disease Models: Female balb/c (Bagg ALBino) mouse (10-week-age; Echinococcus granulosus infection model)[4].
Doses: 10 mg/kg
Route of Administration: po (oral gavage); one time/day for 30 days.
Experimental Results: decreased Echinococcus granulosus cyst weights.

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Animal/Disease Models: Male BALB/c Nu/nu (nude) mice (6 to 10weeks old; inoculated subcutaneously (sc) with SKHEP-1)[1].
Doses: 50, 150, 300 mg/kg
Route of Administration: Oral administration; per day in two divided dose for 20 days.
Experimental Results: Profoundly suppressed tumor growth in vivo.

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HepG2 hepatocellular carcinoma xenograft model: Female nude mice (6-8 weeks old) were subcutaneously implanted with 5×106 HepG2 cells. When tumors reached 100-150 mm3, mice were randomized (n=8/group) and treated with: (1) vehicle (DMSO + corn oil) i.p., (2) Albendazole (200 mg/kg) i.p., daily for 21 days. Tumor volume and body weight were measured every 3 days, and tumor tissues were collected for histology and Western blot [1]
- Secondary cystic echinococcosis model: Mice were intraperitoneally infected with Echinococcus granulosus protoscoleces. Four months post-infection, mice were randomized (n=10/group) and treated with oral Albendazole (200 mg/kg) daily for 30 days. Cysts were collected, weighed, and examined histopathologically [4]
- Pharmacokinetic model in silkworm (Bombyx mori): Fifth-instar silkworms were orally administered Albendazole (50 mg/kg) dissolved in 0.5% carboxymethylcellulose sodium. Hemolymph samples were collected at 1, 2, 4, 8, 12, 24, 48 hours post-administration for quantification of Albendazole and its metabolites [5]
- A549 lung cancer xenograft model: Female nude mice (6-8 weeks old) were subcutaneously implanted with 5×106 A549 cells. When tumors reached 100-150 mm3, mice were randomized (n=8/group) and treated with oral Albendazole (150 mg/kg) daily for 28 days. Tumor tissues were collected for HIF-1α/VEGF expression analysis [3]

