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Gliclazide binds to the _ cell sulfonyl urea receptor (SUR1). This binding subsequently blocks the ATP sensitive potassium channels. The binding results in closure of the channels and leads to a resulting decrease in potassium efflux leads to depolarization of the _ cells. This opens voltage-dependent calcium channels in the _ cell resulting in calmodulin activation, which in turn leads to exocytosis of insulin containing secretorty granules.
Gliclazide is a second generation sulphonylurea which acts as a hypoglycemic agent. It stimulates _ cells of the islet of Langerhans in the pancreas to release insulin. It also enhances peripheral insulin sensitivity. Overall, it potentiates insulin release and improves insulin dynamics.
Extensively metabolized in the liver. Less than 1% of the orally administered dose appears unchanged in the urine. Metabolites include oxidized and hydroxylated derivates, as well as glucuronic acid conjugates.
LD50=3000 mg/kg (orally in mice). Gliclazide and its metabolites may accumulate in those with severe hepatic and/or renal dysfunction. Symptoms of hypoglycemia include: dizziness, lack of energy, drowsiness, headache and sweating.
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LGM currently offers Monoclonal Antibodies (mAbs) for non-GMP/R&D use. Please inquire about Monoclonal Antibodies produced under GMP conditions.
Questions? Call our customer API support number 1-(800)-881-8210.