英国药典【BP】兰索拉唑【Lansoprazole】
LansoprazoleGeneral Notices(Ph Eur monograph 2219)It shows polymorphism (5.9).IDENTIFICATIONInfrared absorption spectrophotometry (2.2.24).Comparison lansoprazole CRS.If the spectra obtained in the solid state show differences, dissolve the substance to be examined and the reference substance separately in anhydrous ethanol R, evaporate toexamined and the reference substance separately in anhydrous ethanol R, evaporate to dryness and record new spectra using the residues.TESTSAppearance of solutionThe solution is clear (2.2.1) and not more intensely coloured than reference solution B2 or BY2 (2.2.2, Method II).Dissolve 1.0 g in dimethylformamide R and dilute to 20 ml with the same solvent.Related substancesLiquid chromatography (2.2.29). Prepare the solutions immediately before use and protect them from light.Solvent mixture Mix 1 volume of triethylamine R with 60 volumes of water R; adjust the pH to 10.5 using phosphoric acid R; mix the solution obtained with 40 volumes of acetonitrile R1.Test solution Dissolve 10 mg of the substance to be examined in the solvent mixture and dilute to 10 ml with the solvent mixture.Reference solution (a)Dissolve the contents of a vial of lansoprazole for peak identification CRS (containing impurities A and B) in 1.0 ml of the solvent mixture.Reference solution (b)Dilute 2.0 ml of the test solution to 100.0 ml with the solvent mixture. Dilute 1.0 ml of this solution to 10.0 ml with the solvent mixture.Reference solution (c)Dissolve 5 mg of 2-mercaptobenzimidazole R (impurity E) and 5 mg of 2-hydroxybenzimidazole R (impurity D) in the solvent mixture and dilute to 100 ml with the solvent mixture. Dilute 1 ml of this solution to 10 ml with the solvent mixture.Column:— size: l = 0.25 m, Ø = 4.6 mm;— stationary phase: amidohexadecylsilyl silica gel for chromatography R (5 µm).Mobile phase Mix 1 volume of triethylamine R with 60 volumes of water R; adjust the pH to 6.2 using phosphoric acid R; mix the solution obtained with 40 volumes of acetonitrile R1. Flow rate 1.2 ml/min.Detection Spectrophotometer at 285 nm.Injection10 µl.Run time 3 times the retention time of lansoprazole.Identification of impurities Use the chromatogram supplied with lansoprazole for peak identification CRS and the chromatogram obtained with reference solution (a) to identify the peaks due to impurities A and B; use the chromatogram obtained with reference solution (c) to identify the peaks due to impurities D and E.Relative retention With reference to lansoprazole (retention time = about 7 min): impurity D = about 0.4; impurity A = about 0.5; impurity E = about 0.6; impurity B = about 1.2.System suitability Reference solution (a):— resolution: minimum 3.0 between the peaks due to lansoprazole and impurity B.Limits:Limits:— correction factor: for the calculation of content, multiply the peak area of impurity E by 0.4;— impurity B: not more than twice the area of the principal peak in the chromatogram obtained with reference solution (b) (0.4 per cent);— impurities A, D, E: for each impurity, not more than 0.5 times the area of the principal peak in the chromatogram obtained with reference solution (b) (0.1 per cent);— unspecified impurities: for each impurity, not more than 0.5 times the area of the principal peak in the chromatogram obtained with reference solution (b) (0.10 per cent);— total: not more than 3 times the area of the principal peak in the chromatogram obtained with reference solution (b) (0.6 per cent);— disregard limit: 0.25 times the area of the principal peak in the chromatogram obtained with reference solution (b) (0.05 per cent).Water (2.5.32)Maximum 0.1 per cent, determined on 1.000 g.Sulphated ash (2.4.14)Maximum 0.1 per cent, determined on 1.0 g.ASSAYDissolve 0.300 g in 40 ml of ethanol (96 per cent) R and dilute to 50 ml with water R. Titrate with 0.1 M sodium hydroxide, determining the end-point potentiometrically (2.2.20).1 ml of 0.1 M sodium hydroxide is equivalent to 36.94 mg of C16H14F3N3O2S.STORAGEIn an airtight container, protected from light.IMPURITIESSpecified impurities A, B, D, E.Other detectable impurities(The following substances would, if present at a sufficient level, be detected by one or other of the tests in the monograph. They are limited by the general acceptance criterion for other/unspecified impurities and/or by the general monograph Substances for pharmaceutical use (2034). It is therefore not necessary to identify these impurities for demonstration of compliance. See also 5.10. Control of impurities in substances for pharmaceutical use): C, F.A. 2-[(RS)-[[3-methyl-1-oxido-4-(2,2,2-trifluoroethoxy)pyridin-2-yl]methyl]sulphinyl]-1H-benzimidazole,B. X = SO2: 2-[[[3-methyl-4-(2,2,2-trifluoroethoxy)pyridin-2-yl]methyl]sulphonyl]-1H-benzimidazole,C. X = S: 2-[[[3-methyl-4-(2,2,2-trifluoroethoxy)pyridin-2-yl]methyl]sulphanyl]-1H-benzimidazole,D. R = OH: 1H-benzimidazol-2-ol,E. R = SH: 1H-benzimidazole-2-thiol,Lauroyl Macrogolglycerides。
兰索拉唑片(可意林)的说明书
兰索拉唑片(可意林)的说明书生活交际当中难免遇到吃喝聚会，因此一部分人的胃肠疾病也就接踵而至了。
目前治疗胃肠疾病最好的药物当属兰索拉唑片(可意林)了，它对于人体没有任何副作用，您可以放心使用。
针对胃肠疾病比较严重的患者，我们极力推荐您使用兰索拉唑片(可意林)进行治疗，其效果立竿见影。
【药品名称】通用名称：兰索拉唑片商品名称：兰索拉唑片(可意林)英文名称：Lansoprazole Tablets拼音全码：LanSuoLaZuoPian(KeYiLin)【主要成份】本品主要成份为兰索拉唑。
化学名：（+）-2[3—甲基—4—（2,2,2—三氟乙氧基）—2吡啶基]—1H—苯并咪唑。
【成份】分子式：C16H14F3N3O2S分子量：369.37【性状】该品为肠溶片，除去包衣后显白色或类白色。
【适应症/功能主治】胃溃疡、十二指肠溃疡、反流性食管炎、佐-艾（Zollinger-Ellison）综合征（胃泌素瘤）。
【规格型号】15mg*14s【用法用量】治疗胃溃疡和十二指肠溃疡，每日清晨口服1次，一次15~30mg。
或遵医嘱。
【不良反应】本品副作用轻微，主要表现为口干、头晕、恶心。
【禁忌】孕妇、哺乳期妇女忌用。
【注意事项】1、治疗过程中应注意观察，因长期使用的经验不足，暂不推荐用于维持治疗。
2、本品服用时请不要嚼碎，应整片用水吞服。
3、下列患者慎重用药。
（1）曾发生药物过敏症的患者。
（2）肝肾功能障碍的患者。
4、因本药会掩盖胃癌的症状，所以须先排除胃癌，方可给药。
【儿童用药】遵医嘱。
【老年患者用药】遵医嘱。
【孕妇及哺乳期妇女用药】孕妇、哺乳期妇女忌用。
【药物相互作用】如与其他药物同时使用可能会发生药物相互作用，详情请咨询医师或药师。
【药物过量】尚不明确。
【药理毒理】该品为新型的抑制胃酸分泌的药物，它作用于胃壁细胞的H+-K+-ATP酶，使壁细胞的H+不能转运到胃中去，以致胃液中胃酸量大为减少，临床上用于十二指肠溃疡、胃溃疡、反流性食管炎，佐-艾（Zollinger-Ellison）综合征（胃泌素瘤）的治疗，疗效显著，对幽门螺杆菌有抑制作用。
兰索拉唑
【药物名称】兰索拉唑Lansoprazole [国家基本药物]【药物类别】抗消化性溃疡药其结构式为：分子式：C16H14F3N3O2S 分子量：369.37【性状】【性状】略带褐色的白色结晶性粉末。
