Fibre bundle formulation of nonrelativistic quantum mechanics. IV. Mixed states and evoluti
菲律宾仿制药注册清单
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药物国际非专利名称所用词干
国际非专利名称〔INN〕所用词干-abine -他滨-ac 抗感染药 -酸异丁芬酸衍生物Aceclofenac 醋氯芬酸Alclofenac 阿氯芬酸Amfenac 氨芬酸Anirolac 阿尼罗酸Bendazac 苄达酸Bromfenac 溴芬酸Bufexamac 丁苯羟酸Bufezolac 丁苯唑酸Cinfenoac 辛芬酸Clidanac 环氯茚酸Clofurac 氯呋酸Clopirac 氯吡酸Dexpemedolac 右培美酸Diclofenac 双氯芬酸Eltenac 依尔替酸Etodolac 依托度酸Felbinac 联苯乙酸Fenclofenac 芬氯酸Fenclorac 苯克洛酸Fentiazac 芬替酸Furofenac 呋罗芬酸Ibufenac 异丁芬酸 Isofezolac 三苯唑酸 Isoxepac 伊索克酸Ketorolac 酮咯酸 Lexofenac 来克芬酸 Lonazolac 氯那唑酸Mofezolac 莫苯唑酸 Nepafenac 奈帕芬胺 Oxepinac 奥昔平酸Oxindanac 羟吲达酸 Pemedolac 培美酸 Pirazolac 吡拉唑酸Sulindac 舒林酸 Tianafac 噻那酸 Tifurac 替呋酸Tiopinac 硫平酸 Trifezolac 曲非唑酸 Zomepirac 佐美酸-zolac -唑酸Bufezolac 丁苯唑酸Isofezolac 三苯唑酸Lonazolac 氯那唑酸Pirazolac 吡拉唑酸Trifezolac 曲非唑酸-acetam 〔见-racetam〕 -西坦-actide 类促皮质激素合成多肽-克肽Alsactide 阿沙克肽ricosactide 曲可克肽Codactide 可达克肽Tosactide 托沙克肽Giractide 吉拉克肽Norleusactide 正亮克肽Seractide 丝拉克肽Tetracosactide 替可克肽-adol 止痛药 -多Acetylmethadol 醋美沙多Alimadol 阿利马多Alphacetylmethadol 阿醋美沙多Alphamethadol 阿法美沙多Axomadol 阿索马多Betacetylmethadol 倍醋美沙多Betamethadol 倍他美沙多Ciprefadol 环丙法多Ciramadol 西拉马多Cloracetadol 氯西他多Dibusadol 地布沙多Dimenoxadol 地美沙多Diproxadol 地丙沙多Filenadol 非来那多Flumexadol 氟甲沙多Gaboxadol 加波沙多Hexapradol 己普拉醇Levacetylmethadol 左醋美沙多Levonantradol 左南曲多Lorcinadol 洛西那多Myfadol 麦法多Nafoxadol 萘克沙多Nantradol 南曲多Nerbacadol 那巴卡多Noracymethadol 诺美沙多Oxapadol 奥沙帕多Picenadol 哌西那多Pipradimadol 哌地马多Pipramadol 哌马多Profadol 普罗法多Quinestradol 奎雌醇Tapentadol 他喷他多Tolpadol 托帕多Tramadol 曲马多-adom 止痛药 -多替氟多类衍生物Lufuradom 鲁夫拉多Tifluadom 替氟多-fenone 抗心律失常药-非农<酮> 普罗帕酮类衍生物Alprafenone 阿普非农Berlafenone 柏拉非农Diprafenone 地丙苯酮Etafenone 依他苯酮Nizofenone 尼唑苯酮Pitofenone 吡托非农Propafenone 普罗帕酮Romifenone 罗米芬酮-afil 血管扩药 -非Beminafil 贝米那非Dasantafil 达生他非Sildenafil 那非Tadalafil 他达拉非Vardenafil 伐地那非-aj- 抗心律失常药 -义西萝芙木碱类衍生物Ajmaline* 阿义马林Detajmium Bitartrate 重酒石酸地他义铵Lorajmine 劳拉义明-al -醛-aldrate 抗酸药 -铝Carbaldrate 卡巴铝Magaldrate 镁加铝Potassium Glucaldrate 葡铝酸钾Simaldrate 硅镁铝Sodium Glucaspaldrate 葡柳铝酸钠-alol <见-olol> -洛尔-alox <见-ox>-铝-amivir <见-vir> -米韦-ampanel AMPA受体阻滞药 -帕奈Becampanel 贝坎帕奈 Irampanel 伊仑帕奈 Talampanel 他仑帕奈Zonampanel 唑南帕奈andr 雄激素类药雄Andrographolide 穿心莲酯 Androisoxazole 雄异唑 Androstanolone 雄诺龙Androstenediol 雄烯二醇 Androsterone 雄酮-anib 血管生成抑制药 -尼Pegaptanib 培加他尼 Semaxanib 司马沙尼 Vandetanib 凡德他尼 Vatalanib 伐他拉尼-anide 利尿药 -尼特苯吡磺苯酸衍生物-oxanide抗蠕虫药 -沙奈水酰苯胺衍生物Bromoxanide 溴沙奈Clioxanide 氯碘沙奈Diloxanide 二氯沙奈Nitazoxanide 硝唑沙奈Rafoxanide 雷复沙奈-anserin 5-羟色胺拮抗药 -色林Adatanserin 阿达色林 Altanserin 阿坦色林 Blonanserin 布南色林Butanserin 布坦色林 Cinanserin 辛那色林 Eplivanserin 依利色林Fananserin 法南色林 Flibanserin 氟班色林 Glemanserin 格来色林Iferanserin 艾夫色林 Ketanserin 酮色林 Lidanserin 利丹色林Mianserin 米安色林 Pelanserin 培兰色林 Pruvanserin 普凡色林Ritanserin 利坦色林 Seganserin 司更色林 Tropanserin 托烷色林-antel抗蠕虫药 -太尔Amidantel 阿米太尔Carbantel 卡班太尔Closantel 氯生太尔Epsiprantel 依西太尔Febantel 非班太尔Flurantel 氟仑太尔Morantel 莫仑太尔Oxantel 奥克太尔Pexantel 哌克太尔Resorantel 雷琐太尔Salantel 沙仑太尔Zilantel 齐仑太尔-apine <见-pine> -氮平<平>-<ar>abine 抗肿瘤药 -拉滨阿拉伯糖苷衍生物Ancitabine 安西他滨Capecitabine 卡培他滨Clofarabine 氯法拉滨Cytarabine 阿糖胞苷Decitabine 地西他滨Elvucitabine 艾夫他滨Emtricitabine 恩曲他滨Enocitabine 依诺他滨Fazarabine 法扎拉滨Fengabine 酚加宾Fiacitabine 非西他滨Fludarabine 氟达拉滨Flurocitabine 氟西他滨Galocitabine 加洛他滨Gemcitabine 吉西他滨Ibacitabine 伊巴他滨Nelzarabine 奈拉滨Retigabine 瑞替加滨Tezacitabine 替扎他滨Tiagabine 噻加宾Torcitabine 托西他滨Troxacitabine 曲沙他滨Valtorcitabine 伐托他滨Vidarabine 阿糖腺苷Zalcitabine 扎西他滨-arit消炎镇痛药 -<扎>利Actarit 阿克他利Bindarit 宾达利Clobuzarit 氯丁扎利Lobenzarit 氯苯扎利Romazarit 氯马扎利-arol抗凝血药-香豆素双香豆素衍生物Acenocoumarol 醋硝香豆素 Clocoumarol 氯香豆素 Cloridarol 氯达香豆素Coumetarol 库美香豆素 Cyclocoumarol 环香豆素 Dicoumarol 双香豆素Ethylidenedicoumarol 乙双香豆素 Fluindarol 氟茚香豆素Tioclomarol 噻氯香豆素 Xylocoumarol 甲苄香豆素-arone -隆<酮>Amiodarone 胺碘酮 Benzarone 苯扎隆 Benzbromarone 苯溴马隆Benziodarone 苯碘达隆 Brinazarone 布吲扎酮 Bucromarone 布色酮Diarbarone 地阿巴隆 Dronedarone 决奈达隆 Etabenzarone 依他扎隆Fantofarone 泛托法隆 Furidarone 呋碘达隆 Inicarone 吡香豆酮Mecinarone 美西那隆 Pyridarone 吡达隆 Rilozarone 利洛扎隆-arotene -罗汀Betacarotene 倍他胡萝卜素 Bexarotene 贝沙罗汀 Etarotene 依他罗汀Linarotene 林那罗汀 Mofarotene 莫法罗汀 Sumarotene 舒马罗汀Tamibarotene 他米巴罗汀 Tazarotene 他扎罗汀 Temarotene 替马罗汀arte-抗疟药<青>蒿- 青蒿素衍生物Artemether蒿甲醚 Artemisinin青蒿素 Artemotil蒿乙醚Artenimol青蒿醇Artesunate青蒿琥酯-ase -酶Alfimeprase 阿非普酶 Alglucerase 阿糖脑苷酶 Alpha Amylase 阿法淀粉酶Alteplase 阿替普酶 Amediplase 安地普酶 Anistreplase 阿尼普酶Asparaginase 门冬酰胺酶 Brinase 纤维蛋白酶 Cellulase 纤维素酶Cocarboxylase 辅羧酶 Desmoteplase 去氨普酶 Desoxyribonuclease 去氧核糖核酸酶Diastase 淀粉酶 Duteplase 度替普酶 Elastase 弹性酶 Epafipase依帕非酶Eufauserase 尤福丝酶 Hyalosidase 透明糖酶 Hyaluronidase 玻璃酸酶Idusulfase 艾度硫酸酯酶 Imiglucerase 伊米苷酶 Kallidinogenase 血管舒缓素Lanoteplase 拉诺普酶 Laronidase 拉罗尼酶 Ledismase 来地酶Monteplase 孟替普酶 Nasaruplase 那沙普酶 Nateplase 那替普酶Pamiteplase 帕米普酶 Pancrelipase 胰脂肪酶 Pegademase 培加酶Pegaspargase 培门冬酶 Penicillinase 青霉素酶 Promelase 普罗米酶Ranpirnase 豹蛙酶 Rasburicase 拉布立酶 Reteplase 瑞替普酶Rizolipase 根霉脂肪酶 Saruplase 沙芦普酶 Serrapeptase 舍雷肽酶Sfericase 司非立酶 Silteplase 西替普酶 Streptodornase 链道酶Streptokinase 链激酶 Sudismase 超氧歧化酶 Tenecteplase 替奈普酶Tilactase 半乳糖苷酶 Urokinase 尿激酶-ast 镇咳平喘药、抗过敏药 -司特Acitazanolast 阿扎司特 Acreozast 阿克瑞司特 Andolast 安多司特Asobamast 阿索司特 Ataquimast 阿喹司特 Bamaquimast 巴马司特Batebulast 巴布司特 Binizolast 比尼司特 Bunaprolast 布那司特Cilomilast 西洛司特 Cinalukast 西那司特 Dametralast 达美司特Dazoquinast 达唑司特 Doqualast 多夸司特 Eclazolast 乙唑司特Eflumast 乙氟司特 Enofelast 乙诺司特 Enoxamast 依诺司特Fenprinast 苯呤司特 Filaminast 非明司特 Ibudilast 异丁司特Idenast 艾地司特 Lirimilast 利米司特 Loxanast 洛沙司特Melquinast 甲喹司特 Ontazolast 昂唑司特 Oxalinast 草氨司特Pemirolast 吡嘧司特 Piclamilast 吡拉米司特 Picumast 哌香豆司特Pirodomast 吡咯司特 Quazolast 喹唑司特 Quinotolast 喹托司特Raxofelast 雷索司特 Repirinast 瑞吡司特 Revenast 瑞那司特Roflumilast 罗氟司特 Scopinast 司考匹司特 Tazanolast 他扎司特Tetomilast 替托司特 Tetrazolast 四唑司特 Tiacrilast 硫克司特Tibenelast 硫苯司特 Tioxamast 噻草司特 Tiprinast 替普司特Tofimilast 妥非司特 Tranilast 曲尼司特 Zaprinast 扎普司特-lukast -鲁司特Ablukast 阿鲁司特 Cinalukast 西那司特 Iralukast 伊拉司特Montelukast 孟鲁司特 Pobilukast 泊比司特 Pranlukast 普仑司特Ritolukast 利托司特 Sulukast 硫鲁司特 Tomelukast 托鲁司特Verlukast 维鲁司特 Zafirlukast 扎鲁司特-trodast-曲司特Imitrodast 咪曲司特 Seratrodast 塞曲司特- astride<见-ster-> -雄胺Dutasteride 度他雄胺 Finasteride 非那雄胺-astine 抗组胺药 -斯汀Acrivastine 阿伐斯汀 Alinastine 阿利那斯汀 Azelastine 氮斯汀Bamirastine 巴麦斯汀 Barmastine 巴马斯汀 Bepiastine 贝匹斯汀Bepotastine 贝他斯汀 Bermastine 哌马斯汀 Bilastine 比拉斯汀Cabastine 卡巴斯汀 Carebastine 卡瑞斯汀 Clemastine 氯马斯汀Cloperastine 氯哌斯汀 Dorastine 多拉斯汀 Ebastine 依巴斯汀Emedastine 依美斯汀 Epinastine 依匹斯汀 Flezelastine 氟斯汀Levocabastine 左卡巴斯汀 Linetastine 利奈他斯汀 Mapinastine 马哌斯汀Mizolastine 咪唑斯汀 Moxastine 莫沙斯汀 Noberastine 诺柏斯汀Octastine 辛斯汀 Perastine 哌拉斯汀 Piclopastine 吡氯斯汀Rocastine 罗卡斯汀 Setastine 司他斯汀 Talastine 他拉斯汀Temelastine 替美斯汀 Vinblastine 碱 Zepastine 帕斯汀-azam <见-azepam> -占Arfendazam 阿芬达占 Clobazam 氯巴占 Lofendazam 洛芬达占Razobazam 雷唑巴占 Triflubazam 三氟巴占 Zomebazam 唑美巴占-azenil苯二氮类拮抗药-西尼.