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Glyburide (Glibenclamide)

Alias:
Cat No.:V1678 Purity: ≥98%
Glyburide (formerly HB419; HB420;Glibenclamide;Micronase; Diabeta; Maninil; Micronase; Neogluconin) is a selective blocker of vascular ATP-sensitive K+ channels (KATP) that has been approved as an antidiabetic sulfonylurea drug used for the treatment of type 2 diabetes.
Glyburide (Glibenclamide)
Glyburide (Glibenclamide) Chemical Structure CAS No.: 10238-21-8
Product category: Potassium Channel
This product is for research use only, not for human use. We do not sell to patients.
Size Price Stock Qty
2g
5g
10g
50g
100g
Other Sizes

Other Forms of Glyburide (Glibenclamide):

  • Glyburide-d3 (Glyburide-d3)
  • Glyburide-d11 (glyburide d11)
  • Glibenclamide potassium (Glyburide potassium)
Official Supplier of:
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Top Publications Citing lnvivochem Products
Purity & Quality Control Documentation

Purity: ≥98%

Product Description

Glyburide (formerly HB419; HB420; Glibenclamide; Micronase; Diabeta; Maninil; Micronase; Neogluconin) is a selective blocker of vascular ATP-sensitive K+ channels (KATP) that has been approved as an antidiabetic sulfonylurea drug used for the treatment of type 2 diabetes. Its actions are similar to those of chlorpropamide that can potentially be used to decrease cerebral edema.

