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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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Male volunteers ( n=12) participated in a randomised, two-period, crossover trial evaluating the effect of multiple doses of 600 mg rifampicin once daily for 7 days on repaglinide metabolism. Subjects were, after baseline measurements of repaglinide pharmacokinetics, randomised to receive, on either day 7 or day 8 of the rifampicin administration period, a single dose of 4 mg repaglinide and vice versa in the following period.

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Two new sulfonylureas being investigated are repaglinide, which has a rapid onset of action, rapid reversal, and potential usefulness as a preprandial treatment of NIDDM, and glimepiride, the most potent sulfonylurea on a weight basis with an efficacy similar to that for glyburide. Metformin, an orally administered biguanide hypoglycemic agent, decreases blood glucose levels by 50 to 100 mg/dL and consistently improves triglyceride levels. Another agent for NIDDM therapy is acarbose, an a-glucosidase inhibitor. This agent avidly binds to intestinal disaccharidases and limits the postprandial increase in blood glucose. Troglitazone, a member of the thiazolidinedione class of insulin sensitizers, enhances insulin action and lowers blood glucose and blood pressure levels. In overweight patients with diabetes, fenfluramine has been the most effective centrally acting weight reduction agent.

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Patients with diabetes are at risk of early renal function decline. Therefore, kidney function needs monitoring at least once per year. Once the glomerular filtration rate (GFR) is less than 60 ml/min, the pharmacokinetics of antidiabetic drugs may be altered. Sulfonylurea and glinide therapies are associated with a risk of hypoglycaemia which is increased in the presence of renal impairment. Most sulfonylureas must be discontinued once GFR is <60 ml/min. Some glinides may be continued beyond this threshold, in particular repaglinide, which may be used in dialysis patients. In the absence of comorbidities, metformin can be continued at lower doses until a GFR of 45 ml/min, but must be withdrawn in case of dehydration or during the administration of a nephrotoxic drug including dye for radiological investigations. Glitazones may worsen water and sodium retention in patients with renal impairment. The pharmacokinetics of all DPP-IV inhibitors except linagliptin are altered with impaired renal function. Only sitagliptin, saxagliptin and linagliptin may be used in advanced kidney disease, but experience is as yet very limited. GLP-1 agonists are contraindicated in moderate to advanced kidney disease.

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Short-term costs required to provide comprehensive diabetes care and achieve glycemic goals can be substantial. The model suggests a sulphonylurea strategy may provide similar effectiveness with cost savings over other agents and should be considered when selecting an initial drug therapy in newly diagnosed patients with type 2 diabetes mellitus.

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In this single-centre, open-label, phase-I trial, six healthy male volunteers received 2 mg of the prandial glucose regulator, repaglinide, four times daily for 13 days, 15 min before meals. On the morning of day 7, breakfast was omitted and the dose was given as an oral solution containing 2 mg of (14)C-repaglinide.

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The subject matter of this case report is "sudden deterioration" of glycemic control in a thus far well-complying patient with type 2 diabetes. It describes possible impacts of glucometer technical failure associated with other unfavorable circumstances. An error in displaying glycemia was discovered when analyzing data from glucometer in a computer using software (DIABASS PRO, Mediaspect GmbH, Konstanz, Germany) for data evaluation, and other possible complications (especially hypoglycemia episodes) resulting from inadequate treatment correction were thus prevented.

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Diabetic prevalence in nursing homes is high, and institutionalised patients are elderly, long-standing diabetics, with both macro- and microvascular complications, and have a significant level of mental and functional disabilities.

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Pharmacokinetic profiles of single- and multiple-dose regimens of repaglinide were evaluated in 12 elderly subjects with type 2 diabetes. On day 1, following a 10-hour fast, subjects received a single 2-mg dose of repaglinide. Starting on day 2 and continuing for 7 days, each subject received a 2-mg dose of repaglinide 15 minutes before each of the three main meals. On day 9, subjects received a single 2-mg dose of repaglinide. Pharmacokinetic profiles, including area under the curve (AUC), log(AUC), maximal concentration (Cmax), log(Cmax), time to maximal concentration (Tmax), and half-life (T(1/2)), were determined at completion of the single- and multiple-dose regimens (days 1 and 9, respectively). Trough repaglinide values were collected on days 2 through 7. The mean log(AUC) values after multiple dosing were significantly higher than the values obtained after a single dose. The mean values for log(Cmax), and Tmax were comparable after each dosing regimen. The T(1/2) of repaglinide after multiple dosing was 1.7 hours. The trough values for repaglinide were low. No hypoglycemic events were reported. The pharmacokinetic profiles of repaglinide after single- and multiple-dose regimens were similar, and repaglinide was well tolerated by elderly subjects with type 2 diabetes.

