Miglitol

207.22

207.22

276-661-6

0V5436JAQW

DTXSID0023323

C61847

White to pale-yellow powder|Crystals from ethanol

A - Alimentary tract and metabolism

29333990

104

-2.6

1.5±0.1 g/cm3

114 °C

453.7°C at 760 mmHg

284.3±27.4 °C

1.598

H2O: soluble

-20°C Freezer

7.33X10-10 mm Hg at 25 deg C (est)

Henry's Law constant = 4.34X10-15 atm-cu m/mol at 25 °C (est)

5.9|pKa = 5.9

141 Ų [M+H]+ [CCS Type: TW, Method: calibrated with polyalanine and drug standards]

Hydroxyl radical reaction rate constant = 1.54X10-10 cu cm/molec-sec at 25 °C (est)

NONH for all modes of transport

3

TN4350170

P201, P202, P260, P264, P280, P281, P301+P330+P331, P302+P352, P303+P361+P353, P304+P340, P305+P351+P338, P308+P313, P310, P321, P332+P313, P337+P313, P362, P363, P405, P501

H314

SRP: Expired or waste pharmaceuticals shall carefully take into consideration applicable DEA, EPA, and FDA regulations. It is not appropriate to dispose by flushing the pharmaceutical down the toilet or discarding to trash. If possible return the pharmaceutical to the manufacturer for proper disposal being careful to properly label and securely package the material. Alternatively, the waste pharmaceutical shall be labeled, securely packaged and transported by a state licensed medical waste contractor to dispose by burial in a licensed hazardous or toxic waste landfill or incinerator.|SRP: At the time of review, regulatory criteria for small quantity disposal are subject to significant revision, however, household quantities of waste pharmaceuticals may be managed as follows: Mix with wet cat litter or coffee grounds, double bag in plastic, discard in trash.

The Approved Drug Products with Therapeutic Equivalence Evaluations identifies currently marketed prescription drug products, including miglitol, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act.

|Danger|H314 (100%): Causes severe skin burns and eye damage [Danger Skin corrosion/irritation]|P201, P202, P260, P264, P280, P281, P301+P330+P331, P302+P352, P303+P361+P353, P304+P340, P305+P351+P338, P308+P313, P310, P321, P332+P313, P337+P313, P362, P363, P405, and P501|The GHS information provided by 1 company from 1 notification to the ECHA C&L Inventory.

Unlike sulfonylureas or insulin, an overdose will not result in hypoglycemia. An overdose may result in transient increases in flatulence, diarrhea, and abdomi-nal discomfort. Because of the lack of extra-intestinal effects seen with miglitol, no serious systemic reactions are expected in the event of an overdose.

In several large clinical trials, serum aminotransferase elevations were no more common with miglitol than with placebo, and all elevations that occurred were asymptomatic and resolved rapidly with stopping therapy. Neither during these studies nor since approval and wide clinical use have reports of clinically apparent liver injury due to miglitol been published. Thus, liver injury from miglitol must be very rare if it occurs at all. There also have been no reports of patients who developed liver injury while on acarbose being switched to miglitol.

