Alpha-glucosidase (IC50 = 11 nM)

The effects of Acarbose (1, 2, and 3 μM) on TNF-α-induced VSMC migration and proliferation were dose- and time-dependent. Acarbose (1, 2 and 3 μM) dose-dependently decreased β-galactosidase and Ras expression while increasing p-AMPK expression in A7r5 cells that had been pretreated with TNF-α [2].

In diabetic rats, acarbose (300 mg/60 kg body weight) can lower fasting blood glucose and control glucose tolerance without causing weight loss. DM rats' blood levels of TNF-α and IL6 are dramatically inhibited by acarbose [1]. Neointimal IL-6, TNF-α, and iNOS staining intensity were considerably and dose-dependently reduced by acarbose (2.5 and 5.0 mg/kg), but neointimal p-AMPK staining intensity was dramatically raised. In HCD-fed rabbits with no weight loss, acarbose (2.5 and 5.0 mg/kg) substantially and dose-dependently decreased neointimal Ras and β-galactosidase expression [2].

The inhibitory effects of natural and synthetic inhibitors on the intestinal membrane-bound hydrolase, alpha-glucosidase (AGH), were evaluated by using an immobilized cyanogen bromide-activated Sepharose 4B support. Immobilized AGH (iAGH) inhibition study by synthetic inhibitors (acarbose and voglibose) revealed that the magnitude of inhibition differed from that in the free AGH (fAGH) study: IC50 value of acarbose in iAGH-maltase assay system, 340-430 nM; fAGH, 11 nM. iAGH-maltase inhibition by both inhibitors was influenced by blocking reagents with different functional groups (COOH, OH, CH3, and NH2 groups). On the other hand, significant iAGH-sucrase inhibitory activity was observed only when using the negatively charged support induced by 0.1 M beta-alanine. The Km values obtained in the iAGH assay system were similar to those from the fAGH method. With natural inhibitors, the iAGH-sucrase inhibitory activity of D-Xylose, with in vivo glucose suppression, increased twice compared to that in fAGH. Green tea extract gave almost the same inhibition for both AGH assay systems. [3]

Cell viability analysis [5]
Cell viability was determined using the 3-(4,5-dimethylthiazol-2-yl)-2,5- diphenyltetrazolium bromide (MTT) assay44. Cells were seeded in 24-well culture plates at a density of 2 × 104 cells/well, incubated for 48 h, treated with acarbose at varying concentrations (0.5, 1.0, 2.0, 3.0, and 5.0 μM) for 24 h; or pre-treated with TNF-α (20 ng/ml) for either 24 h or 48 h to evaluate the dose-dependent effects of acarbose on VSMC growth and viability, cultured with 0.5 mg/ml MTT at 37 °C in a humidified atmosphere of 5% CO2 for another 4 h, and solubilized with isopropanol. The viable cell number varied directly with the concentration of formazan product measured spectrophotometrically at 563 nm.

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Wound healing [5]
A7r5 cells were seeded at a density of 1 × 106 ml in 6-well culture plates and incubated for 48 h. A sterile 100-μl pipette tip was used to make a straight scratch in the cell monolayer in each well45. The non-adhering cells were washed out with PBS, and the remaining cells were treated with TNF-α (0, 10, 20, 50 and 100 ng/ml) at 37 °C in a humidified atmosphere of 5% CO2. Under a 40X lens, images of the linear wound (9 fields per well) were taken at 24 and 48 h. Migrated cells were counted per well and the counts were averaged.

