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Prandin (Repaglinide)

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Prandin is an efficacious medical preparation in fight against type 2 diabetes. Prandin acts by controlling and decreasing glucose (sugar in blood).

Other names for this medication:

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Also known as:  Repaglinide.


Prandin is created with extremely active ingredients with aim to make Prandin ideal remedy against type 2 diabetes. Target of Prandin is to control sugar level in blood.

Prandin acts by controlling and decreasing glucose (sugar in blood). You can use it in case exercise and diet does not help.

Prandin is also known as Repaglinide, Eurepa, GlucoNorm, NovoNorm, Rapilin.

Prandin is an oral anti-diabetic drug. It can be taken together with anti-diabetic medication as Glucophage.

Prandin is not taken to treat type 1 diabetes.

You can normally take insulin while using Prandin.


It is better to take Prandin orally every day at the same time.

Usual Prandin dosage is 0.5mg - 4mg, which is taken 2-4 times a day before meal.

If you want to achieve most effective results do not stop taking Prandin suddenly.


If you overdose Prandin and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Prandin overdosage: troublesome, retching, flushing, migraine, short breath, weakness, sweating, coma, fainting, muscle pain, hunger, pain of stomach, tremors, extreme fatigue, dizziness, seizure, slow heartbeat, dyspepsia, feeling cold, lack of appetite, fast heartbeat.


Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Prandin are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.


Do not take Prandin if you are allergic to Prandin components.

Be careful with Prandin if you're pregnant or you plan to have a baby, or you are a nursing mother.

Prandin is not taken to treat type 1 diabetes.

You can normally take insulin while using Prandin.

Do not use Prandin in case of having type 1 diabetes, diabetic ketoacidosis, liver disease, poor adrenal, pituitary function.

Try to be careful with Prandin in case of using such medication as sulfa drugs (Gantanol); isoniazid; niacin (Nicobid); water pills (thiazide diuretics HydroDIURIL, Dyazide); beta blockers (blood pressure medications as Tenormin, Inderal); barbiturates (sedatives as Nembutal, Seconal); calcium channel blockers (blood pressure medications as Procardia, Cardizem); Rifampin (Rimactane, Rifadin); oral contraceptives; ketoconazole (Nizoral); chloramphenicol (Chloromycetin); nonsteroidal anti-inflammatory drugs (Voltaren, Motrin, Advil, Naprosyn); blood thinners (Miradon, Dicumarol); steroids as prednisone; furosemide as Lasix; clarithromycin as Biaxin; thyroid medications as Synthroid; phenytoin as Dilantin; Probenecid (ColBENEMID, Benemid); estrogens (Premarin); aspirin; erythromycin (PCE, Eryc, Ery-Tab); MAO inhibitors (antidepressants Parnate, Marplan, Nardil); glucose lowering agents (Micronase, Glucotrol); carbamazepine (Tegretol); major tranquilizers (Stelazine, Mellaril).

You can use Prandin in case exercise and diet does not help.

Prandin can be taken together with anti-diabetic medication as Glucophage.

Try to avoid unhealthy food.

Avoid consuming alcohol.

Do not stop taking Prandin suddenly.

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There is a rising worldwide prevalence of diabetes, especially type 2 diabetes mellitus (T2DM), which is one of the most challenging health problems in the 21st century. The associated complications of diabetes, such as cardiovascular disease, peripheral vascular disease, stroke, diabetic neuropathy, amputations, renal failure, and blindness result in increasing disability, reduced life expectancy, and enormous health costs. T2DM is a polygenic disease characterized by multiple defects in insulin action in tissues and defects in pancreatic insulin secretion, which eventually leads to loss of pancreatic insulin-secreting cells. The treatment goals for T2DM patients are effective control of blood glucose, blood pressure, and lipids (if elevated) and, ultimately, to avert the serious complications associated with sustained tissue exposure to excessively high glucose concentrations. Prevention and control of diabetes with diet, weight control, and physical activity has been difficult. Treatment of T2DM has centered on increasing insulin levels, either by direct insulin administration or oral agents that promote insulin secretion, improving sensitivity to insulin in tissues, or reducing the rate of carbohydrate absorption from the gastrointestinal tract. This review presents comprehensive and up-to-date information on the mechanism(s) of action, efficacy, pharmacokinetics, pleiotropic effects, drug interactions, and adverse effects of the newer antidiabetic drugs, including (1) peroxisome proliferator-activated-receptor-γ agonists (thiazolidinediones, pioglitazone, and rosiglitazone); (2) the incretin, glucagon-like peptide-) receptor agonists (incretin-mimetics, exenatide. and liraglutide), (3) inhibitors of dipeptidyl-peptidase-4 (incretin enhancers, sitagliptin, and vildagliptin), (4) short-acting, nonsulfonylurea secretagogue, meglitinides (repaglinide and nateglinide), (5) amylin anlog-pramlintide, (6) α-glucosidase inhibitors (miglitol and voglibose), and (7) colesevelam (a bile acid sequestrant). In addition, information is presented on drug candidates in clinical trials, experimental compounds, and some plants used in the traditional treatment of diabetes based on experimental evidence. In the opinion of this reviewer, therapy based on orally active incretins and incretin mimetics with long duration of action that will be efficacious, preserve the β-cell number/function, and block the progression of diabetes will be highly desirable. However, major changes in lifestyle factors such as diet and, especially, exercise will also be needed if the growing burden of diabetes is to be contained.

