Pharmaceutical Raw Material API CAS 122320-73-4 Rosiglitazone

Superiority:

Rosiglitazone achieves durable glycemic control by directly reducing insulin resistance and improving beta cell function. It is a highly selective and potent peroxisome proliferator-activated receptor gamma (PPARγ) agonist. The receptor is a protein found in adipose, skeletal muscle and liver tissue in insulin-sensitive tissues. The absolute bioavailability of rosiglitazone is 99%. Rosiglitazone was rapidly absorbed in healthy volunteers, reaching peak concentrations on average 1 hour after taking the drug. It can increase insulin content in pancreatic islets without affecting insulin secretion. Rosiglitazone prevents beta cell depletion by reducing cell death, and these evidences suggest that rosiglitazone has a protective effect on beta cells. Rosiglitazone reduces hyperinsulinemia and plasma free fatty acid levels. Decreased plasma insulin levels suggest that rosiglitazone reduces the burden on pancreatic beta cells. Since high free fatty acid levels have toxic effects on the pancreas, lowering free fatty acid levels also has a protective effect on pancreatic beta cell function. Therefore, the basic physiological link for type 2 diabetes is to reduce insulin resistance and improve β-cell function to control blood sugar.

1. More effective blood sugar control. It was reported that 493 patients with type 2 diabetes (failed by diet control or previously treated) participated. Baseline was a mean fasting blood glucose of approximately 225 mg/dl and a mean HbA1c of 8.9%. After 4W, patients were randomized to receive rosiglitazone 4mg/d or 8mg/d or placebo for a total of 26W. Compared with placebo, rosiglitazone (4 mg/d or 8 mg/d) significantly reduced fasting intracellular blood glucose by 58 mg/dl and 76 mg/dl, respectively, and reduced HbA1c by 1.2% and 1.5%, respectively. 2. Significantly reduce postprandial hyperglycemia, an 8W study on the effect of rosiglitazone monotherapy on patients with type 2 diabetes. The results showed that the postprandial blood glucose level of patients with type 2 diabetes was significantly reduced, and the rosiglitazone 8 mg/d treatment group was more obvious. It is important to demonstrate that the insulin-sensitizing effect of rosiglitazone improves peripheral glucose utilization. Reducing postprandial blood glucose is important because chronic postprandial hyperglycemia increases the risk of myocardial infarction and mortality. 3. Combination with metformin can significantly lower blood sugar. Works by increasing skeletal muscle and adipose tissue glucose uptake and metformin in hepatic glucose output. The results of the study confirmed that rosiglitazone combined with metformin has a complementary effect in reducing hyperglycemia. It indicated that metformin plus rosiglitazone 4mg/d or 8mg/d significantly reduced fasting blood glucose and HbA1c compared with metformin alone. In addition to glycemic control, free fatty acids were also reduced by 2.6 mg/dl and 4.3 mg/dl, respectively, from baseline. The main pathogenic mechanisms associated with abnormal metabolism in type 2 diabetes mellitus in combination with sulfonylureas are: insulin resistance in target tissues, especially skeletal muscle and liver, decreased abnormal glucose uptake and increased hepatic glucose output. 4. Combination of rosiglitazone and sulfonylureas to confirm that the combination of a drug that reduces insulin resistance and another drug that promotes insulin secretion is more effective than the two drugs alone. The results confirmed that the combination of the two drugs could further improve hyperglycemia. Combination with sulfonylureas significantly reduces fasting blood glucose and HbA1c. It also significantly reduced free fatty acid levels. 5. Combined use with insulin: Rosiglitazone is a powerful insulin sensitizer, which can reduce the demand for endogenous insulin when blood sugar is controlled within the normal range. Significant improvement in fasting blood glucose and HbA1c.

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1. Thiazolidinediones insulin sensitizers. It is suitable for the treatment of non-insulin-dependent (type II) diabetes mellitus.

2. For the treatment of diabetes