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Western blot analysis [5]
Western blot analysis46 was used to assess the expressions and/or activities of these migration-related proteins and thereby the mechanisms underlying the anti-migratory effects of acarbose on VSMCs. Specific antibodies were used to evaluate the expressions of iNOS, Ras, p-AMPK, AMPKα1/2, and TNF-α and β-galactosidase. After pre-treatment with TNF-α (20 ng/ml) for 24 h, the cells were treated with acarbose (0, 1, 2, and 3 μM) for 24 h and lysed. Cell lysates (50 μg of protein) were separated by electrophoresis on 8–12% SDS polyacrylamide gels and transferred to nitrocellulose membranes. The membranes were incubated with Tris-buffered saline (TBS) containing 1% (w/v) nonfat-milk and 0.1% (v/v) Tween-20 (TBST) for 1 h to block non-specific binding, washed with TBST for 30 min, incubated with the appropriate primary antibody for 2 h, incubated with horseradish peroxidase-conjugated second antibody for 1 h, developed using ECL chemiluminescence, and analyzed by densitometry using AlphaImager Series 2200 software. Compound C (an AMPK inhibitor, 5 μM) and L-NAME (iNOS inhibitor, 0.5 mM) were used to confirm AMPK and iNOS expression in TNF-α-pretreated acarbose-treated (1, 2 and 3 μM for 24 h) cells. Results are representative of at least 3 independent experiments.

Animal Models, Grouping, and Treatment [4]
Male Sprague-Dawley rats (280–320 g) were used. As previously described, diabetic rats were fed a high-fat diet (40% of calories as fat) for 4 weeks, and then were administered a single dose of streptozotocin (STZ, 50 mg/kg, tail vein) formulated in 0.1 mmol/L citrate buffer, pH 4.5. One week after the STZ injection, the random blood glucose level of the diabetic rats was measured to confirm hyperglycemia. Random blood glucose above 16.7 mmol/L was used to define rats as diabetic. Diabetic rats were fed a high-fat diet throughout the experiment. Diabetic rats with a similar degree of hyperglycemia were randomly divided into three groups: vehicle, low dose acarbose (AcarL), and high dose acarbose (AcarH) groups (n = 10, in each group). The typical human daily dose of acarbose is 300 mg/60 kg body weight. According to the formula: drat = dhuman × 0.71/0.11, the corresponding dose of acarbose for rats is 32.28 mg/kg per day. Therefore, we selected 30 and 60 mg/kg per day as low and high dosages, respectively. The control (n = 10) and the diabetic group received 0.5% saline, whereas the AcarL and AcarH groups were given acarbose at doses of 30 and 60 mg/kg in a 0.5% saline solution, respectively. The drug was administered once daily for 8 weeks using a gastric gavage. All animals were housed in an environmentally controlled room at 25°C with a 12 h light-dark cycles and were given free access to food and water throughout the experimental period. Fasting animals were allowed free access to water. After 6 weeks of treatment, an oral glucose tolerance test (OGTT) was performed. After 8 weeks of treatment, blood samples were taken from rats after anesthesia. The rats were then sacrificed. Some terminal ileums were collected for performing the microarray and quantitative real-time reverse transcription PCR (qRT-PCR) analysis. Other terminal ileums were fixed in 10% neutralized formalin for immunohistochemical staining.

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Animals and diets [5]
Twenty-four male New Zealand white rabbits, weighing 2500 g were used. They were individually housed in metal cages in an air-conditioned room (22 ± 2 °C, 55 ± 5% humidity), under a 12 h light/12 h dark cycle with free access to food and water. All rabbits were randomly assigned to four groups of 6 animals each and were fed either standard chow (Group I), high cholesterol diet (HCD; containing 95.7% standard Purina chow + 3% lard oil + 0.5% cholesterol) (Group II), HCD diet and 2.5 mg kg−1 per day acarbose (Group III), or HCD diet and 5.0 mg kg−1 per day acarbose (Group IV). At the end of the 25 weeks, all rabbits were sacrificed by exsanguination under deep anesthesia with pentobarbital (30 mg kg−1 i.v.) injected via the marginal ear vein. Serum was stored at −80 °C prior to measurement of serum values. The aortic arch and thoracic aortas were carefully removed to protect the endothelial lining, and were collected and freed of adhering soft tissue.