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HbA1c is 6 %. On the basis of positive family history for diabetes, normal body weight and negative antibodies against islet-cell antigens, we perform blood molecular genetic analyses with the suspicion of a genetic form of diabetes. Genetic tests reveal a monogenic form of diabetes (MODY, Maturity Onset Diabetes of the Young) due to an heterozygous mutation in exon 6 of the glucokinase (GCK) gene. The same mutation is subsequently detected in the patient's mother.

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Human oral therapeutic doses of ritonavir and repaglinide were extrapolated to rats based on the body surface area. Ritonavir (20 mg/kg, p.o.), alone and along with repaglinide (0.5 mg/kg, p.o.), was given to normal, diabetic and hepatic impaired rats, and the PK/PD were studied.

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Neither the mean AUC(0-infinity) (geometric mean ratio: 1.01; 95% CI: 0.93-1.1, P = 0.88) nor the mean C(max) (geometric mean ratio: 1.05; 95% CI: 0.94-1.2, P = 0.35) of repaglinide were statistically significantly different in the group carrying the CYP2C8*3 mutant allele compared with wild-types. Grapefruit juice caused a 19% decrease in the geometric mean ratio of the 3-hydroxyquinidine to quinidine ratio (difference: 0.81; 95% CI: 0.75-0.87, P < 0.0001), which was used as an index of CYP3A4 activity, and an increase in the mean AUC(0-infinity) of repaglinide (geometric mean ratio: 1.13; 95% CI: 1.04-1.2, P = 0.0048), but had no statistically significant effect on the t(1/2). There was no statistically significant difference in blood glucose concentration in subjects who had or had not ingested grapefruit juice. The effect was more pronounced at the low dose of repaglinide (0.25 mg) than at the therapeutic dose of 2 mg.

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To evaluate the efficacy and safety of nateglinide, a new antidiabetic agent, in the treatment of type 2 diabetes.

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The placental transfer of repaglinide from mother to fetus was low. Since a higher transfer rate of repaglinide was observed in fetal-to-maternal than maternal-to-fetal direction, active transport by OATP-transporters may be an important factor in fetal exposure to repaglinide.

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Repaglinide is the first stimulator of insulin secretion from the new meglitinide family. Via specific binding to the ATP-sensitive potassium channel of the beta cell membrane, it stimulates the rapid release of insulin. In preclinical studies, the insulin-stimulating effect of repaglinide has been found to be 10 to 20 times more potent than that of glibenclamide. Repaglinide is rapidly absorbed and has a short action, which makes it particularly well suited for the regulation of prandial blood glucose and meal-related dose adjustment. Since repaglinide is eliminated almost exclusively by non-renal routes, it can be used without danger in patients with moderately reduced renal function. Repaglinide is a suitable agent for first-line monotherapy in patients whose glucose metabolism cannot be optimally controlled by increasing physical activity and appropriate dietary measures. Repaglinide is clearly superior to glibenclamide in reducing postprandial hyperglycemia, and has a lower hypoglycemia risk than all the sulphonylureas. The flexibility of repaglinide makes it possible for good oral meal-related treatment.

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Type 2 diabetes mellitus (T2DM) is one of the most common chronic diseases worldwide, presenting a great challenge to the public health systems due to high morbidity and mortality, because of frequent micro-/macro-vascular complications. Many treatment options are now available, with different efficacy as well as mechanisms of action to improve deranged glucose metabolism. We review some of the available data on derivatives of meglitinide, namely nateglinide and repaglinide. These two compounds increase insulin secretion by a mechanism similar to the one of sulfonylureas, but with a shorter half-life. Nateglinide and repaglinide, derivatives of meglitinides, have characteristic pharmacodynamic and pharmacokinetic properties that, together with their proposed mechanism of action, make them useful for type 2 diabetes mellitus, especially when used in combination therapy.