Biological Activity I Assay Protocols (From Reference)
Targets
ATP-sensitive K+ channel (KATP)
ln Vitro
Glibenclamide (brown adipocytes; 10 μM; 1 day) has no effect on adipocyte differentiation. Glibenclamide (Ucp1-2A-GFP brown adipocyte) dramatically increases UCP1 expression. Glibenclamide directly binds to and inhibits the SUR1 subunit of ATP-dependent potassium channels (KATP), consequently boosting insulin production from pancreatic beta cells [2]. Glibenclamide interferes with mitochondrial bioenergetics by allowing Cl- to enter the inner mitochondrial membrane and boosting Cl-/K+ co-transport in the mitochondrial network [4]. Glibenclamide-induced autophagy limits its beneficial effect on β-cell insulin secretion [5].
ln Vivo
Glibenclamide (2 mg/kg; po) quickly lowers blood glucose levels and enhances the release of insulin [2]. Body weight and body composition do not significantly alter when using glibeenclamide (50 μg/kg; po) [2].
Enzyme Assay
Glibenclamide is well known to interact with the sulphonylurea receptor (SUR) and has been shown more recently to inhibit the cystic fibrosis transmembrane conductance regulator protein (CFTR), both proteins that are members of the ABC [adenosine 5'-triphosphate (ATP)-binding cassette] transporters. The effect of glibenclamide and two synthetic sulphonylcyanoguanidine derivatives (dubbed BM-208 and BM-223) was examined on P-glycoprotein, the major ABC transporter responsible for multidrug resistance (MDR) in cancer cells. To this end, we employed different cell lines that do or do not express P-glycoprotein, as confirmed by Western blotting: first, a tumour cell line (VBL600) selected from a human T-cell line (CEM) derived from an acute leukaemia; second, an epithelial cell line derived from a rat colonic adenocarcinoma (CC531(mdr+)) and finally, a non tumour epithelial cell line derived from the proximal tubule of the opossum kidney (OK). Glibenclamide and the two related derivatives inhibited P-glycoprotein because firstly, they acutely increased [3H]colchicine accumulation in P-glycoprotein-expressing cell lines only; secondly BM-223 reversed the MDR phenomenon, quite similarly to verapamil, by enhancing the cytotoxicity of colchicine, taxol and vinblastine and thirdly, BM-208 and BM-223 blocked the photoaffinity-labelling of P-glycoprotein by [3H]azidopine. Furthermore, glibenclamide is itself a substrate for P-glycoprotein, since the cellular accumulation of [3H]glibenclamide was low and substantially increased by addition of P-glycoprotein substrates (e. g., vinblastine and cyclosporine) only in the P-glycoprotein-expressing cell lines. We conclude that glibenclamide and two sulphonylcyanoguanidine derivatives inhibit P-glycoprotein and that sulphonylurea drugs would appear to be general inhibitors of ABC transporters, suggesting an interaction with some conserved motif.[3]
The interference of glibenclamide, an antidiabetic sulfonylurea, with mitochondrial bioenergetics was assessed on mitochondrial ion fluxes (H+, K+, and Cl-) by passive osmotic swelling of rat liver mitochondria in K-acetate, KNO3, and KCl media, by O2 consumption, and by mitochondrial transmembrane potential (Deltapsi). Glibenclamide did not permeabilize the inner mitochondrial membrane to H+, but induced permeabilization to Cl- by opening the inner mitochondrial anion channel (IMAC). Cl- influx induced by glibenclamide facilitates K+ entry into mitochondria, thus promoting a net Cl-/K+ cotransport, Deltapsi dissipation, and stimulation of state 4 respiration rate. It was concluded that glibenclamide interferes with mitochondrial bioenergetics of rat liver by permeabilizing the inner mitochondrial membrane to Cl- and promoting a net Cl-/K+ cotransport inside mitochondria, without significant changes on membrane permeabilization to H+[4].
Cell Assay
