Drug/Small Molecule:
glibenclamide

last updated 08/10/2011

Dutch Pharmacogenetics Working Group Guideline for glibenclamide and CYP2C9

Summary

There are currently no dosing recommendations for glibenclamide based on CYP2C9 genotype.

Annotation

The Royal Dutch Pharmacists Association - Pharmacogenetics Working Group has evaluated therapeutic dose recommendations for glibenclamide based on CYP2C9 genotype (PMID:21412232). They conclude that there are no recommendations at this time.

Genotype Therapeutic Dose Recommendation Level of Evidence Clinical Relevance
CYP2C9 *1/*2 None Published controlled studies of moderate quality* relating to phenotyped and/or genotyped patients or healthy volunteers, and having relevant pharmacokinetic or clinical endpoints. Clinical effect (NS) Kinetic effect (NS)
CYP2C9 *2/*2 None Published controlled studies of moderate quality* relating to phenotyped and/or genotyped patients or healthy volunteers, and having relevant pharmacokinetic or clinical endpoints. Clinical effect (NS) Kinetic effect (NS)
CYP2C9 *1/*3 None Published controlled studies of moderate quality* relating to phenotyped and/or genotyped patients or healthy volunteers, and having relevant pharmacokinetic or clinical endpoints. Clinical effect (S): short-lived discomfort (< 48 hr) without permanent injury: e.g. reduced decrease in resting heart rate; reduction in exercise tachycardia; decreased pain relief from oxycodone; ADE resulting from increased bioavailability of atomoxetine (decreased appetite, insomnia, sleep disturbance etc); neutropenia > 1.5x109/l; leucopenia > 3.0x109/l; thrombocytopenia > 75x109/l; moderate diarrhea not affecting daily activities; reduced glucose increase following oral glucose tolerance test.
CYP2C9 *2/*3 None Published controlled studies of moderate quality* relating to phenotyped and/or genotyped patients or healthy volunteers, and having relevant pharmacokinetic or clinical endpoints. Clinical effect (NS) Kinetic effect (NS)
CYP2C9 *3/*3 None Published controlled studies of moderate quality* relating to phenotyped and/or genotyped patients or healthy volunteers, and having relevant pharmacokinetic or clinical endpoints. Minor clinical effect (S): QTc prolongation (<450 ms females, <470 ms males); INR increase < 4.5
  • *See Methods or PMID: 18253145 for definition of "moderate" quality.
  • S: statistically significant difference.

PharmGKB gathers information regarding PGx on FDA drug labels from the FDA's "Table of Pharmacogenomic Biomarkers in Drug Labels", and from FDA-approved FDA and EMA-approved (European Medicines Agency) EMA labels brought to our attention. Excerpts from the label and downloadable highlighted label PDFs are manually curated by PharmGKB.

Please note that some drugs may have been removed from or added to the FDA's "Table of Pharmacogenomic Biomarkers in Drug Labels" without our knowledge. We periodically check the table for additions to this table and update PharmGKB accordingly.

There is currently no such list for European drug labels - we are working with the EMA to establish a list of European Public Assessment Reports (EPAR)s that contain PGx information. We are constructing this list by initially searching for drugs for which we have PGx-containing FDA drug labels - of these 44 EMA EPARs were identified and are being curated for pgx information.

We welcome any information regarding drug labels containing PGx information approved by the FDA, EMA or other Medicine Agencies around the world - please contact feedback.


last updated 12/17/2013

FDA Label for glibenclamide and G6PD

This label is on the FDA Biomarker List
Actionable PGx

Summary

Although the glibenclamide (glyburide; GLYNASE PresTab) drug label does not specifically mention genetic testing, the FDA highlight precaution labeling prior to initiating treatment with glibenclamide for G6PD deficient individuals due to risk of hemolytic anemia. Treatment of patients with glucose 6-phosphate dehydrogenase (G6PD) deficiency with sulfonylurea agents can lead to hemolytic anemia; caution should be used in patients with G6PD deficiency and a non-sulfonylurea alternative should be considered.

Annotation

Although the glibenclamide (glyburide; GLYNASE PresTab) drug label does not specifically mention genetic testing, the FDA highlight precaution labeling prior to initiating treatment with glibenclamide for G6PD deficient individuals due to risk of hemolytic anemia.

Excerpt from the glibenclamide (GLYNASE PresTab) drug label:

Hemolytic Anemia: Treatment of patients with glucose 6-phosphate dehydrogenase (G6PD) deficiency with sulfonylurea agents can lead to hemolytic anemia. Because GLYNASE PresTab belongs to the class of sulfonylurea agents, caution should be used in patients with G6PD deficiency and a non-sulfonylurea alternative should be considered.

