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Renabetic

Renabetic - General Information

An antidiabetic sulfonylurea derivative with actions similar to those of chlorpropamide. [PubChem]

 

Pharmacology of Renabetic

Renabetic (INN), also known as glyburide (USAN), a second-generation sulfonylurea antidiabetic agent, appears to lower the 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, glibenclamide produces a mild diuresis by enhancement of renal free water clearance. Renabetic is twice as potent as the related second-generation agent glipizide.

 

Renabetic for patients

Patients should be informed of the potential risks and advantages of MICRONASE and of alternative modes of therapy. They also should be informed about the importance of adherence to dietary instructions, of a regular exercise program, and of regular testing of urine and/or blood glucose.

The risks of hypoglycemia, its symptoms and treatment, and conditions that predispose to its development should be explained to patients and responsible family members. Primary and secondary failure also should be explained.

 

Renabetic Interactions

The hypoglycemic action of sulfonylureas may be potentiated by certain drugs including nonsteroidal anti-inflammatory agents and other drugs that are highly protein bound, salicylates, sulfonamides, chloramphenicol, probenecid, coumarins, monoamine oxidase inhibitors, and beta adrenergic blocking agents. When such drugs are administered to a patient receiving MICRONASE, the patient should be observed closely for hypoglycemia. When such drugs are withdrawn from a patient receiving MICRONASE, the patient should be observed closely for loss of control.

Certain drugs tend to produce hyperglycemia and may lead to loss of control. These drugs include the thiazides and other diuretics, corticosteroids, phe-nothiazines, thyroid products, estrogens, oral contraceptives, phenytoin, nicotinic acid, sympathomimet-ics, calcium channel blocking drugs, and isoniazid. When such drugs are administered to a patient receiving MICRONASE, the patient should be closely observed for loss of control. When such drugs are withdrawn from a patient receiving MICRONASE, the patient should be observed closely for hypoglycemia.

A possible interaction between glyburide and ciprofloxacin, a fluoroquinolone antibiotic, has been reported, resulting in a potentiation of the hypoglycemic action of glyburide. The mechanism for this interaction is not known.

A potential interaction between oral miconazole and oral hypoglycemic agents leading to severe hypoglycemia has been reported. Whether this interaction also occurs with the intravenous, topical or vaginal preparations of miconazole is not known. Metformin: In a single-dose interaction study in NIDDM subjects, decreases in glyburide AUC and Cmax were observed, but were highly variable. The single-dose nature of this study and the lack of correlation between glyburide blood levels and pharmaco-dynamic effects, makes the clinical significance of this interaction uncertain. Coadministration of gly-buride and metformin did not result in any changes in either metformin pharmacokinetics or pharmaco-dynamics.

 

Renabetic Contraindications

MICRONASE Tablets are contraindicated in patients with:

1.Known hypersensitivity or allergy to the drug.

2.Diabetic ketoacidosis, with or without coma. This condition should be treated with insulin.

3.Type I diabetes mellitus, as sole therapy.

 

Additional information about Renabetic

Renabetic Indication: 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 satisfactorily controlled by diet alone.
Mechanism Of Action: Sulfonylureas such as glibenclamide likely bind to ATP-sensitive potassium-channel receptors 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.
Drug Interactions: Acebutolol The beta-blocker decreases the symptoms of hypoglycemia
Atenolol The beta-blocker decreases the symptoms of hypoglycemia
Bevantolol The beta-blocker decreases the symptoms of hypoglycemia
Betaxolol The beta-blocker decreases the symptoms of hypoglycemia
Bisoprolol The beta-blocker decreases the symptoms of hypoglycemia
Carteolol The beta-blocker decreases the symptoms of hypoglycemia
Carvedilol The beta-blocker decreases the symptoms of hypoglycemia
Esmolol The beta-blocker decreases the symptoms of hypoglycemia
Labetalol The beta-blocker decreases the symptoms of hypoglycemia
Metoprolol The beta-blocker decreases the symptoms of hypoglycemia
Nadolol The beta-blocker decreases the symptoms of hypoglycemia
Oxprenolol The beta-blocker decreases the symptoms of hypoglycemia
Penbutolol The beta-blocker decreases the symptoms of hypoglycemia
Pindolol The beta-blocker decreases the symptoms of hypoglycemia
Practolol The beta-blocker decreases the symptoms of hypoglycemia
Propranolol The beta-blocker decreases the symptoms of hypoglycemia
Sotalol The beta-blocker decreases the symptoms of hypoglycemia
Timolol The beta-blocker decreases the symptoms of hypoglycemia
Trisalicylate-choline The salicylate increases the effect of sulfonylurea
Salsalate The salicylate increases the effect of sulfonylurea
Salicylate-magnesium The salicylate increases the effect of sulfonylurea
Salicylate-sodium The salicylate increases the effect of sulfonylurea
Bismuth Subsalicylate The salicylate increases the effect of sulfonylurea
Aspirin The salicylate increases the effect of sulfonylurea
Bosentan Increased risk of hepatic toxicity
Dicumarol The agent increases the effect of sulfonylurea
Chloramphenicol The agent increases the effect of sulfonylurea
Clofibrate The agent increases the effect of sulfonylurea
Cyclosporine The sulfonylurea increases the effect of cyclosporine
Diazoxide Diazoxide/sulfonylurea: antagonism of action
Glucosamine Possible hyperglycemia
Isocarboxazid The MAO inhibitor increases the effect of the hypoglycemic agent
Phenelzine The MAO inhibitor increases the effect of the hypoglycemic agent
Phenylbutazone Phenylbutazone increases the effect of the hypoglycemic agent
Repaglinide Similar mode of action - questionable association
Rifampin Rifampin decreases the effect of sulfonylurea
Tranylcypromine The MAO inhibitor increases the effect of the hypoglycemic agent
Food Interactions: Avoid alcohol.
Avoid sugar and sugary food.
Take 30-60 minutes before breakfast.
Generic Name: Glibenclamide
Synonyms: Glibenclamidum [INN-Latin]; Glibenclamida [INN-Spanish]; Glyburide; Apo-Glibenclamide
Drug Category: Antiarrhythmic Agents; Hypoglycemic Agents; Sulfonylureas
Drug Type: Small Molecule; Approved

Other Brand Names containing Glibenclamide: 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; Sugril; Suraben; Tiabet; Yuglucon; Semi-Daonil;
Absorption: Significant absorption within 1 hour and peak plasma levels are reached within 4 hours.
Toxicity (Overdose): Oral rat LD50: > 20,000 mg/kg. Oral mouse LD50: 3250 mg/kg.
Protein Binding: Extensively bound to serum proteins
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 contribute no significant hypoglycemic action in humans as they are only weakly active.
Half Life: 10 hours
Dosage Forms of Renabetic: Tablet Oral
Chemical IUPAC Name: 5-chloro-N-[2-[4-(cyclohexylcarbamoylsulfamoyl)phenyl]ethyl]-2-methoxybenzamide
Chemical Formula: C23H28ClN3O5S
Glibenclamide on Wikipedia: https://en.wikipedia.org/wiki/Glibenclamide
Organisms Affected: Humans and other mammals