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Acarbose (Precose)

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Generic Precose is used for treating type 2 diabetes in adults whose diabetes cannot be managed with diet alone. Generic Precose may be used alone, in combination with other oral diabetes medicines, or with insulin.

Other names for this medication:
Acarbosa, Acarbosum, Asucrose, Byetta, Carbose, Decarbay, Deglu, Diabose, Dorobay, Glicobase, Glucar, Glucobay, Gluconase, Glucor, Glumida, Glynose, Incardel, Prandase, Sincrosa

Similar Products:
Glucophage, Actos, Avandia, Amaryl, Glucovance, Micronase, Glycomet


Also known as:  Precose.


Generic Precose is used for treating type 2 diabetes in adults whose diabetes cannot be managed with diet alone. Generic Precose may be used alone, in combination with other oral diabetes medicines, or with insulin.

Generic Precose is a glucosidase inhibitor. It works by slowing down the enzyme that turns carbohydrates into glucose; it decreases blood sugar levels following a meal.

Precose is also known as Acarbose, Glucobay, Glucor, Rebose.

Generic name of Generic Precose is Acarbose.

Brand name of Generic Precose is Precose.


Take Generic Precose by mouth with food.

If you also take charcoal or digestive enzyme preparations, do not take them within 2 to 4 hours before after taking Generic Precose.

Temporary insulin therapy may be necessary during stressful periods (such as fever, trauma, infection, or surgery).

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


If you overdose Generic Precose and you don't feel good you should visit your doctor or health care provider immediately.


Store at room temperature below 25 degrees C (77 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 Acarbose 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 Generic Precose if you are allergic to Generic Precose components.

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

Do not take Generic Precose if you have blockage of the stomach or intestine or are at risk for these problems.

Do not take Generic Precose if you have long-term (chronic) bowel inflammation, colon ulcers, or stomach or intestine problems that interfere with digestion or nutrient absorption.

Do not take Generic Precose if you have cirrhosis of the liver or unexplained abnormal liver function tests.

Do not take Generic Precose if you have diabetic ketoacidosis (high ketone levels) or severe kidney problems.

Try to be careful with Generic Precose if you are taking any prescription or nonprescription medicine, herbal preparation, or dietary supplement.

Try to be careful with Generic Precose if you have allergies to medicines, foods, or other substances

if you have stomach or intestinal problems, liver problems, or kidney problems.

Try to be careful with Generic Precose if you are taking anticoagulants (eg, warfarin) because the risk of their side effects, including bleeding, may be increased by Generic Precose; calcium channel blockers (eg, verapamil), corticosteroids (eg, prednisone), diuretics (eg, hydrochlorothiazide), estrogen, isoniazid, nicotinic acid, oral contraceptives (birth control pills), phenothiazines (eg, chlorpromazine), phenytoin, sympathomimetics (eg, pseudoephedrine), or thyroid hormone because they may increase or decrease Precose 's effectiveness; insulin or sulfonylureas (eg, glyburide) because the risk of their side effects may be increased by Generic Precose; digoxin because its effectiveness may be decreased by Generic Precose.

Avoid alcohol.

Do not stop taking Generic Precose suddenly.

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Interactions of wild-type and Trp120-->Phe glucoamylase with maltooligodextrin (Gx) substrates and the tight-binding inhibitor acarbose (A) were investigated here using stopped-flow fluorescence spectroscopy and steady-state kinetic measurements. All wild-type and Trp120-->Phe glucoamylase reactions followed the three-step model E + Gx(or A) (k1) <==> (k-1) EGx (or A) (k2) <==> (k-2) E*Gx(or A) (k3) --> E + P or E-A, previously shown to account for the glucoamylase-maltose system [Olsen, K., Svensson, B., & Christensen, U. (1992) Eur. J. Biochem. 209, 777-784]. K1 = k-1/k1, k2, and k-2, and the catalytic constant, k3, are determined. Binding of maltooligodextrins in the first reaction step is weak, with little difference between wild-type and Trp120-->Phe glucoamylase. The second step, involving a conformational change, in contrast, is strongly influenced by the mutation and by the substrate length. Here wild-type glucoamylase reacts faster and forms more stable intermediates the longer the substrate. In contrast, Trp120-->Phe reacts slower the longer the substrate. The effect of the mutation is thus smallest on maltose. The Trp120-->Phe substitution reduces the fluorescence signal only by 12-20%, indicating that other tryptophanyl residues are important in reporting the conformational change. Trp120 also strongly influences the actual catalytic step, since the mutation decreases the kc values 30-80-fold. Acarbose behaves similar to maltotetraose in the first and the second steps with wild-type but not the Trp120-->Phe glucoamylase. Also, a third step in the acarbose reaction which parallels the catalytic step is strongly affected by the mutation. The rate constant k3 increases 200-fold.

