Glipizide Tablets BP

Name of Medicinal Product
Glipizide Tablets

Pharmaceutical form – Strength and Pack size
  1. Pharmaceutical form: TABLETS 
  2. Description: White, Round, Flat beveled, uncoated tablet embossed with a Breakline on one side and Plain on the other.
  3. Strength: Glipizide BP …. 5mg, per Tablet
  4. Pack Size: 1000’s Bulk

Therapeutic Category
Inhibition of ATP-dependent potassium channels (sulfonylurea); treatment of diabetes mellitus

  • Glipizide is an orally active hypoglycaemic sulphonylurea and has been shown to be effective in the treatment of diabetes mellitus Type II whose hyperglycemia cannot be controlled by diet alone. In certain patients receiving insulin, the concurrent use of Glipizide Tablets allows for a reduction in the daily dose of insulin.
  • Glipizide is indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus

  • Glipizide is contraindicated in patients with:

  1. Hypersensitivity to glipizide or any excipients in the tablets.
  2. Type 1 diabetes, diabetic ketoacidosis, diabetic coma.
  3. Severe renal, hepatic or thyroid impairment; co-existent renal and hepatic disease.
  4. Pregnancy and lactation. Patients treated with miconazole

Precautions / Warnings

  • Since glipizide belongs to the class of sulfonylurea agents, caution should be used in patients with G6PD-deficiency. Treatment of patients with G6PD deficiency with sulfonylurea agents can lead to hemolytic anemia and a nonsulfonylurea alternative should be considered.
  • All sulphonylurea drugs including glipizide are capable of producing severe hypoglycemia which may result in coma and may require hospitalization.
  • Patients experiencing severe hypoglycemia should be managed with appropriate glucose therapy and be monitored for a minimum of 24 to 48 hours. Proper patient selection, dosage, and instructions are important to avoid hypoglycaemic episodes. Regular, timely carbohydrate intake is important to avoid hypoglycaemic events occurring when a meal is delayed or insufficient food is eaten or carbohydrate intake is unbalanced.
  • Renal or hepatic insufficiency may affect the disposition of glipizide and the latter may also diminish gluconeogenic capacity, both of which increase the risk of serious hypoglycaemic reactions. Elderly, debilitated, or malnourished patients and those with adrenal or pituitary insufficiency are particularly susceptible to the hypoglycaemic action of glucose-lowering drugs.
  • Hypoglycemia may be difficult to recognize in the elderly and in people who are taking beta-adrenergic blocking drugs. Hypoglycemia is more likely to occur when calorific intake is deficient, after severe or prolonged exercise, when alcohol is ingested, or when more than one glucose-lowering drug is used.

Loss of control of blood glucose
  • When a patient stabilized on any diabetic regimen is exposed to stress such as fever, trauma, infection or surgery, a loss of control may occur. At such times, it may be necessary to discontinue glipizide and administer insulin.
  • The effectiveness of any oral hypoglycaemic drug, including glipizide, in lowering blood glucose to a desired level decreases in many patients over a period of time. This may be due to the progression of the severity of diabetes or to diminished responsiveness to the drug.
  • This phenomenon is known as secondary failure, to distinguish it from primary failure in which the drug is ineffective in an individual patient when first given. Adequate adjustment of dose and adherence to diet should be assessed before classifying a patient as a secondary failure.

Renal and hepatic disease

  • The pharmacokinetics and/or pharmacodynamics of glipizide may be affected in patients with impaired renal or hepatic function. If hypoglycemia should occur in such patients, it may be prolonged and appropriate management should be instituted.

Information for patients

  • Patients should be informed of the potential risks and advantages of glipizide and of alternative modes of therapy. They should also be informed about the importance of adherence to dietary instructions, of a regular exercise Programme and of regular testing of blood glucose.
  • The risk 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 should also be explained.

Laboratory tests

  • Blood glucose should be monitored periodically. Measurement of glycosylated hemoglobin should be performed and goals assessed by the current standard of care.

Pregnancy and Lactation

  • Glipizide Tablets are contraindicated during pregnancy. Diabetes in pregnancy should be treated with insulin and not sulphonylureas. Recent evidence suggests that hyperglycemia in pregnancy is associated with a higher incidence of congenital abnormalities.