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Sulfonylureas are widely used to treat type 2 diabetes because they stimulate insulin secretion from pancreatic beta-cells. They primarily act by binding to the SUR subunit of the ATP-sensitive potassium (K(ATP)) channel and inducing channel closure. However, the channel is still able to open to a limited extent when the drug is bound, so that high-affinity sulfonylurea inhibition is not complete, even at saturating drug concentrations. K(ATP) channels are also found in cardiac, skeletal, and smooth muscle, but in these tissues are composed of different SUR subunits that confer different drug sensitivities. Thus tolbutamide and gliclazide block channels containing SUR1 (beta-cell type), but not SUR2 (cardiac, smooth muscle types), whereas glibenclamide, glimepiride, repaglinide, and meglitinide block both types of channels. This difference has been exploited to determine residues contributing to the sulfonylurea-binding site. Sulfonylurea block is decreased by mutations or agents (e.g., phosphatidylinositol bisphosphate) that increase K(ATP) channel open probability. We now propose a kinetic model that explains this effect in terms of changes in the channel open probability and in the transduction between the drug-binding site and the channel gate. We also clarify the mechanism by which MgADP produces an apparent increase of sulfonylurea efficacy on channels containing SUR1 (but not SUR2).

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The study comprised three screening visits, followed by a 7-day inpatient period. Thirty-four patients, with normal renal function (n = 12), mild-to-moderate renal dysfunction (n = 12) or severe renal dysfunction (n = 10), received a single 2-mg dose of repaglinide on day 1, followed by preprandial 2-mg doses with main meals (breakfast, lunch and dinner) on each of days 2-4. A final 2-mg dose of repaglinide was administered on day 5.

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To compare the metabolic effects of acarbose and repaglinide in type 2 diabetic patients who are being treated with a sulphonylurea-metformin combination therapy. The primary endpoint of the study was to evaluate which add-on treatment between acarbose and repaglinide is more efficacious in reducing PPG. The second endpoint was to evaluate which of these two treatment is more efficacious in the global management of glucose homeostasis in the enrolled patients.

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76 patients were women and 99 patients suffered from type 2 diabetes. The mean age was 77.8 ± 9.4 years. The HbA1c of the patients with type 2 diabetes at admission was 6.5 ± 1.5 %. The greatest number of hypoglycemia episodes were associated with sulfonylurea and analoga (25), insulin (67), and the combination insulin and sulfonylurea (17). The applied sulfonylureas were in 38 % glibenclamide, in 55 % glimepiride and in 7 % repaglinide. The mean in-hospital stay was 10.4 days after admittance for hypoglycemia, the mean stay was 8.4 days for patients without hypoglycemia. Concerning creatinine there was a normal kidney function in 37.6 % of the patients, the calculated creatinine clearance was normal in only about 15 % of the patients. In 13 patients (12 %) any antidiabetic medication was stopped at time of discharge. 20 patients, chosen randomly, were analyzed concerning the costs associated with the hospital admittance. The mean age of these patients was 76.8 years and their mean stay in hospital was 10.2 day. The costs covered 3,158 €. The mean costs for the other internal patients was 2,716 €.

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In Germany, coverage decisions in the statutory health insurance (SHI) system are based on the principles of evidence-based medicine. Recently, an evidence assessment by the Institute for Quality and Efficiency in Health Care (IQWiG) of the oral antidiabetics of the glinide class showed that their long-term benefit is not proven. Accordingly, the responsible Federal Joint Committee (G-BA) decided to exclude glinides from prescription in the SHI system. This was, however, objected to by the Ministry of Health, which is charged with legal supervision. We use this case to illustrate the path from evidence assessments to coverage decisions in Germany against the background of the latest health reform, which has changed the legal requirements for evidence assessments and the ensuing coverage decisions.

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This review focuses on hypoglycemia in patients with end-stage renal disease (ESRD). It discusses the pathophysiology of glucose metabolism in the kidney, the impact of dialysis on glucose and insulin metabolism, and the challenges of glucose monitoring in ESRD. The clinical relevance of these changes is reviewed in relation to altered blood glucose targets and modification of antidiabetes therapy to prevent hypoglycemia. Based on current data and guidelines, recommendations for the outpatient and inpatient setting are provided for diabetes management in ESRD.

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Monotherapy with the most used ISs, including glimepiride, glibenclamide, glipizide, and tolbutamide, seems to be associated with increased mortality and cardiovascular risk compared with metformin. Gliclazide and repaglinide appear to be associated with a lower risk than other ISs.

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Several studies have shown an increase of mortality in diabetic patients treated with combinations of sulphonylureas and biguanides. Comparisons between different insulin secretagogues in combination with metformin with respect to all-cause mortality have not been reported so far.