Diabetes is a metabolic disease, partly due to hypoinsulinism, which affects ∼8% of the world's adult population. Glibenclamide is known to promote insulin secretion by targeting β cells. Autophagy as a self-protective mechanism of cells has been widely studied and has particular physiological effects in different tissues or cells. However, the interaction between autophagy and glibenclamide is unclear. In this study, we investigated the role of autophagy in glibenclamide-induced insulin secretion in pancreatic β cells. Herein, we showed that glibenclamide promoted insulin release and further activated autophagy through the adenosine 5'-monophosphate (AMP) activated protein kinase (AMPK) pathway in MIN-6 cells. Inhibition of autophagy with autophagy inhibitor 3-methyladenine (3-MA) potentiated the secretory function of glibenclamide further. These results suggest that glibenclamide-induced autophagy plays an inhibitory role in promoting insulin secretion by activating the AMPK pathway instead of altering the mammalian target of rapamycin (mTOR)[5].
Animal Protocol
Animal/Disease Models: Mice[2]
Doses: 2 mg/kg
Route of Administration: Po
Experimental Results: Increased of insulin release and rapid drop of blood glucose level.
Identification of safe and effective compounds to increase or activate UCP1 expression in brown or white adipocytes remains a potent therapeutic strategy to combat obesity. Here we reported that, glyburide, one of the FDA-approved drugs currently used to treat type 2 diabetes, can significantly enhance UCP1 expression in both brown and white adipocytes. Glyburide-fed mice exhibited a clear resistance to high-fat diet-induced obesity, reduced blood triglyceride level, and increased UCP1 expression in brown adipose tissue. Moreover, in situ injection of glyburide to inguinal white adipose tissue remarkably enhanced UCP1 expression and increased thermogenesis. Further mechanistic studies indicated that the glyburide effect in UCP1 expression in adipocytes was KATP channel independent but may involve the regulation of the Ca2+-Calcineurin-NFAT signal pathway. Overall, our findings revealed the significant effects of glyburide in regulating UCP1 expression and thermogenesis in adipocytes, which can be potentially repurposed to treat obesity.[2]
ADME/Pharmacokinetics
Absorption, Distribution and Excretion
Elderly patients taking glyburide reached a Cmax of 211-315ng/mL with a Tmax of 0.9-1.0h, while younger patients reached a Cmax of 144-302ng/mL with a Tmax of 1.3-3.0h. Patients taking glyburide have and AUC of 348ng*h/mL.
Unlike other sulfonylureas, glyburide is 50% excreted in the urine and 50% in the feces. Glyburide is mainly excreted as the metabolite 4-trans-hydroxyglyburide.
Elderly patients have a volume of distribution of 19.3-52.6L, while younger patients have a volume of distribution of 21.5-49.3L.
Elderly patients have a clearance of 2.70-3.55L/h, while younger patients have a clearance of 2.47-4.11L/h.
Metabolism / Metabolites
Glyburide is metabolized mainly by CYP3A4, followed by CYP2C9, CYP2C19, CYP3A7, and CYP3A5. These enzymes metabolize glyburide to 4-trans-hydroxycyclohexyl glyburide (M1), 4-cis-hydroxycyclohexyl glyburide (M2a), 3-cis-hydroxycyclohexyl glyburide (M2b), 3-trans-hydroxycyclohexyl glyburide (M3), 2-trans-hydroxycyclohexyl glyburide (M4), and ethylhydroxycyclohexyl glyburide (M5). The M1 and M2b metabolites are considered active, along with the parent molecule.
Glyburide has known human metabolites that include 3-cis-Hydroxycyclohexyl glyburide, 3-trans-Hydroxycyclohexyl glyburide, 2-trans-hydroxycyclohexyl glyburide, and 4-cis-hydroxycyclohexyl glyburide.
Biological Half-Life
Elderly patients have a terminal elimination half life of 4.0-13.4h, while younger patients have a terminal elimination half life of 4.0-13.9h.
Toxicity/Toxicokinetics
Effects During Pregnancy and Lactation
◉ Summary of Use during Lactation
Limited data indicate that the levels of glyburide in milk are negligible. Monitor breastfed infants for signs of hypoglycemia such as jitteriness, excessive sleepiness, poor feeding, seizures cyanosis, apnea, or hypothermia. If there is concern, monitoring of the breastfed infant's blood glucose is advisable during maternal therapy with hypoglycemic agents.
◉ Effects in Breastfed Infants
The blood glucose level was normal in one breastfed infant whose mothers was taking oral glyburide 5 mg daily.
◉ Effects on Lactation and Breastmilk
Relevant published information was not found as of the revision date.
Protein Binding
Glyburide is 99.9% bound to protein in plasma with >98% accounted for by binding to serum albumin.
References

