Comparative Pharmacology
Head-to-head clinical analysis: ALBENDAZOLE versus STROMECTOL.
Head-to-head clinical analysis: ALBENDAZOLE versus STROMECTOL.
ALBENDAZOLE vs STROMECTOL
Comparing the clinical profiles, pharmacokinetic behaviors, and safety indices of these two therapeutic agents.
Albendazole inhibits tubulin polymerization by binding to beta-tubulin, disrupting microtubule formation, which leads to impaired glucose uptake and depletion of glycogen stores in susceptible parasites, resulting in their immobilization and death.
Ivermectin acts by binding selectively and with high affinity to glutamate-gated chloride ion channels in invertebrate nerve and muscle cells, leading to increased permeability to chloride ions, hyperpolarization of nerve or muscle cells, and death of the parasite. It also interacts with other ligand-gated chloride channels, such as those gated by gamma-aminobutyric acid (GABA).
400 mg orally twice daily for 3-7 days for most indications; for neurocysticercosis, 400 mg orally twice daily for 8-30 days; for hydatid disease, 400 mg orally twice daily for 28-day cycles with 14-day drug-free intervals for 3 cycles.
Oral: 200 mcg/kg once daily for 1-2 days. For strongyloidiasis, 200 mcg/kg/day for 2 days. For onchocerciasis, single dose of 150 mcg/kg.
None Documented
None Documented
Clinical Note
moderateAlbendazole + Digoxin
"Albendazole may decrease the cardiotoxic activities of Digoxin."
Clinical Note
moderateAlbendazole + Digitoxin
"Albendazole may decrease the cardiotoxic activities of Digitoxin."
Clinical Note
moderateAlbendazole + Deslanoside
"Albendazole may decrease the cardiotoxic activities of Deslanoside."
Clinical Note
moderateAlbendazole + Acetyldigitoxin
"Albendazole may decrease the cardiotoxic activities of Acetyldigitoxin."
Terminal half-life of albendazole sulfoxide is 8–12 hours; parent drug half-life is <1 hour. Clinical context: supports once- or twice-daily dosing.
Terminal elimination half-life is approximately 18 hours (range 10–30 hours) in healthy subjects; prolonged in hepatic impairment.
Primarily renal (80%) as inactive metabolites; <2% unchanged in urine. Biliary/fecal excretion accounts for ~20%.
Primarily fecal (90%) as unchanged drug and metabolites; renal excretion accounts for <1% of the dose.
Category D/X
Category C
Anthelmintic
Anthelmintic