Glimepiride (glimepiride)
Last reviewed · Source: First Databank (FDB) drug data
Overview
Glimepiride is a sulfonylurea antidiabetic agent.
Glimepiride is a sulfonylurea antidiabetic agent. The drug is structurally similar to glyburide and glipizide. Like other sulfonylurea antidiabetic agents, glimepiride lowers blood glucose concentration in diabetic patients and in healthy nondiabetic individuals.
Although the hypoglycemic action of the various sulfonylureas generally is similar, the drugs may differ quantitatively and/or possibly qualitatively in the extent to which they produce specific effects, and the effects may vary as a function of duration of treatment. The precise mechanism(s) of hypoglycemic action of sulfonylurea antidiabetic agents has not been clearly established, but the drugs, including glimepiride, initially appear to lower blood glucose concentration principally by stimulating secretion of endogenous insulin from the beta cells of the pancreas. During prolonged administration, sulfonylureas, including glimepiride, provide overall glycemic control without appreciable increases in fasting insulin secretion; therefore, extrapancreatic effects (e.g., enhanced peripheral sensitivity to insulin) appear to contribute substantially to the hypoglycemic action of the drugs.
Like other sulfonylureas, glimepiride alone is ineffective in the absence of functioning beta cells. Following single oral doses as low as 0.5-0.6 mg of the drug in healthy individuals, the hypoglycemic action generally is maximal within 2-3 hours. In patients with type 2 diabetes mellitus receiving 1-8 mg of glimepiride once daily, glycemic effects are maintained over 24 hours.
Following oral administration, peak drug concentration and maximal therapeutic effect is achieved in approximately 2--3 hours. Glimepiride demonstrates linear pharmacokinetics over the dosage range of 1--8 mg. Administration with food decreases the peak plasma concentration and AUC by 8 and 9%, respectively.
Glimepiride is highly protein bound (>99.5%). Glimepiride is completely metabolized by oxidative biotransformation by cytochrome P-450 2C9 to the metabolite M1, which is further metabolized to M2 by cytosolic enzymes. M1 possess approximately one-third of the pharmacological activity in animal models, although it is unclear whether M1 results in clinical meaningful effects on blood glucose in humans; M2 is inactive.
Glimepiride is excreted in the urine (60%) and the feces (40%) as metabolites. In geriatric patients, the mean AUC is reduced by 13% and weight-adjusted clearance is approximately 11% higher than that of younger patients. There is no difference in the pharmacokinetics of glimepiride based on sex (when adjusted for body weight) or race.
The pharmacokinetics of glimepiride do not differ between healthy subjects and patients with diabetes mellitus. In patients with decreased renal function, glimepiride serum concentrations decrease while the AUC and half-lives of the metabolites (M1 and M2) increase. The effect of hepatic impairment on the pharmacokinetics of glimepiride is unknown.
Morbid obesity is associated with a lower maximum plasma concentration and AUC compared to patients with normal body weight. There were no significant differences in the pharmacokinetics of glimepiride between patients with type 2 diabetes who were <=65 years and those >65 years of age.
USES: Glimepiride is used with a proper diet and exercise program to control high blood sugar in people with type 2 diabetes. It may also be used with other diabetes medications. Controlling high blood sugar helps prevent kidney damage, blindness, nerve problems, loss of limbs, and sexual function problems.
Proper control of diabetes may also lessen your risk of a heart attack or stroke. Glimepiride belongs to the class of drugs known as sulfonylureas. It lowers blood sugar by causing the release of your body's natural insulin.
Generic name: glimepiride
Pronunciation: (glye-MEP-ir-ide)
Reference product & biosimilars
No reference, biosimilar or interchangeable associated with this drug.
Today’s intelligence on Glimepiride
Indications
The following indications are listed for Glimepiride:
- Type 2 Diabetes Mellitus
Also known as: Adult Onset Diabetes, Adult Onset Diabetes Mellitus, Adult Onset Dm, Diabetes Mellitus Type 2, Diabetes Mellitus Type Ii, Ketosis-Resistant Diabetes Mellitus, Ketosis-Resistant Dm, Maturity Onset Diabetes, Maturity Onset Diabetes Mellitus, Non-Insulin Dependent Diabetes Mellitus, Non-Insulin-Dependent Diabetes Mellitus, Type Ii Diabetes Mellitus.
Dosing
No dosing information is available for this tab.
Glimepiride is administered orally once daily. Glimepiride should be administered with breakfast or with the first main meal of the day. The fixed combination of glimepiride and pioglitazone is administered orally once daily with the first main meal of the day. See the full prescribing information for additional administration instructions for the combination product. Although food slightly decreases the extent and slightly delays absorption of glimepiride, the manufacturer recommends that the drug be taken with the first meal of the day. Once-daily dosing of glimepiride provides adequate control of blood glucose concentration throughout the day.
Dosage of glimepiride must be individualized carefully based on patient response and tolerance. The goal of therapy should be to reduce both fasting glucose and glycosylated hemoglobin (hemoglobin A1c (HbA1c)) values to normal or near normal using the lowest effective dosage of glimepiride, when used either as monotherapy or in combination with other antidiabetic agents.