苯二氮衍生物Bretazenil 溴他西尼Flumazenil 氟马西尼Nabazenil 大麻折尼Sarmazenil 沙马西尼-carnil苯二氮类拮抗药 -卡尔咔啉衍生物Abecarnil 阿贝卡尔 Gedocarnil 吉多卡尔-quinil苯二氮类拮抗药 -喹尼喹啉衍生物Lirequinil 利瑞喹尼 Resequinil 瑞司奎尼 Terbequinil 特贝喹尼-azepam 安定药-西泮地西泮衍生物Bentazepam 苯他西泮 Bromazepam 溴西泮 Camazepam 卡马西泮Carburazepam 卡布西泮Cinolazepam 西诺西泮Clonazepam 氯硝西泮Clotiazepam 氯噻西泮Cyprazepam 环丙西泮Delorazepam 地洛西泮Diazepam 地西泮Doxefazepam 度氟西泮Elfazepam 依法西泮Fletazepam 氟乙西泮Fludiazepam 氟地西泮Flunitrazepam 氟硝西泮Flurazepam 氟西泮Flutemazepam 氟替马西泮Flutoprazepam 氟托西泮Fosazepam 膦西泮Halazepam 哈拉西泮Iclazepam 伊氯西泮Lopirazepam 氯吡西泮Lorazepam 劳拉西泮Lormetazepam 氯甲西泮Meclonazepam 甲氯西泮Medazepam 美达西泮Menitrazepam 甲硝西泮Metaclazepam 美氯西泮Motrazepam 莫曲西泮Nimetazepam 尼美西泮Nitrazepam 硝西泮Nordazepam 去甲西泮Nortetrazepam 诺替西泮Oxazepam 奥沙西泮Pinazepam 匹那西泮Pivoxazepam 匹伏西泮Prazepam 普拉西泮Premazepam 普瑞西泮Proflazepam 丙氟西泮Quazepam 夸西泮Reclazepam 瑞氯西泮Ripazepam 利帕西泮Sulazepam 硫西泮Temazepam 替马西泮Tetrazepam 四氢西泮Tolufazepam 甲磺西泮Tuclazepam 妥氯西泮Uldazepam 乌达西泮Zolazepam 唑拉西泮-azepide缩胆囊素拮抗药 -西匹<派特>Devazepide 地伐西匹 Pranazepide 普拉那西匹 Tarazepide 他折派特-azocine 镇痛药-佐辛6,7-二苯吗啡衍生物Anazocine 阿那佐辛 Bremazocine 布马佐辛 Butinazocine 布替佐辛Carbazocine 卡巴佐辛 Cogazocine 可加佐辛 Cyclazocine 环佐辛Eptazocine 依他佐辛 Gemazocine 吉马佐辛 Ibazocine 伊巴佐辛Ketazocine 酮佐辛 Metazocine 美他佐辛 Moxazocine 莫沙佐辛Pentazocine 喷他佐辛 Phenazocine 非那佐辛 Quadazocine 夸达佐辛Tonazocine 托那佐辛 Volazocine 伏拉佐辛-azolam <见-azepam> -唑仑Adinazolam 阿地唑仑Alprazolam 阿普唑仑Clazolam 克拉唑仑Climazolam 氯马唑仑Cloxazolam 氯唑仑Estazolam 艾司唑仑Flutazolam 氟他唑仑Haloxazolam 卤沙唑仑Ketazolam 凯他唑仑Loprazolam 氯普唑仑Mexazolam 美沙唑仑Midazolam 咪达唑仑Oxazolam 奥沙唑仑Triazolam 三唑仑-azoline抗组胺药\血管收缩 -唑啉安他唑啉衍生物Aminothiazoline 氨噻唑啉Antazoline 安他唑啉Cilutazoline 西鲁唑啉Cirazoline 西拉唑啉Clonazoline 氯萘唑啉Coumazoline 库马唑啉Diphenazoline 二苯唑啉Domazoline 多马唑啉Fenoxazoline 非诺唑啉Indanazoline 茚唑啉Metrafazoline 美曲唑啉Naphazoline 萘甲唑啉Nemazoline 奈马唑啉Oxymetazoline 羟甲唑啉Phenamazoline 非那唑啉Prednazoline 泼那唑啉Tefazoline 替法唑啉Thibenzazoline 硫苯唑林Tinazoline 替那唑啉Tolazoline 妥拉唑林Tramazoline 曲马唑啉Tymazoline 泰马唑啉Xylometazoline 赛洛唑啉-azone <见-butazone> -宗-azosin 抗高血压药 -唑嗪哌唑嗪衍生物Bunazosin 布那唑嗪 Doxazosin 多沙唑嗪 Neldazosin 奈达唑嗪Prazosin 哌唑嗪 Quinazosin 喹唑嗪 Terazosin 特拉唑嗪Tiodazosin 硫达唑嗪 Trimazosin 曲马唑嗪-bactamβ酰胺酶抑制药 -巴坦Brobactam 溴巴坦 Sulbactam 舒巴坦 Tazobactam 三唑巴坦-bamate 安定药 -氨酯丙二醇类衍生物Chlorphenesin Carbamate 氯苯甘油氨酯 Cyclarbamate 环拉氨酯Difebarbamate 苯巴氨酯 Febarbamate 非巴氨酯 Felbamate 非尔氨酯Lorbamate 劳氨酯 Meprobamate 甲丙氨酯 Nisobamate 尼索氨酯Pentabamate 喷他氨酯 Phenprobamate 苯丙氨酯 Tybamate 泰巴氨酯barb催眠镇静药 -比妥巴比妥类衍生物Allobarbital 阿洛巴比妥 Amobarbital 异戊巴比妥 Aprobarbital 阿普比妥Barbital 巴比妥 Barbital Sodium 巴比妥钠 Benzobarbital 苯佐巴比妥Brallobarbital 溴烯比妥 Brophebarbital 溴苯比妥 Butobarbital 丁巴比妥Carbubarb 卡布比妥 Cyclobarbital 环己巴比妥 Cyclopentobarbital 环戊巴比妥Eterobarb 依特比妥 Ethallobarbital 依沙比妥 Heptabarb 环庚比妥Heptobarbital 苯甲比妥 Hexobarbital 海索比妥 Methylphenobarbital 甲苯比妥Narcobarbital 那可比妥 Nealbarbital 尼阿比妥 Pentobarbital 戊巴比妥Phenobarbital 苯巴比妥 Phenobarbital Sodium 苯巴比妥钠 Probarbital Sodium 普罗比妥钠Proxibarbal 丙羟巴比 Secbutabarbital 仲丁比妥 Secobarbital 司可巴比妥Tetrabarbital 替曲比妥 Thialbarbital 硫烯比妥 Thiotetrabarbital 硫替比妥Vinbarbital 戊烯比妥-benakin <见-kin> -白介素-bendan强心药<见-dan> -本旦Adibendan 阿地本旦 Meribendan 美立苯旦 Pimobendan 匹莫苯旦-bendazole 抗蠕虫药 -苯达唑噻苯达唑类衍生物Albendazole 阿苯达唑 Bisbendazole 双苯达唑 Cambendazole 坎苯达唑Ciclobendazole 环苯达唑 Dribendazole 屈苯达唑 Etibendazole 依苯达唑Fenbendazole 芬苯达唑 Flubendazole 氟苯达唑 Lobendazole 洛苯达唑Luxabendazole 鲁苯达唑 Mebendazole 甲苯达唑 Oxibendazole 奥苯达唑Parbendazole 帕苯达唑 Subendazole 舒苯达唑 Tiabendazole 噻苯达唑Triclabendazole 三氯苯达唑-bermin<见-ermin> -明-betasol <见pred> -倍他索-bersat 抗惊厥药-博沙Carabersat 卡拉博沙 Tidembersat 替旦柏沙 Tonabersat 托那博沙Bol同化激素类药 -勃Bolandiol 勃雄二醇 Bolasterone 勃拉睾酮 Bolazine 勃拉嗪Boldenone 勃地酮 Bolenol 勃来诺 Bolmantalate 勃金刚酯Clostebol 氯司替勃 Dichlorbenzyl Alcobol 二氯苯甲醇 Enestebol 依奈替勃Formebolone 甲酰勃龙 Furazabol 夫拉扎勃 Mebolazine 美勃嗪Mesabolone 美沙勃龙 Metribolone 美曲勃龙 Mibolerone 米勃酮Norboletone 诺勃酮 Norclostebol 诺司替勃 Oxabolone Cipionate 环戊丙羟勃龙Quinbolone 奎勃龙 Roxibolone 罗昔勃龙 Stenbolone 司腾勃龙Tibolone 替勃龙 Trenbolone 群勃龙-bradine减缓心率药-雷定Cilobradine 西洛雷定 Ivabradine 伊伐布雷定 Zatebradine 扎替雷定-brate 降血脂药<见-fibrate> -贝特-bufen 消炎镇痛药 -布芬芳基丁酸类衍生物Fenbufen 芬布芬 Furobufen 呋罗布芬 Indobufen 吲哚布芬Metbufen 甲布芬-butazone 消炎镇痛药<见-buzone> -布宗-buzone消炎镇痛药 -布宗保泰松类衍生物Feclobuzone 苯氯布宗 Kebuzone 凯布宗 Pipebuzone 哌布宗Suxibuzone 琥布宗 Tribuzone 曲布宗-butazoneMofebutazone 莫非布宗 Oxyphenbutazone 羟布宗 Phenylbutazone 保泰松-azoneAmbazone 安巴腙 Aminophenazone 氨基比林 Azapropazone 阿扎丙宗Balaglitazone 巴格列酮 Benhepazone 苯庚宗 Bisfenazone 双苯那宗Bitipazone 比替哌宗 Caroxazone 卡罗沙酮 Cefbuperazone 头孢拉宗Cefoperazone 头孢哌酮 Chlorzoxazone 氯唑沙宗 Ciglitazone 环格列酮Cinnopentazone 辛喷他宗 Ciproquazone 环丙喹宗 Citenazone 氰噻腙Clodazone 氯达酮 Darglitazone 达格列酮 Denpidazone 登匹达酮Dichloralphenazone 氯醛比林 Edaglitazone 依格列宗 Emorfazone 依莫法宗Englitazone 恩格列酮 Famprofazone 泛普法宗 Feprazone 非普拉宗Fluproquazone 氟丙喹宗 Fluquazone 氟喹宗 Furilazone 呋烟腙Gloxazone 格洛沙腙 Halazone 哈拉宗 Ipenoxazone 伊培沙宗Isamfazone 伊胺法宗 Isoprazone 异普拉酮 Meseclazone 美西拉宗Metamfazone 美坦法宗 Metisazone 美替沙腙 Metolazone 美托拉宗Mitoguazone 米托胍腙 Mofebutazone 莫非布宗 Molinazone 吗林那宗Morazone 吗拉宗 Naftazone 萘醌腙 Netoglitazone 萘格列酮Nicothiazone 尼可硫腙 Nifenazone 尼芬那宗 Nifurethazone 硝呋乙宗Nihydrazone 尼海屈腙 Nimazone 尼马宗 Niprofazone 烟丙法宗Nitraquazone 硝喹宗 Oxyphenbutazone 羟布宗 Paraxazone 帕拉沙酮Phenazone 安替比林 Phenopyrazone 非诺吡酮 Pioglitazone 吡格列酮Promepiazone 普罗哌宗 Propyphenazone 异丙安替比林 Proquazone 普罗喹宗Quinethazone 喹乙宗 Ramifenazone 雷米那酮 Rivoglitazone 利格列酮Rosiglitazone 罗格列酮 Ruvazone 芦伐腙 Seclazone 司克拉宗Sulfamazone 磺胺马宗 Sulfinpyrazone 磺吡酮 Thiethazone 硫乙腙Thioacetazone 氨硫脲 Troglitazone 曲格列酮-caine 局部麻醉药 -卡因Ambucaine 氨布卡因 Amoxecaine 阿莫卡因 Amydricaine 戊胺卡因Amylocaine 阿米卡因 Aptocaine 阿托卡因 Articaine 阿替卡因Benzocaine 苯佐卡因 Betoxycaine 贝托卡因 Bucricaine 丁吖卡因Bumecaine 布美卡因 Bupivacaine 布比卡因 Butacaine 布他卡因Butanilicaine 布坦卡因 Chloroprocaine 氯普鲁卡因 Cinchocaine 辛可卡因Clibucaine 氯丁卡因 Clodacaine 氯达卡因 Clormecaine 氯美卡因Cocaine 可卡因 Cyclomethycaine 环美卡因 Dexivacaine 地昔卡因Diamocaine 二胺卡因 Dimethocaine 二甲卡因 Edronocaine 依屈卡因Elucaine 依鲁卡因 Etidocaine 依替卡因 Fexicaine 苯氧卡因Fomocaine 福莫卡因 Fomocaine 福莫卡因 Hexylcaine 海克卡因Hydroxyprocaine 羟普鲁卡因 Hydroxytetracaine 羟丁卡因 Ipravacaine 艾拉卡因Isobucaine 异布卡因 Isobutylcaine 异丁卡因 Ketocaine 凯托卡因Leucinocaine 亮氨卡因 Levobupivacaine 左布比卡因 Lidocaine 利多卡因Lotucaine 洛土卡因 Mepivacaine 甲哌卡因 Meprylcaine 美普卡因Metabutoxycaine 美布卡因 Myrtecaine 麦替卡因 Octacaine 奥他卡因Orthocaine 奥索卡因 Oxetacaine 奥昔卡因 Oxybuprocaine 奥布卡因Parethoxycaine 对乙氧卡因 Paridocaine 哌多卡因 Phenacaine 非那卡因Pinolcaine 哌诺卡因 Piperocaine 哌罗卡因 Piridocaine 匹多卡因Polycaine 泊利卡因 Pramocaine 普莫卡因 Pribecaine 丙贝卡因Prilocaine 丙胺卡因 Procaine 普鲁卡因 Propanocaine 丙泮卡因Propipocaine 丙哌卡因 Propoxycaine 丙氧卡因 Proxymetacaine 丙美卡因Pyrrocaine 吡咯卡因 Quatacaine 夸他卡因 Quinisocaine 奎尼卡因Risocaine 利索卡因 Rodocaine 罗多卡因 Ropivacaine 罗哌卡因Tetracaine 丁卡因 Tolycaine 托利卡因 Trapencaine 曲喷卡因Trimecaine 三甲卡因 Vadocaine 伐多卡因-cain-局部麻醉药 -卡- 普鲁卡因胺、利多卡因类衍生物Acecainide 乙酰卡尼 Asocainol 阿索卡诺 Barucainide 巴芦卡尼Betoxicaine → Betoxycaine Bucainide 布卡尼 Carcainium Chloride 卡氯铵Carocainide 卡罗卡尼 Droxicainide 羟卡尼 Encainide 恩卡尼Epicainide 依吡卡尼 Erocainide 依罗卡尼 Flecainide 氟卡尼Guafecainol 呱非卡诺 Indecainide 英地卡尼 Ketocainol 凯托卡诺Lorcainide 劳卡尼 Milacainide 米拉卡尼 Modecainide 莫地卡尼Murocainide 莫罗卡尼 Nicainoprol 尼卡普醇 Nofecainide 诺非卡尼Pilsicainide 吡西卡尼 Pincainide 平卡尼 Procainamide 普鲁卡因胺Recainam 瑞卡南 Solpecainol 索培卡诺 Stirocainide 司替卡尼Suricainide 舒立卡尼 Tocainide 妥卡尼 Transcainide 群司卡尼Verocainine 维罗卡宁 Zocainone 佐卡酮Calci维生素类药骨化醇维生素D类衍生物Alfacalcidol 阿法骨化醇Atocalcitol 阿托骨化醇Calcifediol 骨化二醇Calcitriol 骨化三醇Doxercalciferol 度骨化醇Falecalcitriol 氟骨化三醇Inecalcitol 依奈骨化醇Lexacalcitol 来沙骨化醇Maxacalcitol 马沙骨化醇Paricalcitol 帕立骨化醇Secalciferol 司骨化醇Seocalcitol 西奥骨化醇Tacalcitol 他卡西醇Tisocalcitate 替索骨化酯-carbef抗生素类药 -头孢Loracarbef氯碳头孢-carnil 苯二氮受体激动药<见-azenil> -卡尔-castat 酶抑制药<见-stat> -卡司他-cavir 抗病毒药<见-vir> -卡韦cef-抗生素类药头孢-Cefalosporannic acid衍生物Cefacetrile头孢乙腈Cefaclomezine头孢氯嗪Cefaclor头孢克洛Cefadroxil头孢羟氨苄Cefalexin头孢氨苄Cefaloglycin头孢来星Cefalonium头孢XXCefaloram头孢洛仑Cefaloridine头孢噻啶Cefalotin头孢噻吩Cefamandole头孢孟多Cefamandole Nafate头孢孟多酯钠Cefaparole头孢帕罗Cefapirin头孢匹林Cefatrizine头孢曲Cefazaflur头孢氮氟Cefazedone头孢西酮Cefazolin头孢唑林Cefbuperazone头孢拉宗Cefcanel头孢卡奈Cefcanel Daloxate头孢卡奈酯Cefcapene头孢卡品Cefclidin头孢克定Cefdaloxime头孢达肟Cefdinir头孢地尼Cefditoren头孢托仑Cefedrolor头孢屈洛Cefempidone头孢吡酮Cefepime头孢吡肟Cefetamet头孢他美Cefetecol头孢替考Cefetrizole头孢三唑Cefivitril头孢维曲Cefixime头孢克肟Cefluprenam头孢瑞南Cefmatilen头孢替林Cefmenoxime头孢甲肟Cefmepidium Chloride头孢氯铵Cefmetazole头孢美唑Cefminox头孢米诺Cefodizime头孢地Cefonicid头孢尼西Cefoperazone头孢哌酮Ceforanide头孢雷特Cefoselis头孢噻利Cefotaxime头孢噻肟Cefotetan头孢替坦Cefotiam头孢替安Cefovecin头孢维星Cefoxazole头孢唑Cefoxitin头孢西丁Cefozopran头孢唑兰Cefpimizole头孢咪唑Cefpiramide头孢匹胺Cefpirome头孢匹罗Cefpodoxime头孢泊肟Cefprozil头孢丙烯Cefquinome头孢喹肟Cefradine头孢拉定Cefrotil头孢罗替Cefroxadine头孢沙定Cefsulodin头孢磺啶Cefsumide头孢舒米Ceftazidime头孢他啶Cefteram头孢特仑Ceftezole头孢替唑Ceftibuten头孢布烯Ceftiofur头孢噻呋Ceftiolene头孢噻林Ceftioxide头孢噻氧Ceftizoxime头孢唑肟Ceftizoxime Alapivoxil头孢唑肟酯Ceftriaxone头孢曲松Cefuracetime头孢呋汀Cefuroxime头孢呋辛Cefuzonam头孢唑南-oxef抗生素类药 -氧头孢 Oxcefalosporannic acid衍生物Flomoxef 氟氧头孢 Latamoxef 拉氧头孢cell-或 cel-纤维素衍生物纤维-Cellulase纤维素酶Celiprolol塞利洛尔cell-ate纤维-酯Cellaburate纤维醋丁酯 Cellacefate纤维醋法酯-cellose -纤维素Cellulose Sodium Phosphate纤维素磷酸钠Cellulose Acetate醋酸纤维素-cic保肝药 -西克<酸>Alonacic 阿洛西克 Bisorcic 比索西克 Limazocic 利马西克Tidiacic 噻二西酸 Timonacic 噻莫西酸-cidin抗生素类药 -菌素<肽>Candicidin 克念菌素Gramicidin 短杆菌肽Methocidin 美索菌素-cillin抗生素类药 -西林 6-aminopenicilanic acid 衍生物Adicillin 阿地西林 Almecillin 阿美西林 Amantocillin 金刚西林Amoxicillin 阿莫西林 Ampicillin 氨苄西林 Apalcillin 阿帕西林Aspoxicillin 阿扑西林 Azidocillin 阿度西林 Azlocillin 阿洛西林Bacampicillin 巴氨西林 Benethamine Penicillin 苯明青霉素Benzathine Benzylpenicillin 苄星青霉素 Benzylpenicillin 青霉素Carbenicillin 羧苄西林 Carfecillin 卡非西林 Carindacillin 卡茚西林Ciclacillin 环己西林 Clemizole Penicillin 克咪西林Clometocillin 氯甲西林 Cloxacillin 氯唑西林 Dicloxacillin 双氯西林Epicillin 依匹西林 Epihetacillin 表海他西林 Fenbenicillin 芬贝西林Fibracillin 非布西林 Flucloxacillin 氟氯西林 Fomidacillin 福米西林Fumoxicillin 呋莫西林 Furbenicillin 呋苄西林 Furbucillin 呋布西林Fuzlocillin 呋洛西林 Hetacillin 海他西林 Isopropicillin 异丙西林Lenampicillin 仑氨西林 Levopropicillin 左普匹西林 Metampicillin 美坦西林Meticillin 甲氧西林 Mezlocillin 美洛西林 Nafcillin 萘夫西林Oxacillin 苯唑西林 Oxetacillin 氧他西林 Penamecillin 培那西林Penethacillin 喷沙西林 Pheneticillin非奈西林 Phenoxymethylpenicillin 青霉素VPhenyracillin 苯拉西林 Piperacillin 哌拉西林 Pirbenicillin 吡苄西林Piroxicillin 匹罗西林 Pivampicillin 匹氨西林 Prazocillin 普唑西林Procaine Benzylpenicillin普鲁卡因青霉素 Propicillin丙匹西林 Quinacillin 喹那西林Rotamicillin 罗坦西林 Sarmoxicillin 沙莫西林 Sarpicillin 沙匹西林Sulbenicillin 磺苄西林 Sultamicillin 舒他西林 Suncillin 森西林Talampicillin 酞氨西林 Tameticillin 他甲西林 Temocillin 替莫西林Ticarcillin 替卡西林 Tifencillin 替芬西林 Tobicillin 托比西林Xantocillin 占托西林-cillide 抗生素类药 -西来Libecillide 利贝西来-cillinam 抗生素类药-西林Bacmecillinam 巴美西林Mecillinam 美西林Pivmecillinam 匹美西林-cilpine <见-pine> -平-cisteine <见-steine> -司坦-citabine抗肿瘤药 -他滨阿糖胞苷类衍生物Ancitabine 安西他滨 Capecitabine 卡培他滨 Decitabine 地西他滨Elvucitabine 艾夫他滨 Emtricitabine 恩曲他滨 Enocitabine 依诺他滨Fiacitabine 非西他滨 Flurocitabine 氟西他滨 Galocitabine 加洛他滨Gemcitabine 吉西他滨 Ibacitabine 伊巴他滨 Tezacitabine 替扎他滨Torcitabine 托西他滨 Troxacitabine 曲沙他滨 Valtorcitabine 伐托他滨Zalcitabine 扎西他滨-clone催眠镇静药 -克隆Barbexaclone 巴比沙隆 Eszopiclone 艾司佐匹克隆 Gestaclone 孕氯酮Pagoclone 帕戈隆 Pazinaclone 帕克隆 Pimeclone 哌美克隆Suproclone 舒普罗酮 Suriclone 舒立克隆 Zopiclone 佐匹克隆-cog凝血因子 -凝血素Eptacog alfa <activated> 依他凝血素α〔活化〕 Moroctocog Alfa 莫罗凝血素αNicogrelate 烟格雷酯 Nonacog Alfa 诺那凝血素α Octocog alfa 辛凝血素αTifacogin 替法可近-conazole抗真菌药 -康唑咪康唑类衍生物Albaconazole 阿巴康唑 Aliconazole 阿利康唑 Alteconazole 阿替康唑Azaconazole 阿扎康唑 Becliconazole 贝康唑 Brolaconazole 溴康唑Butoconazole 布康唑 Cisconazole 顺康唑 Croconazole 氯康唑Democonazole 地莫康唑 Doconazole 多康唑 Eberconazole 依柏康唑Econazole 益康唑 Enilconazole 恩康唑 Fenticonazole 芬替康唑Fluconazole 氟康唑 Fosfluconazole 磷氟康唑 Isoconazole 异康唑Itraconazole 伊曲康唑 Ketoconazole 酮康唑 Lanoconazole 拉诺康唑Luliconazole 氯利康唑 Miconazole 咪康唑 Neticonazole 奈康唑Omoconazole 奥莫康唑 Orconazole 奥康唑 Oxiconazole 奥昔康唑Parconazole 帕康唑 Posaconazole 泊沙康唑 Ravuconazole 雷夫康唑Saperconazole 沙康唑 Sertaconazole 舍他康唑 Sulconazole 硫康唑Terconazole 特康唑 Tioconazole 噻康唑 Valconazole 戊康唑Voriconazole 伏立康唑 Zinoconazole 齐诺康唑 Zoficonazole 佐非康唑cort皮质激素类药 -可特可的松类衍生物Amebucort 安布可特 Anecortave 阿奈可他 Butixocort 布替可特Cicortonide 西可奈德 Clocortolone 氯可托龙 Corticorelin 可的瑞林Corticotrophin 促皮质素 Corticotrophin Zinc Hydroxide 促皮质素锌Cortisone 可的松 Cortisuzol 可的磺唑 Cortivazol 可的伐唑Cortodoxone 可托多松 Deflazacort 地夫可特 Desoxycortone 去氧皮质酮Fluazacort 氟扎可特 Fludrocortisone 氟氢可的松 Fludroxycortide 氟氢缩松Fluocortin 氟可丁 Formocortal 福莫可他 Halocortolone 卤可托龙Hydrocortamate 氢可他酯 Hydrocortisone 氢化可的松Hydrocortisone Aceponate 醋丙氢可的松 Locicortolone Dicibate 地西洛可龙Naflocort 萘非可特 Nicocortonide 尼可奈德 Nivacortol 尼伐可醇Resocortol 瑞索可托 Tetrahydrocortisol 四氢可的索 Tixocortol 替可的松-coxib环氧酶-2抑制药 -考昔Celecoxib 塞来考昔 Cimicoxib 西米考昔 Deracoxib 地拉考昔Etoricoxib 依托考昔 Firocoxib 非罗考昔 Lumiracoxib 芦米考昔Parecoxib 帕瑞考昔 Robenacoxib 罗贝考昔 Rofecoxib 罗非考昔Tilmacoxib 替马考昔 Valdecoxib 伐地考昔-crinat利尿药 -利那依他尼酸类衍生物Brocrinat 溴克利那 Sulicrinat 磺克利那-crine -吖啶吖啶类衍生物Amsacrine 安吖啶 Botiacrine 波替吖啶 Dimetacrine 二甲他林Floxacrine 氟克吖啶 Ipidacrine 伊匹达克林 Mepacrine 米帕林Monometacrine 莫诺吖啶 Nitracrine 尼曲吖啶 Suronacrine 舒罗吖啶Tacrine 他克林 Velnacrine 维吖啶-cromil 抗过敏药 -罗米 cromoglicic acid 类衍生物Ambicromil 安克罗米 Isocromil 异克罗米 Minocromil 米诺罗米Nedocromil 奈多罗米 Probicromil 普克罗米 Proxicromil 普昔罗米Terbucromil 特丁罗米 Texacromil 替沙罗米-curium <见-ium> -司坦-cycline抗生素类药 -环素四环素类衍生物Amicycline 阿米环素 Apicycline 阿哌环素 Cetocycline 西托环素Chlortetracycline 金霉素 Clomocycline 氯莫环素 Colimecycline 多粘环素Demeclocycline 地美环素 Demecycline 去甲环素 Doxycycline 多西环素Etamocycline 乙莫环素 Guamecycline 胍甲环素 Lymecycline 赖甲环素Meclocycline 甲氯环素 Meglucycline 甲葡环素 Metacycline 美他环素Minocycline 米诺环素 Nitrocycline 硝环素 Oxytetracycline 土霉素Pecocycline 哌考环素 Penimepicycline 青哌环素 Penimocycline 培莫环素Pipacycline 匹哌环素 Rolitetracycline 罗利环素 Sancycline 山环素Tetracycline 