"64-77-7"@en . . . . . "Tolbutamida"@en . . "1-Butyl-3-tosylurea"@en . "Humans and other mammals"@en . . . . . "approved"@en . "Tolylsulfonylbutylurea"@en . . "1-Butyl-3-(P-tolylsulfonyl)urea"@en . "Approximately 95% bound to plasma proteins."@en . "For treatment of NIDDM (non-insulin-dependent diabetes mellitus) in conjunction with diet and exercise."@en . . . . . . . "3-(P-Tolyl-4-sulfonyl)-1-butylurea"@en . . . . "N-(4-Methylphenylsulfonyl)-n'-butylurea"@en . . . . . . . "N-(4-Methylbenzenesulfonyl)-n'-butylurea"@en . . . . "# Zhou SF, Zhou ZW, Yang LP, Cai JP: Substrates, inducers, inhibitors and structure-activity relationships of human Cytochrome P450 2C9 and implications in drug development. Curr Med Chem. 2009;16(27):3480-675. Epub 2009 Sep 1. \"Pubmed\":http://www.ncbi.nlm.nih.gov/pubmed/19515014"@en . . . . . . . . . . "Approximately 7 hours with interindividual variations ranging from 4-25 hours. Tolbutamide has the shortest duration of action, 6-12 hours, of the antidiabetic sulfonylureas."@en . . " "@en . . . . . . . . . "Tolbutamide"@en . "N-Butyl-N'-(p-tolylsulfonyl)urea"@en . "Unchanged drug and metabolites are eliminated in the urine and feces. Approximately 75-85% of a single orally administered dose is excreted in the urine principally as the 1-butyl-3-p-carboxyphenylsulfonylurea within 24 hours. "@en . . "N-(P-Methylbenzenesulfonyl)-n'-butylurea"@en . "Orinase (tn)"@en . "1-P-Toluenesulfonyl-3-butylurea"@en . "N-N-Butyl-n'-tosylurea"@en . . . . "Readily absorbed following oral administration. Tolbutamide is detectable in plasma 30-60 minutes following oral administration of a single dose with peak plasma concentrations occurring within 3-5 hours. Absorption is unaltered if taken with food but is increased with high pH."@en . . "Yan-Ping Chen, Pai-Ching Lin, \"Tolbutamide Particle And Preparing Method Thereof And Method Of Reducing A Blood Glucose.\" U.S. Patent US20120121707, issued May 17, 2012."@en . . "1-Butyl-3-(P-methylphenylsulfonyl)urea"@en . "Sulfonylureas lower blood glucose in patients with NIDDM by directly stimulating the acute release of insulin from functioning beta cells of pancreatic islet tissue by an unknown process that involves a sulfonylurea receptor (receptor 1) on the beta cell. Sulfonylureas inhibit the ATP-potassium channels on the beta cell membrane and potassium efflux, which results in depolarization and calcium influx, calcium-calmodulin binding, kinase activation, and release of insulin-containing granules by exocytosis, an effect similar to that of glucose."@en . "Oral, mouse: LD₅₀ = 2600 mg/kg"@en . "N-Butyl-n'-P-toluenesulfonylurea"@en . . . . "N-(Sulfonyl-P-methylbenzene)-n'-N-butylurea"@en . . . "Tolbutamide"@en . . . . . "Tolbutamidum"@en . "N-Butyl-n'-(4-methylphenylsulfonyl)urea"@en . "Tolbutamide is an oral antihyperglycemic agent used for the treatment of non-insulin-dependent diabetes mellitus (NIDDM). It is structurally similar to acetohexamide, chlorpropamide and tolazamide and belongs to the sulfonylurea class of insulin secretagogues, which act by stimulating \u03B2 cells of the pancreas to release insulin. Sulfonylureas increase both basal insulin secretion and meal-stimulated insulin release. Medications in this class differ in their dose, rate of absorption, duration of action, route of elimination and binding site on their target pancreatic \u03B2 cell receptor. Sulfonylureas also increase peripheral glucose utilization, decrease hepatic gluconeogenesis and may increase the number and sensitivity of insulin receptors. Sulfonylureas are associated with weight gain, though less so than insulin. Due to their mechanism of action, sulfonylureas may cause hypoglycemia and require consistent food intake to decrease this risk. The risk of hypoglycemia is increased in elderly, debilitated and malnourished individuals. Tolbutamide appears to be metabolized in the liver. Tolbutamide and its metabolites are excreted in urine (75-85%) and feces. "@en .