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Forty-two patients with type 2 diabetes and chronic stable angina pectoris, and two-vessel or three-vessel disease participated in this study. The patients underwent two consecutive treadmill exercise tests (phase 1). On the day after these exercise tests, 2 mg of oral repaglinide was given to the patients. One week later, two exercise tests were repeated consecutively (phase 2).

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Evidence obtained in the 1990's strongly supports the notion that glycaemic control is important not only in Type I (insulin-dependent), but also in Type II (non-insulin-dependent) diabetes mellitus. Although measurement of HbA(1c) is the standard for assessing the effect of glucose control in the occurrence and prevention of diabetic sequelae, more recent evidence indicates that other glucose parameters are also important. Postchallenge and postprandial hyperglycaemic peaks seem to be prospective determinants of vascular damage in early Type II diabetes. Currently, there is no overall accepted standard approach for the pharmacological management of Type II diabetes. The United Kingdom Prospective Diabetes Study has shown that reaching a near-normal glycaemic target is critically important and the pharmacotherapy of this progressive disease is difficult. Loss of endogenous insulin secretion has been substantiated to cause the progression of Type II diabetes in the United Kingdom Prospective Diabetes Study. Early insulinization, however, was not advantageous over other forms of therapy. The advent of polypharmacy in recent years has greatly strengthened the treatment of this disease. This synergy has been extended of late with the development of early-phase insulin secretion agents. Two such agents, nateglinide and repaglinide, can be used to reduce mealtime glucose excursions and HbA(1c) as monotherapy, and in combination with metformin; their antidiabetic potential is similar to the combination treatment with glibenclamide and metformin. Additional substantiation of their long-term effect on improving life expectancy and reducing diabetic complications in Type II diabetic patients is now required.

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The use of repaglinide or metformin in drug therapy-nai;ve patients with type 2 diabetes over a 12-month period is associated with improvements in both glycaemic control and cardiovascular risk profile. The latter cannot necessarily be attributed to the pharmacotherapy per se, but provides reassurance in the context of initiating oral hypoglycaemic drug therapy with these agents.

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Repaglinide is a novel insulin secretagogue being developed for the management of type 2 (non-insulin-dependent) diabetes mellitus. It stimulates release of insulin from the pancreatic beta-cell, but appears to bind to a different receptor site from sulphonylureas. Repaglinide lowers fasting and postprandial blood glucose levels in animals, healthy volunteers and patients with type 2 diabetes mellitus. Repaglinide is rapidly absorbed and eliminated, which may allow a relatively fast onset and offset of action. Excretion occurs almost entirely by non-renal mechanisms. In comparative clinical trials in patients with type 2 diabetes mellitus, repaglinide 0.5 to 4 mg twice or 3 times daily before meals provided similar glycaemic control to glibenclamide (glyburide) 2.5 to 15 mg/day. Addition of repaglinide to existing metformin therapy resulted in improved glycaemic control. In contrast with glibenclamide, use of repaglinide allowed patients to miss a meal without apparently increasing the risk of hypoglycaemia.

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In ESRD, a combination of impaired insulin clearance, changes in glucose metabolism, and the dialysis process make patients vulnerable to low blood glucose levels. Hypoglycemia accounts for up to 3.6% of all ESRD-related admissions. At admission or during hospitalization, hypoglycemia in ESRD has a poor prognosis, with mortality rates reported at 30%. Several guidelines suggest a modified hemoglobin A1c (A1c) goal of 7 to 8.5% (53 to 69 mmol/mol) and an average blood glucose goal of 150 to 200 mg/dL. Noninsulin antidiabetes agents like dipeptidyl peptidase 4 inhibitors, repaglinide, and glipizide in appropriate doses and reduction of insulin doses up to 50% may help decrease hypoglycemia.

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Two authors independently extracted data and assessed the risk of bias in the included studies.

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Our data demonstrate an important interplay between the actual insulinotropic compounds, VEGF and ambient buy prandin glucose concentration affecting the survival of the vascular endothelial cells. Consequently, this interplay needs to be taken into consideration when designing novel oral antidiabetic compounds.

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PBPK modeling constitutes a useful mechanistic approach for the quantitative prediction of DDI involving simultaneous inducing or inhibitory buy prandin effects on multiple CYPs as often encountered with antiretroviral drugs.

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Prospective case buy prandin -control study.

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Solid lipid nanoparticles ( buy prandin SLNs) are highly susceptible to phagocytosis by reticuloendothelial system (RES). To overcome this problem, a novel hydrogel-coated SLNs structure was developed and evaluated in this study.

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We searched several databases buy prandin including The Cochrane Library, MEDLINE and EMBASE. We also contacted manufacturers and searched ongoing trials databases, and the American Diabetes Association (ADA) and European Association for the Study of Diabetes (EASD) websites.

