部分中文拜唐苹处方资料（仅供参考） 拜唐苹Glucobay  中文别名：阿卡波糖、阿卡波糖，拜糖平 英文别名：Acarbose 生产企业：德国拜耳 药品类别：胰腺激素及其它影响血糖药               性    状 为一种新型口服降糖药。 药理药动 本品是一个α-糖苷酶抑制剂。它结合于碳水化合物分解酶(α-糖苷酶)，从而竞争性和可逆性地抑制了小肠中碳水化合物的分解，使糖的吸收相应减缓，因而拜糖平可以减少饭后血糖浓度的增高。由于小肠内糖吸收的减缓和大肠内糖的调节吸收，使一天内血糖浓度平稳，平均值下降。拜糖平对非胰岛素依赖型糖尿病人单独治疗有明显疗效，可降餐后血糖和空腹血糖。它也适合与其它日服胶降糖药合用，临床试验1年结果，拜糖平对55％已服磺脲类药物的病人和的％已服双胍类药物的病人，均有明显的作用。 适应症 非胰岛素依赖型糖尿病人，当单纯饮食治疗不能控制血糖时，拜糖平应用作一线治疗药。 当现有常规降糖药不能正常控制代谢状态时，拜糖平可加入合并使用。 胰岛素依赖型糖尿病人可配合胰岛素合并使用。 用法用量 每片50mg，初起量为1天3次每次一片，以后可增加到一天3次每次2片。 不良反应 因糖类在小肠内分解及吸收缓慢，停留时间延长，经肠道细菌的酵解而产气增多，因此可引起腹胀、腹痛及腹泻等。 也可引起低血糖。 禁忌症 禁用于对阿卡波糖的过敏反应者； 也不能用于18岁以下的病人； 有明显消化、吸收障碍的慢性肠功能紊乱； 禁用于肠胀气面可能恶化的情况(如严重的疝气、肠梗阻和肠溃疡等)。 孕妇及哺乳期妇女用药 怀孕期间禁服拜糖平，哺乳期也不要服用拜糖平。 Glucobay 50mg tablets 1. Name of the medicinal product Glucobay 50 mg tablets 2. Qualitative and quantitative composition Glucobay 50 mg tablets: 1 tablet contains 50 mg acarbose. For the full list of excipients, see section 6.1. 3. Pharmaceutical form Tablet for oral administration. White to yellow-tinged round, convex tablets of 7 mm diameter and 10 mm radius of curvature with 'G50' on one side and the BAYER-cross on the other side. 4. Clinical particulars 4.1 Therapeutic indications Indications Glucobay is recommended for the treatment of non-insulin dependent (NIDDM) diabetes mellitus in patients inadequately controlled on diet alone, or on diet and oral hypoglycaemic agents. Mode of action Glucobay is a competitive inhibitor of intestinal alpha-glucosidases with maximum specific inhibitory activity against sucrase. Under the influence of Glucobay, the digestion of starch and sucrose into absorbable monosaccharides in the small intestine is dose-dependently delayed. In diabetic subjects, this results in a lowering of postprandial hyperglycaemia and a smoothing effect on fluctuations in the daily blood glucose profile. In contrast to sulphonylureas Glucobay has no stimulatory action on the pancreas. Treatment with Glucobay also results in a reduction of fasting blood glucose and to modest changes in levels of glycated haemoglobin (HbA1, HbA1c). The changes may be a reduction or reduced deterioration in HbA1 or HbA1c levels, depending upon the patient's clinical status and disease progression. These parameters are affected in a dose-dependent manner by Glucobay. Following oral administration, only 1-2% of the active inhibitor is absorbed. 4.2 Posology and method of administration Posology Owing to the great individual variation of glucosidase activity in the intestinal mucosa, there is no fixed dosage regimen, and patients should be treated according to clinical response and tolerance of intestinal side-effects. Adults The recommended initial dose is 50 mg three times a day. However, some patients may benefit from more gradual initial dose titration to minimise gastrointestinal side-effects. This may be achieved by initiating treatment at 50 mg once or twice a day, with subsequent titration to a three times a day regimen. If after six to eight weeks' treatment patients show an inadequate clinical response, the dosage may be increased to 100 mg three times a day. A further increase in dosage to a maximum of 200 mg three times a day may occasionally be necessary. If distressing complaints develop in spite of strict adherence to the diet, the dose should not be increased further and if necessary should be reduced according to the severity of the side-effects and the clinical judgment of the prescriber. Glucobay is intended for continuous long-term treatment. Elderly No modification of the normal adult dosage regimen is necessary. Paediatric population The efficacy and safety of Glucobay in children and adolescents have not been established. Glucobay is not recommended for patients under the age of 18 years. Method of administration Glucobay tablets are taken orally and should be chewed with the first mouthful of food, or swallowed whole with a little liquid directly before the meal. 4.3 Contraindications Hypersensitivity to