  • Although it is not known whether Glipizide is excreted in human milk, some sulphonylurea drugs are known to be excreted in human milk. Therefore Glipizide is contraindicated during lactation.

Side effects / Adverse reactions
The majority of side effects have been dose-related, transient, and have responded to dose reduction or withdrawal of the medication.
However, clinical experience thus far has shown that as with other sulphonylureas some side effects associated with hypersensitivity may be severe and deaths have been reported in some instances.

Blood and Lymphatic System Disorders
  • Leucopenia, thrombocytopenia, hemolytic anemia and pancytopenia have been reported. Aplastic anemia and agranulocytosis have been reported with other sulphonylureas.
Metabolism and Nutritional Disorders
  • Hyponatremia has been reported.
  • Disulfiram-like reactions have been reported with other sulphonylureas.
Psychiatric Disorders
  • Confusion

Nervous System Disorders
  • Dizziness, drowsiness, headache and tremor
Eye Disorders
  • Visual disturbances such as blurred vision, diplopia and abnormal vision including visual impairment and decreased vision have each been reported in patients treated with glipizide.
Gastrointestinal Disorders
  • Nausea, diarrhoea, constipation, and gastralgia. They appear to be dose related and usually disappear on division or reduction of dosage. Abdominal pain and vomiting
Hepatobiliary Disorders
  • Cholestatic jaundice, impaired hepatic function and hepatitis have been reported. Discontinue treatment if jaundice occurs. Hepatic porphyria and porphyria cutanea tarda has been reported.
Skin and Subcutaneous Tissue Disorders
  • Allergic skin reactions including erythema, morbilliform or maculopapular reactions, urticaria, pruritus and eczema have been reported. They frequently disappear with continued therapy. However, if they persist, the drug should be discontinued. As with other sulphonylureas, photosensitivity reactions have been reported
General Disorders and Administration Site Disorders
  • Malaise
Laboratory Investigations
  • Occasional mild to moderate elevations of AST (SGOT), LDH, alkaline phosphatase, BUN and creatinine were noted. The relationship of these abnormalities to glipizide is uncertain and they have rarely been associated with clinical symptoms.

Drug Interactions
The following products are likely to increase the hypoglycaemic effect:

  • Increase in hypoglycaemic effect, possibly leading to symptoms of hypoglycemia or even coma.
  • There have been reports of hypoglycemia following the co-administration of glipizide and fluconazole, possibly the result of an increased half-life of glipizide.
  • Although not studied, voriconazole may increase the plasma levels of sulfonylureas, (e.g. tolbutamide, glipizide, and glyburide) and therefore cause hypoglycemia. Careful monitoring of blood glucose is recommended during co-administration.
Non-steroidal anti-inflammatory agents (NSAIDS) (e.g. phenylbutazone):
  • Increase in the hypoglycaemic effect of sulphonylureas (displacement of
  • sulphonylurea binding to plasma proteins and /or decrease in sulphonylurea elimination).
Salicylates (acetylsalicylic acid):
  • Increase in hypoglycaemic effect by high doses of acetylsalicylic acid (hypoglycaemic action of the acetylsalicylic acid).
  • An increase in a hypoglycaemic reaction can lead to a hypoglycaemic coma.
  • All beta-blockers mask some of the symptoms of hypoglycemia, e.g., palpitations and tachycardia. Most non-cardio selective beta-blockers increase the incidence and severity of hypoglycemia.
Angiotensin-converting enzyme inhibitors:
  • The use of angiotensin-converting enzyme inhibitors may lead to an increased hypoglycaemic effect in diabetic patients treated with sulphonylureas, including glipizide. Therefore, a reduction in glipizide dosage may be required.