四环素 Tigecycline 替吉环素-dan强心药 -旦匹莫苯类衍生物Adibendan 阿地本旦 Bemoradan 贝莫拉旦 Imazodan 伊马唑旦Indolidan 吲哚利旦 Levosimendan 左西孟旦 Meribendan 美立苯旦Nitrodan 硝旦 Pimobendan 匹莫苯旦 Prinoxodan 普啉索旦Senazodan 司那佐旦 Siguazodan 氰胍佐旦 Simendan 西孟旦Tyromedan 甲状米登-dapsone抗麻风药 -苯砜二氨基苯砜类衍生物Acedapsone 醋氨苯砜 Amidapsone 阿米氨苯砜 Dapsone 氨苯砜-decakin免疫抑制药<见-kin> -白介素-dermin<见-ermin> -德明-dil血管舒药 -地尔Alprostadil 前列地尔 Aviptadil 阿肽地尔 Belfosdil 贝磷地尔Bepridil 苄普地尔 Biclodil 二氯地尔 Buflomedil 丁咯地尔Bumepidil 布美地尔 Carprazidil 卡普地尔 Cetiedil 西替地尔Cinepaxadil 桂帕地尔 Dopropidil 多普吡地 Ecipramidil 环丙地尔Eliprodil 依利罗地 Fasudil 法舒地尔 Fenetradil 芬曲地尔Fenoxedil 非诺地尔 Floredil 夫洛地尔 Flosatidil 氟沙地尔Fostedil 福司地尔 Fronepidil 夫罗吡地 Ifenprodil 艾芬地尔Ipramidil 异丙地尔 Levosemotiadil 左司莫地尔 Manozodil 马诺地尔Mefenidil 甲苯地尔 Mepramidil 美普地尔 Metrifudil 腺苷地尔Mibefradil 米贝拉地尔 Minoxidil 米诺地尔 Naftopidil 萘哌地尔Naminidil 纳米尼地尔 Nesapidil 奈沙地尔 Nicorandil 尼可地尔Perfomedil 哌福地尔 Phenobutiodil 碘芬布酸 Pinacidil 吡那地尔Piribedil 吡贝地尔 Pirozadil 吡扎地尔 Pitenodil 哌诺地尔Pretiadil 普硫地尔 Razinodil 雷嗪地尔 Semotiadil 司莫地尔Sinitrodil 西硝地尔 Stevaladil 甾伐地尔 Suloctidil 舒洛地尔Tipropidil 替普地尔 Tixadil 噻吨地尔 Trapidil 曲匹地尔Traxoprodil 曲索罗地 Urapidil 乌拉地尔 Viquidil 维喹地尔-dilol -地洛Carvedilol 卡维地洛 Dioxadilol 地奥地洛 Dramedilol 屈美地洛Flavodilol 黄酮地洛 Mindodilol 明多地洛 Nipradilol 尼普地洛Oberadilol 奥拉地洛 Parodilol 帕地洛 Prizidilol 普齐地洛Tribendilol 曲苯地洛-pendyl -喷地Cloxypendyl 氯羟喷地 Isothipendyl 异西喷地 Oxypendyl 奥昔喷地Prothipendyl 丙硫喷地-dylBisacodyl 比沙可啶 Bunamiodyl 丁碘桂酸 Trihexyphenidyl 苯海索-dilol血管扩药 <见-dil>-地洛Carvedilol 卡维地洛Dioxadilol 地奥地洛Dramedilol 屈美地洛Flavodilol 黄酮地洛Mindodilol 明多地洛Nipradilol 尼普地洛Oberadilol 奥拉地洛Parodilol 帕地洛Prizidilol 普齐地洛Tribendilol 曲苯地洛-dipine钙通道阻滞药 -地平硝苯地平类衍生物Amlodipine 氨氯地平Aranidipine 阿雷地平Azelnidipine 阿折地平Barnidipine 巴尼地平Benidipine 贝尼地平 Budipine 布地品Cilnidipine 西尼地平Clevidipine 氯维地平 Cronidipine 氯硝地平Darodipine 达罗地平Dexniguldipine 右尼古地平 Efonidipine 依福地平Elgodipine 依高地平Elnadipine 依那地平 Felodipine 非洛地平 Flordipine 氟地平Furnidipine 呋尼地平 Iganidipine 伊加地平Isradipine 伊拉地平Lacidipine 拉平 Lemildipine 来米地平Lercanidipine 乐卡地平Manidipine 马尼地平 Mesudipine 甲硫地平Nicardipine 尼卡地平Nifedipine 硝苯地平 Niguldipine 尼古地平 Niludipine 尼鲁地平Nilvadipine 尼伐地平 Nimodipine 尼莫地平 Nisoldipine 尼索地平Nitrendipine 尼群地平 Olradipine 奥拉地平 Oxodipine 奥索地平Palonidipine 帕洛地平 Pranidipine 普拉地平 Prodipine 普罗地平Riodipine 利奥地平 Sagandipine 沙更地平 Sornidipine 索尼地平Teludipine 替鲁地平 Vatanidipine 伐尼地平-dismase酶类药<见-ase> -歧化酶-dodekin <见-kin>-dopa抗震颤麻痹药 -多巴多巴胺类衍生物Carbidopa 卡比多巴 Ciladopa 西拉多巴 Droxidopa 屈昔多巴Etilevodopa 乙左旋多巴 Levodopa 左旋多巴 Melevodopa 美左旋多巴Methyldopa 甲基多巴-opamine多巴胺类药 -巴胺Butopamine 布托巴胺 Cliropamine 克利巴胺 Denopamine 地诺帕明Dopamine 多巴胺 Fosopamine 磷巴胺 Ibopamine 异波帕胺Octopamine 奥克巴胺 Oxidopamine 羟多巴胺 Ractopamine 雷托巴胺Tiopropamine 噻罗帕明 Tolpropamine 托普帕敏 Xylopropamine 赛洛丙胺-dox <见-ox/-alox> -多司Carbadox 卡巴多司 Ciadox 氰多司 Cinoquidox 氰喹多司Drazidox 肼多司 Mequidox 美喹多司 Olaquindox 奥喹多司Temodox 替莫多司-dralazine抗高血压药 -屈嗪衍生物Budralazine 布屈嗪 Cadralazine 卡屈嗪 Dihydralazine 双肼屈嗪Endralazine 恩屈嗪 Hydralazine 肼屈嗪 Mopidralazine 莫哌屈嗪Oxdralazine 奥屈嗪 Picodralazine 吡考屈嗪 Pildralazine 匹尔屈嗪Todralazine 托屈嗪-drine类交感神经药 -君Alifedrine 阿利非君 Benzylephedrine 苄麻黄碱 Bufenadrine 丁苯那胺Butidrine 布替君 Cafedrine 咖啡君 Camphamedrine 樟美君Cinnamedrine 桂美君 Corbadrine 可巴君 Cyclodrine 环戊君Dioxifedrine 二羟非君 Ephedrine 麻黄碱 Etafedrine 乙非君Levopropylhexedrine 左丙己君 Meluadrine美卢君 Methoxyphedrine甲氧非君Methylephedrine 甲麻黄碱 Midodrine 米多君 Norbudrine 诺布君Octodrine 奥托君 Oleandrine 夹竹桃苷 Orphenadrine 奥芬那君Oxyfedrine 奥昔非君 Pholedrine 福来君 Propylhexedrine 丙己君Pseudoephedrine 伪麻黄碱 Racephedrine 消旋麻黄碱 Ritodrine 利托君Tetrandrine 粉防己碱 Theophylline Ephedrine 茶麻黄碱 Tinofedrine 替诺非君Trecadrine 曲卡君-frine 类交感神经药 -福林Berefrine 贝瑞福林Ciclafrine 环拉福林Dimetofrine 二甲福林Dipivefrine 地匹福林Etilefrine 依替福林Gepefrine 吉培福林Norfenefrine 去甲苯福林Oxilofrine 奥洛福林Pivenfrine 新戊福林Racepinefrine 消旋肾上腺素-dronic acid钙代药 -膦酸Alendronic Acid 阿仑膦酸 Butedronic Acid 布替膦酸 Clodronic Acid 氯膦酸Etidronic Acid 依替膦酸 Ibandronic Acid 伊班膦酸 Incadronic Acid 英卡膦酸Lidadronic Acid 利达膦酸 Medronic Acid亚甲膦酸 Minodronic Acid 米诺膦酸Neridronic Acid 奈立膦酸 Olpadronic Acid奥帕膦酸 Oxidronic Acid 奥昔膦酸Pamidronic Acid 帕米膦酸 Piridronic Acid 吡膦酸 Risedronic Acid 利塞膦酸Tiludronic Acid 替鲁膦酸 Zoledronic Acid 唑来膦酸-dutant <见-tant>-dyl <见-dil>-ectin抗寄生虫药 -克丁伊维菌素衍生物Abamectin 阿巴克丁 Dimadectin 地马待克丁 Doramectin 多拉克丁Eprinomectin 依立诺克丁 Fuladectin 呋拉迪克丁 Ivermectin 伊维菌素Latidectin 拉替待克丁 Moxidectin 莫昔克丁 Nemadectin 奈马克丁Selamectin 司拉克丁-elestat<见-stat>-elvekin<见-kin>-emcinal -西那无抗生素活性的红霉素衍生物衍生物Alemcinal 阿兰西那 Idremcinal 伊屈西那 Mitemcinal 米坦西诺-entan 皮素受体阻滞药 -生坦Ambrisentan 安立生坦Atrasentan 阿曲生坦Bosentan 波生坦Clazosentan 克拉生坦Darusentan 达卢生坦Edonentan 艾多南坦Enrasentan 恩拉生坦Fandosentan 泛多生坦Feloprentan 非洛仑坦Nebentan 奈苯坦Sitaxentan 西他生坦Tezosentan 替唑生坦-eptacog <见-cog>erg麦角碱衍生物麦角Acetergamine 醋麦角胺 Amesergide 安麦角 Brazergoline 溴麦角林Bromerguride 溴麦角脲 Cabergoline 卡麦角林 Cianergoline 氰麦角林Delergotrile 地麦角腈 Dihydroergocristine 双氢麦角汀 Dihydroergotamine 双氢麦角胺Dihydroergotamine Mesilate 甲磺双氢麦角胺 Dosergoside度麦角胺 Ergometrine麦角新碱Ergotamine 麦角胺 Etisulergine 乙舒麦角 Lergotrile 麦角腈Lysergide 麦角二乙胺 Mergocriptine 甲麦角隐亭 Mesulergine 美舒麦角Metergoline 甲麦角林 Metergotamine 甲麦角胺 Methylergometrine 甲麦角新碱Methysergide 美西麦角 Nicergoline 尼麦角林 Propisergide 普罗麦角Proterguride 丙麦角脲 Romergoline 罗麦角林 Sergolexole 麦角克索Terguride 特麦角脲 Tiomergine 硫麦角林 Voxergolide 伏高利特-eridine镇痛药 -利定哌替啶类衍生物Anileridine 阿尼利定Carperidine 卡哌利定Diaveridine 二氨藜芦啶Eseridine 依舍立定Etoxeridine 依托利定Meperidine → PethidineMorpheridine 吗哌利定Nexeridine 奈西利定Oxpheneridine 羟芬利定。
英文文献翻译一
在无溶剂的条件下,由一种新的催化剂催化的曼尼希反应岳彩波,伊廷锋,,朱传兵,,刘刚化学与化工学院,安徽工业大学,马鞍山,243002,中国文章信息:文章历史:收稿日期2008年9月29日认可时间2009年2月13日COO](吡啶鎓三氟乙酸盐)被合成和使用于各摘要:一种酸性催化剂—[Py][CF3种芳香醛,芳香酮和芳族胺的曼尼希反应。
在无溶剂的条件下,在室温下进行曼尼希反应可得到理想收率的β-氨基羰基化合物。
通过简单地水洗和去水后,该产品可以从催化剂中分离,催化剂最多可以回收和重复使用达四次,并且不明显降低催化活性。
Crown版权所有由Elsevier BV代表韩国工业协会和工程化学出版。
保留所有权利。
关键词:曼尼希反应吡啶三氟乙酸β-氨基羰基化合物无溶剂条件1.介绍曼尼希类的反应为β-氨基酮醛的制备提供了一种最经典的和有用的方法,他们组成各种药品,自然产品,多功能合成的中间体[1–4]。
在醛,酮和芳香胺的直接曼尼希反应中传统上习惯使用路易斯酸和质子酸。
但是,这些催化剂有一些严重的缺点。
比如,这些路易斯酸催化的反应,只在严格的无水条件下进行。
此外,许多亚胺在水中不稳定。
再者,从产品中分离常规催化剂也有一定的毒害和困难。
因此,在过去的几十年里,对曼尼希反应新型催化剂的研究已经在合成化学中获得了普及。
如今,已经发现该反应也可以由其他各种各样的催化剂,如脯氨酸[5–8],布朗斯台德酸性离子液[9–12],,稀土全氟辛烷[13–15],盐[16–23]等催化。
无溶剂反应在有机合成中非常重要,因为他减少了对环境的污染,节约能源,降低处理成本,简化工作方法[24]。
这里,一种盐,带有弱酸性的[Py][CF3COO](三氟乙酸吡啶盐)在无水和室温条件下,被用来连续催化三种反应物—芳香醛,芳香酮和芳族胺一锅煮式的曼COO]催化曼尼希反应在公尼希反应(方案一)。
据我们所知,以前没有[Py][CF3开文献的报告。
4a: R1 = H, R2 = H, R3 = H; 4b: R1 = H, R2 = H, R3 = p-CH3; 4c:R1 = H, R2 = H, R3 = p-OCH3; 4d: R1 = H, R2 = H, R3 = p-NO2; 4e:R1 = H,R2 = H,R3 = p-Cl; 4f: R1 = p-CH3, R2 = H,R3 = H; 4g: R1 = p-Cl,R2 = H,R3 = H; 4h: R1 = p-NO2, R2 = H,R3 = H; 4i: R1 = H,R2 = p-CH3,R3 = H; 4j: R1 = H, R2 = p-Cl, R3 = H; 4k: R1 = H, R2 = p-NO2, R3 = H.2. 实验2.1 材料和方法显微镜热板熔点测定仪(未校正),布鲁克500MHz光谱仪(CDCl3为溶剂,TMS为内标准)测氢核磁波谱。
非富勒烯小分子受体不稳定单元