the active substance or to any of the excipients listed in section 6.1, pregnancy and in nursing mothers. Glucobay is also contra-indicated in patients with inflammatory bowel disease, colonic ulceration, partial intestinal obstruction or in patients predisposed to intestinal obstruction. In addition, Glucobay should not be used in patients who have chronic intestinal diseases associated with marked disorders of digestion or absorption and in patients who suffer from states which may deteriorate as a result of increased gas formation in the intestine, e.g. larger hernias. Glucobay is contra-indicated in patients with severe hepatic impairment. As Glucobay has not been studied in patients with severe renal impairment, it should not be used in patients with a creatinine clearance < 25 ml/min/1.73 m2. 4.4 Special warnings and precautions for use Hypoglycaemia: Glucobay has an antihyperglycaemic effect, but does not itself induce hypoglycaemia. If Glucobay is prescribed in addition to other blood glucose lowering drugs (e.g sulphonylureas metformin, or insulin) a fall of the blood glucose values into the hypoglycaemic range may require a dose adaption of the respective co-medication. If acute hypoglycemia develops glucose should be used for rapid correction of hypoglycaemia (see section 4.5). Episodes of hypoglycaemia occurring during therapy must, where appropriate, be treated by the administration of glucose, not sucrose. This is because acarbose will delay the digestion and absorption of disaccharides, but not monosaccharides. Transaminases: Cases of fulminant hepatitis have been reported during Glucobay therapy. The mechanism is unknown, but Glucobay may contribute to a multifactorial pathophysiology of liver injury. It is recommended that liver enzyme monitoring is considered during the first 6 to 12 months of treatment (see section 4.8). If elevated liver enzymes are observed, a reduction in dosage or withdrawal of therapy may be warranted, particularly if the elevations persist. In such circumstances, patients should be monitored at weekly intervals until normal values are established. The administration of antacid preparations containing magnesium and aluminium salts, e.g. hydrotalcite, has been shown not to ameliorate the acute gastrointestinal symptoms of Glucobay in higher dosage and should, therefore, not be recommended to patients for this purpose. 4.5 Interaction with other medicinal products and other forms of interaction When administered alone, Glucobay does not cause hypoglycaemia. It may, however, act to potentiate the hypoglycaemic effects of insulin, metformin and sulphonylurea drugs, and the dosages of these agents may need to be modified accordingly. In individual cases hypoglycaemic shock may occur (i.e. clinical sequelae of glucose levels < 1 mmol/L such as altered conscious levels, confusion or convulsions). Episodes of hypoglycaemia occurring during therapy must, where appropriate, be treated by the administration of glucose, not sucrose. This is because acarbose will delay the digestion and absorption of disaccharides, but not monosaccharides. Sucrose (cane sugar) and foods containing sucrose often cause abdominal discomfort or even diarrhoea during treatment with Glucobay tablets as a result of increased carbohydrate fermentation in the colon. Intestinal adsorbents (e.g. charcoal) and digestive enzyme preparations containing carbohydrate splitting enzymes (e.g. amylase, pancreatin) may reduce the effect of Glucobay and should not therefore be taken concomitantly. The concomitant administration of neomycin may lead to enhanced reductions of postprandial blood glucose and to an increase in the frequency and severity of gastro-intestinal side-effects. If the symptoms are severe, a temporary dose reduction of Glucobay may be warranted. The concomitant administration of colestyramine may enhance the effects of Glucobay, particularly with respect to reducing postprandial insulin