For the complete drug label text with sections containing pharmacogenetic information highlighted, see the glibenclamide drug label.

*Disclaimer: The contents of this page have not been endorsed by the FDA and are the sole responsibility of PharmGKB.

Full label available at DailyMed

Genes and/or phenotypes found in this label

  • Diabetes Mellitus
    • Indications & usage section, Contraindications section, Warnings section, Precautions section
    • source: PHONT
  • Diabetes Mellitus, Type 2
    • Contraindications section, Warnings section, Precautions section
    • source: PHONT
  • G6PD
    • Precautions section, toxicity
    • source: FDA Label

PharmGKB contains no Clinical Variants that meet the highest level of criteria.

To see more Clinical Variants with lower levels of criteria, click the button at the bottom of the page.

Disclaimer: The PharmGKB's clinical annotations reflect expert consensus based on clinical evidence and peer-reviewed literature available at the time they are written and are intended only to assist clinicians in decision-making and to identify questions for further research. New evidence may have emerged since the time an annotation was submitted to the PharmGKB. The annotations are limited in scope and are not applicable to interventions or diseases that are not specifically identified.

The annotations do not account for individual variations among patients, and cannot be considered inclusive of all proper methods of care or exclusive of other treatments. It remains the responsibility of the health-care provider to determine the best course of treatment for a patient. Adherence to any guideline is voluntary, with the ultimate determination regarding its application to be made solely by the clinician and the patient. PharmGKB assumes no responsibility for any injury or damage to persons or property arising out of or related to any use of the PharmGKB clinical annotations, or for any errors or omissions.

? = Mouse-over for quick help

This is a non-comprehensive list of genetic tests with pharmacogenetics relevance, typically submitted by the manufacturer and manually curated by PharmGKB. The information listed is provided for educational purposes only and does not constitute an endorsement of any listed test or manufacturer.

A more complete listing of genetic tests is found at the Genetic Testing Registry (GTR).

PGx Test Variants Assayed Gene?

The table below contains information about pharmacogenomic variants on PharmGKB. Please follow the link in the "Variant" column for more information about a particular variant. Each link in the "Variant" column leads to the corresponding PharmGKB Variant Page. The Variant Page contains summary data, including PharmGKB manually curated information about variant-drug pairs based on individual PubMed publications. The PMIDs for these PubMed publications can be found on the Variant Page.

The tags in the first column of the table indicate what type of information can be found on the corresponding Variant Page.

Links in the "Gene" column lead to PharmGKB Gene Pages.

Gene ? Variant?
(138)
Alternate Names / Tag SNPs ? Drugs ? Alleles ?
(+ chr strand)
Function ? Amino Acid?
Translation
No VIP available No VIP available VA CYP2C9 *1 N/A N/A N/A
No VIP available No VIP available VA CYP2C9 *2 N/A N/A N/A
No VIP available No VIP available VA CYP2C9 *3 N/A N/A N/A
No VIP available CA VA G6PD A- 202A_376G N/A N/A N/A
No VIP available CA No VIP available G6PD B (wildtype) N/A N/A N/A
No VIP available No Clinical Annotations available VA
rs1057910 1075A>C, 47545517A>C, 47639A>C, 96741053A>C, CYP2C9*3, CYP2C9*3:Ile359Leu, CYP2C9: I359L, CYP2C9:359Ile>Leu, CYP2C9:Ile359Leu, Ile359Leu, mRNA 11A>C
A > C
Missense
Ile359Leu
No VIP available No Clinical Annotations available VA
rs1799853 430C>T, 47506511C>T, 8633C>T, 96702047C>T, Arg144Cys, CYP2C9*2, CYP2C9:144Arg>Cys, CYP2C9:Arg144Cys, mRNA 455C>T
C > T
Missense
Arg144Cys
rs5030868 153762634G>A, 18154C>T, 4680572G>A, 563C>T, 653C>T, Mediterranean, Ser188Phe, Ser218Phe
G > A
Not Available
Ser218Phe
No VIP available No Clinical Annotations available VA
rs5215 1009G>A, 17348630C>T, 17408630C>T, 6577G>A, 748G>A, Val250Ile, Val337Ile
C > T
Missense
Val250Ile
No VIP available No Clinical Annotations available VA
rs5219 -16-179A>G, 17349572T>C, 17409572T>C, 5635A>G, 67A>G, E23K, KCNJ11: Lys23Glu, KCNJ11:67A>G, KCNJ11:E23K, Lys23Glu
T > C
Intronic
Lys23Glu
No VIP available No Clinical Annotations available VA
rs757110 17358477C>A, 17418477C>A, 4105G>T, 84973G>T, Ala1369Ser
C > A
Missense
Ala1369Ser
No VIP available No Clinical Annotations available VA
rs889299 23321914G>A, 23381914G>A, 73324G>A, 881-706G>A
G > A
Intronic
Alleles, Functions, and Amino Acid Translations are all sourced from dbSNP 138
2D structure from PubChem
provided by PubChem

