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Glucotrol (Glipizide)

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Glucotrol is a medication consists in a class of drugs called sulfonylureas. Glucotrol is used to treat type 2 diabetes. Glucotrol may be used along with diet, exercise and insulin therapy. Glucotrol works by controlling blood sugar levels in your organism.

Other names for this medication:
Actine, Antidiab, Beapizide, Diactin, Diasef, Dipazide, Euglizip, Gabaz, Glibenese, Glide, Glidiab, Glimerol, Glipicontin, Glipizid, Glipizida, Glipizidum, Glipom, Gluco-rite, Glucolip, Glucopress, Glucotrol, Glutrol, Glynase, Glyzip, Luditec, Melizid, Melizide, Mindiab, Minodiab, Ozidia, Singloben, Sucrazide, Xiprine, Zitrol xr

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Also known as:  Glipizide.


Glucotrol is a medication consists in a class of drugs called sulfonylureas.

Glucotrol is used to treat type 2 diabetes. Glucotrol may be used along with diet, exercise and insulin therapy.

Glucotrol is also known as Glipizide, Glytop SR.

Glucotrol works by controlling blood sugar levels in your organism.

Generic name of Glucotrol is Glipizide.

Brand names of Glucotrol are Glucotrol, Glucotrol XL.


Take Glucotrol orally.

Do not chew, divide or crush the tablet. Swallow it whole.

Glucotrol is usually taken before breakfast if it is taken once a day, or before meals if it is taken several times each day.

Take each dose of Glucotrol with a full glass of water.

The dosage and the kind of tablets depend on the disease and its prescribed treatment.

While taking Glucotrol follow diet, medication and exercise routines closely.

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


If you overdose Glucotrol and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Glucotrol overdosage: hunger, nausea, anxiety, cold sweats, weakness, drowsiness, unconsciousness, coma.


Store at room temperature below 30 degrees C (86 degrees F) away from moisture and heat. 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 Glucotrol 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 Glucotrol if you are allergic to Glucotrol components.

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

Be careful with Glucotrol if you have kidney disease, liver disease, thyroid disease, type 1 diabetes, serious infection, illness, or injury.

Be careful with Glucotrol if you take aspirin or another salicylate such as magnesium/choline salicylate (Trilisate), salsalate (Disalcid, others), choline salicylate (Arthropan), magnesium salicylate (Magan) or bismuth subsalicylate (Pepto-Bismol); nonsteroidal anti-inflammatory drug (NSAID) such as ibuprofen (Motrin, Advil, Nuprin, others), ketoprofen (Orudis, Orudis KT, Oruvail), diclofenac (Voltaren, Cataflam), etodolac (Lodine), indomethacin (Indocin), nabumetone (Relafen), oxaprozin (Daypro), naproxen (Anaprox, Naprosyn, Aleve) and others; sulfa-based drug such as sulfamethoxazole-trimethoprim (Bactrim, Septra), sulfisoxazole (Gantrisin), or sulfasalazine (Azulfidine); monoamine oxidase inhibitor (MAOI) such as isocarboxazid (Marplan), tranylcypromine (Parnate) or phenelzine (Nardil); beta-blocker such as propranolol (Inderal), atenolol (Tenormin), acebutolol (Sectral), metoprolol (Lopressor) and others; diuretic (water pill) such as hydrochlorothiazide (HCTZ, Hydrodiuril), chlorothiazide (Diuril) and others; steroid medicine such as prednisone (Deltasone, Orasone, others), methylprednisolone (Medrol, others), prednisolone (Prelone, Pediapred, others) and others; phenothiazine such as chlorpromazine (Thorazine), fluphenazine (Prolixin, Permitil), prochlorperazine (Compazine), promethazine (Phenergan) and others; phenytoin (Dilantin); isoniazid (Nydrazid); prescription, over-the-counter, or herbal cough, cold, allergy or weight loss medications.

Avoid alcohol.

Do not stop taking Glucotrol suddenly.

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To determine the pharmacokinetics and pharmacodynamics of glipizide after a single dose and 12 weeks of dosing in patients with type II diabetes mellitus, and evaluate the influence of aging.

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Insulin action was assessed by measuring insulin-mediated glucose disposal (KI) in 13 non-ketotic diabetic patients both before treatment and after normalization of plasma glucose by diet (5 patients) or sulfonylurea (glipizide) therapy (8 patients). While the KI of the diet-treated group was unchanged by therapy, that of the glipizide-treated group was significantly increased. The data show that chronic glipizide therapy is associated with a potentiation of insulin action, which may account for the major anti-diabetic effect of this drug.

