Comparative Pharmacology
Head-to-head clinical analysis: ACETOHEXAMIDE versus GLUCOTROL.
Peer-Reviewed Evidence
Head-to-head clinical analysis: ACETOHEXAMIDE versus GLUCOTROL.
ACETOHEXAMIDE vs GLUCOTROL
Comparing the clinical profiles, pharmacokinetic behaviors, and safety indices of these two therapeutic agents.
Sulfonylurea that stimulates insulin release from pancreatic beta cells by binding to the sulfonylurea receptor (SUR1) on ATP-sensitive potassium channels (K_ATP), causing membrane depolarization, calcium influx, and exocytosis of insulin-containing granules. Also may increase peripheral insulin sensitivity.
Stimulates insulin secretion from pancreatic beta cells by binding to sulfonylurea receptor 1 (SUR1) on ATP-sensitive potassium channels, causing depolarization and calcium influx. Also may increase peripheral insulin sensitivity.
Initial: 250 mg orally once daily; maintenance: 250-1500 mg orally once daily or in divided doses twice daily.
Initial dose 5 mg orally once daily, increased by 2.5-5 mg increments weekly based on glycemic response; maximum 20 mg daily as single or divided doses (for doses >15 mg, administer in divided doses).
None Documented
None Documented
Terminal elimination half-life: 6-12 hours (parent drug); ~5-6 hours (active metabolite hydroxyhexamide); clinical context: prolonged in renal impairment due to accumulation of active metabolite
Terminal elimination half-life: 2-4 hours (mean 3.4 hours) in normal subjects; extended up to 8-12 hours in elderly or hepatic impairment due to reduced clearance.
Renal: 85-90% (60-70% as unchanged drug, remainder as hydroxylated metabolite); biliary/fecal: <10%
Primarily renal: ~80% as metabolites (mainly 4-trans-hydroxyglipizide and 3-cis-hydroxyglipizide) and ~10% unchanged; fecal: ~10%.
Category C
Category C
Sulfonylurea Antidiabetic
Sulfonylurea Antidiabetic