Absorption, Distribution and Excretion
The oral bioavailability of acarbose is extremely minimal, with less than 1-2% of orally administered parent drug reaching the systemic circulation. Despite this, approximately 35% of the total radioactivity from a radiolabeled and orally administered dose of acarbose reaches the systemic circulation, with peak plasma radioactivity occurring 14-24 hours after dosing - this delay is likely reflective of metabolite absorption rather than absorption of the parent drug. As acarbose is intended to work within the gut, its minimal degree of oral bioavailability is therapeutically desirable.
Roughly half of an orally administered dose is excreted in the feces within 96 hours of administration. What little drug material is absorbed into the systemic circulation (approximately 34% of an orally administered dose) is excreted primarily by the kidneys, suggesting renal excretion would be a significant route of elimination if the parent drug was more readily absorbed - this is further supported by data in which approximately 89% of an intravenously administered dose of acarbose was excreted in the urine as active drug (in comparison to <2% following oral administration) within 48 hours.
In a study of 6 healthy men, less than 2% of an oral dose of acarbose was absorbed as active drug, while approximately 35% of total radioactivity from a 14C-labeled oral dose was absorbed. An average of 51% of an oral dose was excreted in the feces as unabsorbed drug-related radioactivity within 96 hours of ingestion. Because acarbose acts locally within the gastrointestinal tract, this low systemic bioavailability of parent compound is therapeutically desired.
Following oral dosing of healthy volunteers with 14C-labeled acarbose, peak plasma concentrations of radioactivity were attained 14-24 hours after dosing, while peak plasma concentrations of active drug were attained at approximately 1 hour. The delayed absorption of acarbose-related radioactivity reflects the absorption of metabolites that may be formed by either intestinal bacteria or intestinal enzymatic hydrolysis.
Acarbose is metabolized exclusively within the gastrointestinal tract, principally by intestinal bacteria, but also by digestive enzymes. A fraction of these metabolites (approximately 34% of the dose) was absorbed and subsequently excreted in the urine.
The fraction of acarbose that is absorbed as intact drug is almost completely excreted by the kidneys. When acarbose was given intravenously, 89% of the dose was recovered in the urine as active drug within 48 hours. In contrast, less than 2% of an oral dose was recovered in the urine as active (i.e., parent compound and active metabolite) drug. This is consistent with the low bioavailability of the parent drug.
For more Absorption, Distribution and Excretion (Complete) data for Acarbose (6 total), please visit the HSDB record page.

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Metabolism / Metabolites
Acarbose is extensively metabolized within the gastrointestinal tract, primarily by intestinal bacteria and to a lesser extent by digestive enzymes, into at least 13 identified metabolites. Approximately 1/3 of these metabolites are absorbed into the circulation where they are subsequently renally excreted. The major metabolites appear to be methyl, sulfate, and glucuronide conjugates of 4-methylpyrogallol. Only one metabolite - resulting from the cleavage of a glucose molecule from acarbose - has been identified as having alpha-glucosidase inhibitory activity.
Acarbose is metabolized exclusively within the gastrointestinal tract, principally by intestinal bacteria, but also by digestive enzymes. ... At least 13 metabolites have been separated chromatographically from urine specimens. The major metabolites have been identified as 4-methylpyrogallol derivatives (i.e., sulfate, methyl, and glucuronide conjugates). One metabolite (formed by cleavage of a glucose molecule from acarbose) also has alpha-glucosidase inhibitory activity. This metabolite, together with the parent compound, recovered from the urine, accounts for less than 2% of the total administered dose.

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Biological Half-Life
In healthy volunteers, the plasma elimination half-life of acarbose is approximately 2 hours.
The plasma elimination half-life of acarbose activity is approximately 2 hours in healthy volunteers.

Hepatotoxicity
In several large clinical trials, serum enzyme elevations above 3 times the upper limit of normal were more common with acarbose therapy (2% to 5%) than with placebo, but all elevations were asymptomatic and resolved rapidly with stopping therapy. These studies reported no instances of clinically apparent liver injury. Subsequent to approval and with wide clinical use, however, at least a dozen instances of clinically apparent liver injury have been linked to acarbose use. The liver injury typically arises 2 to 8 months after starting therapy and is associated with a hepatocellular pattern of serum enzyme elevations with marked increases in serum ALT levels, suggestive of acute viral hepatitis. Immunoallergic features and autoantibody formation are not typical. While most cases are mild, some are associated with marked jaundice and cases with a fatal outcome have been reported to the sponsor. No cases of chronic liver injury or vanishing bile duct syndrome have been linked to acarbose use, and most large series of cases of drug induced liver injury and acute liver failure have not identified cases due to acarbose. Rechallenge has been carried out in several instances and resulted in recurrence with a shortening of the time to onset.
Likelihood score: B (rare but likely cause of clinically apparent liver injury).