非富勒烯小分子受体不稳定单元英文回答:Non-fullerene small molecule acceptors (NF-SMAs) have attracted considerable attention as promising alternatives to fullerenes in organic solar cells (OSCs) due to their tunable optoelectronic properties, ease of synthesis, and low cost. However, the instability of NF-SMAs under ambient conditions remains a major challenge that hinders their practical application. The instability of NF-SMAs is primarily attributed to the presence of labile chemical bonds, such as C-C and C-H bonds, which are susceptible to attack by oxygen and moisture.Several strategies have been developed to improve the stability of NF-SMAs. One approach involves theintroduction of bulky side chains or steric hindrance around the labile bonds. This approach can effectively reduce the accessibility of these bonds to oxygen and moisture, thereby enhancing the stability of the NF-SMAs.Another approach involves the use of cross-linking agents to form covalent bonds between the NF-SMAs and the polymer matrix. This approach can prevent the NF-SMAs fromdiffusing out of the active layer and improve the long-term stability of the OSCs.The development of stable NF-SMAs is crucial for the commercialization of OSCs. By addressing the instability issues, NF-SMAs have the potential to become a viable alternative to fullerenes and enable the development of high-performance, low-cost OSCs.中文回答:非富勒烯小分子受体(NF-SMA)由于其可调的光电性能、易于合成和低成本,作为有机太阳能电池(OSC)中富勒烯的有希望的替代品而备受关注。
EP 5.1.4 非无菌制剂和药用物质的微生物质量标准(中英文)
01/2011:50104 5.1.4. MICROBIOLOGICAL QUALITY OF NON-STERILE PHARMACEUTICAL PREPARATIONS AND SUBSTANCES FOR PHARMACEUTICAL USE (1) 非无菌制剂和药用物质的微生物质量The presence of certain micro-organisms in non-sterile preparations may have the potential to reduce or even inactivate the therapeutic activity of the product and has a potential to adversely affect the health of the patient.在非无菌制剂中如果存在某些微生物,可能会降低或抑制药物的治疗活性,可能会对病人健康有潜在不良影响。
Manufacturers therefore have to ensure a low bioburden of finished dosage forms by implementing current guidelines on Good Manufacturing Practice during the manufacture, storage and distribution of pharmaceutical preparations.因此,生产商应在药品生产、存贮和销售过程中遵守现行GMP指南,来保证制剂的微生物在一个较低的水平。
Microbial examination of non-sterile products is performed according to the methods given in general chapters 2.6.12 and 2.6.13. Acceptance criteria for non-sterile pharmaceutical products based upon the total aerobic microbial count (TAMC) and the total combined yeasts/moulds count (TYMC) are given in Tables 5.1.4-1 and 5.1.4-2. Acceptance criteria are based on individual results or on the average of replicate counts when replicate counts are performed (e.g. direct plating methods).非无菌产品微生物检查应依据通则2.6.12和2.6.13中指定的方法进行。
加拿大拟定肟菌酯的最大残留限量
加拿大拟定肟菌酯的最大残留限量
2008年5月20日,加拿大卫生部有害生物管理局(PMRA)拟定肟菌酯(Trifloxystrobin)最大残留限量。
目前,加拿大的最大残留限量是通过官方公报进行磋商后,根据食品药物法规(FDR)制定的。
通过Bill C-28对食品药物法的修订,预计于2008年生效,这将允许按照有害生物控制产品法合法的制定杀虫剂最大残留限量,而无须经过FDA所属法规的批准。
本文件的目的是对所列肟菌酯(Trifloxystrobin),包括代谢物CGA-321113的MRLs进行咨询,这些限量是在PCPA于2008年6月28日生效后由PMRA拟定的。
咨询活动已经在Bill C-28生效之前开始,以便在FDA被修改后尽快合法的制定本文件所列的MRLs。
(注意:在将有关杀虫剂最大残留限量立法从食品药物法案过渡为有害生物控制产品法案(对拟定最大残留限量的磋商(PMRL2006-01))的文件中拟定的0.04ppm最大残留限量在G/SPS/N/CAN/276中通报)。
所列产品补充了作物14组核果的最大残留限量。
活性物质联合[发明专利]
专利名称:活性物质联合
专利类型:发明专利
发明人:H·H·布施曼,B·古蒂雷茨斯尔瓦,J·霍兰茨,A·法雷格米斯
申请号:CN200580018312.4
申请日:20050405
公开号:CN1976722A
公开日:
20070606
专利内容由知识产权出版社提供
摘要:本发明涉及一种包含至少一种取代的甲醇化合物与至少一种阿片样物质的活性物质联合,一种包含所述活性物质联合的药物,一种包含所述活性物质联合的药物制剂,以及所述活性物质联合在制备药物中的应用。
申请人:埃斯特韦实验室有限公司
地址:西班牙巴塞罗那
国籍:ES
代理机构:中国专利代理(香港)有限公司
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非蒸散型吸气剂工艺流程
非蒸散型吸气剂工艺流程英文回答:Non-evaporative inhalants are a type of medication that is inhaled through the mouth or nose to provide relief for respiratory conditions such as asthma or chronicobstructive pulmonary disease (COPD). Unlike evaporative inhalants, which are inhaled as a mist or vapor, non-evaporative inhalants are inhaled as a dry powder or aerosol.The process of manufacturing non-evaporative inhalants involves several steps. First, the active ingredient is mixed with other excipients, such as lactose or magnesium stearate, to create a uniform powder. This powder is then compressed into tablets or filled into capsules.Next, the tablets or capsules are coated with a protective layer to prevent degradation of the active ingredient and to enhance the stability of the product. Thecoating may also be used to control the release of the medication, allowing for a sustained effect.After coating, the tablets or capsules are inspectedfor quality control purposes. This includes checking forany defects or inconsistencies in size, shape, or color.Any defective products are removed from the batch.Once the tablets or capsules pass inspection, they are packaged into blister packs or bottles for distribution.The packaging is designed to protect the medication from moisture and light, which can degrade the active ingredient.Finally, the packaged inhalants are labeled with the necessary information, such as the name of the medication, dosage instructions, and expiration date. This ensures that patients have access to important information about the medication and can use it safely and effectively.中文回答:非蒸散型吸气剂是一种通过口腔或鼻腔吸入的药物,用于缓解哮喘或慢性阻塞性肺疾病(COPD)等呼吸系统疾病。
非囊泡转运名词解释
非囊泡转运名词解释
非囊泡转运(non-vesicular transport)是一种细胞内物质运输的方式,与通过囊泡(vesicle)进行的运输方式相对。
在非囊泡转运中,细胞内的物质直接从一个区域移动到另一个区域,而不经过膜包裹的囊泡。
这种转运方式通常涉及细胞骨架系统,如微管(microtubules)和细胞质流(cytoplasmic streaming),以及各种细胞内囊泡的直接转移。
非囊泡转运在细胞内物质的分布和运输中起到关键作用,尤其是在快速适应环境变化或应激反应时。
例如,在神经元中,非囊泡转运帮助快速地运输神经递质和受体,以快速响应神经活动。
以上内容仅供参考,建议查阅关于非囊泡转运的专业书籍或文献,获取更准确的信息。
一种非泼罗尼中间体的合成方法与流程
一种非泼罗尼中间体的合成方法与流程下载温馨提示:该文档是我店铺精心编制而成,希望大家下载以后,能够帮助大家解决实际的问题。
文档下载后可定制随意修改,请根据实际需要进行相应的调整和使用,谢谢!并且,本店铺为大家提供各种各样类型的实用资料,如教育随笔、日记赏析、句子摘抄、古诗大全、经典美文、话题作文、工作总结、词语解析、文案摘录、其他资料等等,如想了解不同资料格式和写法,敬请关注!Download tips: This document is carefully compiled by theeditor.I hope that after you download them,they can help yousolve practical problems. The document can be customized andmodified after downloading,please adjust and use it according toactual needs, thank you!In addition, our shop provides you with various types ofpractical materials,such as educational essays, diaryappreciation,sentence excerpts,ancient poems,classic articles,topic composition,work summary,word parsing,copy excerpts,other materials and so on,want to know different data formats andwriting methods,please pay attention!精细化工技术:非泼罗尼关键中间体的高效合成路径在现代药物化学中,非泼罗尼作为一种高效的杀虫剂和医药成分,其合成过程中的中间体优化对于提高整体生产效率和降低成本至关重要。
非诺贝酸说明书(FDA)2009.8
