Nateglinide

The main ingredient of this product is nateglinide. Chemical name: N-(trans-4-isopropylcyclohexyl-1-formyl)-D-phenylalanine

Data from in vivo and in vitro studies indicate that nateglinide is metabolized primarily by the cytochrome P450 enzyme CYP2C9 (70%) and partially by CYP3A4 (30%). Nateglinide can inhibit the in vitro metabolism of tolbutamide (a substrate of CYP2C9). In vitro studies have shown that the drug has no inhibitory effect on the metabolic reaction of CYP3A4. These findings suggest that the potential for clinically significant pharmacokinetic interactions between the drug and other drugs is low. Nateglinide has no effect on the pharmacokinetic characteristics of the following drugs: warfarin (a substrate of CYP3A4 and CYP2C9), diclofenac (a substrate of CYP2C9), troglitazone (a CYP3A4 inducer), and digoxin. Therefore, no dose adjustment is required for nateglinide, digoxin, warfarin, or diclofenac when used together. Similarly, there are no clinically significant pharmacokinetic interactions between nateglinide and other oral antidiabetic drugs, such as metformin or glyburide. When co-administered with sulfinpyrazone (a highly potent and selective CYP2C9 inhibitor), a modest increase in the AUC of nateglinide (28%) was observed in healthy subjects, whereas the mean Cmax and elimination half-life did not change. A prolonged duration of action and the risk of hypoglycemia cannot be excluded when nateglinide is co-administered with CYP2C9 inhibitors. Nateglinide is highly bound to serum proteins (98%), mainly to albumin. In vitro displacement studies with highly protein-bound drugs have shown that they have no effect on the protein binding of nateglinide. These drugs are furosemide, propranolol, captopril, nicardipine, pravastatin, glyburide, warfarin, phenytoin, acetylsalicylic acid, tolbutamide and metformin. Similarly, nateglinide had no effect on the serum protein binding of propranolol, glyburide, nicardipine, warfarin, phenytoin, acetylsalicylic acid and tolbutamide. Physicians should consider the interaction of some drugs that affect glucose metabolism with nateglinide: The hypoglycemic effect of oral antidiabetic drugs can be enhanced by certain drugs, including nonsteroidal anti-inflammatory drugs, salicylates, monoamine oxidase inhibitors and non-selective beta-adrenergic blockers. The hypoglycemic effect of oral antidiabetic drugs can be weakened by certain drugs, including thiazides, cortisone, thyroid preparations and sympathomimetics. Patients receiving nateglinide should be closely observed for changes in blood sugar when adding or stopping the above drugs.

The main ingredient of this product is nateglinide. Chemical name: N-(trans-4-isopropylcyclohexyl-1-formyl)-D-phenylalanine

Data from in vivo and in vitro studies indicate that nateglinide is metabolized primarily by the cytochrome P450 enzyme CYP2C9 (70%) and partially by CYP3A4 (30%). Nateglinide can inhibit the in vitro metabolism of tolbutamide (a substrate of CYP2C9). In vitro studies have shown that the drug has no inhibitory effect on the metabolic reaction of CYP3A4. These findings suggest that the potential for clinically significant pharmacokinetic interactions between the drug and other drugs is low. Nateglinide has no effect on the pharmacokinetic characteristics of the following drugs: warfarin (a substrate of CYP3A4 and CYP2C9), diclofenac (a substrate of CYP2C9), troglitazone (a CYP3A4 inducer), and digoxin. Therefore, no dose adjustment is required for nateglinide, digoxin, warfarin, or diclofenac when used together. Similarly, there are no clinically significant pharmacokinetic interactions between nateglinide and other oral antidiabetic drugs, such as metformin or glyburide. When co-administered with sulfinpyrazone (a highly potent and selective CYP2C9 inhibitor), a modest increase in the AUC of nateglinide (28%) was observed in healthy subjects, whereas the mean Cmax and elimination half-life did not change. A prolonged duration of action and the risk of hypoglycemia cannot be excluded when nateglinide is co-administered with CYP2C9 inhibitors. Nateglinide is highly bound to serum proteins (98%), mainly to albumin. In vitro displacement studies with highly protein-bound drugs have shown that they have no effect on the protein binding of nateglinide. These drugs are furosemide, propranolol, captopril, nicardipine, pravastatin, glyburide, warfarin, phenytoin, acetylsalicylic acid, tolbutamide and metformin. Similarly, nateglinide had no effect on the serum protein binding of propranolol, glyburide, nicardipine, warfarin, phenytoin, acetylsalicylic acid and tolbutamide. Physicians should consider the interaction of some drugs that affect glucose metabolism with nateglinide: The hypoglycemic effect of oral antidiabetic drugs can be enhanced by certain drugs, including nonsteroidal anti-inflammatory drugs, salicylates, monoamine oxidase inhibitors and non-selective beta-adrenergic blockers. The hypoglycemic effect of oral antidiabetic drugs can be weakened by certain drugs, including thiazides, cortisone, thyroid preparations and sympathomimetics. Patients receiving nateglinide should be closely observed for changes in blood sugar when adding or stopping the above drugs.

The main ingredient of this product is nateglinide, and its chemical name is: N-(trans-4-isopropylcyclohexanecarbonyl)-D-phenylalanine.

In vitro studies have shown that nateglinide is mainly metabolized by the cytochrome P450 enzyme CYP2C9 (70%) and partially by CYP3A4 (30%). In vitro experiments have shown that it can inhibit the metabolism of mesitylbutazone, based on which it is judged that nateglinide is a potential inhibitor of CYP2C9 in vivo. In vitro experiments have shown that the drug has no inhibitory effect on the metabolic reaction of CYP3A4. In summary, these findings indicate that the potential for clinically significant pharmacokinetic interactions between this drug and other drugs is low. Nateglinide has no effect on the pharmacokinetic characteristics of the following drugs: warfarin (a substrate of CYP3A4 and CYP2C9), diclofenac sodium (a substrate of CYP2C9), troglitazone (a CYP3A4 inducer), and digoxin. Therefore, no dose adjustment is required for nateglinide, digoxin, warfarin, or diclofenac sodium when used together. Similarly, there is no clinically significant pharmacokinetic interaction between nateglinide and other oral antidiabetic drugs, such as metformin or glyburide. Nateglinide is highly bound to serum proteins (98%), primarily to albumin. In vitro displacement studies with highly protein-bound drugs have shown that they have no effect on the protein binding of nateglinide. These drugs are: furosemide, propranolol, captopril, nicardipine, pravastatin, glyburide, warfarin, phenytoin sodium acetylsalicylic acid, tolbutamide, and metformin. Similarly, nateglinide has no effect on the serum protein binding of propranolol, glyburide, nicardipine, warfarin, phenytoin sodium, acetylsalicylic acid, and tolbutamide. Physicians should consider the interaction of some drugs that affect glucose metabolism with nateglinide: The hypoglycemic effect of oral antidiabetic drugs can be potentiated by certain drugs, including nonsteroidal anti-inflammatory drugs, salicylates, monoamine oxidase inhibitors, and non-selective beta-adrenergic blocking agents. The hypoglycemic effect of oral antidiabetic drugs can be weakened by certain drugs, including thiazides, cortisone, thyroid preparations and sympathomimetics. Patients receiving nateglinide should be closely monitored for changes in blood sugar when adding or stopping the above drugs.