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Effects During Pregnancy and Lactation
◉ Summary of Use during Lactation
Because less than 2% of a dose of acarbose is absorbed from the mother's gastrointestinal tract, it is unlikely that any drug reaches the infant through breastmilk.
◉ Effects in Breastfed Infants
Relevant published information was not found as of the revision date.
◉ Effects on Lactation and Breastmilk
Relevant published information was not found as of the revision date.

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Protein Binding
As only 1-2% of an orally administered dose is absorbed into the circulation, acarbose is unlikely to be subject to clinically relevant protein binding.

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Interactions
... A possible interaction between digoxin and acarbose was reported. In these reports, absorption of digoxin was decreased dramatically by coadministration of acarbose. The hypoglycemic action of acarbose stems from the reversible and competitive inhibition of alpha-glucosidase that hydrolyzes oligosaccharides absorbed later as glucose molecules. Acarbose functions exclusively in intestine, and most of it appears unchanged in feces. Digoxin is a well-known medication used in the treatment of heart failure and/or chronic atrial fibrillation. Acarbose delays the digestion of sucrose and starch in humans; as a result, a disturbance of gastrointestinal transit, causing loose stools, follows. Therefore, it is possible that gastrointestinal motility is increased, and absorption of digoxin decreased, by coadministration with acarbose. It is also possible that acarbose interferes with the hydrolysis of digoxin before its absorption, resulting in alteration in the release of the corresponding genine and thus affecting the reliability of the digoxin laboratory test. These case reports indicate that the absorption of digoxin is decreased by the administration of acarbose. ...
In a single-centre, placebo-controlled, clinical study, the influence of an antacid containing magnesium hydroxide and aluminium hydroxide (Maalox 70; 10 mL) on the pharmacodynamics of the oral antidiabetic drug acarbose (Glucobay 100, Bay g 5421, CAS 56180; 100 mg) was tested in 24 healthy male volunteers. The drugs were given alone or in combination and were compared with placebo. Volunteers were randomized into four different treatment groups. The daily medication over 4 days was 1 x 1 placebo tablet, or 1 x 1 tablet containing 100 mg acarbose, or 1 x 1 tablet containing 100 mg acarbose plus 10 mL antacid suspension, or 1 x 1 placebo tablet plus 10 ml antacid suspension, interrupted by wash-out phases of 6-10 days between successive treatments. Efficacy was assessed on the basis of postprandial blood glucose and serum insulin levels after administration of 75 g sucrose, and was measured as maximal concentrations and 'area under the curve' (0-4 hr). No influence of the antacid on the blood glucose and insulin-lowering effect of acarbose could be detected. Hence, there does not appear to be a significant interaction between acarbose and the antacid tested. Antacids similar to that tested do not need to be classified as a contraindication when used in combination with acarbose.
To investigate whether treatment with acarbose alters the pharmacokinetics (PK) of coadministered rosiglitazone. Sixteen healthy volunteers (24-59-years old) received a single 8-mg dose of rosiglitazone on day 1, followed by 7 days of repeat dosing with acarbose [100 mg three times daily (t.i.d.) with meals]. On the last day of acarbose t.i.d. dosing (day 8), a single dose of rosiglitazone was given with the morning dose of acarbose. PK profiles following rosiglitazone dosing on days 1 and 8 were compared, and point estimates (PE) and associated 95% confidence intervals (CI) were calculated. Rosiglitazone absorption [as measured with peak plasma concentration (Cmax) and time to peak concentration (Tmax)] was unaffected by acarbose. The area under the concentration-time curve from time zero to infinity [AUC(0-infinity)] was on average 12% lower (95% CI-21%, -2%) during rosiglitazone + acarbose coadministration and was accompanied by an approximate 1-hr (23%) reduction in terminal elimination half-life (4.9 hr versus 3.8 hr). This small decrease in AUC(0-infinity) appears to be due to an alteration in systemic clearance of rosiglitazone and not changes in absorption. These observed changes in AUC(0-infinity) and half-life are not likely to be clinically relevant. Coadministration of rosiglitazone and acarbose was well tolerated. Acarbose administered at therapeutic doses has a small, but clinically insignificant, effect on rosiglitazone pharmacokinetics.