Overview

Generic Names
  • Apo-Glibenclamide
  • Glibenclamida [INN-Spanish]
  • Glibenclamidum [INN-Latin]
  • Glyburide
  • glibenclamide
Trade Names
  • Abbenclamide
  • Adiab
  • Azuglucon
  • Bastiverit
  • Benclamin
  • Betanase
  • Betanese 5
  • Calabren
  • Cytagon
  • Daonil
  • Debtan
  • Dia-basan
  • Diabeta
  • Diabiphage
  • Dibelet
  • Duraglucon
  • Euclamin
  • Euglucan
  • Euglucon
  • Euglucon 5
  • Euglykon
  • GBN 5
  • Gen-Glybe
  • Gewaglucon
  • Gilemal
  • Glamide
  • Glibadone
  • Gliban
  • Gliben
  • Gliben-Puren N
  • Glibenbeta
  • Glibenclamid AL
  • Glibenclamid Basics
  • Glibenclamid Fabra
  • Glibenclamid Genericon
  • Glibenclamid Heumann
  • Glibenclamid Riker M.
  • Glibenclamid-Cophar
  • Glibenclamid-Ratiopharm
  • Glibenil
  • Glibens
  • Glibesyn
  • Glibet
  • Glibetic
  • Glibil
  • Gliboral
  • Glicem
  • Glidiabet
  • Glimel
  • Glimide
  • Glimidstata
  • Glisulin
  • Glitisol
  • Glubate
  • Gluben
  • Gluco-Tablimen
  • Glucobene
  • Glucohexal
  • Glucolon
  • Glucomid
  • Glucoremed
  • Glucoven
  • Glyben
  • Glybenclamide
  • Glybenzcyclamide
  • Glycolande
  • Glycomin
  • Glynase
  • Hexaglucon
  • Humedia
  • Lederglib
  • Libanil
  • Lisaglucon
  • Malix
  • Maninil
  • Med-Glionil
  • Melix
  • Micronase
  • Miglucan
  • Nadib
  • Neogluconin
  • Norglicem 5
  • Normoglucon
  • Novo-Glyburide
  • Orabetic
  • Pira
  • Praeciglucon
  • PresTab
  • Prodiabet
  • Renabetic
  • Semi-Daonil
  • Sugril
  • Suraben
  • Tiabet
  • Yuglucon
Brand Mixture Names
  • Glucovance (Metformin + Glibenclamide)

PharmGKB Accession Id:
PA449782

Description

Glyburide is an oral antihyperglycemic agent used for the treatment of non-insulin-dependent diabetes mellitus (NIDDM). It belongs to the sulfonylurea class of insulin secretagogues, which act by stimulating beta 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 beta 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. Glyburide has been shown to decrease fasting plasma glucose, postprandial blood glucose and glycosolated hemoglobin (HbA1c) levels (reflective of the last 8-10 weeks of glucose control). Glyburide appears to be completely metabolized, likely in the liver. Although its metabolites exert a small hypoglycemic effect, their contribution to glyburide's hypoglycemic effect is thought to be clinically unimportant. Glyburide metabolites are excreted in urine and feces in approximately equal proportions. The half-life of glyburide appears to be unaffected in those with a creatinine clearance of greater than 29 ml/min/1.73m 2.

Source: Drug Bank

Indication

Indicated as an adjunct to diet to lower the blood glucose in patients with NIDDM whose hyperglycemia cannot be satisfactorily controlled by diet alone.

Source: Drug Bank

Other Vocabularies

Information pulled from DrugBank has not been reviewed by PharmGKB.

Pharmacology, Interactions, and Contraindications

Mechanism of Action

Sulfonylureas such as glyburide bind to ATP-sensitive potassium channels 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.