H2 Receptor Antagonists:
  • The use of H2 receptor antagonists may potentiate the hypoglycaemic effects of sulphonylureas, including glipizide.
  • The hypoglycaemic action of sulphonylureas in general may also be potentiated by monoamine oxidase inhibitors and drugs that are highly protein-bound, such as sulphonamides, chloramphenicol, probenecid, and coumarins.
  • When such drugs are administered to (or withdrawn from) a patient receiving glipizide, the patient should be observed closely for hypoglycemia (or loss of control).
  • In vitro binding studies with human serum proteins indicate that glipizide binds to different sites on albumin than does tolbutamide and does not interact with salicylate or dicoumarol. However, caution must be exercised in extrapolating these findings to the clinical situation in the use of glipizide with these drugs.
  • The following products could lead to hyperglycemia:
Danazol: Diabetogenic effect of danazol. If it cannot be avoided, warn the patient and step up self-monitoring of blood glucose and urine. Possibly adjust the dosage of the antidiabetic agent during treatment with danazol and after its discontinuation
Phenothiazines (e.g. chlorpromazine) at high doses (> 100mg per day of chlorpromazine): Elevation in blood glucose (reduction in insulin release).
Corticosteroids: Elevation in blood glucose.
Sympathomimetics (e.g., ritodrine, salbutamol, terbutaline): Elevation in blood glucose due to beta-2-adrenoceptor stimulation. Other drugs that may produce hyperglycemia and lead to a loss of control include the thiazides and other diuretics, thyroid products, estrogens, progestogens, oral contraceptives, phenytoin, nicotinic acid, calcium channel blocking drugs and isoniazid. When such drugs are withdrawn from (or administered to) a patient receiving glipizide, the patient should be observed closely for hypoglycemia (or loss of control).

Dosage & Administration

Route of administration: Oral.

  • There is no fixed dosage regimen for the management of diabetes mellitus with Glipizide or any other hypoglycaemic agent. In addition to the usual monitoring of urinary glucose, the patient’s blood glucose must also be monitored periodically to determine the minimum effective dose for the patient, to detect primary failure: i.e. inadequate lowering of blood glucose at the maximum recommended dose of medication, and to detect secondary failure, i.e. loss of adequate blood-glucose-lowering response after an initial period of effectiveness. Glycosylated hemoglobin levels may also be of value in monitoring the patient’s response to therapy.
  • Short-term administration of Glipizide may be sufficient during periods of transient loss of control in patients usually controlled well on diet.
  • In general, Glipizide should be given approximately 30 minutes before a meal to achieve the greatest reduction in postprandial hyperglycemia. Concomitant food intake may delay absorption and administration: therapeutic effects are usually seen within 30 minutes and peak at about 60 minutes. Glipizide is rapidly metabolised and excreted mainly in the urine and therefore it is unlikely that delayed hypoglycaemic episodes will occur.
  • When administered in divided daily doses Glipizide can be considered as having a physiological action as its peak effect coincides with post-prandial peak blood-sugar levels.

Initial dose:

  • The recommended starting dose is 5mg, given before breakfast or the midday meal. Elderly patients and other patients at risk for hypoglycemia may be started on 2.5mg
  • Dosage adjustments should ordinarily be in increments of 2.5 or 5mg, as determined by blood glucose response. At least several days should elapse between titration steps. The maximum recommended single dose is 15mg.
  • Doses above 15mg should ordinarily be taken in 2 divided doses before meals. Multiple divided doses (2 or 3 daily) are recommended for patients who experience particularly high post-prandial blood glucose peaks.
  • Some patients may be effectively controlled on a once-a-day regimen. Total daily dosage above 15mg should ordinarily be divided. Patients can usually be stabilized on a dosage ranging from 2.5 to 20mg daily. The maximum recommended daily dosage is 20mg.

Use in the elderly and in high-risk patients:

  • Elderly diabetics are more sensitive to the hypoglycaemic effects of sulphonylurea drugs and should therefore be prescribed a low starting dose of 2.5mg daily. The elderly are also particularly susceptible to the effects of hypoglycemia. Hypoglycemia may be difficult to recognize in the elderly.
  • To decrease the risk of hypoglycemia in patients at risk including elderly, debilitated or malnourished patients, patients with irregular calorie intake, and patients with impaired renal or hepatic function, the initial maintenance dosing should be conservative to avoid hypoglycaemic reactions.

Use in children:

  • Safety and effectiveness in children have not been established.