[1]. A review of the safety and efficacy of acarbose in diabetes mellitus. Pharmacotherapy. 1996;16(5):792-805.

[2]. Acarbose: oral anti-diabetes drug with additional cardiovascular benefits [published correction appears in Expert Rev Cardiovasc Ther. 2009 Mar;7(3):330]. Expert Rev Cardiovasc Ther. 2008;6(2):153-163.

[3]. Evaluation of alpha-glucosidase inhibition by using an immobilized assay system. Biol Pharm Bull. 2000;23(9):1084-1087.

[4]. Acarbose Reduces Blood Glucose by Activating miR-10a-5p and miR-664 in Diabetic Rats. PLoS One. 2013 Nov 18;8(11):e79697.

[5]. Pleiotropic effects of acarbose on atherosclerosis development in rabbits are mediated via upregulating AMPK signals. Sci Rep. 2016 Dec 7;6:3864.

(2R,3R,4R,5S,6R)-5-[[(2R,3R,4R,5S,6R)-5-[[(2R,3R,4S,5S,6R)-3,4-dihydroxy-6-methyl-5-[[(1S,4R,5S,6S)-4,5,6-trihydroxy-3-(hydroxymethyl)-1-cyclohex-2-enyl]amino]-2-oxanyl]oxy]-3,4-dihydroxy-6-(hydroxymethyl)-2-oxanyl]oxy]-6-(hydroxymethyl)oxane-2,3,4-triol is a glycoside and an amino cyclitol.
Acarbose is a complex oligosaccharide that acts as an inhibitor of several enzymes responsible for the breakdown of complex carbohydrates in the intestines. It inhibits both pancreatic alpha-amylase and membrane-bound alpha-glucosidases - including intestinal glucoamylase, sucrase, maltase, and isomaltase - which are responsible for the metabolism of complex starches and oligo-, tri-, and disaccharides into absorbable simple sugars. By inhibiting the activity of these enzymes, acarbose limits the absorption of dietary carbohydrates and the subsequent postprandial increase in blood glucose and insulin levels. Acarbose is therefore used in conjunction with diet, exercise, and other pharmacotherapies for the management of blood sugar levels in patients with type 2 diabetes. Acarbose is one of only two approved alpha-glucosidase inhibitors (the other being [miglitol]), receiving its first FDA approval in 1995 under the brand name Precose (since discontinued). This class of antidiabetic therapy is not widely used due to their relatively modest impact on A1c, their requirement for thrice-daily dosing, and the potential for significant gastrointestinal adverse effects.
Acarbose is an alpha glucosidase inhibitor which decreases intestinal absorption of carbohydrates and is used as an adjunctive therapy in the management of type 2 diabetes. Acarbose has been linked to rare instances of clinically apparent acute liver injury.
Precose has been reported in Hintonia latiflora, Hericium erinaceus, and Xylaria feejeensis with data available.
Acarbose is a pseudotetrasaccharide and inhibitor of alpha-glucosidase and pancreatic alpha-amylase with antihyperglycemic activity. Acarbose binds to and inhibits alpha-glucosidase, an enteric enzyme found in the brush border of the small intestines that hydrolyzes oligosaccharides and disaccharides into glucose and other monosaccharides. This prevents the breakdown of larger carbohydrates into glucose and decreases the rise in postprandial blood glucose levels. In addition, acarbose inhibits pancreatic alpha-amylase which hydrolyzes complex starches to oligosaccharides in the small intestines.
An inhibitor of ALPHA-GLUCOSIDASES that retards the digestion and absorption of DIETARY CARBOHYDRATES in the SMALL INTESTINE.
See also: Acarbose (annotation moved to).