levels. Simultaneous administration of Glucobay and colestyramine should, therefore, be avoided. In the rare circumstance that both Glucobay and colestyramine therapy are withdrawn simultaneously, care is needed as a rebound phenomenon has been observed with respect to insulin levels in non-diabetic subjects. In individual cases Glucobay may affect digoxin bioavailability, which may require dose adjustment of digoxin. Monitoring of serum digoxin levels should be considered. In a pilot study to investigate a possible interaction between Glucobay and nifedipine, no significant or reproducible changes were observed in the plasma nifedipine profiles. 4.6 Fertility, pregnancy and lactation Glucobay should not be administered during pregnancy as no information is available from clinical studies on its use in pregnant women. After the administration of radioactively marked acarbose to nursing rats, a small amount of radioactivity was recovered in the milk. To date there have been no similar findings in humans. Nevertheless, as the possibility of drug induced effects on nursing infants can not be excluded, the prescription of Glucobay is not recommended during breast-feeding. 4.7 Effects on ability to drive and use machines None known. 4.8 Undesirable effects The frequencies of adverse drug reactions (ADRs) reported with Glucobay, based on placebo-controlled studies (Glucobay N = 8,595; placebo N = 7,278), are summarised in the table below. Within each frequency grouping, undesirable effects are presented in order of decreasing seriousness. Frequencies are defined as very common (≥ 1/10), common (≥ 1/100 to < 1/10), uncommon (≥ 1/1,000 to < 1/100) and rare (≥ 1/10,000 to < 1/1,000). The ADRs identified during postmarketing surveillance only and for which a frequency could not be estimated, are listed under “Not known”. System Organ Class (MedDRA) Very common Common Uncommon Rare Not known Blood and lymphatic system disorders Thrombocytopenia Immune system disorders Drug hypersensivity and hypersensivity (rash, erythema, exanthema, urticaria) Vascular disorders Oedema Gastrointestinal disorders Flatulence Diarrhoea Gastrointestinal and abdominal pains Nausea Vomiting Dyspepsia Subileus/Ileus Pneumatosis cystoides intestinalis Hepatobiliary disorders Increase in transaminases Jaundice Hepatitis Skin and subcutaneous tissue disorders Acute generalised exanthematous pustulosis In postmarketing, cases of liver disorder, hepatic function abnormal, and liver injury have been reported. Individual cases of fulminant hepatitis with fatal outcome have also been reported, particularly from Japan. In patients receiving the recommended daily dose of 150 to 300 mg Glucobay, clinically relevant abnormal liver function tests (three times above upper limit of normal range) were rarely observed. Abnormal values may be transient under ongoing Glucobay therapy (see section 4.4). If the prescribed diabetic diet is not observed the intestinal side effects may be intensified. If strongly distressing symptoms develop in spite of adherence to the diabetic diet prescribed, the doctor must be consulted and the dose temporarily or permanently reduced. Reporting of suspected adverse reactions Reporting suspected adverse reactions after authorisation of the medicinal product is important. It allows continued monitoring of the benefit/risk balance of the medicinal product. Healthcare professionals are asked to report any suspected adverse reactions via the Yellow Card Scheme at: www.mhra.gov.uk/yellowcard. 4.9 Overdose When Glucobay tablets are taken with drinks and/or meals containing carbohydrates overdose may lead to meteorism, flatulence and diarrhoea. If Glucobay tablets are taken in overdose independently of food, excessive intestinal symptoms need not be anticipated. No specific antidotes to Glucobay are known. Intake of carbohydrate-containing meals or beverages should be avoided for 4-6 hours. Diarrhoea should be treated by standard conservative measures. 