Several studies investigated the possible interaction between miglitol and glyburide. In six healthy volunteers given a single dose of 5-mg glyburide on a background of 6 days treatment with miglitol (50 mg 3 times daily for 4 days followed by 100 mg 3 times daily for 2 days) or placebo, the mean Cmax and AUC values for glyburide were 17% and 25% lower, respectively, when glyburide was given with miglitol. In a study in diabetic patients in which the effects of adding miglitol 100 mg 3 times daily x 7 days or placebo to a background regimen of 3.5 mg glyburide daily were investigated, the mean AUC value for glyburide was 18% lower in the group treated with miglitol, although this difference was not statistically significant. Further information on a potential interaction with glyburide was obtained from one of the large U.S. clinical trials (Study 7) in which patients were dosed with either miglitol or placebo on a background of glyburide 10 mg twice daily. At the 6-month and 1-year clinic visits, patients taking concomitant miglitol 100 mg 3 times daily exhibited mean Cmax values for glyburide that were 16% and 8% lower, respectively, compared to patients taking glyburide alone. However, these differences were not statistically significant. Thus, although there was a trend toward lower AUC and Cmax values for glyburide when co-administered with miglitol, no definitive statement regarding a potential interaction can be made based on the foregoing three studies.|The effect of miglitol on the pharmacokinetics of a single 1000-mg dose of metformin was investigated in healthy volunteers. Mean AUC and Cmax values for metformin were 12% to 13% lower when the volunteers were given miglitol as compared with placebo, but this difference was not statistically significant.|In a healthy volunteer study, co-administration of miglitol 3 times daily together with digoxin reduced the average plasma concentrations of digoxin by 19% and 28%, respectively. However, in diabetic patients under treatment with digoxin, plasma digoxin concentrations were not altered by co-administration of miglitol ...|Other healthy volunteer studies have demonstrated that miglitol may significantly reduce the bioavailability of ranitidine and propranolol by 60% and 40%, respectively. No effect of miglitol was observed on the pharmacokinetics or pharmacodynamics of nifedipine.|For more Interactions (Complete) data for Miglitol (9 total), please visit the HSDB record page.

Miglitol is contraindicated in patients with known hypersensitivity to the drug or diabetic ketoacidosis. The drug is also contraindicated in patients with inflammatory bowel disease, colonic ulceration, partial intestinal obstruction or predisposition to this condition, chronic intestinal diseases associated with marked disorders of digestion or absorption, and coexisting conditions that may deteriorate as a result of increased intestinal gas formation.

The protein binding of miglitol is negligible (<4.0%).

Miglitol has been shown to be excreted in human milk to a very small degree. Total excretion into milk accounted for 0.02% of a 100-mg maternal dose. The estimated exposure to a nursing infant is approximately 0.4% of the maternal dose.

Miglitol has been shown to be excreted in human milk to a very small degree. Total excretion into milk accounted for 0.02% of a 100-mg maternal dose. The estimated exposure to a nursing infant is approximately 0.4% of the maternal dose.

For use as an adjunct to diet to improve glycemic control in patients with non-insulin-dependent diabetes mellitus (NIDDM) whose hyperglycemia cannot be managed with diet alone.

Miglitol is an alpha glucosidase inhibitor which delays intestinal absorption of carbohydrates and is used as an adjunctive therapy in the management of type 2 diabetes. Miglitol has not been linked to instances of clinically apparent acute liver injury.

Antidiabetic Agents

1-Deoxynojirimycin/*analogs & derivatives; alpha-Glucosidases/antagonists & inhibitors; Enzyme Inhibitors|Reduction in postprandial blood glucose concentrations persists for 3-4 hours following a single dose in healthy individuals.|Miglitol is indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus./Included in US product label/

Miglitol is contraindicated in patients with known hypersensitivity to the drug or diabetic ketoacidosis. The drug is also contraindicated in patients with inflammatory bowel disease, colonic ulceration, partial intestinal obstruction or predisposition to this condition, chronic intestinal diseases associated with marked disorders of digestion or absorption, and coexisting conditions that may deteriorate as a result of increased intestinal gas formation.|Miglitol should not cause hypoglycemia when administered alone in the fasting or postprandial state. There is an increased risk of hypoglycemia when miglitol is used concomitantly with insulinor a sulfonylurea antidiabetic agent. If hypoglycemia occurs, dosage of these agents should be adjusted appropriately.|Oral glucose (dextrose) should be used for the treatment of mild to moderate hypoglycemia instead of sucrose (table sugar, a disaccharide); absorption of oral glucose (a monosaccharide) is not delayed by miglitol. Severe hypoglycemia may require the use of either iv glucose infusion or parenteral glucagon.|There is a risk of possible loss of glycemic control in patients receiving miglitol during periods of stress (e.g., fever, trauma, infection, surgery); temporary administration of insulin may be required.|For more Drug Warnings (Complete) data for Miglitol (11 total), please visit the HSDB record page.