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This study assessed the effect of postprandial glucose reduction by acarbose on insulin sensitivity and biomarkers of systemic inflammation.

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We have established a new method for the enzymatic diagnosis of glycogen storage disease type II (Pompe disease or acid maltase deficiency) using mixed leukocytes. The method employs glycogen and 4-methylumbelliferyl-alpha-D-glucopyranoside (4MU-alphaGlc) as substrates for measuring the lysosomal acid alpha-glucosidase (acid alphaGlu) activity, and incorporates acarbose to eliminate the interference of unrelated alpha-glucosidases (predominantly maltase-glucoamylase). It is shown that 3.0 micromol/L acarbose completely inhibits the maltase-glucoamylase activity at pH 4.0, but the lysosomal acid alphaGlu activity by less than 5%. With this method, we determined the acid alphaGlu activity in mixed leukocytes from 25 patients with glycogen storage disease type II (2 infantile and 23 late-onset cases), one GAA2/GAA2 homozygote and 30 healthy subjects. In the assay with glycogen as substrate, the addition of acarbose created a clear separation between the patient and the control ranges. In the assay with 4MU-alphaGlc as substrate, the two ranges were fully separated but remained very close despite the use of acarbose. The separation of the patient and normal ranges was improved considerably by taking the ratio of acarbose-inhibited over uninhibited activity. A GAA2/GAA2 homozygote was correctly diagnosed with 4MU-alphaGlc but misdiagnosed as patient when glycogen was used as substrate. We conclude that the inclusion of 3.0 micromol/L acarbose in the assays with glycogen and 4MU-alphaGlc substrates at pH 4.0 allows for the specific measurement of lysosomal acid alphaGlu activity in mixed leukocytes, thus enabling a reliable diagnosis of glycogen storage disease type II in this specimen.

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Besides lifestyle, various pharmacological treatments have proven their efficacy to reduce the incidence of type 2 diabetes in high-risk individuals, especially in those with impaired glucose tolerance (IGT) and/or impaired fasting glucose (IFG). Major placebo-controlled clinical trials demonstrated favourable effects of various glucose-lowering drugs generally used for the treatment of type 2 diabetes, i.e. metformin, acarbose and thiazolidinediones (glitazones). These trials showed a lower rate of progression to overt diabetes and a higher regression rate to a normal glucose status with active treatment as compared to placebo after a follow up of several years. Ongoing trials should confirm such a favourable effect with those drugs and may demonstrate a similar protective effect with other pharmacological approaches such as glinides or even basal insulin regimen. However, the reported favourable effects were generally observed while the subjects were still on treatment, and partially vanished after a rather short period of wash-out of several weeks. Therefore, the distinction between a true preventing effect and simply a masking effect is difficult with glucose-lowering drugs. In addition, as type 2 diabetes is a progressive disease, it is still questionable whether the effect corresponds to a prevention effect or only to a postponing of the development of the disease. Owing to the pathophysiology of the disease, the only way to block the progression of type 2 diabetes is probably to avoid the progressive loss of beta-cell function and/or mass. Whatsoever, these data obtained in large clinical trials bring further argument to support early treatment of diabetes, even at a prediabetic state, in order to stop the vicious circle leading to an inevitable deterioration of glycaemia in predisposed subjects.