5. Pharmacological properties 5.1 Pharmacodynamic properties Pharmacotherapeutic group: drugs used in diabetes, alpha-glusosidase inhibitors, ATC code: A10BF01 In all species tested, acarbose exerts its activity in the intestinal tract. The action of acarbose is based on the competitive inhibition of intestinal enzymes (α-glucosidases) involved in the degradation of disaccharides, oligosaccharides, and polysaccharides. This leads to a dose-dependent delay in the digestion of these carbohydrates. Glucose derived from these carbohydrates is released and taken up into the blood more slowly. In this way, acarbose reduces the postprandial rise in blood glucose, thus reducing blood glucose fluctuations. 5.2 Pharmacokinetic properties Following administration, only 1-2% of the active inhibitor is absorbed. The pharmacokinetics of Glucobay were investigated after oral administration of the 14C-labelled substance (200mg) to healthy volunteers. On average, 35% of the total radioactivity (sum of the inhibitory substance and any degradation products) was excreted by the kidneys within 96 h. The proportion of inhibitory substance excreted in the urine was 1.7% of the administered dose. 50% of the activity was eliminated within 96 hours in the faeces. The course of the total radioactivity concentration in plasma was comprised of two peaks. The first peak, with an average acarbose-equivalent concentration of 52.2 ± 15.7μg/l after 1.1 ± 0.3 h, is in agreement with corresponding data for the concentration course of the inhibitor substance (49.5 ± 26.9μg/l after 2.1 ± 1.6 h). The second peak is on average 586.3 ± 282.7μg/l and is reached after 20.7 ± 5.2 h. The second, higher peak is due to the absorption of bacterial degradation products from distal parts of the intestine. In contrast to the total radioactivity, the maximum plasma concentrations of the inhibitory substance are lower by a factor of 10-20. The plasma elimination half-lives of the inhibitory substance are 3.7 ± 2.7 h for the distribution phase and 9.6 ± 4.4 h for the elimination phase. A relative volume of distribution of 0.32 l/kg body-weight has been calculated in healthy volunteers from the concentration course in the plasma. 5.3 Preclinical safety data Acute toxicity LD50 studies were performed in mice, rats and dogs. Oral LD50 values were estimated to be > 10 g/kg body-weight. Intravenous LD50 values ranged from 3.8 g/kg (dog) to 7.7 g/kg (mouse). Sub-chronic toxicity Three month studies have been conducted in rats and dogs in which acarbose was administered orally by gavage. In rats, daily doses of up to 450 mg/kg body-weight were tolerated without drug-related toxicity. In the dog study, daily doses of 50-450 mg/kg were associated with decreases in body-weight. This occurred because dosing of the animals took place shortly before the feed was administered, resulting in the presence of acarbose in the gastro-intestinal tract at the time of feeding. The pharmacodynamic action of acarbose led to a reduced availability of carbohydrate from the feed, and hence to weight loss in the animals. A greater time interval between dosing and feeding in the rat study resulted in most of the drug being eliminated prior to feed intake, and hence no effect on body-weight development was observed. Owing to a shift in the intestinal α-amylase synthesis feedback mechanism a reduction in serum α-amylase activity was also observed in the dog study. Increases in blood urea concentrations in acarbose-treated dogs also occurred, probably as a result of increased catabolic metabolism associated with the weight loss. Chronic toxicity In rats treated for one year with up to 4500 ppm acarbose in their feed, no drug-related toxicity was observed. In dogs, also treated for one year with daily doses of up to 400 mg/kg by gavage, a pronounced reduction in body-weight development was observed, as seen in the sub-chronic study. Again this effect was