Source: Drug Bank

Pharmacology

Glyburide, a second-generation sulfonylurea antidiabetic agent, lowers blood glucose acutely by stimulating the release of insulin from the pancreas, an effect dependent upon functioning beta cells in the pancreatic islets. With chronic administration in Type II diabetic patients, the blood glucose lowering effect persists despite a gradual decline in the insulin secretory response to the drug. Extrapancreatic effects may be involved in the mechanism of action of oral sulfonyl-urea hypoglycemic drugs. The combination of glibenclamide and metformin may have a synergistic effect, since both agents act to improve glucose tolerance by different but complementary mechanisms. In addition to its blood glucose lowering actions, glyburide produces a mild diuresis by enhancement of renal free water clearance. Glyburide is twice as potent as the related second-generation agent glipizide.

Source: Drug Bank

Food Interaction

Avoid alcohol.|Take 30-60 minutes before breakfast.

Source: Drug Bank

Absorption, Distribution, Metabolism, Elimination & Toxicity

Biotransformation

Primarily hepatic (mainly cytochrome P450 3A4). The major metabolite is the 4-trans-hydroxy derivative. A second metabolite, the 3-cis-hydroxy derivative, also occurs. These metabolites do not contribute clinically significant hypoglycemic action in humans as they are only weakly active; however, retention of 4-trans-hydroxyglyburide may prolong the hypoglycemic effect of the agent in those with severe renal impairment.

Source: Drug Bank

Protein Binding

Unchanged drug is ~99% bound to serum proteins; 4-trans-hydroxyglyburide is greater than 97% bound to serum proteins. Protein binding is primarily nonionic making glyburide and is less likely to displace or be displaced by drugs that bind via an ionic mechanism.

Source: Drug Bank

Absorption

Significant absorption within 1 hour and peak plasma levels are reached in 2 to 4 hours. Onset of action occurs within one hour.

Source: Drug Bank

Half-Life

1.4-1.8 hours (unchanged drug only); 10 hours (metabolites included). Duration of effect is 12-24 hours.

Source: Drug Bank

Toxicity

Oral rat LD 50: > 20,000 mg/kg. Oral mouse LD 50: 3250 mg/kg.

Source: Drug Bank

Clearance

78 ml/hr/kg in healthy adults. Clearance may be substantially decreased in those with severe renal impairment.

Source: Drug Bank

Route of Elimination

Glyburide is excreted as metabolites in the bile and urine, approximately 50% by each route.
This dual excretory pathway is qualitatively different from that of other sulfonylureas, which are excreted primarily in the urine.

Source: Drug Bank

Volume of Distribution

Steady state V d=0.125 L/kg; V d during elimination phase=0.155 L/kg.

Source: Drug Bank

Chemical Properties

Chemical Formula

C23H28ClN3O5S

Source: Drug Bank

Isomeric SMILES

COc1ccc(cc1C(=O)NCCc2ccc(cc2)S(=O)(=O)NC(=O)NC3CCCCC3)Cl

Source: OpenEye

Canonical SMILES

COC1=C(C=C(Cl)C=C1)C(=O)NCCC1=CC=C(C=C1)S(=O)(=O)NC(=O)NC1CCCCC1

Source: Drug Bank

Average Molecular Weight

494.004

Source: Drug Bank

Monoisotopic Molecular Weight

493.143819418

Source: Drug Bank

Genes that are associated with this drug in PharmGKB's database based on (1) variant annotations, (2) literature review, (3) pathways or (4) information automatically retrieved from DrugBank, depending on the "evidence" and "source" listed below.

Curated Information ?

Drug Targets

Gene Description
ABCA1 (source: Drug Bank)
ABCB11 (source: Drug Bank)
ABCC1 (source: Drug Bank)
ABCC3 (source: Drug Bank)
ABCC8 (source: Drug Bank)
ABCC9 (source: Drug Bank)
CFTR (source: Drug Bank)
KCNJ1 (source: Drug Bank)
KCNJ11 (source: Drug Bank)
KCNJ5 (source: Drug Bank)