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Spectrofluorimetric and high-performance liquid chromatography methods for estimation of repaglinide were developed. These methods were validated for estimation of repaglinide in tablets as well as in receptor fluid obtained during in vitro permeation studies. Repaglinide was observed to exhibit emission and excitation wavelengths, respectively, at 379 nm and 282 nm with linearity in the concentration range of 5-80 µg/ml. High-performance liquid chromatography analysis of repaglinide yielded retention time of 6.14 min with linearity ranging from 0.1-1.2 µg/ml concentration. Spectrofluorimetric analysis of repaglinide in tablets yielded results comparable to high performance liquid chromatography.

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In all cystic fibrosis patients with an age of 10 years or older, an oral glucose tolerance test is recommended. The result of this test is classified according to the WHO cut off values. It is required to have two diabetes positive oral glucose tolerance tests for the diagnosis of diabetes mellitus.This study is a multi-national, multicentre, open labelled, randomized and prospective controlled parallel group's trial, with 24 months treatment.The primary objective of this trial is to compare the glycaemic control of oral therapy with Repaglinide with insulin injections in patients with cystic fibrosis related diabetes after 2 years of treatment.The trial should include 74 subjects showing cystic fibrosis related diabetes newly diagnosed by oral glucose tolerance test during annual screening for cystic fibrosis related diabetes.Patients are randomised by central fax randomisation.Primary endpoint is mean HbA1c after 24 months of treatment. Secondary endpoints are change in FEV1% predicted and change in BMI-Z-score.

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We conducted a meta-analysis to compare the efficacy and safety of repaglinide plus metformin with metformin alone on type 2 diabetes. Twenty-two studies were included in this meta-analysis. Results showed combination therapy was safe and could gain better outcomes in glycemic control. Well-designed studies are required to confirm this conclusion.

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Prandial glucose regulation has the potential for achieving good metabolic control with a low risk of hypoglycaemia and increased flexibility with regard to eating patterns. Comparative studies have suggested that the prandial glucose regulator repaglinide is at least equivalent to sulphonylureas in terms of efficacy, but incurs a lower risk of major hypoglycaemia. However, these trials employed fixed dosing and mealtime regimens, so repaglinide was not used as intended. This prospective investigation in a daily clinical setting aimed to assess the efficacy and tolerability profile of flexible prandial glucose regulation with repaglinide in Type 2 diabetes.

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This single-dose study found that the test and reference formulations of repaglinide met the regulatory criteria for bioequivalence in these fasting, healthy Chinese male volunteers. Both formulations appeared to be well tolerated. identifier: 2012L01684.

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The aim of this study was to evaluate the pharmacogenetic variability in the disposition of repaglinide in healthy Chinese subjects.

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To further explore the mechanism underlying the interaction between repaglinide and gemfibrozil, alone or in combination with itraconazole.

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The NCS (neuronal calcium sensor) proteins, including neurocalcins, recoverins and visinin-like proteins are members of a family of Ca2+-sensitive regulators, each with three Ca2+-binding EF-hand motifs. In plants, lily CCaMK [chimaeric Ca2+/CaM (calmodulin)-dependent protein kinase] and its PpCaMK ( Physcomitrella patens CCaMK) homologue are characterized by a visinin-like domain with three EF-hands. In the present study, in an effort to discover NCS antagonists, we screened a total of 43 compounds using Ca2+-dependent drug affinity chromatography and found that the insulinotropic agent repaglinide targets the NCS protein family. Repaglinide was found to bind to NCS proteins, but not to CaM or S100 proteins, in a Ca2+-dependent manner. Furthermore, the drug antagonized the inhibitory action of recoverin in a rhodopsin kinase assay with IC50 values of 400 microM. Moreover, repaglinide tightly bound to the visinin-like domain of CCaMK and PpCaMK in a Ca2+-dependent manner and antagonized the regulatory function of the domain with IC50 values of 55 and 4 microM for CCaMK and PpCaMK respectively. Although both repaglinide and a potent insulin secretagogue, namely glibenclamide, blocked K(ATP) channels with similar potency, glibenclamide had no antagonizing effect on the Ca2+-stimulated CCaMK and PpCaMK autophosphorylation, mediated by their visinin-like domain. In addition, a typical CaM antagonist, trifluoperazine, had no effect on the CCaMK and PpCaMK autophosphorylation. Repaglinide appears to be the first antagonist of NCS proteins and visinin-like domain-bearing enzymes. It may serve as a useful tool for evaluating the physiological functions of the NCS protein family. In addition, since repaglinide selectively targets NCS proteins among the EF-hand Ca2+-binding proteins, it is a potential lead compound for the development of more potent NCS antagonists.