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In this study, the amorphization of glipizide was systematically investigated through high-energy ball milling at different temperatures. The results of solid-state amorphization through milling indicated that glipizide underwent direct crystal-to-glass transformation at 15 and 25°C and crystal-to-glass-to-crystal conversion at 35°C; hence, milling time and temperature had significant effects on the amorphization of glipizide, which should be effectively controlled to obtain totally amorphous glipizide. Solid forms of glipizide were detailedly characterized through analyses of X-ray powder diffraction, morphology, thermal curves, vibrational spectra, and solid-state nuclear magnetic resonance. The physical stability of solid forms was investigated under different levels of relative humidity (RH) at 25°C. Forms I and III are kinetically stable and do not form any new solid-state forms at various RH levels. By contrast, Form II is kinetically unstable, undergoing direct glass-to-crystal transformation when RH levels higher than 32.8%. Therefore, stability investigation indicated that Form II should be stored under relatively dry conditions to prevent rapid crystallization. High temperatures can also induce the solid-state transformation of Form II; the conversion rate increased with increasing temperature.

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Onychomycosis and dermatomycoses can result in serious complications in patients with underlying chronic diseases such as diabetes. To avoid these complications, these dermatological disorders need to be treated efficiently, for example with the triazole antifungal itraconazole. Itraconazole can inhibit the metabolism of drugs by CYP 3A4 and therefore might affect the efficacy of antidiabetic agents.

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CYP2C9 polymorphisms leading to decreased enzyme activity show a modest impact on the risk of mild hypoglycaemia attacks during oral antidiabetic treatment, with a significant association in patients treated with gliclazide.

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To examine whether hyperglycaemia impairs the absorption of sulphonylurea agents, glipizide, which is rapidly and completely absorbed, was measured in plasma from 12 healthy young subjects during various levels of experimentally-induced hyperglycaemia. An increase in the plasma glucose concentration above 7 mmol/l was associated with a dose-dependent delay in the absorption of glipizide; at a concentration above 11 mmol/l, the plasma glipizide concentration was reduced by 50%. The data indicate that hyperglycaemia may delay the absorption of sulphonylurea agents, probably because it impairs gastric motility and/or gastric emptying. This delay of absorption may be clinically relevant, since the efficacy of short-acting sulphonylureas is dependent upon the absorption rate of the drug.

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Ezetimibe is the first lipid-lowering drug that inhibits intestinal uptake of dietary and biliary cholesterol without affecting the absorption of fat-soluble nutrients. Following oral administration, ezetimibe is rapidly absorbed and extensively metabolised (>80%) to the pharmacologically active ezetimibe-glucuronide. Total ezetimibe (sum of 'parent' ezetimibe plus ezetimibe-glucuronide) concentrations reach a maximum 1-2 hours post-administration, followed by enterohepatic recycling and slow elimination. The estimated terminal half-life of ezetimibe and ezetimibe-glucuronide is approximately 22 hours. Consistent with the elimination half-life of ezetimibe, an approximate 2-fold accumulation is observed upon repeated once-daily administration. The recommended dose of ezetimibe 10 mg/day can be administered in the morning or evening without regard to food. There are no clinically significant effects of age, sex or race on ezetimibe pharmacokinetics and no dosage adjustment is necessary in patients with mild hepatic impairment or mild-to-severe renal insufficiency. The major metabolic pathway for ezetimibe consists of glucuronidation of the 4-hydroxyphenyl group by uridine 5'-diphosphate-glucuronosyltransferase isoenzymes to form ezetimibe-glucuronide in the intestine and liver. Approximately 78% of the dose is excreted in the faeces predominantly as ezetimibe, with the balance found in the urine mainly as ezetimibe-glucuronide. Overall, ezetimibe has a favourable drug-drug interaction profile, as evidenced by the lack of clinically relevant interactions between ezetimibe and a variety of drugs commonly used in patients with hypercholesterolaemia. Ezetimibe does not have significant effects on plasma levels of HMG-CoA reductase inhibitors commonly known as statins (atorvastatin, fluvastatin, lovastatin, pitavastatin, pravastatin, rosuvastatin, simvastatin), fibric acid derivatives (gemfibrozil, fenofibrate), digoxin, glipizide, warfarin and triphasic oral contraceptives (ethinylestradiol and levonorgestrel). Concomitant administration of food, antacids, cimetidine or statins had no significant effect on ezetimibe bioavailability. Although coadministration with gemfibrozil and fenofibrate increased the bioavailability of ezetimibe, the clinical significance is thought to be minor considering the relatively flat dose-response curve of ezetimibe and the lack of dose-related increase in adverse events. In contrast, coadministration with the bile acid binding agent colestyramine significantly decreased ezetimibe oral bioavailability (based on area under the plasma concentration-time curve of total ezetimibe). Hence, ezetimibe and colestyramine should be administered several hours apart to avoid attenuating the efficacy of ezetimibe. Finally, higher ezetimibe exposures were observed in patients receiving concomitant ciclosporin, and ezetimibe caused a small but statistically significant effect on plasma levels of ciclosporin. Because treatment experience in patients receiving ciclosporin is limited, physicians are advised to exercise caution when initiating ezetimibe in the setting of ciclosporin coadministration, and to carefully monitor ciclosporin levels.