熔点（分解）166℃；易溶于二甲基甲酰胺，可溶于甲醇，难溶于无水乙醇，极难溶于乙醚，几乎不溶于水。
【药物别名】达克普隆，兰素拉唑Takepron、Prevacid【分子式成分】2-[3-甲基-4-(2,2,2-村氟乙氧基)-2-吡啶基]亚磺酰]-1H-苯并咪唑。
本品为结晶,M.P.178-182℃。
【制剂规格】胶囊：15mg、30mg。
【药理毒理】本药转移到胃粘膜壁细胞的酸分泌细管后，在酸性条件下，转变为活性体结构，此种活性物与质子泵((H+＋K+)-ATPase)的SH基结合，从而抑制该酶的活性，故能抑制胃酸的分泌。
1.(H+＋K+)-ATPase活性抑制作用兰索拉唑可抑制狗胃粘膜内微粒体的(H+＋K+)-ATPase活性(体外实验)。
2.壁细胞酸生成抑制作用兰索拉唑对狗胃粘膜离体壁细胞由组胺、乙酰胆碱及胃泌素的刺激所产生的酸分泌，皆具有抑制作用(体外实验)。
3.胃酸分泌抑制作用1)对胃泌素刺激引起的酸分泌：于健康成人，1天1次兰索拉唑30mg口服给药，连续7天，可明显地抑制由胃泌素引起的酸分泌，且此作用能持续24小时。
2)对胰岛素刺激引起的酸分泌：于健康成人，1天1次兰索拉唑30mg口服给药，连续7天，可明显地抑制由胰岛素引起的酸分泌。
3)对夜间的酸分泌：于健康成人，1天1次兰索拉唑30mg口服给药，连续7天，具有明显地抑制夜间胃酸分泌的作用。
4)对24小时的酸分泌：于健康成人24小时胃液采样试验，以1天1次兰索拉唑30mg口服给药连续7天，24小时的胃酸分泌明显地受到抑制。
5)24小时胃内pH值的监测：对健康成人以及十二指肠溃疡患者，以1天1次兰索拉唑30mg口服给药连续7天，24小时的胃酸分泌皆明显地受到抑制。
兰索拉唑肠溶片有关物质测定方法比较
兰索拉唑肠溶片有关物质测定方法比较尚海巍;葛会奇【摘要】目的比较研究测定兰索拉唑肠溶片有关物质的两种标准测定方法.方法这两种方法分别收载于中国药典2010年版增补本和英国药典(BP2010).两种方法均使用高效液相色谱法(HPLC),色谱柱分别为Kromasil C18(250 mm×4.6mm,5μm)和ECOSIL C18(250 mm ×4.6 mm,5μm),流动相分别为甲醇-水-三乙胺-磷酸溶液和乙腈-水-三乙胺-磷酸溶液.结果英国药典中的高效液相色谱法测定兰索拉唑肠溶片有关物质优于中国药典标准.结论建议测定兰索拉唑肠溶片有关物质时推广使用英国药典中的高效液相色谱法.【期刊名称】《辽宁科技学院学报》【年(卷),期】2015(017)002【总页数】3页(P31-33)【关键词】兰索拉唑;有关物质;方法比较【作者】尚海巍;葛会奇【作者单位】辽宁科技学院生物医药与化学工程学院,辽宁本溪117004;辽宁科技学院生物医药与化学工程学院,辽宁本溪117004【正文语种】中文【中图分类】R927.2兰索拉唑(lansoprazole)是新一代质子泵抑制剂，大量的临床应用证明其对消化性溃疡有很好的治疗效果，广泛用于治疗各种与酸分泌相关的消化功能紊乱性疾病。
它可以抑制各种原因引起的胃酸分泌，保护并促进胃粘膜溃疡愈合〔1〕。
兰索拉唑为2[[[3-甲基-4-(2,2,2-三氟乙氧基)-2-吡啶基]甲基]亚硫酰基]苯并咪唑，苯并咪唑结构的存在使其对光、热、湿均不稳定。
兰索拉唑及其已知杂质(A-F)结构见图1。
兰索拉唑肠溶片质量标准收载于《中国药典》2010版增补本〔2〕(ChP 2010)，《英国药典》2010版〔3〕(BP 2010)、《英国药典》2012增补本〔4〕(BP 2012 Supplement)。
以上方法均采用高效液相色谱法对有关物质进行了检查，并且BP 2010兰索拉唑肠溶片、BP 2012 Updated 兰索拉唑肠溶片有关物质方法色谱条件完全相同。
兰索拉唑药物简析
兰索拉唑药物简析lansoprazole Drug Report一、摘要信息药物英文名：lansoprazole药物中文名：兰索拉唑药物别名：A-65006; AG-1749; Agopton; Bamalite; Dakar; Ilsatec; Lansone; Lansox; Lanzo; Lanzor; Laprazol; Limpidex; Ogast; Ogastro; Opiren; Prevacid; Prezal; Takepron; Zoton原研单位：Takeda (Originator), Almirall Prodesfarma (Licensee), Salvat (Licensee), TAP (Licensee), Wyeth Pharmaceuticals (Licensee)全球最高状态：1995年批准上市中国是否上市：是二、药物概述本品最初由武田制药合成，1984年武田申请专利，1991年本品上市，1995 年首次获得美国食品和药物管理局（FDA）批准。
自2009年以来，本品已作为美国非处方药，由诺华公司以Prevacid 24HR销售，在澳大利亚由辉瑞以Zoton销售[CK020192]。
本品可以用来治疗胃溃疡或反流性食道炎及其它胃酸过多引起的病症。
它能够抑制胃壁细胞内昊有催化作用的蛋白质称为ATP酶（ATPase）的作用，使胃酸生产的最后步骤受到阻碍，最后直接减少胃酸的产生并降低胃或食道的刺激，使得溃疡部份渐渐地得到休息康复。
此药也可与其它抗生素一起服用，治疗由H.pylori细菌感染所造成的胃渍疡[CK020193]。
三、API信息四、合成线路合成线路1：合成线路2：五、药理作用ATC分类：A02BC03 消化道及代谢 > 治疗与胃酸分泌相关疾病的药物 > 消化道溃疡和胃食管返流病治疗药物 > 质子泵抑制药作用靶点：PPI参考靶点：Potassium-transporting ATPase alpha chain 1; Microtubule-associated protein tau 作用机制：Lansoprazole belongs to a class of antisecretory compounds, the substituted benzimidazoles, that do not exhibit anticholinergic or histamine H2-receptor antagonist properties, but rather suppress gastric acid secretion by specific inhibition of the (H+,K+)-ATPase enzyme system at the secretory surface of the gastric parietal cell. Because this enzyme system is regarded as the acid (proton) pump within the parietal cell, Lansoprazole has been characterized as a gastric acid-pump inhibitor, in that it blocks the final step of acid production. This effect is dose-related and leads to inhibition of both basal and stimulated gastric acid secretion irrespective of the stimulus.六、中国临床试验数据库（29条）七、国外药典在线（35条）八、美国FDA橙皮书数据库（62条）九、参比制剂备案数据库（37条）十、美国FDA药品说明书（109条）以上是整理的部分关于“兰索拉唑药物”的数据信息，内容中只选取了部分数据库及部分内容作为展示，如需要兰索拉唑药物更详细的报告，请进入药智论坛下载，或者购买药智数据VIP账号进入直接下载完整报告。
兰索拉唑的代谢原理
兰索拉唑的代谢原理
兰索拉唑（Lansoprazole）是一种质子泵抑制剂，通过抑制胃酸分泌起作用。
其代谢原理如下：
1. 吸收：兰索拉唑在胃酸的存在下，可被迅速吸收。
在胃中，兰索拉唑会转化为活性代谢物，即兰索拉唑砷酮（lansoprazole sulfone）。
2. 转化：兰索拉唑砷酮是兰索拉唑的主要代谢产物，它也具有质子泵抑制作用，能够抑制胃酸分泌。
这种转化是通过肝脏中的细胞色素P450酶（CYP2C19和CYP3A4）介导的。
3. 消除：兰索拉唑砷酮的半衰期较长，为约1.5-2.0小时。
它主要通过肝脏和肾脏的代谢和排泄来清除体内。
总的来说，兰索拉唑在胃中被转化为活性代谢物，然后通过抑制胃酸分泌来发挥作用。
最终，代谢产物被排泄出体外，完成药物的消除过程。
兰索拉唑萘普生
(No. 1546)PRV0509 R9, May 2009PREVACID® NapraPAC ®500(lansoprazole delayed-release 15 mg capsules and naproxen 500 mg tablets kit)Rx onlyCardiovascular Risk• NSAIDs (a nonsteroidal anti-inflammatory drug) may cause an increased risk of serious cardiovascular thrombotic events, myocardial infarction, and stroke, which can be fatal. This risk may increase with duration of use. Patients with cardiovascular disease or risk factors for cardiovascular disease may be at greater risk (see WARNINGS).• PREVACID NapraPAC is contraindicated for the treatment of peri-operative pain in the setting of coronary artery bypass graft (CABG) surgery (see WARNINGS).Gastrointestinal (GI) Risk• NSAIDs cause an increased risk of serious GI adverse events including bleeding and perforation of the stomach and intestines, which can be fatal. These events can occur at any time during use and without warning symptoms. Patients with a history of gastric and/or duodenal ulcers (especially patients with a history of bleeding or perforation) and geriatric patients are at greater risk for serious GI events (see WARNINGS and CLINICAL STUDIES, Risk Reduction of NSAID-Associated Gastric Ulcer(s)). PREVACID® NapraPAC ®500 is a combination package containing two individual drug products: PREVACID® (lansoprazole) Delayed-Release Capsules, a proton pump inhibitor (PPI), and NAPROSYN® (naproxen tablets), a nonsteroidal anti-inflammatory drug (NSAID) with analgesic and antipyretic properties. The information described in this labeling concerns only the use of these products as indicated in this combination package and does not include all individual use information. For information on use of the components when dispensed as individual medications outside this combination package, please see the package inserts for PREVACID Delayed-Release Capsules and NAPROSYN Tablets.DESCRIPTIONPREVACID NapraPAC 500 is a combination package containing NAPROSYN 500 mg tablets and PREVACID 15 mg capsules.NAPROSYNNaproxen is a proprionic acid derivative related to the arylacetic acid group of NSAIDs. The chemical name for naproxen is (S)-6-methoxy-α-methyl-2-naphthaleneacetic acid and naproxen has the following structure:O N H NS CH 2 N H 3C2CF 3Naproxen has a molecular weight of 230.26 and a molecular