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Type 2 diabetes mellitus is a chronic metabolic disorder that results from defects in both insulin secretion and insulin action. An elevated rate of basal hepatic glucose production in the presence of hyperinsulinemia is the primary cause of fasting hyperglycemia; after a meal, impaired suppression of hepatic glucose production by insulin and decreased insulin-mediated glucose uptake by muscle contribute almost equally to postprandial hyperglycemia. In the United States, five classes of oral agents, each of which works through a different mechanism of action, are currently available to improve glycemic control in patients with type 2 diabetes. The recently completed United Kingdom Prospective Diabetes Study (UKPDS) has shown that type 2 diabetes mellitus is a progressive disorder that can be treated initially with oral agent monotherapy but will eventually require the addition of other oral agents, and that in many patients, insulin therapy will be needed to achieve targeted glycemic levels. In the UKPDS, improved glycemic control, irrespective of the agent used (sulfonylureas, metformin, or insulin), decreased the incidence of microvascular complications (retinopathy, neuropathy, and nephropathy). This review examines the goals of antihyperglycemic therapy and reviews the mechanism of action, efficacy, nonglycemic benefits, cost, and safety profile of each of the five approved classes of oral agents. A rationale for the use of these oral agents as monotherapy, in combination with each other, and in combination with insulin is provided.

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Repaglinide is an antidiabetic drug metabolised by cytochrome P450 (CYP) 2C8 and CYP3A4 enzymes. To clarify the mechanisms of observed repaglinide drug interactions, we determined the contribution of the two enzymes to repaglinide metabolism at different substrate concentrations, and examined the effect of fibrates and rifampicin on CYP2C8, CYP3A4 and repaglinide metabolism in vitro. We studied repaglinide metabolism using pooled human liver microsomes, recombinant CYP2C8 and recombinant CYP3A4 enzymes. The effect of quercetin and itraconazole on repaglinide metabolism, and of gemfibrozil, bezafibrate, fenofibrate and rifampicin on CYP2C8 (paclitaxel 6alpha-hydroxylation) and CYP3A4 (midazolam 1-hydroxylation) activities and repaglinide metabolism were studied using human liver microsomes. At therapeutic repaglinide concentrations (<0.4 microM), CYP2C8 and CYP3A4 metabolised repaglinide at similar rates. Quercetin (25 microM) and itraconazole (3 microM) inhibited the metabolism of 0.2 microM repaglinide by 58% and 71%, and that of 2 microM repaglinide by 56% and 59%, respectively. The three fibrates inhibited CYP2C8 (Ki: bezafibrate 9.7 microM, gemfibrozil 30.4 microM and fenofibrate 92.6 microM) and repaglinide metabolism (IC50: bezafibrate 37.7 microM, gemfibrozil 111 microM and fenofibrate 164 microM), but had no effect on CYP3A4. Rifampicin inhibited CYP2C8 (Ki 30.2 microM), CYP3A4 (Ki 18.5 microM) and repaglinide metabolism (IC50 13.7 microM). In conclusion, both CYP2C8 and CYP3A4 are important in the metabolism of therapeutic concentrations of repaglinide in vitro, but their predicted contributions in vivo are highly dependent on the scaling factor used. Gemfibrozil is only a moderate inhibitor of CYP2C8 and does not inhibit CYP3A4; inhibition of CYP-enzymes by parent gemfibrozil alone does not explain its interaction with repaglinide in vivo. Rifampicin competitively inhibits both CYP2C8 and CYP3A4, which can counteract its inducing effect in humans.