Miglitol, an oral alpha-glucosidase inhibitor, is a desoxynojirimycin derivative that delays the digestion of ingested carbohydrates, thereby resulting in a smaller rise in blood glucose concentration following meals. As a consequence of plasma glucose reduction, miglitol reduce levels of glycosylated hemoglobin in patients with Type II (non-insulin-dependent) diabetes mellitus. Systemic nonenzymatic protein glycosylation, as reflected by levels of glycosylated hemoglobin, is a function of average blood glucose concentration over time. Because its mechanism of action is different, the effect of miglitol to enhance glycemic control is additive to that of sulfonylureas when used in combination. In addition, miglitol diminishes the insulinotropic and weight-increasing effects of sulfonylureas. Miglitol has minor inhibitory activity against lactase and consequently, at the recommended doses, would not be expected to induce lactose intolerance.

Substances which lower blood glucose levels. (See all compounds classified as Hypoglycemic Agents.)|Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction. (See all compounds classified as Enzyme Inhibitors.)|Compounds that inhibit or block the activity of GLYCOSIDE HYDROLASES such as ALPHA-AMYLASES and ALPHA-GLUCOSIDASES. (See all compounds classified as Glycoside Hydrolase Inhibitors.)

Absorption of miglitol is saturable at high doses with 25 mg being completely absorbed while a 100-mg dose is only 50-70% absorbed. No evidence exists to show that systemic absorption of miglitol adds to its therapeutic effect.|Miglitol is not metabolized in man or in any animal species studied. It is eliminated by renal excretion as an unchanged drug.|0.18 L/kg|Absorption of miglitol is saturable at high doses: a dose of 25 mg is completely absorbed, whereas a dose of 100 mg is only 50% - 70% absorbed. For all doses, peak concentrations are reached in 2-3 hours.|Therapeutic effects principally result from local actions on the small intestine; there is no evidence that systemic absorption contributes to therapeutic response.|The protein binding of miglitol is negligible (<4.0%). Miglitol has a volume of distribution of 0.18 L/kg, consistent with distribution primarily into the extracellular fluid.|Miglitol is distributed principally into extracellular fluid and concentrated in enterocytes of the small intestine.|For more Absorption, Distribution and Excretion (Complete) data for Miglitol (9 total), please visit the HSDB record page.

Miglitol is not metabolized in man or in any animal species studied.|Miglitol is not metabolized in man or in any animal species studied. No metabolites have been detected in plasma, urine, or feces, indicating a lack of either systemic or pre-systemic metabolism.

The elimination half-life of miglitol from plasma is approximately 2 hours.|... Miglitol is rapidly eliminated from plasma with apparent elimination half-lives of 0.4-1.8 hr. ... At very low concentration levels a terminal elimination phase of radioactivity characterized by half-lives of 50-110 hr...