[1]. The anti-diabetic drug trelagliptin induces vasodilation via activation of Kv channels and SERCA pumps. Life Sci. 2021;283:119868.

[2]. Glyburide Regulates UCP1 Expression in Adipocytes Independent of KATP Channel Blockade. iScience. 2020;23(9):101446.

[3]. P-glycoprotein inhibition by glibenclamide and related compounds. Pflugers Arch. 1999;437(5):652-660.

[4]. Glibenclamide interferes with mitochondrial bioenergetics by inducing changes on membrane ion permeability. J Biochem Mol Toxicol. 2004;18(3):162-169.

[5]. Glibenclamide-Induced Autophagy Inhibits Its Insulin Secretion-Improving Function in β Cells. Int J Endocrinol. 2019;2019:1265175.

Additional Infomation
Glyburide is an N-sulfonylurea that is acetohexamide in which the acetyl group is replaced by a 2-(5-chloro-2-methoxybenzamido)ethyl group. It has a role as a hypoglycemic agent, an anti-arrhythmia drug, an EC 2.7.1.33 (pantothenate kinase) inhibitor and an EC 3.6.3.49 (channel-conductance-controlling ATPase) inhibitor. It is a N-sulfonylurea and a member of monochlorobenzenes.
Glyburide is a second generation sulfonylurea used to treat patients with diabetes mellitus type II. It is typically given to patients who cannot be managed with the standard first line therapy, [metformin]. Glyburide stimulates insulin secretion through the closure of ATP-sensitive potassium channels on beta cells, raising intracellular potassium and calcium ion concentrations. Glyburide was granted FDA approval on 1 May 1984. A formulation with metformin was granted FDA approval on on 31 July 2000.
Glyburide is a Sulfonylurea.
Glyburide is a sulfonamide urea derivative with antihyperglycemic activity that can potentially be used to decrease cerebral edema. Upon administration, glyburide binds to and blocks the sulfonylurea receptor type 1 (SUR1) subunit of the ATP-sensitive inwardly-rectifying potassium (K(ATP)) channels on the membranes of pancreatic beta cells. This prevents the inward current flow of positively charged potassium (K+) ions into the cell, and induces a calcium ion (Ca2+) influx through voltage-sensitive calcium channels, which triggers exocytosis of insulin-containing granules. In addition, glyburide also inhibits the SUR1-regulated nonselective cation (NC) Ca-ATP channel, melastatin 4 (transient receptor potential cation channel subfamily M member 4; (TRPM4)), thereby preventing capillary failure and brain swelling. SUR1-TRPM4 channels are formed by co-assembly of SUR1 with TRPM4 in neurons, astrocytes, and capillary endothelium during cerebral ischemia. Upon ischemia-induced ATP depletion, channels open which results in sodium influx, cytotoxic edema formation, capillary fragmentation and necrotic cell death. SUR1-TRPM4 is not expressed in normal, uninjured tissues.
An antidiabetic sulfonylurea derivative with actions like those of chlorpropamide
See also: Glyburide; Metformin Hydrochloride (component of).
Drug Indication
Glyburide is indicated alone or as part of combination product with metformin, as an adjunct to diet and exercise, to improve glycemic control in adults with type 2 diabetes mellitus.
Amglidia is indicated for the treatment of neonatal diabetes mellitus, for use in newborns, infants and children. Sulphonylureas like Amglidia have been shown to be effective in patients with mutations in the genes coding for the β-cell ATP-sensitive potassium channel and chromosome 6q24-related transient neonatal diabetes mellitus.
Treatment of large hemispheric infarction
Treatment of neonatal diabetes mellitus
Mechanism of Action
Glyburide belongs to a class of drugs known as sulfonylureas. These drugs act by closing ATP-sensitive potassium channels on pancreatic beta cells. The ATP-sensitive potassium channels on beta cells are known as sulfonylurea receptor 1 (SUR1). Under low glucose concentrations, SUR1 remains open, allowing for potassium ion efflux to create a -70mV membrane potential. Normally SUR1 closes in response to high glucose concentrations, the membrane potential of the cells becomes less negative, the cell depolarizes, voltage gated calcium channels open, calcium ions enter the cell, and the increased intracellular calcium concentration stimulates the release of insulin containing granules. Glyburide bypasses this process by forcing SUR1 closed and stimulating increased insulin secretion.
Pharmacodynamics
Glyburide is a second generation sulfonylurea that stimulates insulin secretion through the closure of ATP-sensitive potassium channels on beta cells, raising intracellular potassium and calcium ion concentrations. Glibenclamide has a long duration of action as it is given once daily, and a wide therapeutic index as patients are started at doses as low as 0.75mg but that can increase as high as 10mg or more. Patients taking glyburide should be cautioned regarding an increased risk of cardiovascular mortality as seen with tolbutamide, another sulfonylurea.
These protocols are for reference only. InvivoChem does not independently validate these methods.
Physicochemical Properties
Molecular Formula
C23H28CLN3O5S
Molecular Weight
494
Exact Mass
493.143
Elemental Analysis
C, 55.92; H, 5.71; Cl, 7.18; N, 8.51; O, 16.19; S, 6.49
CAS #
10238-21-8
Related CAS #
Glyburide-d3;1219803-02-7;Glyburide-d11;1189985-02-1; 52169-36-5 (potassium salt)
PubChem CID
3488
Appearance
White to off-white solid powder
Density
1.4±0.1 g/cm3
Boiling Point
705.7±70.0 °C at 760 mmHg
Melting Point
173-175°C
Flash Point
380.6±35.7 °C
Vapour Pressure
0.0±2.4 mmHg at 25°C
Index of Refraction
1.623
LogP
5.19
Hydrogen Bond Donor Count
3
Hydrogen Bond Acceptor Count
5
Rotatable Bond Count
8
Heavy Atom Count
33
Complexity
746
Defined Atom Stereocenter Count
0
InChi Key
ZNNLBTZKUZBEKO-UHFFFAOYSA-N
InChi Code
InChI=1S/C23H28ClN3O5S/c1-32-21-12-9-17(24)15-20(21)22(28)25-14-13-16-7-10-19(11-8-16)33(30,31)27-23(29)26-18-5-3-2-4-6-18/h7-12,15,18H,2-6,13-14H2,1H3,(H,25,28)(H2,26,27,29)
Chemical Name
5-chloro-N-[2-[4-(cyclohexylcarbamoylsulfamoyl)phenyl]ethyl]-2-methoxybenzamide
Synonyms