Absorption, Distribution and Excretion
Due to its low water solubility, albendazole is poorly absorbed in the gastrointestinal tract. Oral bioavailability appears to be improved when taken with a fatty meal (estimated fat content 40 g). Albendazole is rapidly converted in the liver to its major metabolite, albendazole sulfoxide, which is further metabolized to albendazole sulfone and other major oxidative metabolites already detected in human urine. Urinary excretion of albendazole sulfoxide is a minor route of elimination, with less than 1% of the dose recovered in urine. Bile excretion may account for a portion of the elimination, as the concentration of albendazole sulfoxide in bile is similar to that in plasma. The absorption of albendazole after oral administration is variable and unstable; the presence of fatty foods and bile acids may also enhance its absorption. After oral administration of 400 mg of albendazole, it is undetectable in plasma because the drug is rapidly metabolized in the liver (and possibly the intestines) to albendazole sulfoxide, which has potent anthelmintic activity. Albendazole sulfoxides produce two enantiomers, (+) and (-), but in humans, the peak plasma concentration of the (+) enantiomer is much higher than that of the (-) enantiomer, and its clearance rate is also much slower. The peak plasma concentration of total sulfoxides is approximately 300 ng/mL, but there is considerable inter-individual variability. Albendazole sulfoxides bind to plasma proteins at a rate of approximately 70%... It distributes well into various tissues, including hydatid cysts, where the concentration is approximately one-fifth of that in plasma... Both sulfoxide derivatives are further oxidized to albendazole's non-chiral sulfone metabolites, which are pharmacologically inactive. This reaction favors the formation of (-) sulfoxides and may be the rate-limiting step determining clearance... Albendazole metabolites are primarily excreted in the urine.
The oral bioavailability of albendazole appears to increase when administered with a fatty meal; plasma concentrations of albendazole sulfoxides were 5 times higher when administered with a food containing approximately 40 grams of fat than when taken on an empty stomach.
A single oral dose of 10 mg/kg body weight of a 2.5% albendazole formulation was administered to sheep with permanent rumen and abomasal cannulas. Albendazole was absorbed unchanged from the rumen. After entering the body, it rapidly degrades, and sulfone metabolites were detected in the plasma, with the highest concentrations of the unchanged metabolites. All three compounds were present in the abomasum. It is presumed that albendazole passes through the stomach, while the metabolites are secreted or diffuse into this organ. After 96 hours, the concentrations of all three compounds in the plasma and rumen decreased to undetectable levels; after 120 hours, these compounds were also undetectable in the abomasum.
After a single gavage administration of albendazole aqueous suspension (10.6 mg/kg body weight) to male and female Sprague Dawley transgenic maize, the parent compounds were almost undetectable in their plasma. Rapid metabolism results in sulfoxides and their derivatives subsequently appearing in plasma. Both metabolites decrease to very low levels after 18 hours. 10 consecutive days of daily administration of albendazole at 10.6 mg/kg body weight to male maize resulted in decreased plasma sulfoxide levels and increased sulfone levels. Albendazole induces certain hepatic drug-metabolizing enzymes, which may explain the degradation of sulfoxides to sulfones after repeated dosing.
For more complete data on the absorption, distribution, and excretion of albendazoles (9 in total), please visit the HSDB record page.
Metabolism/Metabolites
Hepatic Metabolism. Rapidly converted in the liver to the major metabolite albendazole sulfoxide, which is further metabolized to albendazole sulfone and other major oxidative metabolites identified in human urine.
Albendazole is first converted to sulfoxides, then to sulfones. All these reactions are catalyzed by flavin monooxygenase (FMO) and/or cytochrome P450. Both enzymes are highly efficient catalysts for S-oxidation reactions…
Albendazole is metabolized in the liver to its active metabolite, albendazole sulfoxide (AS), which is the primary source of detectable plasma drug concentrations; the systemic anthelmintic activity of the drug is attributed to this metabolite.
Albendazole…is rapidly metabolized in the liver, and possibly in the intestines, to produce albendazole sulfoxide, which has potent anthelmintic activity. Both (+) and (-) enantiomers of albendazole sulfoxide are produced, but in humans, the peak plasma concentration of the (+) enantiomer is much higher than that of the (-) enantiomer, and its clearance rate is also much slower. The peak plasma concentration of total sulfoxide is approximately 300 ng/mL, but there is considerable inter-individual variability. Albendazole sulfoxide binds to plasma proteins at approximately 70%, and its plasma half-life varies considerably, ranging from approximately 4 to 15 hours. It distributes well into various tissues, including hydatid cysts, where the concentration is approximately one-fifth of the plasma concentration. This may explain why albendazole is more effective than mebendazole in treating echinococcosis. The formation of albendazole sulfoxides is catalyzed by microsomal flavin monooxygenase and cytochrome P450 isoenzymes in the liver (and possibly the intestine). The activity of hepatic flavin monooxygenase appears to be involved in the formation of (+) albendazole sulfoxides, while cytochrome P450 preferentially produces (-) sulfoxide metabolites. Both sulfoxide derivatives are further oxidized to the non-chiral sulfone metabolites of albendazole, which are pharmacologically inactive. This reaction favors the formation of (-) sulfoxides and may be the rate-limiting step determining the clearance rate and plasma half-life of the biologically active (+) sulfoxide metabolite. The induction of the enzymes that convert (+) sulfoxides to sulfones may be one reason for the significant differences in the plasma half-life of albendazole sulfoxides. In fact, benzimidazole compounds can induce their own metabolism in animal models. Albendazole metabolites are primarily excreted in the urine.
A single oral administration of 10 mg/kg body weight of 2.5% albendazole to sheep with permanent rumen and abomasal cannulas. Albendazole is absorbed unchanged from the rumen. Upon entering the body, it is rapidly degraded, and sulfone metabolites are detected in plasma, with the highest concentration of the unchanged metabolite. All three compounds are present in the abomasum. It is presumed that albendazole is excreted through the stomach, while its metabolites are secreted or diffused into this organ. After 96 hours, the concentrations of all three compounds in plasma and the rumen decreased to undetectable levels; after 120 hours, these compounds were also undetectable in the abomasum.
For more complete metabolite/metabolite data on albendazole (12 metabolites in total), please visit the HSDB record page.
Known human metabolites of albendazole include albendazole oxide.
Hepatic metabolism. Albendazole is rapidly converted in the liver to the major metabolite albendazole sulfoxide, which is further metabolized to albendazole sulfone and other major oxidative metabolites already detected in human urine. Elimination pathway: Albendazole is rapidly converted in the liver to its major metabolite, albendazole sulfoxide (AS), which is further metabolized to albendazole sulfone and other major oxidative metabolites already detected in human urine. Urinary excretion of AS is minimal, with less than 1% of the administered dose recovered in urine. Bile excretion is likely a partial drug clearance pathway, as evidenced by bile concentrations of AS similar to those in plasma. Half-life: The terminal elimination half-life is 8 to 12 hours (single dose, 400 mg). Albendazole is rapidly metabolized to albendazole sulfoxide, whose plasma half-life varies considerably, ranging from approximately 4 to 15 hours. Both (+) and (-) sulfoxide derivatives are further oxidized to achiral sulfone metabolites. This reaction favors the formation of (-) sulfoxide and may be the rate-limiting step determining the plasma half-life of the biologically active (+) sulfoxide metabolite. Induction of enzymes involved in the sulfone formation from (+) sulfoxide may be one of the reasons for the significant differences in the plasma half-life of albendazole sulfoxide.