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To test the possibility that a fast-onset promoting agent repaglinide may initiate prandial insulin secretion through the mechanism of cephalic-phase insulin release, we explored the expression and distribution character of sulfonylurea receptors in rat taste buds. Twenty male Wistar rats aged 10 weeks old were killed after general anesthesia. The circumvallate papillae, fungiform papillae and pancreas tissues were separately collected. Immunohistochemical staining was used to detect the expression and distribution of sulfonylurea receptor 1 (SUR1) or sulfonylurea receptor 2 (SUR2) in rat taste buds. Reverse transcriptase polymerase chain reaction (RT-PCR) was used to analyze the expression of SUR1 or SUR2 mRNA. The pancreatic tissues from the same rat were used as positive control. This is the first study to report that SUR1 is uniquely expressed in the taste buds of fungiform papillae of each rat tongue, while the expression of SUR1 or SUR2 was not detected in the taste buds of circumvallate papillae. SUR1 is selectively expressed in rat taste buds, and its distribution pattern may be functionally relevant, suggesting that the rapid insulin secretion-promoting effect of repaglinide may be exerted through the cephalic-phase secretion pathway mediated by taste buds.

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All components of the glucose triad (ie, FPG, HbA1c, and PPG) should be considered in the management of type 2 diabetes. Therapy targeted at PPG has been shown to improve glucose control and to reduce the progression of atherosclerosis and CV events; therefore, physicians should consider monitoring and targeting PPG, as well as HbA1c and FPG, in patients with type 2 diabetes.

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age, sex, prevalence of diabetes, duration of diabetes, complications, macrovascular complications, retinopathy, nephropathy, and neuropathy. Metabolic control: frequency of baseline blood glucose and HbA1c determinations. Metabolic complications suffered.

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The Cystic Fibrosis Foundation recommends both short-term and long-acting insulin therapy when cystic fibrosis-related diabetes has been diagnosed. Diagnosis is based on: an elevated fasting blood glucose level greater than 6.94 mmol/liter (125 mg/deciliter); or symptomatic diabetes for random glucose levels greater than 11.11 mmol/liter (200 mg/deciliter); or glycated hemoglobin levels of at least 6.5%.

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A combination therapy of metformin hydrochloride (MH) and repaglinide (RG) achieves a perfect glycemic control; however, the combination formulation of immediate release must be taken several times a day, compromising the therapeutic benefits and causing inconveniences to the patients. Herein, a bilayer matrix tablet that aimed at continuously releasing both MH and RG over time was developed, in which the two drugs were formulated into two separated layers. The tablets were prepared by wet granulation method, and the optimized formulation was obtained by evaluating the factors that affected the drug release. The bilayer tablets simultaneously released the two drugs over 12 h; and a better in vivo performance with a steady plasma concentration, markedly lower Cmax, prolonged Tmax, and perfect absorption was obtained. Summarily, the bilayer matrix tablets sustained both MH and RG release over time, thereby prolonging the actions for diabetic therapy and producing better health outcomes.

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Aim of this prospective study is to evaluate the effect of repaglinide t.i.d. (three times a day) plus single-dose insulin glargine regimen in low-risk type 2 diabetic patients during Ramadan fasting. Participants had been taking the regimen for at least 3 months. Patients with a history of diabetic coma, severe hypoglycemic crisis or repeating attacks of hypoglycemia were excluded. Hypoglycemic unawareness, kidney or liver disease or HbA1c over 8% were also accepted as exclusion criteria. Eleven patients who insisted on this worship and eight non-fasting cases were involved. All were told to make home-glucose-monitorisation weekly and report any hypoglycemic event throughout Ramadan. Fasting blood glucose (FBG), post-prandial blood glucose (PBG) and fructosamine levels, body weights and blood pressures were recorded just before and after Ramadan. Seven patients in each group concluded the follow-up. Any significant change was detected in the parameters in either groups (P>0.05). Glucose control remained unchanged; fructosamine 318.14+/-65.38 versus 317.28+/-52.80 mmol/L in fasting group, 290.71+/-38.48 versus 290+/-38.56 mmol/L in non-fasting group. None of them exhibited either a major or a minor hypoglycemic event. The results of this pilot study indicated that repaglinide t.i.d. plus single-dose insulin glargine regimen was safe for low-risk type 2 diabetic patients who insisted on fasting during Ramadan.

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Lipid changes as a result of improved glycaemic control are not uniform findings associated with anti-diabetic therapy. Only metformin, acarbose, voglibose, rosiglitazone and pioglitazone had significant effects on the lipid profile. These effects should be considered when selecting OAMs for patients with type 2 diabetes.