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The results of the Diabetes Control and Complications Trial (DCCT) and UK Prospective Diabetes Study trials in type 1 and type 2 diabetes, respectively, have proved the importance of intensive glucose management in the prevention of microvascular complications (retinopathy, nephropathy, and neuropathy). Both trials showed encouraging trends for a decrease in macrovascular complications, and this is buy prandin being pursued in new studies. These findings have led to more strict goals for glucose control. As glucose levels are aimed to be closer to the normal range, the risk for hypoglycemia also increases dramatically. The choice of the agent therefore is more influenced currently by the risk for hypoglycemia. There are presently four classes of oral antihyperglycemic agents. These agents differ greatly in terms of mechanisms of action, efficacy, side effect profiles, and cost. Except for Acarbose, all classes decrease the glycosylated hemoglobin by a similar magnitude: 1.0 to 1.5%. In chronic renal failure, the oral agents that can be used therefore include the insulin secretagogues repaglinide and nateglinide and the thiazolidinediones (rosiglitazone and pioglitazone) with caution. Insulin also can be used safely in renal failure.

prandin gel 2015-10-09

[symbol: see text] Nateglinide (Starlix-Novartis) and [symbol: see text] repaglinide (NovoNorm-Novo Nordisk) are two of a new class of orally active antidiabetic drugs, the meglitinides. They have a rapid-onset and short-lasting stimulating effect on insulin secretion. Both are licensed for combination therapy with metformin in patients with type 2 diabetes mellitus who are inadequately controlled by maximally tolerated doses of metformin alone. In addition, repaglinide is licensed for use as monotherapy in patients with type 2 diabetes whose hyperglycaemia can no longer be controlled satisfactorily by diet, weight reduction and exercise. Here we buy prandin discuss whether repaglinide and nateglinide offer worthwhile advantages in the management of patients with type 2 diabetes.

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The effect of 17 extracts on metabolism was examined in a human liver microsome assay by HPLC and individual cytochrome P450s 2C9, 2C19, 2C8 and 3A4 in a microplate fluorometric assay. Gliclazide, rhaponticin and its aglycone derivative, rhapontigenin were also examined in the fluorometric assay. The effect on transport was examined with 11 extracts using the intestinal epithelial Caco-2 differentiated cell monolayer model at buy prandin times up to 180 min.

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The area under the plasma concentration-time curve from time 0 to infinity (AUC((0-inf))) of repaglinide was significantly higher in subjects possessing the MDR1 2677GT and 2677TT alleles than in those with the MDR1 2677GG and 2677TA alleles buy prandin (p = 0.007). The mean AUCs and peak plasma concentration were higher in subjects with the 521TC allele than in those with the OATP1B1 521TT allele, and the OATP1B1 388A allele is associated with a reduced trend of pharmacokinetic exposure; however, these trends were not statistically significant. The pharmacokinetics of repaglinide was not associated with MDR1 C1236T, MDR1 C3435T, and CYP3A4*18.

prandin renal dose 2015-11-30

Prandial glucose regulation represents a new concept in the management of type 2 diabetes: targeting postprandial glycaemic excursions as a means of achieving long-term glycaemic control. Although control of the overall glycaemic load is the most important factor for the success of long-term management of type 2 diabetes, control of postprandial hyperglycaemia also has positive implications for preventing the development of diabetic complications. Repaglinide is the first prandial glucose regulator to become available in the clinical setting. It has a rapid and short-lived insulinotropic action and can therefore reduce postprandial glucose excursions without increasing the risk of hypoglycaemia. Short-term clinical studies showed that repaglinide is superior to glibenclamide in improving postprandial glycaemic control. Longer-term studies confirmed that improved PGR is accompanied by improved overall glycaemic control that is at least equivalent to that achieved by sulphonylurea treatment. Moreover, because repaglinide can be used with flexible meal patterns without compromising glucose control, it can improve quality of life as indicated by overall treatment satisfaction, well-being and health status. Repaglinide has few contraindications or drug interactions and can be used in a wide range of patients. Although careful titration of repaglinide dose is recommended for patients with mild to moderate renal impairment, no dosage adjustment is otherwise needed in the elderly. In addition to being an effective first-line hypoglycaemic agent, repaglinide is highly effective in combination therapy for patients with type 2 diabetes who require more intensive treatment. When glucose targets are not met using repaglinide monotherapy, the combination of repaglinide with metformin can further improve glycaemic control by enhancing insulin secretion and improving insulin sensitivity. Similarly, when required combination of repaglinide with troglitazone or NPH-insulin can produce better glycaemic control than monotherapy alone. Given that most patients with type 2 diabetes require a multitherapy approach to achieve and sustain adequate glycaemic control, repaglinide will be an important element in buy prandin future intensive therapy regimens.