formula of C 14H 14O 3.Naproxen is an odorless, white to off-white crystalline substance. It is lipid-soluble, practically insolublein water at low pH and freely soluble in water at high pH. The octanol/water partition coefficient ofnaproxen at pH 7.4 is 1.6 to 1.8.NAPROSYN (naproxen tablets) is available as yellow tablets containing 500 mg of naproxen for oral administration. The inactive ingredients are croscarmellose sodium, iron oxides, povidone, and magnesium stearate.PREVACID The active ingredient in PREVACID Delayed-Release capsules is lansoprazole, a substitutedbenzimidazole, 2-[[[3-methyl-4-(2,2,2-trifluoroethoxy)-2-pyridyl]methyl] sulfinyl] benzimidazole, a compound that inhibits gastric acid secretion. Its empirical formula is C 16H 14F 3N 3O 2S with a molecular weight of 369.37. PREVACID has the following structure: CH 3 3 Lansoprazole is a white to brownish-white odorless crystalline powder which melts with decomposition at approximately 166°C. Lansoprazole is freely soluble in dimethylformamide; soluble in methanol; sparingly soluble in ethanol; slightly soluble in ethyl acetate, dichloromethane and acetonitrile; very slightly soluble in ether; and practically insoluble in hexane and water.Lansoprazole is stable when exposed to light for up to two months. The rate of degradation of the compound in aqueous solution increases with decreasing pH. The degradation half-life of the drug substance in aqueous solution at 25ºC is approximately 0.5 hour at pH 5 and approximately 18 hours at pH 7.PREVACID Delayed-Release capsules contain enteric-coated granules consisting of 15 mg of lansoprazole (active ingredient) and the following inactive ingredients: sugar sphere, sucrose,methacrylic acid copolymer, low substituted hydroxypropyl cellulose, starch, magnesium carbonate, talc, polyethylene glycol, titanium dioxide, polysorbate 80, hydroxypropyl cellulose, colloidal silicon dioxide, D&C Red No. 28, FD&C Blue No. 1, FD&C Green No. 3, and FD&C Red No. 40.CLINICAL PHARMACOLOGYPharmacokineticsNAPROSYNAbsorptionNaproxen is rapidly and completely absorbed from the GI tract with an in vivo bioavailability of 95%. After administration of NAPROSYN tablets, peak plasma levels are attained in 2 to 4 hours. The elimination half-life of naproxen ranges from 12 to 17 hours. Steady-state levels of naproxen are reached in 4 to 5 days, and the degree of naproxen accumulation is consistent with this half-life.DistributionNaproxen has a volume of distribution of 0.16 L per kg. At therapeutic levels, naproxen is greater than 99% albumin-bound. At doses of naproxen greater than 500 mg per day, there is less than proportional increase in plasma levels due to an increase in clearance caused by saturation of plasma protein binding at higher doses (average trough concentrations at steady state were 36.5, 49.2 and 56.4 mg per L with 500, 1000, and 1500 mg daily doses of naproxen, respectively).The naproxen anion has been found in the milk of lactating women at a concentration equivalent to approximately 1% of the maximum naproxen concentration in plasma (see PRECAUTIONS, Nursing Mothers).MetabolismNaproxen is extensively metabolized in the liver to 6-0-desmethyl naproxen, and both parent and metabolites do not induce metabolizing enzymes. Both naproxen and 6-0-desmethyl naproxen are further metabolized to their respective acylglucuronide conjugated metabolites.ExcretionThe clearance of naproxen is 0.13 mL per min per kg. Approximately 95% of the naproxen from any dose is excreted in the urine, primarily as naproxen (less than 1%), 6-0-desmethyl naproxen (less than 1%) or their conjugates (66% to 92%). The plasma half-life of the naproxen anion in humans ranges from 12 to 17 hours. The corresponding half-lives of both naproxen’s metabolites and conjugates are shorter than 12 hours, and their rates of excretion have been found to coincide closely with the rate of naproxen disappearance from the plasma. Small amounts, 3% or less of the administered dose, are excreted in the feces. In patients with renal failure metabolites may accumulate (see WARNINGS, Renal Effects).Special PopulationsPediatric PatientsThe combination of naproxen and lansoprazole has not been studied in pediatric patients (see CLINICAL PHARMACOLOGY, PREVACID Special Populations – Pediatric Use).Geriatric PatientsStudies indicate that although total plasma concentration of naproxen is unchanged, the unbound plasma fraction of naproxen is increased in the elderly, although the unbound fraction is less than 1% of the total naproxen concentration. Unbound trough naproxen concentrations in elderly subjects have beenreported to range from 0.12% to 0.19% of total naproxen concentration, compared with 0.05% to 0.075% in younger subjects. The clinical significance of this finding is unclear; although, it is possible that the increase in free naproxen concentration could be associated with an increase in the rate of adverse events per a given dosage in some elderly patients.RacePharmacokinetic differences due to race have not been studied.Hepatic InsufficiencyNaproxen pharmacokinetics has not been determined in subjects with hepatic insufficiency.Renal InsufficiencyNaproxen pharmacokinetics has not been determined in subjects with renal insufficiency. Given that naproxen, its metabolites and conjugates are primarily excreted by the kidney, the potential exists for naproxen metabolites to accumulate in the presence of renal insufficiency (see CLINICAL PHARMACOLOGY, PREVACID Special Populations -Renal Insufficiency). Elimination of naproxen is decreased in patients with severe renal impairment. Naproxen-containing products are not recommended for use in patients with moderate to severe and severe renal impairment – (creatinine clearance less than 30 mL per min – see WARNINGS, Renal Effects).PREVACIDPREVACID Delayed-Release capsules contain an enteric-coated granule formulation of lansoprazole. Absorption of lansoprazole begins only after the granules leave the