In contrast to sulfonylureas, miglitol does not enhance insulin secretion. The antihyperglycemic action of miglitol results from a reversible inhibition of membrane-bound intestinal a-glucoside hydrolase enzymes. Membrane-bound intestinal a-glucosidases hydrolyze oligosaccharides and disaccharides to glucose and other monosaccharides in the brush border of the small intestine. In diabetic patients, this enzyme inhibition results in delayed glucose absorption and lowering of postprandial hyperglycemia.|Miglitol is a desoxynojirimycin derivative that delays the digestion of ingested carbohydrates, thereby resulting in a smaller rise in blood glucose concentration following meals. As a consequence of plasma glucose reduction, miglitol tablets reduce levels of glycosylated hemoglobin in patients with Type II (non-insulin-dependent) diabetes mellitus. Systemic nonenzymatic protein glycosylation, as reflected by levels of glycosylated hemoglobin, is a function of average blood glucose concentration over time.|Miglitol inhibits alpha-glucosidase enzymes (e.g., sucrase, glucoamylase, maltase, isomaltase) that hydrolyze oligosaccharides, trisaccharides, and disaccharides to glucose and other monosaccharides in the small intestinal brush border. The drug has little or no inhibitory effect on trehalase, lactase, or pancreatic alpha-amylase; it is not expected to produce lactose intolerance. Miglitol delays carbohydrate breakdown and glucose absorption and reduces postprandial hyperglycemia in diabetic patients; fasting blood glucose concentrations are mildly decreased.|In contrast to sulfonylurea antidiabetic agents, miglitol does not enhance insulin secretion. The drug does not produce hypoglycemia when given as monotherapy in the fasted or postprandial state. When used in combination with sulfonylurea antidiabetic agents, miglitol reduces the insulinotropic and weight-increasing effects of sulfonylureas. Miglitol does not produce clinically important weight loss.|Oral administration of miglitol has been reported to produce glucagon-like peptide 1 (GLP-1). /The authors/ hypothesized that p.o. administration of miglitol, an absorbable antidiabetic drug, reduces myocardial infarct size by stimulating GLP-1 receptors and inhibiting glycogenolysis in the myocardium. The effects of p.o. and i.v. administration of miglitol on myocardial infarct size were compared in a rabbit model of ischemia induced by 30 min of coronary occlusion and 48 hr of reperfusion. The levels of phospho(p)-PI3kinase and p-Akt were measured in cardiac tissue by use of Western blot analysis. Both p.o. and i.v. administration of miglitol reduced the infarct size, and this effect was greater after p.o. than after i.v. administration under similar plasma miglitol concentrations. The reduction in infarct size induced by p.o. miglitol but not that induced by i.v. miglitol was partially inhibited by treatment with exendin(9-39), a GLP-1 receptor blocker. Both p.o. and i.v. miglitol improved ejection fraction and +/-dP/dt after myocardial infarction. Miglitol administered p.o. but not i.v. up-regulated the myocardial expression of phospho(p)-PI3kinase and p-Akt following myocardial infarction; an effect that was inhibited by exendin(9-39). Administration of miglitol p.o. reduces myocardial infarct size through stimulation of GLP-1 receptors and activation of PI3kinase-Akt pathway in addition to the inhibition of glycogenolysis. These findings may have clinical implications for the p.o. administration of miglitol for the treatment of patients with diabetes mellitus combined with coronary artery disease.|Imino sugars are used to treat type 2 diabetes mellitus (miglitol (Glyset)) and lysosomal storage disorders (miglustat (Zavesca)) based on the inhibition of alpha-glucosidases and glucosyltransferases. In this substrate specificity study, /investigators/ examined the interactions of imino sugars with a novel human glucose sensor, sodium/glucose cotransporter type 3 (hSGLT3), using expression in Xenopus laevis oocytes and electrophysiology. The results for hSGLT3 are compared with those for alpha-glucosidases and human SGLT type 1 (hSGLT1), a well characterized sodium/glucose cotransporter of the SGLT family. In general, substrates have lower apparent affinities (K0.5) for hSGLT3 than hSGLT1 (D-glucose, alpha-methyl-D-glucose, 1-deoxy-D-glucose, and 4-deoxy-4-fluoro-D-glucose exhibit K0.5 values of 19, 21, 43, and 17 mM, respectively, for hSGLT3, and 0.5, 0.7, 10, and 0.07 mM, respectively, for hSGLT1). However, specificity of hSGLT3 binding is greater (D-galactose and 4-deoxy-4-fluoro-D-galactose are not hSGLT3 substrates, but have hSGLT1 K0.5 values of 0.6 and 1.3 mM). An important deviation from this trend is potent hSGLT3 activation by the imino sugars 1-deoxynojirimycin (DNJ), N-hydroxylethyl-1-deoxynojirimycin (miglitol), N-butyl-1-deoxynojirimycin (miglustat), N-ethyl-1-deoxynojirimycin, and 1-deoxynojirimycin-1-sulfonic acid, with K0.5 values of 0.5 to 9 microM. The diastereomer 1-deoxygalactonojirimycin activates hSGT3 with a K0.5 value of 11 mM, a 3000-fold less potent interaction than is observed for DNJ (4 microM). These imino sugar binding characteristics are similar to those for alpha-glucosidases, but there are no interactions with hSGLT1. This work provides insights into hSGLT3 and -1 substrate binding interactions, establishes a pharmacological profile to study endogenous hSGLT3, and may have important ramifications for the clinical application of imino sugars.

