Source: Pharmaceutical Benefits Scheme (AU) Revision Year: 2020 Publisher: Pfizer Australia Pty Ltd, Level 17, 151 Clarence Street, Sydney NSW 2000, Toll Free Number: 1800 675 229, www.pfizer.com.au
MINIDIAB is a sulphonylurea hypoglycaemic agent. The primary mode of action of MINIDIAB in experimental animals appears to be the stimulation of insulin secretion from the beta cells of pancreatic islet tissue and is thus dependent on functioning beta cells in the pancreatic islets. In humans MINIDIAB 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. The mechanism by which MINIDIAB lowers blood glucose during long-term administration has not been clearly established. In man, stimulation of insulin secretion by MINIDIAB in response to a meal is undoubtedly of major importance. Fasting insulin levels are not elevated even on long-term MINIDIAB administration, but the postprandial insulin response continues to be enhanced after at least 6 months of treatment.
The insulinotropic response to a meal occurs within 30 minutes after an oral dose of MINIDIAB in diabetic patients, but elevated insulin levels do not persist beyond the time of the meal challenge. Extrapancreatic effects may play a part in the mechanism of action of oral sulphonylurea hypoglycaemic drugs. Some patients fail to respond initially, or gradually lose their responsiveness to sulphonylureas, including MINIDIAB. Alternatively, MINIDIAB may be effective in some patients who have not responded, or have ceased to respond to other sulphonylureas.
Clinical studies show that blood sugar control persists in some patients for up to 24 hours after a single dose of MINIDIAB, even though plasma levels have declined to a small fraction of peak levels by that time.
No data available.
Gastrointestinal absorption of MINIDIAB in humans is uniform, rapid, and essentially complete. Peak plasma concentrations occur 1 to 3 hours after a single oral dose. The halflife of elimination ranges from 2 to 4 hours in normal subjects, whether given intravenously or orally. Total absorption and disposition of an oral dose were unaffected by food in normal volunteers, but absorption was delayed by about 40 minutes. Thus MINIDIAB 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 MINIDIAB and found to be 92 to 99% one hour after either route of administration. The apparent volume of distribution of MINIDIAB after intravenous administration was 5-11 L, indicative of localisation within the extracellular fluid compartment. In mice neither MINIDIAB nor metabolites were detectable autoradiographically in the brain or spinal cord of males or females, nor in the fetuses of pregnant females. In another study, however, very small amounts of radioactivity were detected in the fetuses of rats given the labelled drug.
The metabolism of MINIDIAB 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 3.0-4.3% unchanged MINIDIAB is found in the urine. The metabolic and excretory patterns are similar with both oral and IV routes of administration, indicating that first-pass metabolism is not significant. MINIDIAB does not accumulate in plasma on repeated oral administration.
No data available.
No data available.
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