HB-420; Glyburide; Glybenclamide; Glynase; Euglucon; Glibenclamide; HB419; HB420;Micronase; Diabeta; Maninil; Micronase; Neogluconin

HS Tariff Code
2934.99.9001
Storage

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Shipping Condition
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
Solubility Data
Solubility (In Vitro)
DMSO: 99 mg/mL (200.4 mM)
Water:<1 mg/mL
Ethanol:<1 mg/mL
Solubility (In Vivo)
Solubility in Formulation 1: ≥ 2.08 mg/mL (4.21 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

Solubility in Formulation 2: ≥ 2.08 mg/mL (4.21 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

 (Please use freshly prepared in vivo formulations for optimal results.)
Preparing Stock Solutions 1 mg 5 mg 10 mg
1 mM 2.0243 mL 10.1215 mL 20.2429 mL
5 mM 0.4049 mL 2.0243 mL 4.0486 mL
10 mM 0.2024 mL 1.0121 mL 2.0243 mL

*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.

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Clinical Trial Information
Metabolic Analysis for Treatment Choice in Gestational Diabetes Mellitus
CTID: NCT03029702
Phase: Phase 4    Status: Completed
Date: 2024-11-29
Glyburide Advantage in Malignant Edema and Stroke Pilot
CTID: NCT01268683
Phase: Phase 1/Phase 2    Status: Completed
Date: 2024-11-22
Metformin Compared to Glyburide in Gestational Diabetes
CTID: NCT00965991
Phase: N/A    Status: Completed
Date: 2024-11-19
Glyburide Advantage in Malignant Edema and Stroke - Remedy Pharmaceuticals
CTID: NCT01794182
Phase: Phase 2    Status: Completed
Date: 2024-11-12
Glyburide (RP-1127) for Traumatic Brain Injury (TBI)
CTID: NCT01454154
Phase: Phase 2    Status: Completed
Date: 2024-11-12
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Spinal Cord Injury Neuroprotection With Glyburide
CTID: NCT05426681
Phase: Phase 1    Status: Recruiting
Date: 2024-10-15