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Drug Indication
Acarbose is indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus.
FDA Label

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Mechanism of Action
Alpha-glucosidase enzymes are located in the brush-border of the intestinal mucosa and serve to metabolize oligo-, tri-, and disaccharides (e.g. sucrose) into smaller monosaccharides (e.g. glucose, fructose) which are more readily absorbed. These work in conjunction with pancreatic alpha-amylase, an enzyme found in the intestinal lumen that hydrolyzes complex starches to oligosaccharides. Acarbose is a complex oligosaccharide that competitively and reversibly inhibits both pancreatic alpha-amylase and membrane-bound alpha-glucosidases - of the alpha-glucosidases, inhibitory potency appears to follow a rank order of glucoamylase > sucrase > maltase > isomaltase. By preventing the metabolism and subsequent absorption of dietary carbohydrates, acarbose reduces postprandial blood glucose and insulin levels.
In contrast to sulfonylureas, acarbose does not enhance insulin secretion. The antihyperglycemic action of acarbose results from a competitive, reversible inhibition of pancreatic alpha-amylase and membrane-bound intestinal alpha-glucoside hydrolase enzymes. Pancreatic alpha-amylase hydrolyzes complex starches to oligosaccharides in the lumen of the small intestine, while the membrane-bound intestinal alpha-glucosidases hydrolyze oligosaccharides, trisaccharides, and disaccharides to glucose and other monosaccharides in the brush border of the small intestine. In diabetic patients, this enzyme inhibition results in a delayed glucose absorption and a lowering of postprandial hyperglycemia. Because its mechanism of action is different, the effect of acarbose to enhance glycemic control is additive to that of sulfonylureas, insulin or metformin when used in combination. In addition, acarbose diminishes the insulinotropic and weight-increasing effects of sulfonylureas. Acarbose has no inhibitory activity against lactase and consequently would not be expected to induce lactose intolerance.
Acarbose represents a pharmacological approach to achieving the metabolic benefits of a slower carbohydrate absorption in diabetes, by acting as a potent, competitive inhibitor of intestinal alpha-glucosidases. Acarbose molecules attach to the carbohydrate binding sites of alpha-glucosidases, with an affinity constant that is much higher than that of the normal substrate. Because of the reversible nature of the inhibitor-enzyme interaction, the conversion of oligosaccharides to monosaccharides is only delayed rather than completely blocked. Acarbose has the structural features of a tetrasaccharide and does not cross the enterocytes after ingestion. Thus, its pharmacokinetic properties are well suited to the pharmacological action directed exclusively towards the intestinal glucosidases. ...
The aim of the present study was to reveal the possible involvement of thyroid hormones in the antihyperglycaemic and antiperoxidative effects of acarbose. The effects of acarbose on changes in serum concentration of thyroid hormones, insulin and glucose in dexamethasone-induced type 2 diabetic mice were investigated. Simultaneously, changes in lipid peroxidation (LPO), reduced glutathione (GSH) content and the activity of associated endogenous anti-oxidant enzymes, such as superoxide dismuatase (SOD) and catalase (CAT), were investigated in renal and cardiac tissues, which are commonly affected in diabetes mellitus. Although administration of dexamethasone (1.0 mg/kg, i.m., for 22 days) caused hyperglycaemia with a parallel increase in serum insulin and tissue LPO, it decreased thyroid hormone concentrations and the activity of SOD and CAT. When dexamethasone-induced hyperglycemic mice were treated with acarbose (10 mg/kg per day, p.o., for 15 days), levels of thyroid hormones were increased and most of the abnormalities, including serum insulin and glucose levels, tissue LPO, SOD and CAT activity and GSH content, were reversed. These findings suggest the involvement of thyroid hormones in the mode of action of acarbose in amelioration of type 2 diabetes mellitus.

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Acarbose is a novel oral anti-hyperglycemic agent approved for the treatment of noninsulin-dependent diabetes mellitus. It inhibits alpha-glucosidases in the small intestine, an action that delays the digestion and absorption of complex carbohydrates. Subsequently, there is a smaller rise in the postprandial plasma glucose levels and an overall decrease in the glycosylated hemoglobin by 0.5-1.0%. Potential advantages of acarbose include a greater effectiveness in controlling postprandial hyperglycemia, a low risk of hypoglycemia, and a possible delay in initiating insulin therapy. Acarbose can potentiate the hypoglycemic effects of sulfonylureas or insulin. It has not been associated with weight gain and hyperinsulinemia, both of which can occur with sulfonylureas or insulin. Gastrointestinal adverse effects are common with acarbose, and may decrease with continued treatment. Although rare, elevated serum transaminase levels have been reported.[1]

