| Compound Information | SONAR Target prediction |
| Name: | Glipizide |
| Unique Identifier: | LOPAC 00194 |
| MolClass: | Checkout models in ver1.5 and ver1.0 |
| Molecular Formula: | C21H27N5O4S |
| Molecular Weight: | 418.322 g/mol |
| X log p: | 10.429 (online calculus) |
| Lipinksi Failures | 1 |
| TPSA | 101.38 |
| Hydrogen Bond Donor Count: | 0 |
| Hydrogen Bond Acceptors Count: | 9 |
| Rotatable Bond Count: | 10 |
| Canonical Smiles: | Cc1cnc(cn1)C(=O)NCCc1ccc(cc1)S(=O)(=O)NC(=O)NC1CCCCC1 |
| Class: | K+ Channel |
| Action: | Blocker |
| Selectivity: | ATP-sensitive |
| Generic_name: | Glipizide |
| Chemical_iupac_name: | N-[2-[4-(cyclohexylcarbamoylsulfamoyl)phenyl]ethyl]-5-methyl-pyridine-2-carboxamide |
| Drug_type: | Approved Drug |
| Pharmgkb_id: | PA449762 |
| Kegg_compound_id: | D00335 |
| Drugbank_id: | APRD00436 |
| Melting_point: | 208-209 oC |
| H2o_solubility: | 37.2 mg/L |
| Logp: | 1.763 |
| Isoelectric_point: | 5.9 |
| Cas_registry_number: | 29094-61-9 |
| Drug_category: | Hypoglycemic Agents; ATC:A10BB07 |
| Indication: | For use as an adjunct to diet for the control of hyperglycemia and its associated symptomatology in patients with non-insulin-dependent diabetes mellitus (NIDDM; type II), formerly known as maturity-onset diabetes, after an adequate trial of dietary therapy has proved unsatisfactory. |
| Pharmacology: | Glipizide, a second-generation sulfonylurea, is used with diet to lower blood glucose in patients with diabetes mellitus type II. The primary mode of action of glipizide in experimental animals appears to be the stimulation of insulin secretion from the beta cells of pancreatic islet tissue and is thus dependent on functioning beta cells in the pancreatic islets. In humans glipizide appears to lower the blood glucose acutely by stimulating the release of insulin from the pancreas, an effect dependent upon functioning beta cells in the pancreatic islets. In man, stimulation of insulin secretion by glipizide in response to a meal is undoubtedly of major importance. Fasting insulin levels are not elevated even on long-term glipizide administration, but the postprandial insulin response continues to be enhanced after at least 6 months of treatment. Some patients fail to respond initially, or gradually lose their responsiveness to sulfonylurea drugs, including glipizide. |
| Mechanism_of_action: | Sulfonylureas likely bind to ATP-sensitive potassium-channel receptors on the pancreatic cell surface, reducing potassium conductance and causing depolarization of the membrane. Depolarization stimulates calcium ion influx through voltage-sensitive calcium channels, raising intracellular concentrations of calcium ions, which induces the secretion, or exocytosis, of insulin. |
| Organisms_affected: | Humans and other mammals |
| Found: 24 nonactive as graph: single | with analogs | 1 2 3 4 5 6 7 8 9 10 Next >> [24] |
| Species: | 4932 |
| Condition: | BY4741 |
| Replicates: | 8 |
| Raw OD Value: r im | 0.7991±0.0724808 |
| Normalized OD Score: sc h | 0.9894±0.0184667 |
| Z-Score: | -0.4592±0.697479 |
| p-Value: | 0.570056 |
| Z-Factor: | -25.5253 |
| Fitness Defect: | 0.562 |
| Bioactivity Statement: | Nonactive |
| ps |
| DBLink | Rows returned: 1 |
| 3478 | N-[2-[4-(cyclohexylcarbamoylsulfamoyl)phenyl]ethyl]-5-methyl-pyrazine-2-carboxamide |
| internal high similarity DBLink | Rows returned: 0 |
| active | Cluster 5012 | Additional Members: 11 | Rows returned: 1 |
| Prest1231 | 0.48936170212766 |
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