Store glimepiride tablets at 20-25degreesC in well-closed containers with safety closures.
No dosing information is available for this tab.
No dosing information is available for this tab.
Drug interactions
Glimepiride is metabolized by cytochrome P-450 (CYP) isoenzyme 2C9.
There are no contraindication interactions for this drug.
There are no severe interactions for this drug.
There are no moderate interactions for this drug.
Contraindications
*Hypersensitivity to glimepiride or any ingredient in the formulation.
*Hypersensitivity to sulfonamide derivatives.
There are no contraindication contraindications for this drug.
There are no severe contraindications for this drug.
There are no moderate contraindications for this drug.
Adverse reactions
The most common adverse effects of glimepiride (>=5% of patients and more common than placebo) reported in clinical trials were hypoglycemia, headache, nausea, and dizziness.
There are no severe adverse reactions for this drug.
There are no less severe adverse reactions for this drug.
Precautions
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Glimepiride is not recommended in pediatric patients because of its adverse effects on body weight and hypoglycemia.
The pharmacokinetics of a single dose of glimepiride were evaluated in 30 pediatric patients (aged 10--17 years) with type 2 diabetes mellitus. The results of this study found that the maximum plasma concentration, AUC, and half-life were comparable to historical data in adults. The safety and efficacy of glimepiride in pediatric patients were evaluated in a single-blind, 24-week trial that randomized 272 patients (aged 8--17 years) with type 2 diabetes to receive either glimepiride or metformin. Treatment naive and previously treated patients were enrolled; previously treated patients were required to discontinue other oral antidiabetic agents at randomization. After 24 weeks, the overall mean treatment difference in glycosylated hemoglobin (hemoglobin A1c; HbA1c) was 0.2%, favoring metformin. Based on this result, the trial did not meet its primary objective of showing a similar reduction in HbA1c with glimepiride compared to metformin. Adverse effects reported in pediatric patients treated with glimepiride were similar to those reported in adult patients. Hypoglycemic events documented by a blood glucose <36 mg/dL were observed in 4% of patients treated with glimepiride compared to 1% treated with metformin. One patient in each treatment group experienced a severe hypoglycemic episode.
Available data from a small number of published studies and decades of postmarketing experience with glimepiride in pregnancy have not identified any drug associated risk for major birth defects, miscarriage, or adverse maternal outcomes. However, sulfonylureas (including glimepiride) cross the placenta and have been associated with neonatal adverse reactions such as hypoglycemia. Prolonged hypoglycemia, lasting 4--10 days, has been reported in neonates born to mothers receiving a sulfonylurea at the time of delivery and has been reported with the use of agents with a prolonged half-life.
In animal studies, there was no increase in congenital anomalies, but an increase in fetal deaths occurred in rats and rabbits at glimepiride doses 50 times and 0.1 times the maximum recommended human dose (based on body surface area), respectively. This fetotoxicity was observed only at doses inducing maternal hypoglycemia and is believed to be directly related to the pharmacologic (hypoglycemic) action of glimepiride, as has been similarly noted with other sulfonylureas.
Poorly controlled diabetes in pregnancy is associated with risks to both the mother and fetus. Poorly controlled diabetes in pregnancy is associated with increased maternal risk for diabetic ketoacidosis, preeclampsia, spontaneous abortions, preterm delivery, and delivery complications. Poorly controlled diabetes also increases the fetal risk for major birth defects, still birth, and macrosomia-related morbidity.
Due to reports of prolonged hypoglycemia in neonates born to mothers receiving a sulfonylurea at the time of delivery, glimepiride should be discontinued at least 2 weeks before expected delivery. Observe newborns for symptoms of hypoglycemia and respiratory distress and manage accordingly.
There is no information regarding the presence of glimepiride in human milk or the effects on milk production. Glimepiride is distributed into milk in rats. During prenatal and postnatal studies in rats, significant concentrations of glimepiride were present in breast milk and the serum of the pups. Offspring of rats exposed to high levels of glimepiride during pregnancy and lactation developed skeletal deformities consisting of shortening, thickening, and bending of the humerus during the postnatal period. These skeletal deformities were determined to be the result of nursing from mothers exposed to glimepiride.
The developmental and health benefits of breastfeeding should be considered along with any potential adverse effects on the breast-fed child from glimepiride or from the underlying maternal condition. Breast-fed infants of lactating women using glimepiride should be monitored for symptoms of hypoglycemia (e.g., jitters, cyanosis, apnea, hypothermia, excessive sleepiness, poor feeding, seizures).
In clinical trials of glimepiride, 1053 of 3491 patients (30%) were >65 years of age. No overall differences in safety or effectiveness were observed between these patients and younger patients, but greater sensitivity of some older individuals cannot be ruled out. There were no significant differences in the pharmacokinetics of glimepiride between patients with type 2 diabetes <=65 years and those >65 years of age.
Glimepiride is substantially excreted by the kidney. Geriatric patients are more likely to have renal impairment. Additionally, hypoglycemia may be difficult to recognize in geriatric patients. Use caution when initiating glimepiride and increasing the dosage of glimepiride in geriatric patients.
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Last reviewed · Source: First Databank (FDB) drug data
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