Comparison Between Metformin and Glyburide in the Management of Gestational Diabetes
CTID: NCT06589141
Phase: N/A    Status: Not yet recruiting
Date: 2024-09-19
Efficacy and Safety of Insulin Aspart Versus Glibenclamide in Type 2 Diabetes
CTID: NCT00267683
Phase: Phase 3    Status: Terminated
Date: 2023-11-02
Glycaemic & Cardiovascular Treatment Outcomes of Voglibose Vs Glibenclamide Added to Metformin in T2DM Patients
CTID: NCT05688332
Phase: Phase 3    Status: Not yet recruiting
Date: 2023-07-03
Oral Glibenclamide in Preterm Infants With Hyperglycaemia (GALOP)
CTID: NCT05687500
Phase: Phase 2    Status: Recruiting
Date: 2023-06-18
Safety and Efficacy of Glibenclamide Combined With Rt-PA in Acute Cerebral Embolism
CTID: NCT03284463
Phase: Phase 2/Phase 3    Status: Completed
Date: 2023-06-12
Assessment of Dapagliflozin Effect on Diabetic Endothelial Dysfunction of Brachial Artery
CTID: NCT02919345
Phase: Phase 4    Status: Completed
Date: 2023-03-10
Glyburide vs Placebo as Prophylaxis Against Cerebral Edema in Patients Receiving Radiosurgery for Brain Metastases (RAD 1502/UAB 1593)
CTID: NCT02460874
Phase: Phase 1/Phase 2    Status: Terminated
Date: 2022-09-21
Spinal Cord Injury Neuroprotection With Glyburide
CTID: NCT02524379
Phase: Phase 1/Phase 2    Status: Terminated
Date: 2022-07-05
Glibenclamide Advantage in Treating Edema After Intracerebral Hemorrhage
CTID: NCT03741530
Phase: N/A    Status: Completed
Date: 2022-04-08
Evaluate the Use of Glibenclamide on Acute aSAH
CTID: NCT05137678
Phase: Phase 4    Status: Unknown status
Date: 2022-02-14
To Evaluate the Effect of Glibenclamide in Reducing Brain Edema of TBI
CTID: NCT05148403
Phase: Phase 1/Phase 2    Status: Unknown status
Date: 2021-12-08
A Study to Evaluate the DDI of DBPR108 With Metformin,Glibenclamide,Valsartan, or Simvastatin in Healthy Subjects
CTID: NCT04859452
Phase: Phase 1    Status: Completed
Date: 2021-07-20
The Hemodynamic Effects of PACAP38 After Glibenclamide Administration in Healthy Volunteers
CTID: NCT04960657
Phase: N/A    Status: Completed
Date: 2021-07-14
Safety Study of RP-1127 (Glyburide for Injection) in Healthy Volunteers
CTID: NCT01132703
Phase: Phase 1    Status: Completed
Date: 2021-06-21
Glyburide vs Glucovance in the Treatment of GDM
CTID: NCT02726490
PhaseEarly Phase 1    Status: Terminated
Date: 2020-10-12
The Hemodynamic Effects of CGRP After Glibenclamide Administration in Healthy Volunteers
CTID: NCT04231617
Phase: N/A    Status: Completed
Date: 2020-09-09
Treatment of Mild Gestational Diabetes With Glyburide Versus Placebo
CTID: NCT00744965
Phase: Phase 4    Status: Completed
Date: 2020-03-12
Glibentek in Patients With Neonatal Diabetes Secondary to Mutations in K+-ATP Channels
CTID: NCT02375828
Phase: Phase 3    Status: Completed
Date: 2019-08-30
Study to Evaluate the Effect of IW-3718 on the Pharmacokinetics of Oral Contraceptive, Levothyroxine, Glyburide, and Digoxin in Healthy Adult Volunteers
CTID: NCT03856970
Phase: Phase 1    Status: Completed
Date:
A Feasibility study looking at the use of Glibenclamide and metfoRmin versus stAndard Care in gEstational diabeteS
CTID: null
Phase: Phase 4    Status: Completed
Date: 2014-04-02
Randomized, open label, two parallel arms, intervention trial comparing the effect of DPP-IV inhibitor Vildagliptin vs. Glibenclamide on circulating EPCs.
CTID: null
Phase: Phase 4    Status: Completed
Date: 2013-01-22
Glibenclamide treatment in hypotonia-cystinuria syndrome
CTID: null
Phase: Phase 2    Status: Completed