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In silkworm hemolymph, after oral administration of albendazole (50 mg/kg), the Cmax of the parent drug was 3.2 μM, and the Cmax values of the metabolites albendazole sulfoxide (ABZ-SO) and albendazole sulfone (ABZ-SO2) were 8.5 μM and 4.1 μM, respectively [5]
- The terminal half-life (t1/2) of the parent drug albendazole in silkworm hemolymph was 4.2 hours, while the t1/2 values of ABZ-SO and ABZ-SO2 were 8.5 hours and 12.3 hours, respectively [5]
- Albendazole is rapidly metabolized in vivo. Albendazole is oxidized to ABZ-SO (the major active metabolite) and ABZ-SO2 (a minor metabolite) [5]
- The bioavailability of oral abendazole in mice is approximately 30%, and it has good tissue penetration into tumor and cyst tissues [1][4]

Toxicity Summary
Albendazole binds to the colchicine-sensitive sites of tubulin, inhibiting its polymerization or assembly into microtubules, leading to degenerative changes in worm epidermal and intestinal cells. Loss of cytoplasmic microtubules results in impaired glucose uptake in susceptible larvae and adults, depleting their glycogen reserves. Degenerative changes in the endoplasmic reticulum and germinal layer mitochondria, followed by lysosomal release, lead to reduced production of adenosine triphosphate (ATP), the energy required for worm survival. Due to reduced energy production, the parasite loses its motility and eventually dies. Hepatotoxicity
Up to 50% of patients treated with albendazole experience transient and asymptomatic elevations in serum transaminase levels after several weeks of treatment. These abnormalities improve rapidly upon discontinuation of the drug, which is rare (approximately 4%). Albendazole is also associated with rare cases of clinically significant liver injury. The onset of damage can range from a few days to up to two months after the start of treatment, or even faster after multiple courses of treatment. Damage may also occur 1 to 2 weeks after a short period (1 to 3 days) of albendazole administration. Elevated serum enzymes are typically hepatocellular or mixed. Allergic symptoms (rash, fever, eosinophilia) may occur, but are usually mild. Most cases are mild and recover rapidly after discontinuation of the drug. There have been reports of rapid relapse after re-administration, but with similar severity. Cases leading to acute liver failure and ultimately requiring emergency liver transplantation or death have also been reported.
Probability Score: B (Highly probable cause of clinically significant liver damage).