stomach. Absorption is rapid, with mean peak plasma levels of lansoprazole occurring after approximately 1.7 hours. After a single-dose administration of 15 mg to 60 mg of oral lansoprazole, the peak plasma concentrations (C max) of lansoprazole and the area under the plasma concentration curves (AUCs) of lansoprazole were approximately proportional to the administered dose. Lansoprazole does not accumulate and its pharmacokinetics are unaltered by multiple dosing.AbsorptionThe absorption of lansoprazole is rapid, with the mean C max occurring approximately 1.7 hours after oral dosing, and the absolute bioavailability is over 80%. In healthy subjects, the mean (± SD) plasma half-life was 1.5 (± 1.0) hours. Both the C max and AUC are diminished by about 50 to 70% if lansoprazole is given 30 minutes after food, compared to the fasting condition. There is no significant food effect if lansoprazole is given before meals.DistributionLansoprazole is 97% bound to plasma proteins. Plasma protein binding is constant over the concentration range of 0.05 to 5 mcg per mL.MetabolismLansoprazole is extensively metabolized in the liver. Two metabolites have been identified in measurable quantities in plasma (the hydroxylated sulfinyl and sulfone derivatives of lansoprazole). These metabolites have very little or no antisecretory activity. Lansoprazole is thought to betransformed into two active species which inhibit acid secretion by blocking the proton pump [(H+,K+)ATPase enzyme system] at the secretory surface of the gastric parietal cell. The two active species are not present in the systemic circulation. The plasma elimination half-life of lansoprazole is less than 2 hours while the acid inhibitory effect lasts more than 24 hours. Therefore, the plasma elimination half-life of lansoprazole does not reflect its duration of suppression of gastric acid secretion.EliminationFollowing single-dose oral administration of PREVACID, virtually no unchanged lansoprazole was excreted in the urine. In one study, after a single oral dose of14C-lansoprazole, approximately one-third of the administered radiation was excreted in the urine and two-thirds was recovered in the feces. This implies a significant biliary excretion of the lansoprazole metabolites.Special PopulationsPediatric UseThe combination of lansoprazole and naproxen has not been studied in pediatric patients (see CLINICAL PHARMACOLOGY, NAPROSYN Special Populations – Pediatric Use).Geriatric UseThe clearance of lansoprazole is decreased in the elderly, with elimination half-life increased approximately 50% to 100%. Because the mean half-life in the elderly remains between 1.9 to2.9 hours, repeated once daily dosing does not result in accumulation of lansoprazole. Peak plasma levels were not increased in the elderly.GenderIn a study comparing 12 male and 6 female human subjects who received lansoprazole, no gender differences were found in pharmacokinetics and intragastric pH results (see PRECAUTIONS, PREVACID Use in Women).Renal InsufficiencyIn patients with severe renal insufficiency, plasma protein binding decreased by 1% to 1.5% after administration of 60 mg of lansoprazole. Patients with renal insufficiency had a shortened elimination half-life and decreased total AUC (free and bound). The AUC for free lansoprazole in plasma, however, was not related to the degree of renal impairment; and the C max and T max (time to reach the maximum concentration) were not different than the C max and T max from subjects with normal renal function (see CLINICAL PHARMACOLOGY, NAPROSYN Special Populations -Renal Insufficiency).Hepatic InsufficiencyIn patients with various degrees of chronic hepatic disease, the mean plasma half-life of lansoprazole was prolonged from 1.5 hours to 3.2 to 7.2 hours. An increase in the mean AUC of up to 500% was observed at steady state in hepatically-impaired patients compared to healthy subjects. Dose reductionin patients with severe hepatic disease should be considered.RaceThe pooled mean pharmacokinetic parameters of PREVACID from twelve U.S. Phase I studies (N=513) were compared to the mean pharmacokinetic parameters from two Asian studies (N=20). The meanAUCs of PREVACID in Asian subjects were approximately twice that seen in pooled U.S. data; however, the inter-individual variability was high. The C max values were comparable. PharmacodynamicsNAPROSYNNaproxen is a NSAID with analgesic and antipyretic properties. The mechanism of action of the naproxen anion, like that of other NSAIDs, is not completely understood but may be related to prostaglandin synthetase inhibition.PREVACIDMechanism of ActionPREVACID (lansoprazole) belongs to a class of antisecretory compounds, the substituted benzimidazoles, that suppress gastric acid secretion by specific inhibition of the (H+,K+)-ATPase enzyme system at the secretory surface of the gastric parietal cell. Because this enzyme system is regarded as the acid (proton) pump within the parietal cell, lansoprazole has been characterized as a gastric acid-pump inhibitor, in that it blocks the final step of acid production. This effect is dose-related and leads to inhibition of both basal and stimulated gastric acid secretion irrespective of the stimulus. Lansoprazole does not exhibit anticholinergic or histamine type-2 antagonist activity.Antisecretory ActivityAfter oral administration, lansoprazole was shown to significantly decrease the basal acid output and significantly increase the mean gastric pH and percent of time the gastric pH was greater than 3 and greater than 4. Lansoprazole also significantly reduced meal-stimulated gastric acid output and secretion volume, as well as pentagastrin-stimulated acid output. In patients with hypersecretion of acid, lansoprazole significantly reduced basal and pentagastrin-stimulated gastric acid secretion. Lansoprazole inhibited the normal increases in secretion volume, acidity and acid output induced by insulin.The intragastric pH results of a five-day, pharmacodynamic, crossover study of 15 mg and 30 mg of once daily lansoprazole are presented in Table 1.Table 1: Mean Antisecretory Effects after single andmultiple daily PREVACID dosingPREVACIDParameter BaselineValue15 mgDay 1 Day 530 mgDay 1 Day 5Mean 24-Hour pH Mean Nighttime pH % Time Gastric pH>3 % Time Gastric pH>42.11.918122.7+ 4.0+2.43.0+33+ 59+22+ 49+3.6*4.9*2.63.8*51* 72*41* 66*NOTE: An intragastric pH of greater than 4 reflects a reduction in gastric acid by 99%. *(p<0.05) versus baseline and lansoprazole 15 mg.