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| Clinical data | |
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| Trade names | Glucotrol, Glucotrol XL, others |
| AHFS/Drugs.com | Monograph |
| MedlinePlus | a684060 |
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| Routes of administration | By mouth |
| Drug class | Sulfonylurea |
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| Pharmacokinetic data | |
| Bioavailability | 100% (regular formulation) 90% (extended release) |
| Protein binding | 98 to 99% |
| Metabolism | Liverhydroxylation |
| Eliminationhalf-life | 2 to 5 hours |
| Excretion | Kidney and fecal |
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| ECHA InfoCard | 100.044.919 |
| Chemical and physical data | |
| Formula | C21H27N5O4S |
| Molar mass | 445.54 g·mol−1 |
| 3D model (JSmol) | |
| Melting point | 208 to 209 °C (406 to 408 °F) |
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Glipizide, sold under the brand nameGlucotrol among others, is ananti-diabetic medication of thesulfonylurea class used to treattype 2 diabetes.[1][2] It is used together with adiabetic diet and exercise.[1][2] It is not indicated for use by itself intype 1 diabetes.[1][2] It is takenby mouth.[1][2] Effects generally begin within half an hour and can last for up to a day.[1]
Common side effects include nausea,diarrhea,low blood sugar, andheadache.[1] Other side effects include sleepiness, skin rash, and shakiness.[3] The dose may need to be adjusted in those withliver orkidney disease.[1] Use duringpregnancy orbreastfeeding is not recommended.[3] It works by stimulating thepancreas to releaseinsulin and increases tissue sensitivity to insulin.[1]
Glipizide was approved for medical use in the United States in 1984.[1] It is available as ageneric medication.[1] In 2023, it was the 42nd most commonly prescribed medication in the United States, with more than 15 million prescriptions.[4][5]
Glipizide sensitizes thebeta cells of pancreaticislets of Langerhans insulin response, meaning that more insulin is released in response to glucose than would be without glipizide ingestion.[2] Glipizide acts by partially blockingpotassium channels among beta cells of pancreatic islets of Langerhans. By blockingpotassium channels, the cell depolarizes, which results in the opening of voltage-gated calcium channels. The resulting calcium influx encourages insulin release from beta cells.[6]
It was patented in 1969, and approved for medical use in 1971.[7] Glipizide was approved for medical use in the United States in 1984.[1]