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Patients with type 2 diabetes (n = 256) who had inadequate glycemic control (HbA1c > or =7.0%) during previous monotherapy were randomly assigned to receive repaglinide (0.5-4.0 mg at meals), troglitazone (200-600 mg once daily), or a combination of repaglinide (1-4 mg at meals) and troglitazone (200-600 mg once daily). After a 4-6 week washout period, the trial assessed 22 weeks of treatment: 3 weeks (weeks 0-2) of forced titration, 11 weeks of fixed-dose treatment (weeks 3-13), and buy prandin 8 weeks (weeks 14-21) of titration to maximum dose. Changes in HbA1c and fasting plasma glucose (FPG) values were measured.

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Repaglinide (Prandin), NovoNorm, GlucoNorm, an oral insulin secretagogue, was the first meglitinide analogue to become available for use in patients with type 2 diabetes mellitus. The drug lowers postprandial glucose excursions by targeting early-phase insulin release, an effect thought to be important in reducing long-term cardiovascular complications of diabetes. Repaglinide provided similar overall glycaemic control to that achieved with glibenclamide (glyburide), as assessed by glycosylated haemoglobin (HbA(1c)) and fasting blood glucose levels, and was generally well tolerated in well designed clinical trials. Its rapid onset and relatively short duration of action allow for flexible meal schedules. Two modelled US cost-effectiveness analyses projected lifetime costs and outcomes for a hypothetical cohort of patients with type 2 diabetes. Both analyses projected long-term complications using data on HbA(1c) level changes from short-term clinical trials. Repaglinide plus rosiglitazone was dominant over rosiglitazone in one analysis, and repaglinide plus metformin was dominant over nateglinide plus metformin in the other. A similar Canadian analysis showed a favourable incremental cost-effectiveness ratio (buy prandin confirmation. The prevalence of diabetes mellitus is projected to increase to over 3% of the world's population ( approximate, equals 220 million people) by the year 2010. Globally, 97% of patients with diabetes have type 2 disease, although in industrialised countries the proportion of type 2 disease is about 90%. In 2010, an estimated 14.85 million individuals in the US and 2.88 million in the UK will be diagnosed with type 2 diabetes. In addition, approximately one-third to one-half of individuals with diabetes are unaware that they have the disease, and are therefore undiagnosed. Diabetes is associated with significant morbidity, mortality and economic consequences. For the year 2002 in the US, direct medical costs associated with diabetes (type 1 and 2) were estimated at dollars US 91.8 billion (70% of total costs) and indirect costs at dollars US 39.8 billion (30%), for a total of dollars US 132 billion. Data from more than 7000 patients in eight European countries indicate tha the mean cost per patient with diabetes was dollars US 2928 annually (1999 values), and the proportion of total healthcare expenditure directed toward diabetes ranged from 1.6% to 6.6% depending on the country. Several analyses focusing specifically on type 2 disease showed, not surprisingly, that costs were higher among patients with diabetic complications than in those without complications. Repaglinide, a meglitinide analogue, is an oral insulin secretagogue that reduces postprandial glucose excursions by targeting postprandial insulin release. In clinical trials in patients with type 2 diabetes, repaglinide was usually administered at a dosage of 0.5-4 mg three times daily before meals as monotherapy or in combination with other agents. In placebo-controlled trials of up to 24 weeks' duration in patients with type 2 diabetes, repaglinide achieved statistically significant improvements in glycaemic control, as assessed by glycosylated haemoglobin (HbA(1c)), fasting blood glucose (FBG) and/or postprandial blood glucose (PPBG) levels compared with placebo. Preprandial administration of repaglinide achieved similar glycaemic control to glibenclamide (glyburide) 1.75-15 mg/day and better glycaemic control than glipizide 5-15 mg/day in 1-year, double-blind, randomised trials in patients with type 2 disease, the vast majority of whom had previously received oral antidiabetic therapy. Several randomised, open-label studies have evaluated repaglinide as part of combination therapy over 3-6 months in patients with type 2 diabetes who had inadequate glycaemic control with previous drug therapy. In general, results showed statistically significant improvements in glycaemic control when repaglinide was used in combination with metformin, various thiazolidinediones, or metformin plus bedtime insulin compared with monotherapy with either comparator drug in each study (or metformin plus bedtime insulin in one trial). Other studies in this patient population indicate that metformin plus repaglinide is associated with significantly better glycaemic control than metformin plus nateglinide 60-120 mg three times daily over 16 weeks, and similar glycaemic control to that achieved with metformin in combination with either glibenclamide or glimepiride for up to 1 year. Good glycaemic control has also been achieved with preprandial administration of repaglinide in flexible meal schedules. This was demonstrated in a placebo-controlled trial and in a large, prospective survey of patients receiving repaglinide in a clinical setting. The tolerability profile of repaglinide is characterised by adverse events of mild-to-moderate intensity similar to those associated with sulphonylureas. The most frequently reported adverse events with repaglinide include hypoglycaemia, upper respiratory infection, headache, other respiratory events, musculoskeletal events and gastrointestinal events. Severe episodes of hypoglycaemia are rare with repaglinide and occur approximately 2-2.5 times less frequently than with sulphonylureas. In addition, available data indicate that repaglinide may be less likely to increase bodyweight than various commonly used sulphonylurea agents. In general, repaglinide is also well tolerated when used as part of combination therapy. Repaglinide is metabolised by the cytochrome P450 (CYP) 3A4 enzyme system and therefore has the potential to interact with other CYP3A4 substrates when administered concurrently. A number of studies in healthy volunteers have shown no clinically significant pharmacokinetic drug interactions when repaglinide was administered concomitantly with digoxin, theophylline, warfarin, cimetidine, ketoconazole, rifampicin (rifampin), ethinylestradiol, simvastatin or nifedipine. However, a clinically significant increase in systemic exposure to repaglinide occurs when clarithromycin and repaglinide are administered concurrently, which may necessitate a reduction in repaglinide dosage. Moreover, a potentially hazardous interaction occurs when gemfibrozil (alone or with itraconazole) is used concomitantly with repaglinide. In view of the marked increase in systemic exposure to repaglinide, the combination of repaglinide and gemfibrozil should be avoided if possible. Pharmacoeconomic Analyses of RepaglinideTwo US cost analyses have been conducted with repaglinide in patients with type 2 diabetes (both published in full). One was a retrospective analysis of pharmacy and medical claims data from a large managed care organisation in which costs were adjusted for age, gender and comorbidities. Total adjusted (year 2000) cost per patient over a 9-month period was numerically lower for those treated with a combination of repaglinide plus metformin (dollars US 8924) than for patients who received metformin only (dollars US 9448), metformin plus glibenclamide (dollars US 9576) or repaglinide only (dollars US 11910), although there were no statistically significant differences between treatment groups. The other study, a literature-based decision-tree analysis, projected the proportion of patients achieving a target HbA(1c) level (<7%) and the associated direct medical costs over a 3-year period from the time of diagnosis. Among six different treatment regimens evaluated, costs ranged from dollars US 6106 with glipizide gastrointestinal therapeutic system (GITS) to dollars US 9298 with repaglinide monotherapy (2001/2002 values). Probabilistic sensitivity analysis indicated that first-line therapy with glipizide GITS or metformin would be associated with lower total medical costs than rosiglitazone or repaglinide monotherapy. Three cost-effectiveness analyses, all of which are modelled studies published as abstracts and/or posters, have been conducted with repaglinide in patients with type 2 diabetes. (ABSTRACT TRUNCATED)