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Effects during Pregnancy and Lactation
◉ Overview of Use During Lactation
Albendazole and its active metabolites are rarely excreted into breast milk. An informal advisory group of the World Health Organization concluded that breastfeeding women can take albendazole orally once.
◉ Effects on Breastfed Infants
Two mothers with intestinal parasites received a single oral dose of 400 mg albendazole while exclusively breastfeeding their infants aged 1 to 6 months. No adverse effects on breastfed infants were reported.
◉ Effects on Lactation and Breast Milk
A study compared mothers in Peru who received a single dose of 400 mg albendazole (n = 117) or a matched placebo (n = 99). Infant breast milk intake was measured at 1 month and 6 months postpartum. At 1 month postpartum, 92.5% of participants were exclusively or primarily breastfed. The average daily breast milk intake was 756 ml in the albendazole group and 774 ml in the placebo group, with no statistically significant difference between the two groups. At 6 months, only 10% of infants in both groups were exclusively or primarily breastfed. There was no statistically significant difference in milk intake among their infants.

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Protein Binding
70% bound to plasma proteinsToxicity Data
LD50: 1500 mg/kg (oral, mouse). [MSDS]Interactions
A single-dose annual regimen of albendazole in combination with ivermectin or diethylcarbazine has shown great potential in controlling lymphatic filariasis occurring alone or concurrently with other filariasis infections. This combination therapy also has the added benefit of reducing the incidence of intestinal ascariasis in school-aged children.
...Plasma concentrations of albendazole sulfoxide metabolites can be increased by co-administration with glucocorticoids (and possibly praziquantel).

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Albendazole (1-50 μM) showed low cytotoxicity to normal human cells (L02, NCM460), with an IC50 > 50 μM [1][2]
- No significant histopathological abnormalities were observed in the liver, kidneys, or heart of mice treated with albendazole (150-200 mg/kg, orally/intraperitoneally for 21-30 days), and weight loss <5% [1][3][4]
- At therapeutic concentrations, albendazole and ABZ-SO had 90% and 95% human plasma protein binding rates, respectively. [3]
- No significant hematologic toxicities (e.g., neutropenia, thrombocytopenia) were observed in treated mice [1][4]

[1]. In vitro and in vivo suppression of growth of hepatocellular carcinoma cells by albendazole. Cancer Lett. 2001 Apr 10;165(1):43-9.

[2]. Regulation of apoptosis and autophagy by albendazole in human colon adenocarcinoma cells. Biochimie. 2022 Jul;198:155-166.

[3]. Albendazole inhibits HIF-1α-dependent glycolysis and VEGF expression in non-small cell lung cancer cells. Mol Cell Biochem. 2017 Apr;428(1-2):171-178.

[4]. Efficacy of novel albendazole salt formulations against secondary cystic echinococcosis in experimentally infected mice. Parasitology. 2020 Nov;147(13):1425-1432.

[5]. Determination of albendazole and metabolites in silkworm Bombyx mori hemolymph by ultrafast liquid chromatography tandem triple quadrupole mass spectrometry. PLoS One. 2014 Sep 25;9(9):e105637.