Drug Interactions

Drug Description
glibenclamide Decreased in symptoms of hypoglycemia and increase in time required for the body to compensate for hypoglycemia (source: Drug Bank)
glibenclamide Acebutolol may decrease symptoms of hypoglycemia and increase the time required for the body to compensate for hypoglycemia. (source: Drug Bank)
glibenclamide The salicylate increases the effect of sulfonylurea (source: Drug Bank)
glibenclamide Acetylsalicylic acid increases the effect of the sulfonylurea, glibenclamide. (source: Drug Bank)
glibenclamide The beta-blocker decreases the symptoms of hypoglycemia (source: Drug Bank)
glibenclamide The beta-blocker, atenolol, may decrease symptoms of hypoglycemia. (source: Drug Bank)
glibenclamide The beta-blocker decreases the symptoms of hypoglycemia (source: Drug Bank)
glibenclamide The beta-blocker, bisoprolol, may decrease symptoms of hypoglycemia. (source: Drug Bank)
glibenclamide Increased risk of hepatic toxicity (source: Drug Bank)
glibenclamide Increased risk of hepatic toxicity (source: Drug Bank)
glibenclamide The beta-blocker decreases the symptoms of hypoglycemia (source: Drug Bank)
glibenclamide The beta-blocker, carvedilol, may decrease symptoms of hypoglycemia. (source: Drug Bank)
glibenclamide The agent increases the effect of sulfonylurea (source: Drug Bank)
glibenclamide The agent increases the effect of sulfonylurea (source: Drug Bank)
glibenclamide The agent increases the effect of sulfonylurea (source: Drug Bank)
glibenclamide The agent increases the effect of sulfonylurea (source: Drug Bank)
glibenclamide The sulfonylurea increases the effect of cyclosporine (source: Drug Bank)
glibenclamide The sulfonylurea increases the effect of cyclosporine (source: Drug Bank)
glibenclamide The beta-blocker decreases the symptoms of hypoglycemia (source: Drug Bank)
glibenclamide The beta-blocker, esmolol, may decrease symptoms of hypoglycemia. (source: Drug Bank)
acebutolol The beta-blocker decreases the symptoms of hypoglycemia (source: Drug Bank)
acebutolol The beta-blocker, acebutolol, may decrease symptoms of hypoglycemia. (source: Drug Bank)
aspirin The salicylate increases the effect of sulfonylurea (source: Drug Bank)
aspirin The salicylate increases the effect of sulfonylurea (source: Drug Bank)
atenolol The beta-blocker decreases the symptoms of hypoglycemia (source: Drug Bank)
atenolol The beta-blocker, atenolol, may decrease symptoms of hypoglycemia. (source: Drug Bank)
betaxolol The beta-blocker decreases the symptoms of hypoglycemia (source: Drug Bank)
betaxolol The beta-blocker, betaxolol, may decrease symptoms of hypoglycemia. (source: Drug Bank)
bevantolol The beta-blocker decreases the symptoms of hypoglycemia (source: Drug Bank)
bevantolol The beta-blocker, bevantolol, may decrease symptoms of hypoglycemia. (source: Drug Bank)
bisoprolol The beta-blocker decreases the symptoms of hypoglycemia (source: Drug Bank)
bisoprolol The beta-blocker, bisoprolol, may decrease symptoms of hypoglycemia. (source: Drug Bank)
bosentan Increased risk of hepatic toxicity (source: Drug Bank)
bosentan Increased risk of hepatic toxicity (source: Drug Bank)
carteolol The beta-blocker decreases the symptoms of hypoglycemia (source: Drug Bank)
carteolol The beta-blocker, carteolol, may decrease symptoms of hypoglycemia. (source: Drug Bank)
carvedilol The beta-blocker decreases the symptoms of hypoglycemia (source: Drug Bank)
carvedilol The beta-blocker, carvedilol, may decrease symptoms of hypoglycemia. (source: Drug Bank)
chloramphenicol The agent increases the effect of sulfonylurea (source: Drug Bank)
chloramphenicol The agent increases the effect of sulfonylurea (source: Drug Bank)
clofibrate The agent increases the effect of sulfonylurea (source: Drug Bank)
clofibrate The agent increases the effect of sulfonylurea (source: Drug Bank)
cyclosporine The sulfonylurea increases the effect of cyclosporine (source: Drug Bank)
cyclosporine The sulfonylurea increases the effect of cyclosporine (source: Drug Bank)
diazoxide Diazoxide/sulfonylurea: antagonism of action (source: Drug Bank)
diazoxide Antagonism. (source: Drug Bank)
dicumarol The agent increases the effect of sulfonylurea (source: Drug Bank)
dicumarol The agent increases the effect of sulfonylurea (source: Drug Bank)
esmolol The beta-blocker decreases the symptoms of hypoglycemia (source: Drug Bank)
esmolol The beta-blocker, esmolol, may decrease symptoms of hypoglycemia. (source: Drug Bank)
glucosamine Possible hyperglycemia (source: Drug Bank)
glucosamine Possible hyperglycemia (source: Drug Bank)
isocarboxazid The MAO inhibitor increases the effect of the hypoglycemic agent (source: Drug Bank)
isocarboxazid The MAO inhibitor increases the effect of the hypoglycemic agent (source: Drug Bank)
labetalol The beta-blocker decreases the symptoms of hypoglycemia (source: Drug Bank)
labetalol The beta-blocker, labetolol, may decrease symptoms of hypoglycemia. (source: Drug Bank)
metoprolol The beta-blocker decreases the symptoms of hypoglycemia (source: Drug Bank)
metoprolol The beta-blocker, metoprolol, may decrease symptoms of hypoglycemia. (source: Drug Bank)