/SRP:/ Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on the left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Poisons A and B/|/SRP:/ Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if needed. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . Cover skin burns with dry sterile dressings after decontamination ... . /Poisons A and B/|/SRP:/ Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag valve mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W /SRP: "To keep open", minimal flow rate/. Use 0.9% saline (NS) or lactated Ringer's if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam or lorazepam ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poisons A and B/

/HUMAN EXPOSURE STUDIES/ The inhibitory effect of N- beta-(4-ethoxycarbonylphenoxy-ethyl-1-desoxynojirimycin (BAY o1248) and of N-hydroxyethyl-1-desoxynojirimycin (BAY o1099) was studied in normal men. Nine healthy volunteers (weight range of 82% to 117% of their ideal body weight) ingested a 50 g sucrose load together with placebo, 50 mg BAY m1099, or 10 mg BAY of o1248. Their substrate oxidation rate was measured by continuous indirect calorimetry during four hours. The plasma glucose and plasma insulin peaks were both significantly blunted and the late fall of glycemia reduced. Mean plasma glucose, fructose, and insulin were reduced by both drugs during the first two hours following the sucrose load and led to a decrease of the suprabasal glucose oxidation (oxidation above baseline) during the first two hours of the test. However, the total suprabasal glucose oxidation during the four hours of the test was not significantly different from that of the control. Breath hydrogen, as an index of malabsorption, was shown to increase with both 50 mg BAY m1099 and 10 mg BAY o1248, starting from the third hour. These findings are consistent with a significant delay of sucrose absorption induced by these new alpha-glycohydrolase inhibitors.|/HUMAN EXPOSURE STUDIES/ Postprandial hyperglycemia in diabetic patients can be modified by delaying the digestion and/or absorption of dietary carbohydrates. /Investigators/ have studied an orally active alpha-glucosidase inhibitor, Bay 1099, in normal volunteers to determine whether these inhibitors can decrease postprandial rises in serum glucose without causing gastrointestinal symptoms or significant fecal caloric wastage. Six subjects were given 25, 50, or 100 mg of Bay 1099 or placebo before meals for 1 week, each with a 1-week washout period. Fasting and postprandial concentrations of glucose, insulin, glucagon, enteroglucagon, and gastrointestinal inhibitory peptide (GIP) were measured after the first and last dose of Bay 1099, and the fecal excretions of protein, fat, fiber, and total calories were measured on the last three days of each diet. The passage of unabsorbed carbohydrate into the colon was determined by breath hydrogen analysis three times during each study week. Increasing doses of Bay 1099 were found to decrease the postprandial rise in serum glucose concentration, delay the time to peak insulin concentration, and decrease the output of GIP after the meal. No adaptation was apparent after 1 week of therapy. A dose of /glucosidase/ inhibitor (50 mg tid), which greatly improves postprandial glucose and hormone output in diabetes, was associated with minimal symptoms and no excess fecal caloric losses. Thus, glucosidase inhibitors such as Bay 1099 may be useful in the management of patients with carbohydrate intolerance.|/HUMAN EXPOSURE STUDIES/ alpha-Glucosidase inhibitors delay carbohydrate absorption and have been proposed as adjunctive therapy for diabetes mellitus. To determine the effects of two new alpha-glucosidase inhibitors, miglitol (Bay-m-1099) and Bay-o-1248, on meal carbohydrate and lipid tolerance, plasma glucose, insulin and triglyceride levels were measured at 15-60 min intervals over 12 hr after ingestion of a standard breakfast, lunch and dinner of identical composition in 31 normal volunteers. The volunteers were randomized to receive either Bay-m-1099 (50 or 25 mg) or placebo prior to each meal, or the single administration of Bay-o-1248 (20 or 10 mg) or placebo prior to breakfast. Only Bay-m-1099 at the 50 mg dose reduced significantly the postprandial increase in plasma insulin levels after each meal when compared with placebo (25, 36, 54% at breakfast, lunch, and dinner, respectively; P less than 0.05). Both drugs were well tolerated, with side effects limited to complaints of flatulence. Thus, with the dosage schedule employed, Bay-m-1099, but not Bay-o-1248, significantly reduced postprandial increments in plasma insulin.|/HUMAN EXPOSURE STUDIES/ In this double-blind, cross-over, placebo-controlled, randomized study, possible extraintestinal effects of miglitol, an absorbable alpha-glucosidase inhibitor, were investigated. Sixteen healthy male volunteers underwent two 75 g oral glucose tolerance tests with concomitant administration of miglitol or placebo. Peak and post-peak areas under the curve values for blood glucose, serum insulin and serum C-peptide after miglitol were not different from those found after placebo. The post-peak AUC-ratio (AUC (peak, 180 min) on miglitol/AUC (peak, 180 min) on placebo) was for glucose 1.15 (CI 0.94-1.40, P = 0.16), for insulin 1.12 (CI 0.95-1.33, P = 0.17) and for C-peptide 0.98 (CI 0.81-1.18, P = 0.82). It is concluded that miglitol exerts no clinically relevant extraintestinal effects on glucose control.|For more Human Toxicity Excerpts (Complete) data for Miglitol (8 total), please visit the HSDB record page.