HIGHLIGHTS OF PRESCRIBING INFORMATIONThese highlights do not include all the information needed to use FIBRICOR TM (fenofibric acid) Tablets safely and effectively. See full prescribing information for FIBRICOR.FIBRICOR TM (fenofibric acid)Initial U.S. Approval: 2009--------------------------- INDICATIONS AND USAGE --------------------------- FIBRICOR is a peroxisome proliferator receptor alpha (PPARα) activator indicated:• To reduce triglyceride (TG) levels in patients with severehypertriglyceridemia (> 500 mg/dl) (1.1).• To reduce elevated total cholesterol (TC), low-density-lipoprotein cholesterol (LDL-C), TG and apolipoprotein (Apo) B and toincrease high-density lipoprotein cholesterol (HDL-C) in patientswith primary hyperlipidemia or mixed dyslipidemia (1.2).General Considerations for Treatment: The active moiety of FIBRICOR is fenofibric acid. The pharmacological effects of fenofibric acid have been extensively studied through oral administration of fenofibrate, which is converted in vivo to fenofibric acid (1.3).Limitations of use: Fenofibrate as a dose equivalent to 105 mg of FIBRICOR was not shown to reduce coronary heart disease morbidity and mortality in a large, randomized controlled trial of patients with type 2 diabetes mellitus (1.3).---------------------- DOSAGE AND ADMINISTRATION ----------------------- • FIBRICOR may be taken without regards to meals (2.1).• Severe hypertriglyceridemia: 35 to 105 mg/day; the dose should be adjusted according to patient response (2.2).• Primary hyperlipidemia or mixed dyslipidemia: 105 mg/day (2.2).--------------------- DOSAGE FORMS AND STRENGTHS --------------------- Tablets: 35 mg and 105 mg (3)------------------------------ CONTRAINDICATIONS ----------------------------- • Severe renal dysfunction, including patients receiving dialysis (4)• Active liver disease (4)• Gallbladder disease (4)• Nursing Mothers (4)• Known hypersensitivity to fenofibric acid or fenofibrate (4)FULL PRESCRIBING INFORMATION: CONTENTS*1 INDICATIONS AND USAGE1.1 Severe Hypertriglyceridemia1.2 Primary Hyperlipidemia or Mixed Dyslipidemia1.3 Considerations of Treatment2 DOSAGE AND ADMINISTRATION2.1 Dosing Information2.2 Recommended Adult Dose2.3 RenalImpairment2.4 GeriatricPatients3 DOSAGE FORMS AND STRENGTHS4 CONTRAINDICATIONS5 WARNINGS AND PRECAUTIONS5.1 Abnormal Liver Tests5.2 Cholelithiasis5.3 Concomitant Use with Oral Anticoagulants5.4 Myopathy5.5 Elevated Serum Creatinine5.6 Coronary Heart Disease Morbidity and Mortality5.7 Pancreatitis5.8 Venothromboembolic Disease5.9 Hypersensitivity Reactions5.10 Hematological Changes6 ADVERSE REACTIONS6.1 Clinical Trial Experience6.2 Postmarketing Experience7 DRUG INTERACTIONS7.1 Oral Anticoagulants7.2 Bile-Acid Binding Resins7.3 Immunosuppressants ----------------------- WARNINGS AND PRECAUTIONS -----------------------• Fenofibrate can increase serum transaminases. Monitor liver tests periodically (5.1).• Fenofibrate increases cholesterol excretion into the bile, leading to risk of cholelithiasis. If cholelithiasis is suspected, gallbladder studies are indicated (5.2).• Exercise caution in concomitant treatment with oral coumarin anticoagulants. Adjust the dosage of coumarin anticoagulant to maintain the prothrombin time/INR at the desired level to prevent bleeding complications (5.3).• Myopathy and rhabdomyolysis have been reported in patients taking fenofibrate. The risks of myopathy and rhabdomyolysis appears to be increased in elderly patients and patients with diabetes, renal failure, or hypothyroidism (5.4).• Fenofibrate can reversibly increase serum creatinine levels. Monitor renal function periodically in patients with renal insufficiency (5.5).------------------------------ ADVERSE REACTIONS ------------------------------ Most common adverse reactions (> 2% and greater than placebo) are increased liver tests, abdominal pain, back pain, and headache (6).To report SUSPECTED ADVERSE REACTIONS, contact Mutual Pharmaceutical Company, Inc. at 1-888-351-3786 or FDA at 1-800-FDA-1088 or /medwatch.------------------------------ DRUG INTERACTIONS ------------------------------ • Oral Anticoagulants (7.1)• Bile-Acid Binding Resins (7.2)• Immunosuppressants (7.3)----------------------- USE IN SPECIFIC POPULATIONS ---------------------- • Pediatric use: The safety and effectiveness in pediatric patients have not been established (8.4).• Geriatric use: Determine dose selection based on renal function (8.5).• Renal impairment: Avoid in patients with severe renal impairment; dose reduction required in patients with mild to moderate renal impairment (8.6). • Hepatic impairment: FIBRICOR has not been evaluated in patients with hepatic impairment (8.7).Revised: 8/20098 USE IN SPECIFIC POPULATIONS8.1 Pregnancy8.3 Nursing Mothers8.4 Pediatric Use8.5 Geriatric Use8.6 Renal Impairment8.7 Hepatic Impairment10 OVERDOSAGE11 DESCRIPTION12 CLINICAL PHARMACOLOGY12.1 Mechanism of Action12.2 Pharmacodynamics12.3 Pharmacokinetics13 NONCLINICAL TOXICOLOGY13.1 Carcinogenesis, Mutagenesis, Impairment of Fertility14 CLINICAL STUDIES14.1 Severe Hypertriglyceridemia14.2 Primary Hyperlipidemia (Heterozygous Familial and Nonfamilial)and Mixed Dyslipidemia16 HOW SUPPLIED/STORAGE AND HANDLING17 PATIENT COUNSELING INFORMATION* Sections or subsections omitted from the full prescribing information are not listed.FULL PRESCRIBING INFORMATION response after two months of treatment with themaximum recommended dose of 105 mg per day.1 INDICATIONS AND USAGE1.1 SevereHypertriglyceridemia Consideration should be given to reducing the dosage of FIBRICOR is indicated as adjunctive therapy to diet for FIBRICOR if lipid levels fall significantly below the treatment of severe hypertriglyceridemia (≥ 500 mg/dl). targeted range.Improving glycemic control in diabetic patients showingfasting chylomicronemia will usually obviate the need for 2.2 Recommended Adult Dosepharmacologic intervention. Severe Hypertriglyceridemia: The initial dose is 35 to105 mg per day. Dosage should be individualized Levels of serum triglycerides > 1000 mg/dl may increase according to patient response, and should be adjusted if the risk of developing pancreatitis. The effect of necessary following repeat lipid determinations at 4 to 8 FIBRICOR on reducing this risk has not been studied. week intervals.1.2 Primary Hyperlipidemia or Mixed Dyslipidemia Primary Hyperlipidemia or Mixed Dyslipidemia: TheFIBRICOR is indicated as adjunctive therapy to diet to dose of FIBRICOR is 105 mg per day.reduce elevated LDL-C, total-C, TG, and Apo B, and toincrease HDL-C in patients with primary The maximum dose of FIBRICOR is 105 mg per day.hypercholesterolemia or mixed dyslipidemia.2.3 Renal Impairment1.3 Considerations of Treatment In patients with mild-to-moderate renal impairment,Fenofibrate at a dose equivalent to 105 mg of FIBRICOR treatment with FIBRICOR should be initiated at a dose of was not shown to reduce coronary heart disease morbidity 35 mg/day, and increased only after evaluation of the and mortality in a