due to an excessive pharmacodynamic activity of acarbose and was reversed by increasing the quantity of feed. Carcinogenicity studies In a study in which Sprague-Dawley rats received up to 4500 ppm acarbose in their feed for 24-26 months, malnutrition was observed in animals receiving the drug substance. A dose-dependent increase in tumours of the renal parenchyma (adenoma, hypernephroid carcinoma) was also observed against a background of a decrease in the overall tumour rate. When this study was repeated, an increase in benign tumours of testicular Leydig cells was also observed. Owing to the malnutrition and excessive decrease in bodyweight gain these studies were considered inadequate to assess the carcinogenic potential of acarbose. In further studies with Sprague-Dawley rats in which the malnutrition and glucose deprivation were avoided by either dietary glucose supplementation or administration of acarbose by gavage, no drug-related increases in the incidences of renal or Leydig cell tumours were observed. In an additional study using Wistar rats and doses of up to 4500 ppm acarbose in the feed, neither drug-induced malnutrition nor changes in the tumour profile occurred. Tumour incidences were also unaffected in hamsters receiving up to 4000 ppm acarbose in the feed for 80 weeks (with and without dietary glucose supplementation). Reproductive toxicity There was no evidence of a teratogenic effect of acarbose in studies with oral doses of up to 480 mg/kg/day in rats and rabbits. In rats no impairment of fertility was observed in males or females at doses of up to 540 mg/kg/day. The oral administration of up to 540 mg/kg/day to rats during foetal development and lactation had no effect on parturition or on the young. Mutagenicity The results of a number of mutagenicity studies show no evidence of a genotoxic potential of acarbose. 6. Pharmaceutical particulars 6.1 List of excipients Glucobay tablets contain the following excipients: Microcrystalline cellulose Silica, colloidal anhydrous Magnesium stearate Maize starch 6.2 Incompatibilities None stated. 6.3 Shelf life 3 years 6.4 Special precautions for storage The tablets should be stored in the manufacturer's original container in a dry place at temperatures below 25°C. 6.5 Nature and contents of container Blister strips comprising 300μm polypropylene foil (colourless) with a 20μm soft aluminium backing foil, in cardboard outers. Pack sizes: 90 6.6 Special precautions for disposal and other handling None stated. 7. Marketing authorisation holder Bayer plc Bayer House Strawberry Hill Newbury Berkshire RG14 1JA 8. Marketing authorisation number(s) PL 00010/0171 9. Date of first authorisation/renewal of the authorisation 28 May 1993 / 16 February 2004 10. Date of revision of the text 10/08/2015 附：Glucobay 100 mg tablets（http://www.medicines.org.uk/emc/medicine/19973） --------------------------------------------------------------- 注：以下产品来同规格和不同价格，采购请以咨询为准！ --------------------------------------------------------------- 产地国家: 欧洲共同体国家 原产地英文商品名: GLUCOBAY 100MG/TAB 21TABS/BOX 原产地英文药品名: ACARBOSE 中文参考商品译名: 拜唐苹 100毫克/片 21片/盒 中文参考药品译名: 阿卡波糖 生产厂家中文参考译名: 拜耳 生产厂家英文名: Bayer Vital GmbH Gesch&auml;ftsbereich Pharma --------------------------------------------------------------- 产地国家: 欧洲共同体国家 原产地英文商品名: GLUCOBAY 100MG/TAB 105TABS/BOX 原产地英文药品名: ACARBOSE 中文参考商品译名: 拜唐苹 100毫克/片 105片/盒 中文参考药品译名: 阿卡波糖 生产厂家中文参考译名: 拜耳 生产厂家英文名: Bayer Vital GmbH Gesch&auml;ftsbereich Pharma ---------------------------------------------------------------- 产地国家: 欧洲共同体国家 原产地英文商品名: GLUCOBAY 100MG/TAB 30TABS/BOX 原产地英文药品名: ACARBOSE 中文参考商品译名: 拜唐苹 100毫克/片 30片/盒 中文参考药品译名: 阿卡波糖 生产厂家中文参考译名: 拜耳 生产厂家英文名: Bayer Vital GmbH Gesch&auml;ftsbereich Pharma ----------------------------------------------------------------- 产地国家: 欧洲共同体国家 原产地英文商品名: GLUCOBAY 100MG/TAB 100TABS/BOX 原产地英文药品名: ACARBOSE 中文参考商品译名: 拜唐苹 100毫克/片 100片/盒 中文参考药品译名: 阿卡波糖 生产厂家中文参考译名: 拜耳 生产厂家英文名: Bayer Vital GmbH Gesch&auml;ftsbereich Pharma