BAY m 1099

Glyset (miglitol) tablets are available as 25 mg, 50 mg, and 100 mg white, round, film-coated tablets.

A selective and sensitive, stability-indicating reverse phase high performance liquid chromatography method has been first developed and validated for the estimation of miglitol in bulk and tablet dosages form. Samples were separated on a prepacked, Inertsil amino C18 column (150x4.6 mm i.d.) using a mobile phase comprised of acetonitrile and monobasic sodium phosphate pH 7.5 (80:20, v/v) delivered at 1.5 mL/min flow rate. Detection was performed on a SPD-20A prominence UV/Vis detector at 220 nm. The retention time for miglitol was 13.93 + or -0.0367. The method was validated in terms of linearity, precision, accuracy, ruggedness, and specificity, limit of detection and limit of quantification. The linearity (r2) and percentage recoveries of miglitol were 0.9986 and 99.85%. This method is suitable for routine estimation of miglitol in bulk and tablet dosages form.

A rapid and sensitive method for the determination of miglitol in human plasma was developed using ultra-performance liquid chromatographic separation with tandem mass spectrometry detection. The preparation of samples required a deproteinization step with acetonitrile. Chromatography was performed on a 5 u (50 mm x 4.6 mm, ID.) C18 inertsil column, with the mobile phase consisting of acetonitrile 2 mM and ammonium acetate (pH 3.5) with formic acid. Detection was performed using an Applied Biosystems Sciex API 2000 mass spectrometer set at unit resolution in the multiple reaction monitoring mode. Electrospray ionization was used for ion production. The mean recovery of miglitol was 88.9%, with the lower limit of quantification set at 150 ng/mL. Linearity was established for concentrations in the range of 150-4000 ng/mL, with a coefficient of determination (r(2) ) of 0.9981. This assay method makes use of the increased sensitivity and selectivity of tandem mass spectrometric detection, resulting in high-throughput analysis of miglitol for bioequivalence studies.|A rapid and sensitive method for the determination of miglitol in human plasma using voglibose as internal standard has been developed and validated. Samples of plasma were deproteinated with acetonitrile and washed with dichloromethane before being analyzed by reversed-phase high-performance liquid chromatography (HPLC). Separation was carried out on a short Nucleosil C(18) column (5 microm, 50 x 4.6 mm i.d.) using 10 mmol/L ammonium acetate at 1.0 mL/min as mobile phase. The detector was an Applied Biosystems Sciex API 4000 mass spectrometer using atmospheric pressure chemical ionization (APCI) for ion production. The instrument was operated at unit resolution in the multiple reaction monitoring mode. The assay was linear over the range 5.00-2000 ng/mL with a limit of detection of 1.00 ng/mL. Intra- and inter-day precision were <2.82% and <2.92%, respectively, with accuracy of 93.3-106%. The assay was successfully applied to a clinical pharmacokinetic study of miglitol given as a single oral dose (50 mg) to healthy volunteers.

Human Drugs -> FDA Approved Drug Products with Therapeutic Equivalence Evaluations (Orange Book) -> Active Ingredients