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Using stably transfected cell systems recombinantly expressing the uptake transporters OATP1B1, OATP1B3, OATP2B1, or OCT1, we analyzed whether the antidiabetic drugs repaglinide, rosiglitazone, or metformin influence the transport of substrates and drugs (for OATPs, sulfobromophthalein [BSP] and pravastatin; for OCT1, 1-methyl-4-phenylpyridinium [MPP(+)] and metformin).

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prandin tablets 2017-08-24

A new high-performance liquid chromatography method was developed and validated for the quantitation of gliclazide and repaglinide in pharmaceutical formulations. Determination was performed using a LiChroCART RP-18 column, a mobile phase containing acetonitrile-phosphate buffer (pH 2.1; 60 + 40, v/v), and ultraviolet (UV) detection at 225 nm. Repaglinide was used as an internal standard for gliclazide determination and gliclazide for repaglinide assay. The method was validated with respect to linearity, precision, robustness, ruggedness, accuracy, and specificity. The calibration graphs ranged from 0.015 to 0.09 mg/mL for gliclazide and 0.06 to 0.36 mg/mL for repaglinide. Intra- and interday relative standard deviation values for the standard buy prandin solutions were 0.70 and 1.01% for gliclazide and 0.78 and 0.93% for repaglinide, respectively. Total recoveries of gliclazide and repaglinide from the laboratory-prepared mixtures were 99.82 +/- 0.58 and 101.50 +/- 0.46% for gliclazide and repaglinide, respectively [mean +/- standard deviation (SD)]. In forced degradation studies, the effect of acid, base, oxidation, UV light, and temperature on both drugs was also investigated. Finally, the method was applied for the quality control of commercial gliclazide and repaglinide tablets. Total recovery was 100.40 +/- 0.35 and 104.46 +/- 0.23% for gliclazide and repaglinide, respectively (mean +/- SD).

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Several new pharmacological agents have recently been developed to optimise the management of type 2 (non-insulin-dependent) diabetes mellitus. The aim of this article is to briefly review the various therapeutic agents available for management of patients with type 2 diabetes mellitus and to suggest a potential approach to drug selection. There are three general therapeutic modalities relevant to diabetes care. The first modality is lifestyle adjustments aimed at improving endogenous insulin sensitivity or insulin effect. This can be achieved by increased physical activity and bodyweight reduction with diet and behavioural modification, and the use of pharmacological agents or surgery. This first modality is not discussed in depth in this article. The second modality involves increasing insulin availability by the administration of exogenous insulin, insulin analogues, sulphonylureas and the new insulin secretagogue, repaglinide. The most frequently encountered adverse effect of these agents is hypoglycaemia. Bodyweight gain can also be a concern, especially in patients who are obese. The association between hyperinsulinaemia and premature atherosclerosis is still a debatable question. The third modality consists of agents such as biguanides and thiazolidinediones which enhance insulin sensitivity, or agents that decrease insulin requirements like the alpha-glucosidase inhibitors. buy prandin Type 2 diabetes mellitus is a heterogeneous disease with multiple underlying pathophysiological processes. Therapy should be individualised based on the degree of hyperglycaemia, hyperinsulinaemia or insulin deficiency. In addition, several factors have to be considered when prescribing a specific therapeutic agent. These factors include efficacy, safety, affordability and ease of administration.

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A three-arm multicenter randomized trial compared 1 year of therapy with premeal insulin aspart, repaglinide, or oral placebo in subjects buy prandin with cystic fibrosis who had abnormal glucose tolerance.

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Metformin/repaglinid is an efficient and safe therapeutic regime in the treatment of the type 2 DM that ensure a better control of PBG levels ( buy prandin Tab. 4, Ref. 18).

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The objective of the study was to assess the efficacy and safety of repaglinide compared with placebo in the buy prandin treatment of patients with type 2 diabetes.

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Metformin has been used for the treatment of type 2 diabetes by suppressing hepatic gluconeogenesis. It has been shown that the subclinical inflammatory responses play important roles in the pathogenesis of type 2 diabetes. In the present study, we determined the effects of metformin on the levels of pro-inflammatory cytokines (i.e., IL-6, TNF-α, and buy prandin MCP-1) and anti-inflammatory mediator IL-10 in blood and urine of patients with type 2 diabetes. There were 210 patients with type 2 diabetes, which were randomized into metformin (n = 112) and non-metformin (gliclazide, acarbose, and repaglinide, n = 98) groups. The levels of cytokines were measured by the ELISA.