+(p<0.05) versus baseline only.After the initial dose in this study, increased gastric pH was seen within 1 to 2 hours with 30 mg of lansoprazole and 2 to 3 hours with 15 mg of lansoprazole. After multiple daily dosing, increased gastric pH was seen within the first hour post-dosing with 30 mg of lansoprazole and within 1 to 2 hours post-dosing with 15 mg of lansoprazole.The inhibition of gastric acid secretion as measured by intragastric pH gradually returned to normal over two to four days after multiple doses. There was no indication of rebound gastric acidity. Enterochromaffin-like (ECL) Cell EffectsDuring lifetime exposure of rats with up to 150 mg per kg per day of lansoprazole dosed seven days per week, marked hypergastrinemia was observed followed by ECL cell proliferation and formation of carcinoid tumors, especially in female rats (see PRECAUTIONS, PREVACID Carcinogenesis, Mutagenesis, Impairment of Fertility).Gastric biopsy specimens from the body of the stomach from approximately 150 patients treated continuously with lansoprazole for at least one year did not show evidence of ECL cell effects similar to those seen in rat studies. Longer term data are needed to rule out the possibility of an increased risk of the development of gastric tumors in patients receiving long-term therapy with lansoprazole.Other Gastric Effects in HumansLansoprazole did not significantly affect mucosal blood flow in the fundus of the stomach. Due to the normal physiologic effect caused by the inhibition of gastric acid secretion, a decrease of about 17% in blood flow in the antrum, pylorus, and duodenal bulb was seen. Lansoprazole significantly slowed the gastric emptying of digestible solids. Lansoprazole increased serum pepsinogen levels and decreased pepsin activity under basal conditions and in response to meal stimulation or insulin injection. As with other agents that elevate intragastric pH, increases in gastric pH were associated with increases in nitrate-reducing bacteria and elevation of nitrite concentration in gastric juice in patients with gastric ulcer. No significant increase in nitrosamine concentrations was observed.Serum Gastrin EffectsIn over 2100 patients, median fasting serum gastrin levels increased 50% to 100% from baseline but remained within normal range after treatment with 15 to 60 mg of oral lansoprazole. These elevations reached a plateau within two months of therapy and returned to pretreatment levels within four weeks after discontinuation of therapy.Endocrine EffectsHuman studies for up to one year have not detected any clinically significant effects on the endocrine system. Hormones studied include testosterone, luteinizing hormone (LH), follicle stimulating hormone (FSH), sex hormone binding globulin (SHBG), dehydroepiandrosterone sulfate (DHEA-S), prolactin, cortisol, estradiol, insulin, aldosterone, parathormone, glucagon, thyroid stimulating hormone (TSH), triiodothyronine (T3), thyroxine (T4), and somatotropic hormone (STH). Lansoprazole in oral doses of 15 to 60 mg for up to one year had no clinically significant effect on sexual function. In addition, lansoprazole in oral doses of 15 to 60 mg for two to eight weeks had no clinically significant effect on thyroid function.In 24-month carcinogenicity studies in Sprague-Dawley rats with daily lansoprazole dosages up to150 mg per kg, proliferative changes in the Leydig cells of the testes, including benign neoplasm, were increased compared to control rates.Other EffectsNo systemic effects of lansoprazole on the central nervous system, lymphoid, hematopoietic, renal, hepatic, cardiovascular, or respiratory systems have been found in humans. Among 56 patients who had extensive baseline eye evaluations, no visual toxicity was observed after lansoprazole treatment (up to 180 mg per day) for up to 58 months.After lifetime lansoprazole exposure in rats, focal pancreatic atrophy, diffuse lymphoid hyperplasia in the thymus, and spontaneous retinal atrophy were seen.CLINICAL STUDIESRisk Reduction of NSAID-Associated Gastric Ulcer(s)A large U.S., multicenter, double-blind, placebo- and misoprostol-controlled (misoprostol blinded only to the endoscopist) 12-week study was conducted in patients who required chronic use of an NSAID and had a history of an endoscopically documented gastric ulcer. Patients were randomized to one of the following four treatment groups: PREVACID 15 mg per day, PREVACID 30 mg per day, misoprostol 200 micrograms QID, and placebo. Patients were allowed to take one or more NSAIDs and take concomitant low-dose aspirin (< 325 mg per day) during the study. Patients who had gastric ulcers, duodenal ulcers, erosive esophagitis, or ≥25 gastric/duodenal erosions on baseline upper endoscopy were excluded from participation. Patients had to be H. pylori negative by the CLO test and by histology testing.A total of 537 patients were enrolled in the study, and 535 patients were treated. Patients ranged in age from 23 to 89 years (median age 60 years), with 65% female patients and 35% male patients. Race was distributed as follows: 90% Caucasian, 6% Black, and 4% other. Concomitant low-dose aspirin was used in about 20% of the patients. Additionally, about 99% of the patients had a prior history of a gastric ulcer and about 50% of the patients had a prior history of a duodenal ulcer.The proportion of patients remaining free from gastric ulcers (diagnosed by upper endoscopy) at 4, 8, and 12 weeks was