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Dapagliflozin 10-mg efficacy data from (i) two short-term, active-comparator studies (vs. metformin-XR over 24 weeks and vs. glipizide over 52 weeks), (ii) pooled 24-week analyses of five placebo-controlled trials (as monotherapy or add-on therapy), and (iii) long-term studies over 2 years; dapagliflozin 5- and 10-mg pooled safety data from 12 placebo-controlled trials; and cardiovascular safety and malignancy data from 19 dapagliflozin studies were evaluated.

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In a perfused guinea-pig heart model of myocardial ischaemia, reducing coronary flow by 95% for four successive 6 min periods caused a reproducible net loss of K+ into the coronary perfusate. This was reduced in a concentration-dependent manner by ATP dependent K+ channel blockers (glibenclamide and glipizide) and calcium channel blockers (verapamil and nifedipine). Other K+ channel blockers (UK-66,914, 4-aminopyridine, R56865 and phentolamine) and beta 1-adrenoceptor and beta 2-adrenoceptor antagonists (betaxolol and ICI118551) did not reduce this loss significantly. A single 30 min low-flow period reliably induced K+ release and ventricular fibrillation in control hearts. Glibenclamide, glipizide and phentolamine suppressed ventricular fibrillation but not ischaemic K+ loss in this model. R56865 and 4-aminopyridine and coadministration of betaxolol and ICI118551 yielded similar results while UK-66,914 suppressed neither. In our model, modulation of ischemic K+ loss and suppression of ventricular fibrillation were not closely associated and appeared to occur via separate mechanisms.

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Glipizide was complexed with beta-cyclodextrin in an attempt to enhance the drug solubility. The phase solubility diagram was classified as A(L) type, which was characterized by an apparent 1:1 stability constant that had a value of 413.82 M(-1). Fourier transform infrared spectrophotometry, differential scanning calorimetry, powder x-ray diffractometry and proton nuclear magnetic resonance spectral analysis indicated considerable interaction between the drug and beta-cyclodextrin. A 2(3) factorial design was employed to prepare hydroxypropyl methylcellulose (HPMC) matrix tablets containing the drug or its complex. The effect of the total polymer loads (X1), levels of HPMC K100LV (X9), and complexation (X3) on release at first hour (Y1), 24 h (Y2), time taken for 50% release (Y3), and diffusion exponent (Y4) was systematically analyzed using the F test. Mathematical models containing only the significant terms (P < 0.05) were generated for each parameter by multiple linear regression analysis and analysis of variance. Complexation was found to exert a significant effect on Y1, Y2, and Y3, whereas total polymer loads significantly influenced all the responses. The models generated were validated by developing two new formulations with a combination of factors within the experimental domain. The experimental values of the response parameters were in close agreement with the predicted values, thereby proving-the validity of the generated mathematical models.

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Improved blood-glucose control decreases the progression of diabetic microvascular disease, but the effect on macrovascular complications is unknown. There is concern that sulphonylureas may increase cardiovascular mortality in patients with type 2 diabetes and that high insulin concentrations may enhance atheroma formation. We compared the effects of intensive blood-glucose control with either sulphonylurea or insulin and conventional treatment on the risk of microvascular and macrovascular complications in patients with type 2 diabetes in a randomised controlled trial.

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glucotrol drug class 2017-05-16

We predicted 34 pharmacokinetic drug-drug interactions with the secretagogues, nine moderate and 25 weak. There were 140 and 61 secretagogue-precipitant pairs associated with increased rates of Cymbalta Drug Trials serious hypoglycemia before and after the metformin adjustment, respectively. The results from pharmacokinetic prediction correlated poorly with those from pharmacoepidemiologic screening.

glucotrol medication 2017-04-09

To compare the efficacy, safety and tolerability of Adalat Xl Dose adding rosiglitazone (RSG) vs. sulphonylurea (SU) dose escalation in older type 2 diabetes mellitus (T2DM) patients inadequately controlled on SU therapy.

glucotrol 20 mg 2017-09-25

The objective of this study was to measure the serum insulin and C-peptide concentrations among diabetic patients known to be taking sulfonylurea agents who presented to the emergency department with hypoglycemia thought to be due to therapeutic usage as opposed to overdose. A recently published systematic review of 22 articles involving 76 patients with sulfonylurea-induced hypoglycemia (glucose <49 mg/dL) resulting from accidental ingestion or intentional overdose found that patients had Celexa Normal Dose an average serum insulin concentration of 3.9 μIU/mL or higher and an average serum C-peptide concentration of 1.4 ng/mL or higher.

glucotrol 50 mg 2016-03-07

There is significant variability in human placental transfer rates of the oral hypoglycemics, which strongly correlates with molecular properties. These data suggest Dosage Micardis Plus that less fetal exposure may occur with second-generation sulfonylureas and anticipate that regression models may be useful in selecting agents that minimize placental transport to the fetus.