nadolol The beta-blocker decreases the symptoms of hypoglycemia (source: Drug Bank)
nadolol The beta-blocker, nadolol, may decrease symptoms of hypoglycemia. (source: Drug Bank)
oxprenolol The beta-blocker decreases the symptoms of hypoglycemia (source: Drug Bank)
oxprenolol The beta-blocker, oxprenolol, may decrease symptoms of hypoglycemia. (source: Drug Bank)
penbutolol The beta-blocker decreases the symptoms of hypoglycemia (source: Drug Bank)
penbutolol The beta-blocker, penbutolol, may decrease symptoms of hypoglycemia. (source: Drug Bank)
phenelzine The MAO inhibitor increases the effect of the hypoglycemic agent (source: Drug Bank)
phenelzine The MAO inhibitor increases the effect of the hypoglycemic agent (source: Drug Bank)
phenylbutazone Phenylbutazone increases the effect of the hypoglycemic agent (source: Drug Bank)
phenylbutazone Phenylbutazone increases the effect of the hypoglycemic agent (source: Drug Bank)
pindolol The beta-blocker decreases the symptoms of hypoglycemia (source: Drug Bank)
pindolol The beta-blocker, pindolol, may decrease symptoms of hypoglycemia. (source: Drug Bank)
practolol The beta-blocker decreases the symptoms of hypoglycemia (source: Drug Bank)
practolol The beta-blocker, practolol, may decrease symptoms of hypoglycemia. (source: Drug Bank)
propranolol The beta-blocker decreases the symptoms of hypoglycemia (source: Drug Bank)
propranolol The beta-blocker, propranolol, may decrease symptoms of hypoglycemia. (source: Drug Bank)
repaglinide Similar mode of action - questionable association (source: Drug Bank)
repaglinide Similar mode of action - questionable association (source: Drug Bank)
rifampin Rifampin decreases the effect of sulfonylurea (source: Drug Bank)
rifampin Rifampin decreases the effect of sulfonylurea (source: Drug Bank)
salicylate-magnesium The salicylate increases the effect of sulfonylurea (source: Drug Bank)
salicylate-sodium The salicylate increases the effect of sulfonylurea (source: Drug Bank)
salicylate-sodium The salicylate, salicylate-sodium, increases the effect of the sulfonylurea, glibenclamide. (source: Drug Bank)
salsalate The salicylate increases the effect of sulfonylurea (source: Drug Bank)
salsalate The salicylate, salsalate, increases the effect of the sulfonylurea, glibenclamide. (source: Drug Bank)
somatropin recombinant Somatropin may antagonize the hypoglycemic effect of glibenclamide. Monitor for changes in fasting and postprandial blood sugars. (source: Drug Bank)
sotalol The beta-blocker decreases the symptoms of hypoglycemia (source: Drug Bank)
sotalol The beta-blocker, sotalol, may decrease symptoms of hypoglycemia. (source: Drug Bank)
timolol The beta-blocker decreases the symptoms of hypoglycemia (source: Drug Bank)
timolol The beta-blocker, timolol, may decrease symptoms of hypoglycemia. (source: Drug Bank)
tranylcypromine The MAO inhibitor increases the effect of the hypoglycemic agent (source: Drug Bank)
tranylcypromine The MAO inhibitor increases the effect of the hypoglycemic agent (source: Drug Bank)
trisalicylate-choline The salicylate, trisalicylate-choline, increases the effect of the sulfonylurea, glibenclamide. (source: Drug Bank)
glibenclamide The MAO inhibitor increases the effect of hypoglycemic agent (source: Drug Bank)
glibenclamide The beta-blocker, labetalol, may decrease symptoms of hypoglycemia. (source: Drug Bank)
glibenclamide The beta-blocker decreases the symptoms of hypoglycemia (source: Drug Bank)
glibenclamide The beta-blocker, metoprolol, may decrease symptoms of hypoglycemia. (source: Drug Bank)
glibenclamide The beta-blocker decreases the symptoms of hypoglycemia (source: Drug Bank)
glibenclamide The beta-blocker, nadolol, may decrease symptoms of hypoglycemia. (source: Drug Bank)
glibenclamide The beta-blocker decreases the symptoms of hypoglycemia (source: Drug Bank)
glibenclamide The beta-blocker, oxprenolol, may decrease symptoms of hypoglycemia. (source: Drug Bank)
glibenclamide The MAO inhibitor increases the effect of the hypoglycemic agent (source: Drug Bank)
glibenclamide Phenylbutazone increases the effect of the hypoglycemic agent (source: Drug Bank)
glibenclamide Phenylbutazone increases the effect of the hypoglycemic agent (source: Drug Bank)
glibenclamide The beta-blocker decreases the symptoms of hypoglycemia (source: Drug Bank)
glibenclamide The beta-blocker, pindolol, may decrease symptoms of hypoglycemia. (source: Drug Bank)
glibenclamide The beta-blocker decreases the symptoms of hypoglycemia (source: Drug Bank)
glibenclamide The beta-blocker, propranolol, may decrease symptoms of hypoglycemia. (source: Drug Bank)
glibenclamide Similar mode of action - questionable association (source: Drug Bank)
glibenclamide Rifampin decreases the effect of sulfonylurea (source: Drug Bank)
glibenclamide Rifampin decreases the effect of sulfonylurea (source: Drug Bank)
glibenclamide The beta-blocker decreases the symptoms of hypoglycemia (source: Drug Bank)
glibenclamide The beta-blocker, timolol, may decrease symptoms of hypoglycemia. (source: Drug Bank)