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Repaglinide is a novel insulin secretagogue developed in response to the need buy prandin for a fast-acting, oral prandial glucose regulator for the treatment of type 2 (non-insulin-dependent) diabetes mellitus. Repaglinide is metabolized mainly in the liver; its pharmacokinetics may therefore be altered by hepatic dysfunction. This open, parallel-group study compared the pharmacokinetics and tolerability of a single 4 mg dose of repaglinide in healthy subjects (n = 12) and patients with chronic liver disease (CLD) (n = 12). Values for AUC and Cmax were significantly higher in CLD patients compared with healthy subjects, and the MRT was prolonged in CLD patients. Values for tmax did not differ between the groups, but t1/2 was significantly prolonged in CLD patients compared with previously determined values in healthy subjects. AUC was inversely correlated with caffeine clearance in CLD patients but not in healthy subjects. Blood glucose profiles were similar in both groups. Adverse events (principally hypoglycemia) were similar in the two groups; none was serious. Repaglinide clearance is significantly reduced in patients with hepatic impairment; the agent should be used with caution in this group.

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The study comprised three screening visits, followed buy prandin 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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Fifteen trials involving 3781 participants were included. No studies reported the buy prandin effect of meglitinides on mortality or morbidity. In the eleven studies comparing meglitinides to placebo, both repaglinide and nateglinide resulted in a reductions in glycosylated haemoglobin (0.1% to 2.1% reduction in HbA1c for repaglinide; 0.2% to 0.6% for nateglinide). Only two trials compared repaglinide to nateglinide (342 participants), with greater reduction in glycosylated haemoglobin in those receiving repaglinide. Repaglinide (248 participants in three trials) had a similar degree of effect in reducing glycosylated haemoglobin as metformin. Nateglinide had a similar or slightly less marked effect on glycosylated haemoglobin than metformin (one study, 355 participants). Weight gain was generally greater in those treated with meglitinides compared with metformin (up to three kg in three months). Diarrhoea occurred less frequently and hypoglycaemia occurred more frequently but rarely severely enough as to require assistance.

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Brachial artery endothelial buy prandin function was not influenced by short-term improvements in glycaemic control. The CONTROL DM group was successful in lowering A1C. Future research should explore more intensive and longer-lasting improvements in glycaemic control on endothelial function. Some data previously published in abstract form (Diabetes 2001; 50 (Suppl. 2): A217).

prandin generic 2016-10-08

Post-transplant diabetes mellitus is a frequent complication of solid organ transplantation that generally requires treatment with lifestyle interventions and antidiabetic medication. A number of demonstrated and potential pharmacokinetic drug-drug interactions (DDIs) exist between commonly used immunosuppressants and antidiabetic drugs, which are comprehensively summarized in this review. Cyclosporine (CsA) itself inhibits the cytochrome P450 (CYP) 3A4 enzyme and a variety of drug transporters. As a result, it increases exposure to repaglinide and sitagliptin, will likely increase the exposure to nateglinide, glyburide, saxagliptin, vildagliptin and alogliptin, and could theoretically increase the exposure to gliquidone and several sodium-glucose transporter (SGLT)-2 inhibitors. Currently available data, although limited, suggest that these increases are modest and, particularly with regard to gliptins and SGLT-2 inhibitors, unlikely to result in hypoglycemia. The interaction with repaglinide is more pronounced but does not preclude concomitant use if repaglinide dose buy prandin is gradually titrated. Mycophenolate mofetil and azathioprine do not engage in DDIs with any antidiabetic drug. Although calcineurin inhibitors (CNIs) and mammalian target of rapamycin inhibitors (mTORi) are intrinsically prone to DDIs, their disposition is not influenced by metformin, pioglitazone, sulfonylureas (except possibly glyburide) or insulin. An effect of gliptins on the disposition of CNIs and mTORi is unlikely, but has not been definitively ruled out. Based on their disposition profiles, glyburide and canagliflozin could affect CNI and mTORi disposition although this requires further study. Finally, delayed gastric emptying as a result of glucagon-like peptide-1 agonists seems to have a limited, but not necessarily negligible effect on CNI disposition.