significantly higher with 15 or 30 mg of PREVACID than placebo (see Table 2). The 30 mg dose of PREVACID demonstrated no additional benefit in risk reduction of the NSAID-associated gastric ulcer(s) than the 15 mg dose. In the 12 week study, no patient in any of the treatment groups developed a NSAID-associated serious GI complication (such as bleeding, perforation, or obstruction). However, this study was not designed to demonstrate risk reduction of NSAID-associated serious GI complications. Additionally, this study was not designed to demonstrate risk reduction of duodenal ulcers.Table 2: Proportion of Patients RemainingFree of Gastric Ulcers1PlaceboMisoprostolPREVACIDPREVACID15 mg daily 30 mg daily 200 mcg QIDWeek (N=121) (N=116) (N=106) (N=112)4 90% 92% 96% 66%8 86% 88% 95% 60%12 80% 82% 93% 51%1 % = Life Table Estimate(p<0.001) PREVACID 15 mg daily versus placebo; PREVACID 30 mg daily versus placebo; and misoprostol 200 mcg QID versus placebo.(p<0.05) Misoprostol 200 mcg QID versus PREVACID 15 mg daily; and misoprostol 200 mcg QID versus PREVACID 30 mg dailyOf the 537 patients in the double-blind, placebo- and misoprostol-controlled study, a retrospective subset analysis of 119 patients – whose NSAIDs were naproxen or naproxen and aspirin – was performed. Patients ranged in age from 37 to 84 years (median age 58 years) with 61% female patients and 39% male patients. Race was distributed as follows: 88% Caucasian, 8% Black, and 4% other. Concomitant low-dose aspirin was used in 15% of the patients. Of the 61 patients in the two PREVACID treatment groups: 5, 54, and 2 patients received less than 750 mg, 750 to 1000 mg, and greater than 1000 mg of daily naproxen, respectively.The proportion of patients remaining free from gastric ulcer (diagnosed by upper endoscopy) at 4, 8, and 12 weeks was significantly higher with 15 or 30 mg of PREVACID than placebo (see Table 3). The 30 mg dose of PREVACID demonstrated no additional benefit in risk reduction of the NSAID-associated gastric ulcers than the 15 mg dose.Table 3: Proportion of Patients (whose NSAIDs were Naproxen orNaproxen and Aspirin) Remaining Free of Gastric Ulcers1PlaceboMisoprostolPREVACIDPREVACID15 mg daily 30 mg daily 200 mcg QIDWeek (N=37) (N=24) (N=28) (N=30)4 91% 83% 88% 52%8 89% 83% 88% 52%12 89% 83% 83% 33%1 % = Life Table Estimate(p<0.001) PREVACID 15 mg daily versus placebo; PREVACID 30 mg daily versus placebo; and misoprostol 200 mcg QID versus placebo.NAPROSYNGeneral InformationNaproxen has been studied in patients with rheumatoid arthritis, osteoarthritis, and ankylosing spondylitis. Improvement in patients treated for rheumatoid arthritis was demonstrated by a reduction injoint swelling, a reduction in duration of morning stiffness, a reduction in disease activity as assessed by both the investigator and patient, and by increased mobility as demonstrated by a reduction in walking time. Generally, response to naproxen has not been found to be dependent on age, sex, severity, or duration of rheumatoid arthritis.In patients with osteoarthritis, the therapeutic action of naproxen has been shown by a reduction in joint pain or tenderness, an increase in range of motion in knee joints, increased mobility as demonstrated by a reduction in walking time, and improvement in capacity to perform activities of daily living impaired by the disease.In a clinical trial comparing standard formulations of naproxen 375 mg bid (750 mg a day) vs 750 mg twice daily (1500 mg per day), 9 patients in the 750 mg group terminated prematurely because of adverse events. Nineteen patients in the 1500 mg group terminated prematurely because of adverse events. Most of these adverse events were GI events.In clinical studies in patients with rheumatoid arthritis or osteoarthritis, naproxen has been shown to be comparable to aspirin and indomethacin in controlling the aforementioned measures of disease activity, but the frequency and severity of the milder GI adverse effects (nausea, dyspepsia, heartburn) and nervous system adverse effects (tinnitus, dizziness, lightheadedness) were less in naproxen-treated patients than in those treated with aspirin or indomethacin.In patients with ankylosing spondylitis, naproxen has been shown to decrease night pain, morning stiffness and pain at rest. In double-blind studies the drug was shown to be as effective as aspirin, but with fewer side effects.Naproxen may be used safely in combination with gold salts and/or corticosteroids; however, in controlled clinical trials, when added to the regimen of patients receiving corticosteroids, it did not appear to cause greater improvement over that seen with corticosteroids alone. Whether naproxen has a “steroid-sparing” effect has not been adequately studied. When added to the regimen of patients receiving gold salts, naproxen did result in greater improvement. Its use in combination with salicylates is not recommended because there is evidence that aspirin increases the rate of excretion of naproxen and data are inadequate to demonstrate that naproxen and aspirin produce greater improvement over that achieved with aspirin alone. In addition, as with other NSAIDs, the combination may result in higher frequency of adverse events than demonstrated for either product alone.In 51Cr blood loss and gastroscopy studies with normal volunteers, daily administration of 1000 mg of naproxen as 1000 mg of NAPROSYN (naproxen) has been demonstrated to cause statistically significantly less gastric bleeding and erosion than 3250 mg of aspirin.Geriatric PatientsThe hepatic and renal tolerability of long-term naproxen administration was studied in two double-blind clinical trials involving 586 patients. Of the patients studied, 98 patients were age 65 and older and 10 of the 98 patients were age 75 and older. Naproxen was administered at doses of 375 mg twice daily or 750 mg twice daily for up to 6 months. Transient abnormalities of laboratory tests assessing hepatic and renal function were noted