Glipizide
Glipizide is a second generation sulfonylurea that exhibits anti-diabetic activity. Glipizide inhibits ATP-dependent K+ channels in β cells, forcing cells to remain depolarized, increasing Ca2+ influx and insulin secretion. Glipizide also decreases the metabolic clearance rate of insulin.
References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/18927611
| Cas No. |
29094-61-9 |
|---|---|
| Purity |
≥98% |
| Formula |
C21H27N5O4S |
| Formula Wt. |
445.54 |
| Chemical Name |
N-[2-[4-[[[(Cyclohexylamino)carbonyl]amino]sulfonyl]phenyl]ethyl-5-methylpyrazinecarboxamide |
| IUPAC Name |
N-[2-[4-(cyclohexylcarbamoylsulfamoyl)phenyl]ethyl]-5-methylpyrazine-2-carboxamide |
| Synonym |
Glibenese; Blucotrol; Minidiab; Ozidia |
| Melting Point |
208-209°C |
| Solubility |
Soluble in DMSO (48mg/mL) or methanol (1.9mg/mL).. |
| Appearance |
White or Almost White Crystalline Powder |
Barzilai N, Groop PH, Groop L, et al. A novel mechanism of glipizide sulfonylurea action: decreased metabolic clearance rate of insulin. Acta Diabetol. 1995 Dec;32(4):273-8. PMID: 8750768.
Weinhaus AJ, Poronnik P, Cook DI, et al. Insulin secretagogues, but not glucose, stimulate an increase in [Ca2+]i in the fetal rat beta-cell. Diabetes. 1995 Jan;44(1):118-24. PMID: 7529202.
Heurteaux C, Bertaina V, Widmann C, et al. K+ channel openers prevent global ischemia-induced expression of c-fos, c-jun, heat shock protein, and amyloid beta-protein precursor genes and neuronal death in rat hippocampus. Proc Natl Acad Sci U S A. 1993 Oct 15;90(20):9431-5. PMID: 8415718.
