Save up -80% on Repaglinide
|Note: this is a drug discount program, not an insurance plan.|
|RX BIN: 015558||RX PCN: HT||Group ID: DDN6600||Card Holder ID: DDN6600|
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2019 Price of Prandin
|Price with discount in nearest pharmacy. Price may vary.|
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Repaglinide volume of distribution
Repaglinide pharmacokinetics are characterised by low volume of distribution, 30 L (consistent with distribution into intracellular fluid) and is highly bound to plasma proteins in humans (greater than 98%). Repaglinide is eliminated rapidly within 4 – 6 hours from the blood.
Discount Cards 16,000+
Clients Benefit 29%
Total savings $4,735,080
What is Repaglinide
Repaglinide is an oral antihyperglycemic agent used for the treatment of non-insulin-dependent diabetes mellitus (NIDDM). It belongs to the meglitinide class of short-acting insulin secretagogues, which act by binding to cells of the pancreas to stimulate insulin release. Repaglinide induces an early insulin response to meals decreasing postprandial blood glucose levels. It should only be taken with meals and meal-time doses should be skipped with any skipped meal. Approximately one month of therapy is required before a decrease in fasting blood glucose is seen. Meglitnides may have a neutral effect on weight or cause a slight increase in weight. The average weight gain caused by meglitinides appears to be lower than that caused by sulfonylureas and insulin and appears to occur only in those naive to oral antidiabetic agents. Due to their mechanism of action, meglitinides may cause hypoglycemia although the risk is thought to be lower than that of sulfonylureas since their action is dependent on the presence of glucose. In addition to reducing postprandial and fasting blood glucose, meglitnides have been shown to decrease glycosylated hemoglobin (HbA1c) levels, which are reflective of the last 8-10 weeks of glucose control. Meglitinides appear to be more effective at lowering postprandial blood glucose than metformin, sulfonylureas and thiazolidinediones. Repaglinide is extensively metabolized in the liver and excreted in bile. Repaglinide metabolites do not possess appreciable hypoglycemic activity. Approximately 90% of a single orally administered dose is eliminated in feces and 8% in urine.
Repaglinide mechanism of action
Repaglinide activity is dependent on the presence functioning beta; cells and glucose. In contrast to sulfonylurea insulin secretatogogues, repaglinide has no effect on insulin release in the absence of glucose. Rather, it potentiates the effect of extracellular glucose on ATP-sensitive potassium channel and has little effect on insulin levels between meals and overnight. As such, repaglinide is more effective at reducing postprandial blood glucose levels than fasting blood glucose levels and requires a longer duration of therapy (approximately one month) before decreases in fasting blood glucose are observed. The insulinotropic effects of repaglinide are highest at intermediate glucose levels (3 to 10 mmol/L) and it does not increase insulin release already stimulated by high glucose concentrations (greater than 15 mmol/L). Repaglinide appears to be selective for pancreatic beta; cells and does not appear to affect skeletal or cardiac muscle or thyroid tissue.
Dosage forms of Repaglinide
|Tablet||Oral use||0.5 mg|
AG-EE 388 ZW AG-EE 623 ZW
Actavis Pharma Company
Humans and other mammals
Indication of Repaglinide
As an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus.
Toxicity of Repaglinide
LD sub 50 /sub 1 g/kg (rat) (W. Grell)
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