in some patients, although there were no differences noted in the occurrenceof abnormal values among different age groups.INDICATIONS AND USAGECarefully consider the potential benefits and risks of PREVACID NapraPAC and other treatment options before deciding to use PREVACID NapraPAC. Use the lowest effective dose for the shortest duration consistent with individual patient treatment goals (see WARNINGS).PREVACID NapraPAC is indicated for reducing the risk of NSAID-associated gastric ulcers in patients with a history of documented gastric ulcer(s) who require the use of an NSAID for treatment of the signs and symptoms of rheumatoid arthritis, osteoarthritis, and/or ankylosing spondylitis (see CLINICAL STUDIES and DOSAGE AND ADMINISTRATION). Controlled studies did not extend beyond 12 weeks.CONTRAINDICATIONSPREVACID NapraPAC is contraindicated in patients with known severe hypersensitivity to any component of the formulations of PREVACID (lansoprazole), NAPROSYN (naproxen), or the over-thecounter products containing naproxen.PREVACID NapraPAC is contraindicated in patients who have experienced aspirin- or NSAID-related asthma, urticaria, or allergic-type reactions. Severe, rarely fatal, anaphylactic-like reactions to NSAIDs have been reported in such patients (see WARNINGS, Anaphylactoid Reactions, and PRECAUTIONS –Preexisting Asthma).PREVACID NapraPAC is contraindicated for the treatment of peri-operative pain in the setting of coronary artery bypass graft (CABG) surgery (see WARNINGS).WARNINGSCARDIOVASCULAR EFFECTSCardiovascular Thrombotic EventsClinical trials of several COX-2 selective and nonselective NSAIDs of up to three years duration have shown an increased risk of serious cardiovascular (CV) thrombotic events, myocardial infarction, and stroke, which can be fatal. All NSAIDs, both COX-2 selective and nonselective, may have a similar risk. Patients with known CV disease or risk factors for CV disease may be at greater risk. To minimize the potential risk for an adverse CV event in patients treated with an NSAID, the lowest effective dose should be used for the shortest duration possible. Physicians and patients should remain alert for the development of such events, even in the absence of previous CV symptoms. Patients should be informed about the signs and/or symptoms of serious CV events and the steps to take if they occur.There is no consistent evidence that concurrent use of aspirin mitigates the increased risk of serious CV thrombotic events associated with NSAID use. The concurrent use of aspirin and an NSAID does increase the risk of serious GI events (see GI WARNINGS and CLINICAL STUDIES, Risk Reduction of NSAID-Associated Gastric Ulcer(s)).Two large, controlled, clinical trials of a COX-2 selective NSAID for the treatment of pain in the first 10 to 14 days following CABG surgery found an increased incidence of myocardial infarction and stroke (see CONTRAINDICATIONS).。
兰索拉唑肠溶胶囊BP2010
British Pharmacopoeia V olume IIIFormulated Preparations: Specific MonographsGastro-resistant Lansoprazole CapsulesGeneral NoticesAction and useProton pump inhibitor; treatment of peptic ulcer disease.DefinitionGastro-resistant Lansoprazole Capsules contain Lansoprazole. They are covered with a gastro-resistant coating or prepared from granules or particles covered with a gastro-resistant coating.The capsules comply with the requirements stated under Capsules and with the following requirements.Content of lansoprazole, C16H14F3N3O2S95.0 to 105.0% of the stated amount.IdentificationA. Shake a quantity of the finely powdered contents of the capsules containing30 mg of Lansoprazole with 50 ml of methanol, filter and dilute 1 volume to 50 volumes. The light absorption, Appendix II B, in the range 220 nm to 350 nm exhibits a maximum at 284 nm.B. In the Assay, the chromatogram obtained with solution (1) shows a peak with the same retention time as the principal peak in the chromatogram obtained with solution (2).TestsDissolutionComply with the dissolution test for tablets and capsules , Appendix XII B1.Mix 11 volumes of 0.25m trisodium orthophosphate and 22 volumes of 0.5m anhydrous disodium hydrogen orthophosphate , dilute to 100 volumes with water and adjust the pH, if necessary, to 11.0 with orthophosphoric acid or 10m sodium hydroxide , as appropriate (solution A).Mix 1 volume of 10m sodium hydroxide with 99 volumes of 0.05m phosphate buffer solution pH 4.5 (solution B).test conditions(a) Use Apparatus 2, rotating the paddle at 150 revolutions per minute.(b) Use as the media the solutions described sequentially below.First stage (pH 4.5)Use as the medium 700 ml of 0.05 m phosphate buffer solution pH 4.5 . After 45 minutes, withdraw 5 ml of the medium, filter, dilute to 25 ml with solution A and retain the samples for analysis as described below. Proceed immediately to the final stage.Final stage (pH 6.8)Within 5 minutes, add 200 ml of solution B at 37° to the vessel. Maintain the rotation speed at 150 revolutions per minute and continue to operate the apparatus for 45 minutes. Withdraw 5 ml of the medium, filter, dilute to 25 ml with solution A and retain the samples for analysis as described below.Carry out the method for liquid chromatography , Appendix III D, using the following solutions.(1) Use the sample solutions taken above.(2) Dissolve a sufficient quantity of lansoprazole BPCRS in solution A and dilute with water; the concentration of the final solution should be the same as that expected for solution (1).chromatographic conditionsThe chromatographic conditions described under Related substances may be used. determination of contentCalculate the total content of C16H14F3N3O2S in the medium using the declared content of C16H14F3N3O2S in lansoprazole BPCRS.limitsThe amount of lansoprazole released after the first stage is not more than 10% of the stated amount. The amount of lansoprazole released after the final stage is not less than 75% (Q) of the stated amount.Related substancesCarry out the method for liquid chromatography , Appendix III D, using the following solutions protected from light.solvent aMix 1 volume of triethylamine with 60 volumes of water, adjust the pH to 10.5 using orthophosphoric acid and mix the solution with 40 volumes of acetonitrile.