prandin drug 2015-06-21

Both baseline HbA1c and the decrease of HbA1c were significantly higher in patients with E/K and K/K genotypes of the KCNJ11 E23K variant when compared with E/E homozygotes (P=0.0103 and 0.0221, respectively). The decrease in 2 h Seroquel Overdose Mg postprandial plasma glucose (2hPG) was significantly greater in E/K heterozygotes than E/E homozygotes (P=0.0367). There was a significant difference in the response rate to repaglinide treatment between the E and K alleles (68% vs 82%, P=0.0324). The changes in fasting insulin and the homeostasis model assessment of insulin resistance were significantly greater in patients with ABCC8 exon16-3 C/C versus the T/C and T/T genotypes (P=0.0372 and 0.0274, respectively).

prandin dose range 2017-12-16

The efficacy of repaglinide Tegretol Xr Generic and nateglinide in FBG, postprandial glucose excursion and early-phase insulin secretion is similar. But the effect of repaglinide 1.0 mg t.i.d. on HbA(1c) is stronger than that of nateglinide 90 mg t.i.d.. This trial had shown that nateglinide and repaglinide could comparably improve insulin sensitivity and beta-cell function.

prandin tabs 2015-11-05

Human oral therapeutic doses of ritonavir and repaglinide were extrapolated to rats based on the Nolvadex Cheap Uk body surface area. Ritonavir (20 mg/kg, p.o.), alone and along with repaglinide (0.5 mg/kg, p.o.), was given to normal, diabetic and hepatic impaired rats, and the PK/PD were studied.