Date: 2012-03-16
Multi-center, randomized, open-label, two-parallel arm, intervention trial comparing DPP-IV inhibitor Vildagliptin with Glibenclamide (Glyburide) in achieving and maintaining good blood glucose control in type 2 diabetic patients in treatment failure with Metformin alone
CTID: null
Phase: Phase 4    Status: Prematurely Ended
Date: 2010-09-24
EFFECTS ON INCIDENCE OF CARDIOVASCULAR EVENTS OF THE ADDITION OF PIOGLITAZONE AS COMPARED WITH A SULFONYLUREA IN TYPE 2 DIABETIC PATIENTS INADEQUATELY
CTID: null
Phase: Phase 4    Status: Ongoing
Date: 2010-03-02
A 12-Week, Phase 2, Randomized, Double-Blind, Active-Controlled Study of LY2599506 Given as Monotherapy or in Combination with Metformin in Patients with Type 2 Diabetes Mellitus
CTID: null
Phase: Phase 2    Status: Completed, Prematurely Ended
Date: 2010-02-15
EffectS of PiogLitazone on ENDOthelial progenitoR cells in type 2 diabetic patients with vascular complications - The SPLENDOR Study
CTID: null
Phase: Phase 4    Status: Completed
Date: 2008-02-28
Do sulphponylureas preserve cortical function during hypoglycaemia in patients with type 1 diabetes and hypoglycaemia unawareness?
CTID: null
Phase: Phase 4    Status: Completed
Date: 2007-05-02
A Multicenter, Randomized, Double-Blind, Placebo-Controlled Study to Determine the
CTID: null
Phase: Phase 3    Status: Completed
Date: 2006-05-26
A Parallel-Group, Multi-Centre, Active-Controlled (Glibenclamide) Long Term Extension Study to Evaluate the Safety and Tolerability of oral Tesaglitazar Therapy in Patients with Type 2 Diabetes Mellitus (GALLEX 4)
CTID: null
Phase: Phase 3    Status: Completed
Date: 2005-11-09
A 50 Week Extension to: A Multicenter, Randomized, Double-Blind Factorial Study of the Co-Administration of MK-0431 and Metformin in Patients With Type 2 Diabetes Mellitus Who Have Inadequate Glycemic Control
CTID: null
Phase: Phase 3    Status: Completed
Date: 2005-08-12
An Open, Multi-Centre and Long-Term Extension Study to Evaluate the Safety and Tolerability of oral Tesaglitazar therapy in patients with Type 2 Diabetes.
CTID: null
Phase: Phase 3    Status: Prematurely Ended, Completed
Date: 2005-06-20
The effect of the co-administration of multiple oral doses of the fructose-1,6-bisphosphatase (FBPase) inhibitor CS-917 and glibenclamide on pharmacokinetics, safety and tolerability in diabetic patients (NIDDM)
CTID: null
Phase: Phase 2    Status: Completed
Date: 2005-01-20
A 24-Week Randomized, Double-Blind, Parallel-Group, Multi-Centre, Placebo-Controlled Study to Evaluate the Efficacy, Safety and Tolerability of Tesaglitazar Therapy when Added to the Therapy of Patients with Type 2 Diabetes Poorly Controlled on Sulphonylurea Alone
CTID: null
Phase: Phase 3    Status: Completed
Date: 2004-10-22
A 52-week Randomized, Double-Blind, Parallel-Group, Multi-Centre, Active-Controlled (Glibenclamide) Study to Evaluate the Efficacy, Safety and Tolerability of Tesaglitazar Therapy when Administered to Patients with Type 2 Diabetes
CTID: null
Phase: Phase 3    Status: Completed
Date: 2004-09-10
Tolérance et acceptabilité d'une suspension de glibenclamide (GLIBENTEK) chez des enfants ayant un diabète sucré rare secondaire à une mutation des canaux potassiques ATP-dépendants (Kir6.2 ou SUR1)
CTID: null
Phase: Phase 2    Status: Completed
Date:
The SUGAR-DIP trial: Oral medication strategy versus insulin for diabetes in pregnancy
CTID: null
Phase: Phase 3    Status: Ongoing
Date:

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