large, randomized controlled trial of effects on renal function and lipid levels at this dose. The patients with type 2 diabetes mellitus [see Warnings and use of FIBRICOR should be avoided in patients with Precautions (5.6)]. severe renal impairment [see Use in Specific Populations The active moiety of FIBRICOR is fenofibric acid. The(8.6) and Clinical Pharmacology (12.3)].pharmacological effects of fenofibric acid have been 2.4 GeriatricPatientsextensively studied through oral administration of fenofibrate, which is converted in vivo to fenofibric acid.Dose selection for the elderly should be made on the basis of renal function [see Use in Specific Populations (8.6)].3 DOSAGE FORMS AND STRENGTHS2 DOSAGE AND ADMINISTRATION• 35 mg: White, round tablets. Debossed “AR 787”.2.1 Dosing Information • 105 mg: White, modified oval tablets. DebossedFIBRICOR can be given without regard to meals. “AR 788”.Patients should be placed on an appropriate lipid-lowering 4 CONTRAINDICATIONSdiet before receiving FIBRICOR and should continue this FIBRICOR is contraindicated in patients with:diet during treatment with fenofibric acid. • severe renal impairment, including those receivingdialysis [see Clinical Pharmacology (12.3)].Laboratory studies should be done to ascertain that the • active liver disease, including those with primary lipid levels are consistently abnormal before instituting biliary cirrhosis and unexplained persistent liver FIBRICOR therapy. Every attempt should be made to function abnormalities [see Warnings and Precautions control serum lipids with appropriate diet, exercise, (5.3)].weight loss in obese patients, and control of any medical • preexisting gallbladder disease.problems such as diabetes mellitus and hypothyroidism • known hypersensitivity to fenofibric acid orthat are contributing to the lipid abnormalities. fenofibrate [see Warnings and Precautions (5.9)].Medications known to exacerbate hypertriglyceridemia • FIBRICOR is also contraindicated in nursing mothers (beta blockers, thiazides, estrogens) should be [see Use in Specific Populations (8.3)].discontinued or changed if possible prior to considerationof triglyceride-lowering drug therapy. 5 WARNINGS AND PRECAUTIONSPeriodic determination of serum lipids should be obtained 5.1 Abnormal Liver Testsduring initial therapy in order to establish the lowest Fenofibrate (administered over a range of doses with the effective dose of FIBRICOR. Therapy should be higher dose equivalent to 105 mg fenofibric acid) has withdrawn in patients who do not have an adequate been associated with increases in serum transaminases[AST (SGOT) or ALT (SGPT)].In a pooled analysis of 10 placebo-controlled trials, increases to > 3 times the upper limit of normal of ALT occurred in 5.3% of patients taking fenofibrate versus 1.1% of patients treated with placebo. The incidence of increases in transaminases observed with fenofibrate therapy may be dose related.Chronic active hepatocellular and cholestatic hepatitis associated with fenofibrate therapy have been reported after exposures of weeks to several years. In extremely rare cases, cirrhosis has been reported in association with chronic active hepatitis.Periodic monitoring of liver tests (e.g., ALT) should be performed for the duration of therapy with FIBRICOR, and therapy discontinued if enzyme levels persist above three times the normal limit.5.2 CholelithiasisFIBRICOR, like fenofibrate, clofibrate and gemfibrozil, may increase cholesterol excretion into the bile, leading to cholelithiasis. If cholelithiasis is suspected, gallbladder studies are indicated. FIBRICOR therapy should be discontinued if gallstones are found.5.3 Concomitant Use with Oral Anticoagulants Caution should be exercised when FIBRICOR is given in conjunction with oral anticoagulants. FIBRICOR may potentiate the anticoagulant effects of these agents resulting in prolongation of the prothrombin time/INR. Frequent monitoring of prothrombin time/INR and dose adjustment of the anticoagulant are recommended until the prothrombin time/INR has stabilized in order to prevent bleeding complications [see Drug Interactions (7.1)].5.4 MyopathyFibrates increase the risk for myopathy and have been associated with rhabdomyolysis. The risk for serious muscle toxicity appears to be increased in elderly patients and in patients with diabetes, renal failure, or hypothyroidism.Data from observational studies suggest that the risk for rhabdomyolysis is increased when fibrates, in particular gemfibrozil, are co-administered with an HMG-CoA reductase inhibitor (statin).Myopathy should be considered in any patient with diffuse myalgias, muscle tenderness or weakness, and/or marked elevations of creatine phosphokinase levels. Patients should be advised to report promptly unexplained muscle pain, tenderness or weakness, particularly if accompanied by malaise or fever. CPK levels should be assessed in patients reporting these symptoms, and FIBRICOR therapy should be discontinued if markedly elevated CPK levels occur or myopathy is diagnosed. 5.5 Elevated Serum CreatinineElevations in serum creatinine have been reported in patients on fenofibrate. These elevations tend to return to baseline following discontinuation of fenofibrate. The clinical significance of these observations is unknown. Renal monitoring should be considered for patients with renal impairment and for patients at risk for renal insufficiency, such as the elderly and patients with diabetes.5.6 Coronary Heart Disease Morbidity andMortalityThe effect of FIBRICOR on coronary heart disease morbidity and mortality and non-cardiovascular mortality has not been established.The Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) study was a 5-year randomized, placebo-controlled study of 9795 patients with type 2 diabetes mellitus treated with fenofibrate. Fenofibrate demonstrated a non-significant 11% relative reduction in the primary outcome of coronary heart disease events (hazard ratio [HR] 0.89, 95% CI 0.75–1.05, p=0.16) and a significant 11% reduction in the secondary outcome of total cardiovascular disease events (HR 0.89 [0.80–0.99], p=0.04). There was a non-significant 11% (HR 1.11 [0.95, 1.29], p=0.18) and 19% (HR 1.19 [0.90, 1.57],p=0.22) increase in total and coronary heart disease mortality, respectively, with fenofibrate as compared to placebo.Because of chemical, pharmacological, and clinical similarities between fenofibrate, clofibrate, and gemfibrozil, the adverse findings in 4 large randomized, placebo-controlled clinical studies with these other fibrate drugs may also apply to fenofibric acid.In the Coronary Drug Project, a large study of post myocardial