prandin diabetes medication 2017-10-29

In addition to dietary and lifestyle changes, standing as the cornerstone of type 2 diabetes care, pharmacological treatments, whether as single or multidrug patterns, are often necessary for an efficient blood glucose control. Besides insulin, four different oral antidiabetic drug categories are available, each of them acting through different and potentially synergistic ways. Oral antidiabetic drugs include: 1) biguanides acting through the reduction of hepatic glucose production and are most efficient in obese patients; 2) alpha-glucosidase inhibitors delaying carbohydrate intestinal absorption; 3) thiazolidinediones or "glitazones", acting as insulin sensitizers; 4) insulin secretion enhancers, mainly including sulfonylureas, which increase insulin secretion and are being credited by a long clinical usage; these are now joined by the new generation of insulin secretion enhancers, led by repaglinide, which can mimic the physiological insulin secretion Sinequan Drug Test profile by a specific stimulatory effect on beta-cells characterized by its fast onset and short half-life. Obviously, the combination of these different antidiabetic drugs, by targetting different synergistic and additive pathways, can help to further improve blood glucose.

prandin medication 2017-06-18

The combination of gemfibrozil and itraconazole has only a limited influence on the pharmacokinetics of nateglinide. This is in marked contrast to the substantial effect of this combination on the pharmacokinetics of repaglinide. The findings suggest that in vivo gemfibrozil, probably due to Geodon Dosage its metabolites, is a much more potent inhibitor of CYP2C8 than of CYP2C9.

prandin dosing 2016-09-28

The marketed compound tablet of metformin hydrochloride (MH) and repaglinide (RG) exhibits perfect multidrug therapeutic effect of type 2 diabetes. However, due to the short half life of the drugs, the tablet has to be administered 2 to 3 times a day, causing inconvenience to patient and fluctuations of plasma concentration. Here, a sandwiched osmotic pump tablet was developed to deliver the two drugs simultaneously at zero-order rate, in which MH and RG were loaded in different layers separated by a push layer. The osmotic pump tablet was prepared by a combination of three tableting procedure and film coating method. The factors including type and amount of propellant, osmotic active agents, amount of porogenic agent, coating weight, orifice diameter were optimized. The pharmacokinetic study was performed in beagle dogs, and the drug concentration in plasma samples was assayed by HPLC-MS/MS method. Simultaneous, controlled release of MH Geodon Generic Wikipedia and RG in the first 12 and 8h was achieved from the optimized formulation. A significantly decreased Cmax, prolonged Tmax and satisfactory bioavailability of the osmotic pump tablet were obtained, and a good in vivo-in vitro correlation of the two drugs was also established. In summary, the sandwiched osmotic pump tablet released the MH and RG simultaneously at zero-order rate, and exhibited significant sustained release effect in vivo and good in vivo-in vitro correlation. The designed controlled release system for MH and RG proposed a promising replacement for the marked compound product in the therapy of type 2 diabetes.

prandin generic form 2015-10-23

During the cyclosporine phase, the mean peak repaglinide plasma concentration was 175% (range, 56%--365%; P=.013) and the total area under the plasma concentration-time curve [AUC0--infinity] was 244% (range, 119%--533%; P<.001) of that in the placebo phase. The amount of unchanged repaglinide and its metabolites M2 and M4 excreted in urine were raised 2.7--fold, 7.5--fold, and 5.0--fold, respectively, by cyclosporine (P<.001). The amount of M1 excreted in urine remained unchanged, but cyclosporine reduced the ratio of M1 to repaglinide by 62% (P<.001). Cyclosporine had no significant effect on the elimination half-life or renal clearance of repaglinide. Although the mean blood glucose-lowering effect of repaglinide was unaffected in this low-dose study with frequent carbohydrate intake, the subject with the greatest pharmacokinetic interaction had the greatest increase in blood glucose Glucovance Drug Study -lowering effect. The effect of cyclosporine on repaglinide AUC0-infinity was 42% lower in subjects with the SLCO1B1 521TC genotype than in subjects with the 521TT (reference) genotype (P=.047). In vitro, cyclosporine inhibited the formation of M1 (IC50 [concentration of inhibitor to cause 50% inhibition of original enzyme activity], 0.2 micromol/L) and M2 (IC50, 4.3 micromol/L) but had no effect on M4.

prandin tab 2mg 2017-04-10

To review the new treatment strategies for non-insulin-dependent Casodex Generic Brand diabetes mellitus (NIDDM).

prandin drug class 2016-12-17

Reduction of postprandial hyperglycemia Low Cost Viagra in type 2 diabetic patients is associated with CIMT regression.

prandin dose 2016-04-23

Tacrolimus caused islet cell necrosis, reduced insulin secretion, increased insulin resistance, and increased blood glucose in the model. The blood glucose levels increased in a time-dependent manner. Combination of glargine and repaglinide was Strattera Overdose effective and safe for Chinese patients with post liver transplant diabetes mellitus.