GLIPIZIDE tablet

Land: USA

Sprog: engelsk

Kilde: NLM (National Library of Medicine)

Aktiv bestanddel:

GLIPIZIDE (UNII: X7WDT95N5C) (GLIPIZIDE - UNII:X7WDT95N5C)

Tilgængelig fra:

Direct_Rx

Indgivelsesvej:

ORAL

Recept type:

PRESCRIPTION DRUG

Terapeutiske indikationer:

Glipizide tablets are 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. Known hypersensitivity to the drug. 2. Type 1 diabetes mellitus, diabetic ketoacidosis, with or without coma. This condition should be treated with insulin.

Produkt oversigt:

Glipizide Tablets, USP are supplied as white to off-white, round, scored tablets, imprinted as follows: 5 mg- “APO” on the side and “GLP” over bisect “5” on the other side; 10 mg- “APO” on one side and “GLP” over bisect “10” on the other side. 5 mg Bottles: 100’s 500’s 1,000’s 18,000’s 10 mg Bottles: 100’s 500’s 1,000’s 10,000’s

Autorisation status:

Abbreviated New Drug Application

Produktets egenskaber

GLIPIZIDE- GLIPIZIDE TABLET
DIRECT_RX
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GLIPIZIDE
Glipizide is an oral blood-glucose-lowering drug of the sulfonylurea
class.
The Chemical Abstracts name of glipizide is
1-cyclohexyl-3-[[p-[2-(5-methylpyrazine-
carboxamido)ethyl]phenyl]sulfonyl]urea. The molecular formula is
C21H27N5O4S; the
molecular weight is 445.55; the structural formula is shown below:
Glipizide is a whitish, odorless powder with a pKa of 5.9. It is
insoluble in water and
alcohols, but soluble in 0.1 N NaOH; it is freely soluble in
dimethylformamide. Glipizide
tablets, USP for oral use are available in 5 and 10 mg strengths.
Inert ingredients are: anhydrous lactose; colloidal silicon dioxide;
magnesium stearate;
sodium starch glycolate.
Meets USP Dissolution Test 2.
Mechanism of Action
The primary mode of action of glipizide 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, glipizide 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 glipizide lowers blood glucose during long-term
administration has
not been clearly established. In man, stimulation of insulin secretion
by glipizide in
response to a meal is undoubtedly of major importance. Fasting insulin
levels are not
elevated even on long-term glipizide 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
glipizide 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 sulfonylurea
hypoglycemic drugs.
Blood sugar control persists in some patients for up to 24 hours after
a single dose of
glipizide, even though plasm