Therapeutic Uses
MeSH Title: Anthelmintics, Anti-tapetic Drugs, Antibiotics for Animals
Albendazole is a benzimidazole carbamate used to treat gastrointestinal infections caused by adult roundworms, lungworms, tapeworms, and liver flukes.
Some microsporidia causing intestinal infections in AIDS patients respond partially (to intestinal microsporidia) or completely (to intestinal encephalitis microsporidia and related encephalitis microsporidia); the sulfoxide metabolite of albendazole appears to be particularly effective against these parasites in vitro.
Drug: ...used to treat nematode infections: roundworms, hookworms, hookmouth nematodes, whipworms, pinworms, and systemic nematodes such as trichinella, Gnathostoma spinigerum, and Angiostrongylus cantonensis larvae. It is also used to treat larval infections of Echinococcus granulosus and Echinococcus multilocularis, and to treat neurocysticercosis caused by Taenia solium. For more complete data on the therapeutic uses of albendazole (21 types), please visit the HSDB record page.

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Drug Warnings
The incidence of leukopenia in patients treated with albendazole is less than 1%, and rare cases have been reported with granulocytopenia, pancytopenia, agranulocytosis, or thrombocytopenia. Therefore, blood cell counts should be performed at the start of each 28-day treatment cycle and every 2 weeks during treatment. The manufacturer states that albendazole treatment can continue if a decrease in the total white blood cell count occurs, but the decrease is minor and does not worsen.
Because approximately 16% of patients in clinical trials experienced mild to moderate elevations of liver enzymes after taking albendazole, and because this drug may cause hepatotoxicity, liver function tests should be performed before each initiation of albendazole treatment and at least every 2 weeks during treatment. Albendazole should be discontinued if clinically significant elevations in liver function tests are observed. Once liver enzymes return to pre-treatment levels, treatment can be restarted, but frequent laboratory tests should be performed during repeated treatment. Albendazole may cause harm to the fetus and should only be used during pregnancy if the benefits outweigh the risks to the fetus and there are no other suitable treatment options available clinically. Women of childbearing age should begin treatment only after a negative pregnancy test and should be advised to avoid pregnancy during albendazole treatment or for one month after completion of treatment with this drug. Animal studies (rats and rabbits) have shown that this drug is teratogenic and therefore its use is not recommended for pregnant women or infants under 2 years of age. For more complete data on drug warnings for albendazole (9 in total), please visit the HSDB record page. Pharmacodynamics Albendazole is a broad-spectrum anthelmintic. The primary mechanism of action of albendazole is through the inhibition of tubulin polymerization, leading to the loss of cytoplasmic microtubules. Albendazole is a broad-spectrum benzimidazole anthelmintic with additional antitumor activity [1][4].
Its antitumor mechanism involves a dual action: inhibiting β-tubulin polymerization, inducing G2/M phase cell cycle arrest and apoptosis; and inhibiting HIF-1α-dependent glycolysis and angiogenesis by downregulating the expression of HIF-1α and VEGF[1][2][3].
It can also induce autophagy in colon cancer cells, thereby enhancing their cytotoxicity[2].
Clinically, albendazole is suitable for the treatment of parasitic infections including cystic echinococcosis, ascariasis and hookworm disease[4].
It has the potential to be used as a novel drug to treat certain diseases. Hepatocellular carcinoma, colon adenocarcinoma and non-small cell lung cancer, and has a good safety profile[1][2][3].
Novel albendazole salt formulations have shown higher efficacy against cystic echinococcosis, but their parent drug still retains significant antiparasitic and antitumor activity[4].

C12H15N3O2S

265.33

265.088

54965-21-8

Albendazole sulfoxide;54029-12-8;Albendazole sulfoxide-d3;1448346-38-0;Albendazole-d3;1353867-92-1;Albendazole-d7;1287076-43-0

2082

White to off-white solid powder

1.3±0.1 g/cm3

207-211°C（分解）

1.634

3.07

2

4

5

18

291

0

HXHWSAZORRCQMX-UHFFFAOYSA-N

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)

methyl N-(6-propylsulfanyl-1H-benzimidazol-2-yl)carbamate

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

Solubility in Formulation 1: 2 mg/mL (7.54 mM) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), suspension solution; with sonication.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 2 mg/mL (7.54 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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 (Please use freshly prepared in vivo formulations for optimal results.)