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Tolbutamide (Tolbutamide) - Summary



Tolbutamide is an oral blood-glucose-lowering drug of the sulfonylurea class. Tolbutamide is a pure, white, crystalline compound which is practically insoluble in water.

Tolbutamide is indicated as an adjunct to diet to lower the blood glucose in patients with non-insulin-dependent diabetes mellitus (type II) whose hyperglycemia cannot be controlled by diet alone.

In initiating treatment for non-insulin-dependent diabetes, diet should be emphasized as the primary form of treatment. Caloric restriction and weight loss are essential in the obese diabetic patient. Proper dietary management alone may be effective in controlling the blood glucose and symptoms of hyperglycemia. The importance of regular physical activity should also be stressed, and cardiovascular risk factors should be identified and corrective measures taken where possible.

If this treatment program fails to reduce symptoms and/or blood glucose, the use of an oral sulfonylurea or insulin should be considered. Use of tolbutamide must be viewed by both the physician and patient as a treatment in addition to diet, and not as a substitute for diet or as a convenient mechanism for avoiding dietary restraint. Furthermore, loss of blood glucose control on diet alone may be transient, thus requiring only short-term administration of tolbutamide.

During maintenance programs, tolbutamide should be discontinued if satisfactory lowering of blood glucose is no longer achieved. Judgments should be based on regular clinical and laboratory evaluations.

In considering the use of tolbutamide in asymptomatic patients, it should be recognized that controlling the blood glucose in non-insulin dependent diabetes has not been definitely established to be effective in preventing the long-term cardiovascular or neural complications of diabetes.

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Published Studies Related to Tolbutamide

No relevant interaction with alprazolam, caffeine, tolbutamide, and digoxin by treatment with a low-hyperforin St John's wort extract. [2005.04]
We evaluated the pharmacokinetic interaction between a low-hyperforin St John's wort (SJW) extract and alprazolam, caffeine, tolbutamide, and digoxin. Previous reports on other SJW products had shown remarkably decreased plasma concentrations of certain co-medicated drugs, which was attributed to an inducing effect of SJW on cytochrome P-450 (CYP) and p-glycoprotein (p-gp) activity...

Is acarbose equivalent to tolbutamide as first treatment for newly diagnosed type 2 diabetes in general practice? A randomised controlled trial. [2004.01]
We performed a double blind randomised controlled trial in general practice to assess equivalence between tolbutamide and acarbose with respect to the effect on mean HbA(1c) in newly diagnosed patients with type 2 diabetes. Secondary objectives were to compare the effects of both treatments on fasting and post-load blood glucose and insulin levels, lipids, and adverse events...

Tolbutamide, flurbiprofen, and losartan as probes of CYP2C9 activity in humans. [2003.01]
The metabolic activity of CYP2C9 in 16 subjects expressing four different genotypes (CYP2C9*1/*1, *1/*2, *1/*3, and *2/*2) was evaluated. Single oral doses of tolbutamide, flurbiprofen, and losartan were administered in a randomized, crossover design...

Effects of CYP2C19 and CYP2C9 genetic polymorphisms on the disposition of and blood glucose lowering response to tolbutamide in humans. [2002.03]
Several recent in-vitro data have revealed that CYP2C19, in addition to CYP2C9, is also involved in the 4-methylhydroxylation of tolbutamide. We evaluated the relative contribution of CYP2C9 and CYP2C19 genetic polymorphisms on the disposition of blood glucose lowering response to tolbutamide in normal healthy Korean subjects in order to reappraise tolbutamide as a selective in-vivo probe substrate of CYP2C9 activity...

Fluvoxamine inhibits the CYP2C9 catalyzed biotransformation of tolbutamide. [2001.01]
OBJECTIVE: Our objective was to examine the interaction between fluvoxamine and tolbutamide to confirm that fluvoxamine inhibits CYP2C9... CONCLUSION: Fluvoxamine is a moderate inhibitor of CYP2C9 in vivo.

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Clinical Trials Related to Tolbutamide

A Drug Interaction Study of Tasisulam in Patients With Advanced Cancer or Lymphoma [Recruiting]

Drug Drug Interaction Study Between BI 201335 and BI 207127 in Chronic Hepatitis C Infected Patients [Recruiting]
To evaluate the drug-drug interactions between BI 201335 and BI 207127 as well as their combined effect on CYP probe drug substrates and on tenofovir and raltegravir in treatment naive or prior treatment relapse patients with chronic hepatitis C infection.

Biomarkers of RO4929097and Other Drugs in Treating Patients With Metastatic or Unresectable Solid Tumors [Recruiting]
RATIONALE: Studying samples of blood in the laboratory from patients receiving RO4929097 may help doctors learn more about the effects of RO4929097 on cells. It may also help doctors understand how well patients respond to RO4929097 alone and in combination with other drugs. RO4929097 may stop the growth of tumor cells by blocking some of the enzymes needed for cell growth.

PURPOSE: This randomized study is studying the biomarkers of and best way to give RO4929097 and other drugs in treating patients with metastatic or unresectable solid tumors.

AZD2066 Cocktail Study [Recruiting]

Blockade of Vascular Potassium Channels During Human Endotoxemia [Completed]
Background: Activation of NO-synthase and vascular potassium (K) channels may play a role in the sepsis-induced attenuated sensitivity to norepinephrine. We examined whether various K channel blockers and NO-synthase inhibition could restore norepinephrine sensitivity during experimental human endotoxemia.

Methods and Results: Volunteers received 2ng/kg E. coli endotoxin. The brachial artery was cannulated for infusion of drugs. Forearm blood flow (FBF) was measured using venous occlusion plethysmography. Intrabrachial norepinephrine infusion (1-3-10-30ng/min/dl) decreased FBF to 84▒4, 70▒4, 55▒4, and 38▒4% of baseline ratio, mean▒SEM). Following endotoxin administration, norepinephrine-induced vasoconstriction was attenuated: 101▒4, 92▒4, 83▒6, and 56▒7% (P=0. 0018, pooled data, n=30). Intrabrachial infusion of the K channel blocker tetra-ethyl ammonium (TEA) completely restored the vasoconstrictive effect of norepinephrine: from 104┬▒5, 93┬▒7, 93┬▒12, and 69┬▒12% to 89┬▒9, 73┬▒4, 59┬▒5, and 46┬▒8% (n=6, P=0. 045), whereas other K channel blockers had no effect. NO-synthase inhibitor L-NMMA (0. 2mg/min/dl) also restored the norepinephrine sensitivity (from 92┬▒5, 85┬▒4, 68┬▒11, and 43┬▒13% after endotoxin to 71┬▒3, 66┬▒7, 48┬▒11, and 21┬▒3% in the presence of L-NMMA, n=6, P=0. 009). Furthermore, in the presence of L-NMMA, TEA did not have an additional effect on the norepinephrine-induced vasoconstriction (n=6, P =0. 9).

Conclusions: The K channel blocker TEA completely restores the attenuated vasoconstrictive effects of norepinephrine during experimental human endotoxemia. Co-administration of L-NMMA abolishes this potentiating effect of TEA, suggesting that NO mediates the endotoxin-induced effect on K channels. In the absence of an effect of the selective KATP channel blocker tolbutamide we conclude that endotoxin-induced vasorelaxation is the result of NO-mediated activation of KCa channels.

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Page last updated: 2007-10-18

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