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The pharmacokinetics of repaglinide in subjects carrying the CYP2C8*3 mutant allele did not differ significantly from those in the wild-types. Grapefruit juice increased the bioavailability of repaglinide, suggesting significant intestinal elimination of the drug which was assumed to be primarily mediated buy prandin by CYP3A4 in the gut.

prandin generic price 2015-04-29

Repaglinide showed a strong inhibitory effect on the metabolism of pioglitazone in vitro (Ki  = 0.0757 µm), [I]/Ki  > 0.1. The Simcyp® prediction ratios of AUC and Cmax between the two treatment groups were both about 1.01. The pharmacokinetics of pioglitazone in clinical trials showed no significant difference between these two treatment groups (p > 0.05). buy prandin

prandin drug 2017-10-04

A single dose of repaglinide (0.5-4.0 mg) before breakfast improves insulin secretion and reduces prandial hyperglycemia dose-dependently Administration of repaglinide had no effect on insulin secretion with the second meal, which was consumed buy prandin 4 h after breakfast.

dose of prandin 2017-06-06

Drug consumption Naprosyn Child Dose data should be calculated with the latest DDD value in the time window. The policy of the World Health Organisation to keep changes to the system of DDD to a minimum should be continued.

prandin dose 2016-12-21

To compare the efficacy, safety and compliance of repaglinide Protonix Dosage Form , administered either two or three times daily, regarding glycaemic control in patients with type 2 diabetes mellitus.

prandin similar drugs 2017-09-30

A CGMS was inserted in 14 type 2 diabetic patients on combined oral and insulin therapy at altogether 15 occasions. During Diovan Generic Equivalent the second (48 hours) and third (72 hours) night of registration each subject was observed and plasma glucose was analysed seven times during the night by venous sampling and compared to CGMS. These venous values were not used for calibration of the sensor. Pairs of data were analysed using correlation coefficient, Bland-Altman graphs and Clarke Error Grid analysis.

prandin e gel 2017-09-19

Nateglinide is Combivir Dosage Children similar to repaglinide, but has a quicker onset of action, quicker reversal, and does not usually require dosage titration. Based on the pharmacodynamics of nateglinide and repaglinide, nateglinide produces a more rapid postprandial increase in insulin secretion, and its duration of response is shorter than that of repaglinide. The risk of postabsorptive hypoglycemia should be lower than with either sulfonylureas or repaglinide.

prandin online 2015-06-26

The allele frequencies of CYP2C8*1, *2, *3, *4 and *5 were 95.04, 0.40, 0.40, 0 Cymbalta Depression Dosage and 4.13%, respectively. The frequencies of the CYP3A4*1, *4, *5 and *18 alleles were 97.93, 0, 0 and 2.07%, respectively. CYP2C8 and CYP3A4 genotypes were not significantly associated with repaglinide's blood glucose-lowering effect. However, the CYP3A4 genotype significantly influenced some of repaglinide's pharmacokinetics, where the mean elimination rate constant was 44.0% lower (p = 0.04) and the mean half-life was 33.8% higher (p = 0.04) in subjects with the CYP3A4*1/*18 genotype as compared to those with the normal CYP3A4*1/*1 genotype. This result confirms that CYP3A4 plays a large role in metabolizing repaglinide.

prandin tab 2mg 2017-08-17

Detection and confirmation of the 10 anti-diabetic drugs at 10 ng/mL each in equine plasma and equine urine were achieved by full-scan Epivir Dosing Hemodialysis MS-MS. All of these drugs were detected consistently at this concentration in spiked samples of different plasma and urine (n = 15 each). No significant matrix interferences were observed at the expected retention times of the targeted ions in blank urine samples (n = 30). This method has been used successfully in the analysis of drug-administration samples as well as official racing samples.