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To evaluate the toxicity Chloromycetin Drug Interactions of oral sulfonylurea ingestion in children and the efficacy of treatments instituted in these cases.

glucotrol overdose 2015-08-06

The global heterozygous glucokinase (GK) knockout (gk(wt/del)) male mouse, fed on a high-fat (60% by energy) diet, has provided a robust and reproducible model of hyperglycaemia. This model could be highly relevant to some facets of human type 2 diabetes (T2D). We aimed to investigate the ability of standard therapeutic agents to lower blood glucose at translational doses, and to Cymbalta Overdose Emedicine explore the glucose-lowering potential of novel glucokinase activators (GKAs) in this model.

glucotrol diabetic pills 2016-06-04

Three studies were performed to assess the efficacy of various sulphonylureas in the management of diet-failed NIDDM patients. In the first study, 224 patients inadequately controlled by diet alone or with oral hypoglycaemics received gliclazide in addition to diet or in place of existing drugs for three months. The dosage was adjusted to obtain adequate control or up to the maximum recommended dosage. Good glycaemic control was achieved in 65% of patients. Conversion from other oral hypoglycaemics to gliclazide led to an improvement in control except in cases previously treated with glibenclamide. In the second study, diabetic control was compared in 112 NIDDM patients treated concurrently for one year with chlorpropamide, glipizide, gliquidone, glibenclamide or gliclazide. On the basis of HbA1 levels, the best results were obtained with glibenclamide and gliclazide, leading to normal HbA1 levels in 74% and 80% of patients, respectively. In the third study, secondary failure rates were assessed in 248 NIDDM patients treated for five years with gliclazide, glibenclamide or glipizide. Gliclazide had the lowest secondary failure rate (7%) and was significantly better than glipizide (25.6% failures in five years), but the difference relative to glibenclamide (17.9%) just failed to reach the threshold of significance. The results of these studies show that gliclazide is Motrin Infant Dosage a potent hypoglycaemic agent which compares favourably with others of its type. It has a low incidence of side effects, few problems with hypoglycaemia, and retains its efficacy longer than other sulphonylureas. Gliclazide may therefore be considered a first choice for the therapy of diet-failed NIDDM patients.

glucotrol max dose 2016-01-28

Insulin secretory physiology has been characterized in tumor cell lines derived by primary culture of insulinomas that developed in transgenic mice expressing the large T-antigen of SV40 in pancreatic islet beta-cells. Cells in one of these lines, beta TC-3, contain large amounts of insulin (3100 +/- 294 ng/100 micrograms cellular protein). Constitutive release of insulin over 2 h in static incubation was low at 31.9 ng/100 micrograms protein and was increased 2-fold by glucose (16.7 mM) and 8-fold by depolarizing concentrations of potassium (45 mM). Isobutylmethylxanthine (IBMX; 0.5 mM) and forskolin (5 and 50 microM), which elevated cellular levels of cAMP, were ineffective as secretagogues, but dramatically potentiated glucose and potassium effects on insulin release (6.5- and 4-fold, respectively). A variety of other known insulin secretagogues stimulated insulin release in a manner analogous to their effects in normal islets. The sulfonylurea glipizide (1 microM) and the tumor-promoting phorbol ester 12-O-tetradecanoylphorbol-13-acetate (1 microM) stimulated insulin release 3.4- and 13.7-fold, respectively. The cholinergic agonist carbachol (2 microM) was ineffective alone, but potentiated glucose-induced insulin release 2.8-fold. Comparable stimulation of insulin release by glucose (16.7 mM) Diabecon Dosage and glucose (16.7 mM) plus IBMX (0.5 mM) was noted with several other beta TC lines, which were derived independently from separate transgenic mice. Glucose- and glucose- plus IBMX (0.5 mM)-induced insulin release occurred progressively from 0.15-16.7 mM, indicating that insulin release from beta TC-3 cells occurred at much lower levels than that from normal islets. However, as in the normal islet, the glucose concentration dependency for insulin release was highly correlated (r = 0.93) with the glucose concentration dependency for glucose utilization (measured by 3H2O formation from [5-3H]glucose). This suggests that glucose induces insulin release from beta TC-3 cells by a mechanism similar to that in the normal islet. The high insulin content, the multifold stimulation of insulin release by a variety of secretagogues, their convenient propagation in culture, and the renewable source of these cell lines make the beta TC cells a convenient model for studies of beta-cell function.