Curated Information ?

Publications related to glibenclamide: 36

No Dosing Guideline available No Drug Label available No Clinical Annotation available VA No VIP available No VIP available
CYP2C9, KCNJ11 and ABCC8 polymorphisms and the response to sulphonylurea treatment in type 2 diabetes patients. European journal of clinical pharmacology. 2014. Klen Jasna, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Pharmacoepidemiologic and in Vitro Evaluation of Potential Drug-Drug Interactions of Sulfonylureas with Fibrates and Statins. British journal of clinical pharmacology. 2014. Schelleman H, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available VIP No VIP available
PharmGKB summary: very important pharmacogene information for G6PD. Pharmacogenetics and genomics. 2012. McDonagh Ellen M, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available VA No VIP available No VIP available
The Ser1369Ala variant of ABCC8 and the risk for severe sulfonylurea-induced hypoglycemia in German patients with Type 2 diabetes. Pharmacogenomics. 2012. Holstein Judith Dina, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Genetic risk factors for type 2 diabetes mellitus and response to sulfonylurea treatment. Pharmacogenetics and genomics. 2011. Swen Jesse J, et al. PubMed
No Dosing Guideline available No Drug Label available CA VA No VIP available No VIP available
Diabetes mellitus and glucose-6-phosphate dehydrogenase deficiency: from one crisis to another. Diabetes & metabolism. 2011. Carette C, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available VA No VIP available No VIP available
ABCC8 polymorphism (Ser1369Ala): influence on severe hypoglycemia due to sulfonylureas. Pharmacogenomics. 2010. Sato Ryosuke, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available VA No VIP available No VIP available
Effect of CYP2C9 polymorphisms on prescribed dose and time-to-stable dose of sulfonylureas in primary care patients with Type 2 diabetes mellitus. Pharmacogenomics. 2010. Swen Jesse J, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Medications and glucose-6-phosphate dehydrogenase deficiency: an evidence-based review. Drug safety : an international journal of medical toxicology and drug experience. 2010. Youngster Ilan, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Contributions of human cytochrome P450 enzymes to glyburide metabolism. Biopharmaceutics & drug disposition. 2010. Zhou Lin, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Breast cancer resistance protein (BCRP)-mediated glyburide transport: effect of the C421A/Q141K BCRP single-nucleotide polymorphism. Drug metabolism and disposition: the biological fate of chemicals. 2010. Pollex Erika K, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Role of human placental apical membrane transporters in the efflux of glyburide, rosiglitazone, and metformin. American journal of obstetrics and gynecology. 2010. Hemauer Sarah J, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available VIP No VIP available
Cytochrome P450 2C9-CYP2C9. Pharmacogenetics and genomics. 2010. Van Booven Derek, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Loss-of-function CYP2C9 variants improve therapeutic response to sulfonylureas in type 2 diabetes: a Go-DARTS study. Clinical pharmacology and therapeutics. 2010. Zhou K, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Identification of the major human hepatic and placental enzymes responsible for the biotransformation of glyburide. Biochemical pharmacology. 2009. Zharikova Olga L, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Xenobiotic transporters of the human organic anion transporting polypeptides (OATP) family. Xenobiotica; the fate of foreign compounds in biological systems. 2008. Hagenbuch B, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Glucose-6-phosphate dehydrogenase deficiency. Lancet. 2008. Cappellini M D, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available VA No VIP available No VIP available
Genetic variants in the epithelial sodium channel associate with oedema in type 2 diabetic patients receiving the peroxisome proliferator-activated receptor gamma agonist farglitazar. Pharmacogenetics and genomics. 2007. Spraggs Colin, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