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Acarbose is an alpha-glucosidase inhibitor acting specifically at the level of postprandial glucose excursion. This compound lowers HbA(1c) by 0.5-1% in patients with Type 2 diabetes, either drug naive or in combination with other antidiabetic drugs. In those with impaired glucose tolerance (IGT), it reduces the incidence of newly diagnosed diabetes by 36.4%. Furthermore, it has beneficial effects on overweight, reduces blood pressure and triglycerides, and downregulates biomarkers of low-grade inflammation. In the Study To Prevent Non-Insulin-Dependent-Diabetes-Mellitus (STOP-NIDDM) trial, acarbose significantly reduced the progression of intima media thickness, incidence of cardiovascular events and of newly diagnosed hypertension. In a meta-analysis of patients with Type 2 diabetes (MERIA), acarbose intake was associated with a reduction of cardiovascular events by 35%. Acarbose is a very safe drug but in approximately 30% of patients, it can cause gastrointestinal complaints due to its mode of action, which in the majority disappear after 1-2 months. Acarbose is approved for treatment of IGT in 25 countries. It can be given alone or in combination with other oral antidiabetics and insulin. Acarbose is particularly effective in those with IGT and early diabetes and patients with comorbidities of the metabolic syndrome.[2]

C25H45NO22S

743.683309316635

743.215

1221158-13-9

Acarbose;56180-94-0

127255613

Typically exists as solid at room temperature

16

23

13

49

1030

18

C[C@@H]1[C@H]([C@@H]([C@H]([C@H](O1)O[C@@H]2[C@H](O[C@@H]([C@@H]([C@H]2O)O)O[C@H]([C@@H](CO)O)[C@@H]([C@H](C=O)O)O)CO)O)O)N[C@H]3C=C([C@H]([C@@H]([C@H]3O)O)O)CO.OS(=O)(=O)O

XHZAGRIRYDJUSP-PKCKZCPMSA-N

InChI=1S/C25H43NO18.H2O4S/c1-7-13(26-9-2-8(3-27)14(33)18(37)15(9)34)17(36)20(39)24(41-7)44-23-12(6-30)42-25(21(40)19(23)38)43-22(11(32)5-29)16(35)10(31)4-28;1-5(2,3)4/h2,4,7,9-27,29-40H,3,5-6H2,1H3;(H2,1,2,3,4)/t7-,9+,10+,11-,12-,13-,14-,15+,16-,17+,18+,19-,20-,21-,22-,23-,24-,25-;/m1./s1

(2R,3R,4R,5R)-4-(((2R,3R,4R,5S,6R)-5-(((2R,3R,4S,5S,6R)-3,4-dihydroxy-6-methyl-5-(((1S,4R,5S,6S)-4,5,6-trihydroxy-3-(hydroxymethyl)cyclohex-2-en-1-yl)amino)tetrahydro-2H-pyran-2-yl)oxy)-3,4-dihydroxy-6-(hydroxymethyl)tetrahydro-2H-pyran-2-yl)oxy)-2,3,5,6-tetrahydroxyhexanal sulfate

BAY-g-5421 sulfate; Acarbose sulfate; 1221158-13-9; (2R,3R,4R,5R)-4-[(2R,3R,4R,5S,6R)-5-[(2R,3R,4S,5S,6R)-3,4-dihydroxy-6-methyl-5-[[(1S,4R,5S,6S)-4,5,6-trihydroxy-3-(hydroxymethyl)cyclohex-2-en-1-yl]amino]oxan-2-yl]oxy-3,4-dihydroxy-6-(hydroxymethyl)oxan-2-yl]oxy-2,3,5,6-tetrahydroxyhexanal;sulfuric acid; BAY-g 5421; BAY g-5421 sulfate; Acarbose sulfate; Glucobay; Prandase; Precose

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples

Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.

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Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution.
Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)
Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil)
Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals).

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Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)]
*Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

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Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium)
Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose
Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals).

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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

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Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

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 (Please use freshly prepared in vivo formulations for optimal results.)