(1) Shake a quantity of the finely powdered contents of the capsules containing 50 mg of Lansoprazole with 50 ml of solvent A and filter.(2) Dilute 1 volume of solution (1) to 100 volumes with solvent A and dilute a further 1 volume to 5 volumes with solvent A.(3) 0.01% w/v of lansoprazole impurity standard BPCRS in solvent A.(4) 0.0004% w/v of 2-mercaptobenzimidazole (impurity E) in solvent A. chromatographic conditions(a) Use a stainless steel column (25 cm × 3.0 mm) packed with amidohexadecylsilyl silica gel for chromatography (5 µm) (Supelcosil LC-ABZ is suitable).(b) Use isocratic elution and the mobile phase described below.(c) Use a flow rate of 1.2 ml per minute.(d) Use an ambient column temperature.(e) Use a detection wavelength of 285 nm.(f) Inject 10 µl of each solution.(g) Identify any peaks in the chromatogram obtained with solution (1) corresponding to lansoprazole impurities A and B using solution (3).mobile phase1 volume of triethylamine, 60 volumes of water, adjusted to pH 6.2 using orthophosphoric acid and 40 volumes of acetonitrile.system suitabilityThe test is not valid unless, in the chromatogram obtained with solution (3), the resolution factor between the peaks due to lansoprazole and impurity B is at least 3.0. limitsIn the chromatogram obtained with solution (1):the area of any peak corresponding to impurity A is not greater than 1.5 times the area of the principal peak in the chromatogram obtained with solution (2) (0.3%);the area of any peak corresponding to impurity B is not greater than 2.5 times the area of the principal peak in the chromatogram obtained with solution (2) (0.5%);the area of any peak corresponding to impurity E is not greater than the area of the principal peak in the chromatogram obtained with solution (4) (0.4%);the area of any other secondary peak is not greater than the area of the principal peak in the chromatogram obtained with solution (2) (0.2%);the sum of the areas of all the secondary peaks is not more than 2.0%.Disregard any peak with an area less than 0.25 times the area of the principal peak in the chromatogram obtained with solution (2) (0.05%).AssayCarry out the method for liquid chromatography , Appendix III D, using the following solutions and protect from light.solvent aMix 1 volume of triethylamine with 60 volumes of water, adjust the pH to 10.5 using orthophosphoric acid and mix the solution with 40 volumes of acetonitrile.(1) Add a quantity of the finely powdered mixed contents of 20 capsules containing 20 mg of Lansoprazole to 100 ml of solvent A, shake for 30 minutes and filter.(2) 0.02% w/v of lansoprazole BPCRS.(3) 0.01% w/v of lansoprazole impurity standard BPCRS.chromatographic conditionsThe chromatographic conditions described under Related substances may be used. system suitabilityThe Assay is not valid unless, in the chromatogram obtained with solution (3), the resolution factor between the peaks due to lansoprazole and impurity B is at least 3.0. determination of contentCalculate the content of C16H14F3N3O2S in the capsules , using the declared content of C16H14F3N3O2S in lansoprazole BPCRS .© Crown Copyright 2009。
兰索拉唑肠溶胶囊三国药典释放度测定方法比较
兰索拉唑肠溶胶囊三国药典释放度测定方法比较摘要】确定兰索拉唑肠溶胶囊释放度测定方法。
对中、美、英三国药典中兰索拉唑肠溶胶囊释放度测定方法进行比较。
结果表明，HPLC法测定结果比紫外分光光度(UV)法更准确。
美国药典中缓冲液阶段溶出介质加入了十二烷基硫酸钠，更为合理；英国药典测定时加入了碱溶液可以提高药物稳定性，所得测定结果更为准确、可靠。
综合三国药典，推荐释放度测定采用美国药典方法，溶出液药物含量测定采用英国药典方法。
【关键词】兰索拉唑肠溶胶囊释放度测定药典【中图分类号】R927 【文献标识码】A 【文章编号】2095-1752（2013）07-0024-02兰索拉唑（LSP）是第二代质子泵抑制剂,可选择性、非竞争性的抑制胃壁细胞中H+/K+–ATP酶，从而阻断胃酸分泌的最终环节[1]，在保护和促进胃粘膜溃疡愈合、降低溃疡复发率等方面具有良好作用[2]；主要用于治疗胃溃疡、十二指肠溃疡、吻合口溃疡、反流性食管炎和卓-艾综合症[3]。
由于兰索拉唑难溶于水，在酸性环境下降解明显，故需将其制备成肠溶制剂。
目前新药转正标准第56册、美国药典35版和英国药典2012版均收载了兰索拉唑肠溶胶囊质量标准，但是各自的方法差异很大，得到的结果也很不一致，故有必要对这些方法进行再评价，以指导LSP制剂的开发，所以本实验的目的是利用三国药典收载的释放度测定方法分别对肠溶胶囊进行释放度和酸稳定性测定，通过对比研究得出合适的释放度测定方法。
一仪器与试剂ZRS-8G智能溶出试验仪（天津天大天发科技有限公司）；Agilent1260HPLC色谱仪，紫外检测器（美国安捷伦科技公司）；岛津UV-2401PC可见分光光度计（日本岛津公司）。
兰索拉唑标准品（中国药品生物制品检定所）；兰索拉唑肠溶微丸胶囊（天津武田药品有限公司）；乙腈、甲醇均为色谱纯；去离子水。
二方法（一）《新药转正标准》1 溶出介质酸阶段取氯化钠2.0g，加盐酸7.0ml，加水溶解并稀释至1000 ml，溶液pH 值为1.2。
兰索拉唑肠溶片的说明书
兰索拉唑肠溶片的说明书肠胃不好，生活就不会好，人们的生活总是跟吃分不开关系。
目前患上胃肠疾病的人群很多，正确选择药物就成了您治愈疾病的重要选择了。
兰索拉唑肠溶片是如今治疗胃肠疾病非常好的药物，在众多的胃肠药物当中当属疗效最好的。
那么关于兰索拉唑肠溶片的各种药性和服药原则您了解吗。
【药品名称】通用名称：兰索拉唑片商品名称：兰索拉唑肠溶片拼音全码：LanSuoLaZuoPian【主要成份】本品主要成份为兰索拉唑。
化学名：2-[[[3－甲基－4－（2，2，2－三氟乙氧基）-2-吡啶基]甲基]亚磺酰基]－1H －苯并咪唑。
分子式：C16H14F3N3O2S分子量：369.37【性状】白色肠溶片，除去肠溶衣后显白色或类白色。
【适应症/功能主治】胃溃疡、十二指肠溃疡、反流性食管炎、佐-艾(Zollinger-Ellison)综合征(胃泌素瘤)。
【规格型号】15mg*12s【用法用量】每日清晨口服1次，一次15～30mg，或遵医嘱。
【不良反应】副作用轻微，主要表现为口干、头晕、恶心。
【禁忌】孕妇、哺乳期妇女忌用。
【注意事项】曾发生药物过敏症的患者及肝机能障碍的患者应慎重用药。
【儿童用药】对小儿的安全性尚未被确立(由于在小儿的临床经验极少)。
【老年患者用药】老年患者的胃酸分泌能力和其他生理机能均会降低，故用药期间请注意观察。
【孕妇及哺乳期妇女用药】孕妇、哺乳期妇女忌用。
【药物相互作用】会延迟安定(diazepam)及苯妥英钠(phenytoin Sodium)的代谢与排泄，资料已被发表于类似药物奥美拉唑的报告中。
【药物过量】未进行该项实验且无可靠文献。
【药理毒理】该品为新型的抑制胃酸分泌的药物，它作用于胃壁细胞的H+-K+-ATP酶，使壁细胞的H+不能转运到胃中去，以致胃液中胃酸量大为减少，临床上用于十二指肠溃疡、胃溃疡、反流性食管炎，佐-艾(Zollinger-Ellison)综合征(胃泌素瘤)的治疗，疗效显著，对幽门螺杆菌有抑制作用。
兰索拉唑胶囊说明书
兰索拉唑胶囊说明书兰索拉唑胶囊(南国春)用于胃溃疡、十二指肠溃疡、返流性食道炎、卓-艾综合征(Zollinger-Ellison症候群)、吻合口溃疡。
下面是学习啦小编整理的兰索拉唑胶囊说明书，欢迎阅读。
兰索拉唑胶囊商品介绍通用名：兰索拉唑胶囊生产厂家: 湖北潜龙药业有限公司批准文号：国药准字H20084570药品规格：15mg*7粒药品价格：￥32元兰索拉唑胶囊说明书【通用名称】兰索拉唑胶囊【商品名称】兰索拉唑胶囊(南国春)【英文名称】LansoprazoleCapsules【拼音全码】LanSuoLaZuoJiaoNang(NanGuoChun)【主要成份】兰索拉唑胶囊(南国春)主要成份为兰索拉唑。
化学名：2-[[[3-甲基-4-(2，2，2-三氟乙氧基)-2-吡啶基]甲基]亚磺酰基]-1H-苯并咪唑。
分子式：C16H14F3N3O2S分子量：369.37【性状】兰索拉唑胶囊(南国春)为白色胶囊，内容物为白色或类白色肠溶球状颗粒。
【适应症/功能主治】胃溃疡、十二指肠溃疡、返流性食道炎、卓-艾综合征(Zollinger-Ellison症候群)、吻合口溃疡。
【规格型号】15mg*7s【用法用量】十二指肠溃疡，通常成人每日一次，口服兰索拉唑15mg～30mg，连续服用4～6周;胃溃疡、反流性食管。
【不良反应】1.过敏症：偶有皮疹、瘙痒等症状，如出现上述症状时请停止用药。
2.肝脏：偶有GOT、GPT、AL-P、LDH、γ-GTP上升等现象，所以须细心观察，如有异常现象应采取停药等适应的处置。
3.血液：偶有贫血、白细胞减少，嗜酸球增多等症状，血小板减少之症状极少发生。
4.消化器：偶有便秘，腹泻，口渴，腹胀等症状。
5.精神神经系：偶尔头痛、嗜睡等症状。
失眠，头晕等症状极少发生。
6.其他：偶有发热，总胆固醇上升，尿酸上升等症状。
【禁忌】对兰索拉唑胶囊(南国春)过敏者禁用。
【注意事项】1.治疗过程中应注意观察，因长期使用的经验不足，暂不推荐用于维持治疗。