G6PD deficiency: the genotype-phenotype association. Blood reviews. 2007. Mason Philip J, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Pharmacogenetics of glucose-lowering drug treatment: a systematic review. Molecular diagnosis & therapy. 2007. Bozkurt Ozlem, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Drug-drug interaction between pitavastatin and various drugs via OATP1B1. Drug metabolism and disposition: the biological fate of chemicals. 2006. Hirano Masaru, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available VA No VIP available No VIP available
The E23K variant of KCNJ11 encoding the pancreatic beta-cell adenosine 5'-triphosphate-sensitive potassium channel subunit Kir6.2 is associated with an increased risk of secondary failure to sulfonylurea in patients with type 2 diabetes. The Journal of clinical endocrinology and metabolism. 2006. Sesti Giorgio, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Organic anion transporting polypeptide 2B1 is a high-affinity transporter for atorvastatin and is expressed in the human heart. Clinical pharmacology and therapeutics. 2006. Grube Markus, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
CYP2C9, but not CYP2C19, polymorphisms affect the pharmacokinetics and pharmacodynamics of glyburide in Chinese subjects. Clinical pharmacology and therapeutics. 2005. Yin Ophelia Q P, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Citrus juices inhibit the function of human organic anion-transporting polypeptide OATP-B. Drug metabolism and disposition: the biological fate of chemicals. 2005. Satoh Hiroki, et al. PubMed
Glibenclamide-induced acute haemolytic anaemia revealing a G6PD-deficiency. Diabetes research and clinical practice. 2004. Vinzio St├ęphane, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Identification and relative contributions of human cytochrome P450 isoforms involved in the metabolism of glibenclamide and lansoprazole: evaluation of an approach based on the in vitro substrate disappearance rate. Xenobiotica; the fate of foreign compounds in biological systems. 2004. Naritomi Y, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Sulfonylurea stimulation of insulin secretion. Diabetes. 2002. Proks Peter, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Differential selectivity of insulin secretagogues: mechanisms, clinical implications, and drug interactions. Journal of diabetes and its complications. 2003. Gribble Fiona M, et al. PubMed
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Glyburide and glimepiride pharmacokinetics in subjects with different CYP2C9 genotypes. Clinical pharmacology and therapeutics. 2002. Niemi Mikko, et al. PubMed
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Bosentan, a dual endothelin receptor antagonist, activates the pregnane X nuclear receptor. European journal of pharmacology. 2002. van Giersbergen Paul L M, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Impact of CYP2C9 amino acid polymorphisms on glyburide kinetics and on the insulin and glucose response in healthy volunteers. Clinical pharmacology and therapeutics. 2002. Kirchheiner Julia, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Med-psych drug-drug interactions update. Psychosomatics. 2002. Armstrong Scott C, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Clinical pharmacokinetics of fluvastatin. Clinical pharmacokinetics. 2001. Scripture C D, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Sulfonylurea sensitivity of adenosine triphosphate-sensitive potassium channels from beta cells and extrapancreatic tissues. Metabolism: clinical and experimental. 2000. Gribble F M, et al. PubMed
Glyburide-induced acute haemolysis in a G6PD-deficient patient with NIDDM. British journal of haematology. 1996. Meloni G, et al. PubMed

LinkOuts

Web Resource:
Wikipedia
National Drug Code Directory:
0378-1113-01
DrugBank:
DB01016
ChEBI:
5441
KEGG Compound:
C07022
KEGG Drug:
D00336
PubChem Compound:
3488
PubChem Substance:
167865
46509154
IUPHAR Ligand:
2414
Drugs Product Database (DPD):
2248008
ChemSpider:
3368
Therapeutic Targets Database:
DAP000037
FDA Drug Label at DailyMed:
aeba91ea-3d29-4b8d-af42-0740e7216463

Clinical Trials

These are trials that mention glibenclamide and are related to either pharmacogenetics or pharmacogenomics.

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Sources for PharmGKB drug information: DrugBank, Open Eye Scientific Software.