buy prandin 2015-05-26

The non-sulphonylurea hypoglycaemic agent repaglinide is about one order of magnitude less potent, in terms of insulinotropic efficiency, than S3075, another meglitinide analogue. In the present study, the effects of these two drugs upon 86Rb outflow, 45Ca efflux and insulin release from prelabelled rat pancreatic islets were investigated in a perifusion system. At a concentration of 10 microM, which is sufficient to evoke a maximal secretory response in incubated islets, both agents inhibited 86Rb efflux from islets perifused in the absence of D-glucose, and stimulated both 45Ca efflux and insulin release from islets perifused in the presence of 6 mM D-glucose. The stimulation of 45Ca efflux from prelabelled islets was suppressed in the absence of extracellular Ca2+. The cationic and secretory Starlix Brand Name response to repaglinide differed, however, from that evoked by S3075, in persisting for at least 20 min after removal of the drug from the perifusion medium, whilst the changes in 86Rb outflow, 45Ca efflux and insulin release caused by S3075 were rapidly reversible. These findings indicate that there is no parallel between the insulinotropic efficiency of distinct meglitinide analogues, and the reversibility of their functional effects. Since a comparable dissociation was recently documented in the case of hypoglycaemic sulphonylureas, the present observations reinforce the view that distinct molecular determinants may rule the relative insulinotropic potency of sulphonylureas and structurally related meglitinide analogues, on one hand, and the reversibility of their biological action, on the other hand.

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To review the drug treatments and some of the popular, nontraditional remedies now available for type 2 diabetes mellitus, as well Viagra User Reviews as selected investigational agents; to describe each medication's place in the overall approach to treatment.

prandin diabetes medication 2016-03-04

These findings document the Lopressor Dosing Iv wide variation in utilization patterns associated with pharmacological management of type 2 diabetes, suggesting that opportunity exists to optimize its pharmacological management.

prandin diabetes medicine 2016-03-29

Drug-drug interactions with insulin secretagogues are associated with increased risk of serious hypoglycemia in patients with type 2 diabetes. We aimed to systematically screen for drugs that interact with the five most commonly used secretagogues-glipizide, glyburide, glimepiride, repaglinide, and nateglinide-to cause serious hypoglycemia.

prandin diabetes drug 2017-05-23

Repaglinide is a novel insulin secretagogue that was developed as a prandial glucose regulator for the treatment of people with Type 2 diabetes mellitus. It is used flexibly, taken prior to meals, in order to limit subsequent postprandial blood glucose excursions as well as the dependent basal blood glucose concentration. In theory, the pharmacological profile of repaglinide is well suited for this role. Taken at mealtimes, its relatively rapid-onset and short-duration of action counteract a fundamental pathophysiological aspect of this disease: attenuation of the prandial insulin response. The predominantly hepatic elimination profile and a lack of drug-drug interactions with repaglinide are also properties well suited for patients with Type 2 diabetes. Importantly, the pharmacokinetic properties of repaglinide, are expected to reduce the risk of hypoglycaemia in comparison to the conventional insulin secretagogues (sulphonylureas). A reduced risk of hypoglycaemia carries the advantage that patients are not obliged to consume meals at regular intervals supplemented by snacks, so caloric restriction is feasible and lifestyle not compromised. These theoretical advantages have now been largely borne-out by clinical studies and empirical experience. Placebo-controlled studies have consistently demonstrated the antidiabetic efficacy of repaglinide, with improvements having been shown in all indicators of glycaemic control. Double-blind, active-comparator studies have shown repaglinide to have an antidiabetic efficacy that is at least equivalent to sulphonylureas, even when food intake and dosing intervals were controlled according to the requirements of sulphonylureas. Pooled data from these studies have shown that the risk of severe hypoglycaemia is reduced by 60% (p = 0.03) when repaglinide is used in preference to sulphonylureas. There is also evidence that the blood glucose threshold at which symptoms of hypoglycaemia are perceived by patients may be better preserved during treatment with repaglinide than with sulphonylureas. Studies examining flexible prandial dosing with repaglinide have shown that good glycaemic control and a low risk of hypoglycaemia are achievable goals that are independent of the meal (and, hence, dosing) pattern chosen by the patient. Furthermore, when used in this way, repaglinide has not been associated with weight gain. In combination therapy, repaglinide has been shown to act in synergy with both metformin and troglitazone. The possibility of a 'new' basal-bolus regimen combining repaglinide and exogenous (neutral protamine hagedorn) NPH insulin strategy has also been investigated.

prandin tablets generic 2017-06-02

This analysis shows that the frequency of reported hypoglycaemia within the study cohorts was relatively low. The rates of hypoglycaemia were not equal between drug classes. Treatment with nateglinide or repaglinide was characterized by a higher incidence of hypoglycaemia at the beginning of treatment. Further investigation is necessary to assess whether women treated with TZDs are more prone to hypoglycaemia than men. Findings from this study should be taken into account with other clinical and pharmacoepidemiological studies.