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Type 2 diabetes often has an insidious onset with hyperglycaemia being present for many years before diagnosis is made. It is a progressive disease, due in part to loss of beta-cell function, with the reduction in function probably commencing 10-12 years prior to diagnosis and being aggravated by increasing fasting plasma glucose levels. Earlier intervention in those at risk from type 2 diabetes, aimed at minimizing hyperglycaemia, may prevent or delay overt diabetes and the associated development of micro- and macrovascular disease. Six-year follow-up data from the UK Prospective Diabetes Study, confirm that sulphonylurea, metformin and insulin therapy can reduce hyperglycaemia in individuals with type 2 diabetes. Although none of these agents prevent the subsequent progressive increase in fasting glucose levels, preliminary results with acarbose show that fasting plasma glucose levels can be maintained over 1 year of therapy. Three large-scale studies are currently investigating whether treatment with acarbose at an earlier stage of the disease process, in subjects with varying degrees of glucose intolerance, may be beneficial in helping to prevent or delay the onset of diabetes.

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where to buy acarbose 2017-01-20

The three gliptins showed almost similar glycemic control and incidence of adverse events. However, for FBG control, saxagliptin demonstrated superiority to sitagliptin, while, inferiority to vildagliptin Buy Imdur 30 Mg .

buy acarbose tablets 2015-02-27

Diabetes mellitus type 2 develops worldwide in the dimensions of an epidemic disease. In order to reduce the personal burden of patients and the enormous costs for the health system, which are mainly due to diabetes complications, diabetes prevention is urgently needed. Regarding pathophysiology, type 2 diabetes develops on the basis of insulin resistance, together with increasing reduction of insulin secretion. This leads to postprandial blood glucose peaks (Impaired Glucose Tolerance, IGT), which furthermore increase insulin resistance (metabolic resistance) and decrease insulin secretion, finally resulting in manifestation of diabetes mellitus. Therefore it is a logical way of diabetes prevention, to treat postprandial blood glucose peaks in the early stadium of IGT. The STOP-NIDDM trial showed conclusively that acarbose reduces postprandial hyperglycemia and diabetes incidence for 36% in comparison to placebo in a group of IGT patients. At the same time the incidence of normal glucose tolerance increased significantly for 30%. The NNT ("number needed to treat") for acarbose to avoid one case of diabetes manifestation in patients Buy Domperidone Boots with IGT, is eleven patients in 3.3 years. The preventive effect of acarbose is independent of age, gender or weight of the patients. So acarbose has the potential to reduce postprandial hyperglycemia, which is the driving force for diabetes, and thus can prevent diabetes mellitus type 2.

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Acarbose could be used, either as an alternative or in addition to changes in lifestyle, to delay development of type 2 Rivastigmine Buy Online diabetes in patients with impaired glucose tolerance.

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Current study based on the synthesis of new thiazole derivatives via "one pot" multicomponent reaction, evaluation of their in vitro α-glucosidase inhibitory activities, and in silico studies. All synthetic compounds were fully characterized by (1)H Buy Clomid Discount NMR, (13)C NMR and EIMS. CHN analysis was also performed. These newly synthesized compounds showed activities in the range of IC50=9.06±0.10-82.50±1.70μM as compared to standard acarbose (IC50=38.25±0.12μM). It is worth mentioning that most of the compounds such as 1 (IC50=23.60±0.39μM), 2 (IC50=22.70±0.60μM), 3 (IC50=22.40±0.32μM), 4 (IC50=26.5±0.40μM), 6 (IC50=34.60±0.60μM), 7 (IC50=26.20±0.43μM), 8 (IC50=14.06±0.18μM), 9 (IC50=17.60±0.28μM), 10 (IC50=27.16±0.41μM), 11 (IC50=19.16±0.19μM), 12 (IC50=9.06±0.10μM), 13 (IC50=12.80±0.21μM), 14 (IC50=11.94±0.18μM), 15 (IC50=16.90±0.20μM), 16 (IC50=12.60±0.14μM), 17 (IC50=16.30±0.29μM), and 18 (IC50=32.60±0.61μM) exhibited potent inhibitory potential. Molecular docking study was performed in order to understand the molecular interactions between the molecule and enzyme. Newly identified α-glucosidase inhibitors except few were found to be completely non-toxic.

buy acarbose 2017-09-18

354 patients with non-insulin-dependent diabetes mellitus were recruited; 77 were being treated with diet alone, 83 with diet and metformin, 103 with diet and sulfonylurea, and 91 with diet and insulin. Patients in each treatment group were randomly assigned to either acarbose or placebo for 1 year. Eighty-seven percent of patients receiving acarbose and 92% of those receiving placebo were Buy Brahmi Online India included in the efficacy analysis (n = 316).