3518 Albendazole Albendazole is only found in individuals that have used or taken this drug. It is a benzimidazole broad-spectrum anthelmintic structurally related to mebendazole that is effective against many diseases. (From Martindale, The Extra Pharmacopoeia, 30th ed, p38). Albendazole causes degenerative alterations in the tegument and intestinal cells of the worm by binding to the colchicine-sensitive site of tubulin, thus inhibiting its polymerization or assembly into microtubules. The loss of the cytoplasmic microtubules leads to impaired uptake of glucose by the larval and adult stages of the susceptible parasites, and depletes their glycogen stores. Degenerative changes in the endoplasmic reticulum, the mitochondria of the germinal layer, and the subsequent release of lysosomes result in decreased production of adenosine triphosphate (ATP), which is the energy required for the survival of the helminth. Due to diminished energy production, the parasite is immobilized and eventually dies. 54965-21-8 2082 C12H15N3O2S 265.088500 White to off-white. 208-210°C Practically insoluble Poorly absorbed from the gastrointestinal tract due to its low aqueous solubility. Oral bioavailability appears to be enhanced when coadministered with a fatty meal (estimated fat content 40 g) Albendazole causes degenerative alterations in the tegument and intestinal cells of the worm by binding to the colchicine-sensitive site of tubulin, thus inhibiting its polymerization or assembly into microtubules. The loss of the cytoplasmic microtubules leads to impaired uptake of glucose by the larval and adult stages of the susceptible parasites, and depletes their glycogen stores. Degenerative changes in the endoplasmic reticulum, the mitochondria of the germinal layer, and the subsequent release of lysosomes result in decreased production of adenosine triphosphate (ATP), which is the energy required for the survival of the helminth. Due to diminished energy production, the parasite is immobilized and eventually dies. Hepatic. Rapidly converted in the liver to the primary metabolite, albendazole sulfoxide, which is further metabolized to albendazole sulfone and other primary oxidative metabolites that have been identified in human urine. Route of Elimination: Albendazole is rapidly converted in the liver to the primary metabolite, albendazole sulfoxide, which is further metabolized to albendazole sulfone and other primary oxidative metabolites that have been identified in human urine. Urinary excretion of albendazole sulfoxide is a minor elimination pathway with less than 1% of the dose recovered in the urine. Biliary elimination presumably accounts for a portion of the elimination as evidenced by biliary concentrations of albendazole sulfoxide similar to those achieved in plasma. Half Life: Terminal elimination half-life ranges from 8 to 12 hours (single dose, 400mg). LD50: 1500 mg/kg (oral,mouse). [MSDS] No indication of carcinogenicity to humans (not listed by IARC). For the treatment of parenchymal neurocysticercosis due to active lesions caused by larval forms of the pork tapeworm, <i>Taenia solium</i> and for the treatment of cystic hydatid disease of the liver, lung, and peritoneum, caused by the larval form of the dog tapeworm, <i>Echinococcus granulosus</i>. Symptoms of overdose include elevated liver enzymes, headaches, hair loss, low levels of white blood cells (neutropenia), fever, and itching. 2009-07-30T17:58:36Z 2026-03-31T17:35:01Z Albendazole C01779 16664 ALBENDAZOLE-S-OXIDE Albendazole DB00518 true CCCSC1=CC2=C(C=C1)N=C(NC(=O)OC)N2 C12H15N3O2S 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) HXHWSAZORRCQMX-UHFFFAOYSA-N 265.331 265.088497429 Exogenous Solid 2.7 HMDB14659 CHEMBL1483 1998 <p>Gyurik, R.J. and Theodorides, VJ.; US. Patent 3,915,986; October 28,1975; assigned to<br /> Smith Kline Corp.</p> CHEM002502 DTXSID0022563 NS00009208 methyl N-[6-(propylsulfanyl)-1H-1,3-benzodiazol-2-yl]carbamate