Gliquidone OGB Dexa
Gliquidone OGB Dexa Uses, Dosage, Side Effects, Food Interaction and all others data.
Gliquidone OGB Dexa is a sulfonylurea drug used to treat diabetes mellitus type 2. It is an ATP-dependent K+ (KATP) channel blocker. This block causes a depolarization which leads to activation of voltage-dependent Ca channels and Ca2+ influx, and eventually increases insulin release.
Gliquidone OGB Dexa is an anti-diabetic drug in the sulfonylurea class. In patients with diabetes mellitus, there is a deficiency or absence of a hormone manufactured by the pancreas called insulin. Insulin is the main hormone responsible for the control of sugar in the blood. Gliquidone OGB Dexa is an antidiabetic medication which is used in those patients with adult maturity onset or non-insulin dependent diabetes (NIDDM). It works by lowering blood sugar levels by stimulating the production and release of insulin from the pancreas. It also promotes the movement of sugar from the blood into the cells in the body which need it.
Trade Name | Gliquidone OGB Dexa |
Generic | Gliquidone |
Gliquidone Other Names | Gliquidona, Gliquidone, Gliquidonum |
Type | |
Formula | C27H33N3O6S |
Weight | Average: 527.632 Monoisotopic: 527.209006493 |
Groups | Approved, Investigational |
Therapeutic Class | |
Manufacturer | |
Available Country | Indonesia |
Last Updated: | September 19, 2023 at 7:00 am |
Uses
Gliquidone OGB Dexa is a sulfonylurea drug used in the management of diabetes mellitus type 2.
Used in the treatment of diabetes mellitus type 2.
Gliquidone OGB Dexa is also used to associated treatment for these conditions: Type 2 Diabetes Mellitus
How Gliquidone OGB Dexa works
The mechanism of action of gliquidone in lowering blood glucose appears to be dependent on stimulating the release of insulin from functioning pancreatic beta cells, and increasing sensitivity of peripheral tissues to insulin. Gliquidone OGB Dexa likely binds to ATP-sensitive potassium channel receptors on the pancreatic cell surface, reducing potassium conductance and causing depolarization of the membrane. Membrane depolarization stimulates calcium ion influx through voltage-sensitive calcium channels. This increase in intracellular calcium ion concentration induces the secretion of insulin.
Half Life
The mean terminal half-life was approximately 8 hours (range 5.7-9.4 hours)
Innovators Monograph
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