Gliclazide is an anti-diabetic medication for the treatment of diabetes mellitus type 2. Gliclazide controls hyperglycemia in gliclazide-responsive diabetes mellitus of stable, mild, non-ketosis prone, type 2 diabetes. As an oral antihyperglycemic agent, it is used for the treatment of non-insulin-dependent diabetes mellitus. It has been classified differently according to its drug properties based on its chemical structure. When launched it belonged to the first-generation of sulfonylurea due to the structural presence of a sulfonamide group able to release a proton and the presence of one aromatic group. However, further studies have shown that Gliclazide is a second-generation sulfonylurea, because it has higher potency and a shorter half-life.
Gliclazide is sold under the brand names Diamicron, Diaprel, Azukon, and others.
Gliclazide was first patented in 1966 and approved for medical use in 1972. Due to its efficacy and use around the world, it has been listed on the World Health Organization's List of Essential Medicines.
Gliclazide is not available for sale in the United States.
Forms and dose:
Gliclazide is available as a tablet and extended-release tablet.
In the treatment of type 2 diabetes, the total daily dose recommended varies from 40-320mg. The dose is increased or decreased depending on the response to the therapy. The initial adult dose starts with 40-80mg daily. This can be increased until adequate control is reached. Please note that any single dose should not exceed 160mg. if a patient feels that they need higher doses, it is recommended to take medicine twice a day instead.
The price of Gliclazide:
In India, the lowest price consumers can pay for an 80 mg pill is $0.33. The same supply can cost as low as USD64 for the same supply for medicine.
How does it work?
Gliclazide is in the sulfonylurea family of medications. Its actions increase the release of insulin. It binds to the β cell sulfonylurea receptor subsequently blocking the ATP sensitive potassium channels. The process leads to the closing of channels that leads to a resulting decrease in potassium efflux. This eventually leads to depolarization of the β cells. In the next step, it opens voltage-dependent calcium channels in the β cell resulting in activation of calmodulin. The result of this process is exocytosis of insulin-containing secretory granules.
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