Patients receiving insulin:

  • As with other sulphonylurea-class hypoglycaemics, many stable non-insulin-dependent diabetic patients receiving insulin may be safely placed on Glipizide. When transferring patients from insulin to glipizide, the following general guidelines should be considered:
  • For patients whose daily insulin requirement is 20 units or less, insulin may be discontinued and Glipizide therapy begins at usual dosages. Several days should elapse between Glipizide titration steps.
  • For patients whose daily insulin requirement is greater than 20 units, the insulin dose should be reduced by 50%, and Glipizide therapy initiated at usual dosages. Subsequent reductions in insulin dosage should depend on individual patient responses. Several days should elapse between Glipizide steps.
  • During the insulin withdrawal period, the patient should self-monitor glucose levels. Patients should be instructed to contact the prescriber immediately if these tests are abnormal. In some cases, especially when the patient has been receiving greater than 40 units of insulin daily, it may be advisable to consider hospitalization during the transition period.

Patients receiving other oral hypoglycaemic agents:

  • As with other sulphonylurea class hypoglycaemics, no transition period is necessary when transferring patients to Glipizide. Patients should be observed carefully (1-2 weeks) for hypoglycemia when being transferred from longer half-life sulphonylureas (e.g. chlorpropamide) to Glipizide due to potential overlapping of drug effects.

Combination Use:

  • When adding other blood-glucose-lowering agents to glipizide for combination therapy, the agent should be initiated at the lowest recommended dose and patients should be observed carefully for hypoglycemia. Refer to the product information supplied with the oral agent for additional information.
  • When adding glipizide to other blood-glucose-lowering agents, glipizide can be initiated at 5mg. Those patients who may be more sensitive to hypoglycaemic drugs may be started at a lower dose. Titration should be based on clinical judgment.
  • A biguanide may be added to the treatment if control is not achieved with Glipizide Tablets. The dosage of Glipizide should be maintained and the biguanide added using low doses initially and increasing the dosage of the biguanide progressively until adequate control is achieved or restored.


  • Overdosage of Glipizide can produce hypoglycemia. Mild hypoglycaemic symptoms without loss of consciousness or neurological findings should be treated aggressively with oral glucose and adjustments in drug dosage and/or meal patterns. Close monitoring should continue until the physician is assured that the patient is out of danger.
  • Severe hypoglycaemic reactions with coma, seizure, or other neurological impairment occur infrequently but constitute medical emergencies requiring immediate hospitalization. If a hypoglycaemic coma is diagnosed or suspected, the patient should be given a rapid intravenous injection of concentrated (50%) glucose solution.
  • This should be followed by continuous infusion of a more dilute (10%) glucose solution at a rate that will maintain the blood glucose at a level above 5.6mmol/1 (100mg/dl).
  • Patients should be closely monitored for a minimum of 48 hours and depending on the status of the patient at this time the physician should decide whether further monitoring is required. Clearance of glipizide from plasma would be prolonged in persons with liver disease. Because of the extensive protein binding of glipizide, dialysis is unlikely to be of benefit

Effects on ability to drive and use machines
  • Patients should be informed that their concentration may be affected if their diabetes is not satisfactorily controlled, especially at the beginning of treatment, and should be aware of the symptoms of hypoglycemia and be careful about driving and the use of machinery

Shelf life
  • 24 months from the date of manufacturing

Special precautions for storage
  • Store in a cool place in well-closed container. Protect from light, heat and moisture.
  • Keep out of reach of children.


  • Gastro-intestinal absorption of Glipizide in man is uniform, rapid and essentially complete.
  • Peak plasma concentrations occur 1-3 hours after a single oral dose. The half-life of elimination ranges from 2-4 hours in normal subjects, whether given intravenously or orally. The metabolic and excretory patterns are similar with the two routes of administration, indicating that first-pass metabolism is not significant.
  • Glipizide does not accumulate in plasma on repeated oral administration. Total absorption and disposition of an oral dose were unaffected by food in normal volunteers but absorption was delayed by about 40 minutes. Thus, Glipizide was more effective when administered about 30 minutes before, rather than with a test meal in diabetic patients.
  • Protein binding was studied in serum from volunteers who received either oral or intravenous Glipizide and found to be 98%-99% one hour after either route of administration. The apparent volume of distribution of Glipizide after intravenous administration was 11 liters, indicative of localization within the extracellular fluid compartment.
  • The metabolism of Glipizide is extensive and occurs mainly in the liver. The primary metabolites are inactive hydroxylation products and polar conjugates and are excreted mainly in the urine. Less than 10% unchanged Glipizide is found in the urine.

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