infarction of patients treated for 5 years with clofibrate, there was no difference in mortality seen between the clofibrate group and the placebo group. There was however, a difference in the rate of cholelithiasis and cholecystitis requiring surgery between the two groups (3.0% vs. 1.8%).In a study conducted by the World Health Organization (WHO), 5000 subjects without known coronary artery disease were treated with placebo or clofibrate for 5 years and followed for an additional one year. There was a statistically significant, higher age – adjusted all-cause mortality in the clofibrate group compared with the placebo group (5.70% vs. 3.96%, p<0.01). Excess mortality was due to a 33% increase in non-cardiovascular causes, including malignancy, post-cholecystectomy complications, and pancreatitis. This appeared to confirm the higher risk of gallbladder disease seen in clofibrate-treated patients studied in the Coronary Drug Project.The Helsinki Heart Study was a large (n=4081) study of middle-aged men without a history of coronary artery disease. Subjects received either placebo or gemfibrozil for 5 years, with a 3.5 year open extension afterward. Total mortality was numerically higher in the gemfibrozil randomization group but did not achieve statistical significance (p=0.19, 95% confidence interval for relative risk = 0.91–1.64). Although cancer deaths trended higher in the gemfibrozil group (p=0.11), cancers (excluding basal cell carcinoma) were diagnosed with equal frequency in both study groups. Due to the limited size of the study, the relative risk of death from any cause was not shown to be different than that seen in the 9 year follow-up data from World Health Organization study (relative risk=1.29). Similarly, the numerical excess of gallbladder surgeries in the gemfibrozil group did not differ statistically from that observed in the WHO study.A secondary prevention component of the Helsinki Heart Study enrolled middle-aged men excluded from the primary prevention study because of known or suspected coronary heart disease. Subjects received gemfibrozil or placebo for 5 years. Although cardiac deaths trended higher in the gemfibrozil group, this was not statistically significant (HR 2.2, 95% confidence interval: 0.94–5.05). The rate of gallbladder surgery was not statistically significant between study groups, but did trend higher in the gemfibrozil group, (1.9% vs. 0.3%, p=0.07). There was a statistically significant difference in the number of appendectomies in the gemfibrozil group(6/311 vs. 0/317, p = 0.029).5.7 PancreatitisPancreatitis has been reported in patients taking fenofibrate. This occurrence may represent a failure of efficacy in patients with severe hypertriglyceridemia, a direct drug effect, or a secondary phenomenon mediated through biliary tract stone or sludge formation with obstruction of the common bile duct.5.8 VenothromboembolicDiseaseIn the FIELD trial, pulmonary embolus (PE) and deep vein thrombosis (DVT) were observed at higher rates in the fenofibrate- than the placebo-treated group. Of 9,795 patients enrolled in FIELD, there were 4,900 in the placebo group and 4,875 in the fenofibrate group. For DVT, there were 48 events (1%) in the placebo group and 67 (1%) in the fenofibrate group (p=0.074); and for PE, there were 32 (0.7%) events in the placebo group and 53 (1%) in the fenofibrate group (p=0.022).In the Coronary Drug Project, a higher proportion of the clofibrate group experienced definite or suspected fatal or nonfatal pulmonary embolism or thrombophlebitis than the placebo group (5.2% vs. 3.3% at five years; p < 0.01).5.9 HypersensitivityReactionsAcute hypersensitivity reactions including severe skin rashes such as Stevens-Johnson syndrome and toxicepidermal necrolysis requiring patient hospitalization andtreatment with steroids have been reported in individualstreated with fenofibrate.5.10 Hematological ChangesMild-to-moderate hemoglobin, hematocrit, and whiteblood cell decreases have been observed in patientsfollowing initiation of fenofibrate therapy.Thrombocytopenia and agranulocytosis have beenreported in individuals treated with fenofibrate. Periodicmonitoring of red and white blood cell counts isrecommended during the first 12 months of FIBRICORadministration.6 ADVERSE REACTIONS6.1 Clinical Trial ExperienceBecause clinical trials are conducted under widelyvarying conditions, adverse reaction rates observed in theclinical trials of a drug cannot be directly compared torates in the clinical trials of another drug and may notreflect the rates observed in clinical practice.Adverse reactions reported by 2% or more of patientstreated with fenofibrate (and greater than placebo) duringthe double-blind, placebo-controlled trials are listed inTable 1. Adverse reactions led to discontinuation oftreatment in 5% of patients treated with fenofibrate and in3% treated with placebo. Increases in liver tests were themost frequent events, causing discontinuation offenofibrate treatment in 1.6% of patients.Table 1. Adverse Reactions Reported by 2% or Moreof Patients Treated with Fenofibrate* During theDouble-Blind, Placebo-Controlled TrialsBODY SYSTEMAdverse ReactionsFenofibrate*(N=439)Placebo(N=365)BODY AS A WHOLEAbdominal Pain 4.6% 4.4%Back Pain 3.4% 2.5%Headache 3.2% 2.7% DIGESTIVE Nausea 2.3% 1.9% Constipation 2.1% 1.4% METABOLIC ANDNUTRITIONAL DISORDERSAbnormal Liver Tests 7.5% 1.4%Increased ALT 3% 1.6%Creatine Phosphokinase Increased 3% 1.4%Increased AST 3.4% 0.5% RESPIRATORYRespiratory Disorder 6.2% 5.5%Rhinitis 2.3% 1.1%* Fenofibric acid is the active moiety of fenofibrate; Fenofibrate dosage equivalent to 105 mg fenofibric acid.6.2 Postmarketing ExperienceThe following adverse reactions have been identifiedduring postapproval use of fenofibrate. Because thesereactions are reported voluntarily from a population ofuncertain size, it is not always possible to reliablyestimate their frequency or establish a causal relationshipto drug exposure: myalgia, rhabdomyolysis, increased creatinine phosphokinase, pancreatitis, increased alanine aminotranaminase, increased aspartate aminotranaminase, muscle spasm, acute renal failure, hepatitis, cirrhosis, nausea, abdominal pain, anemia, headache, arthralgia and asthenia. period of organogenesis and allowed to deliver, aborted litters were observed at 150 mg/kg/day (20 times that at the MRHD of fenofibric acid). No developmental findings were observed at 15 mg/kg/day (an exposure to fenofibric acid that is 7 times that at the MRHD of fenofibric acid).7 DRUG INTERACTIONS7.1 OralAnticoagulantsCaution should be exercised when FIBRICOR is given in conjunction with coumarin anticoagulants. FIBRICORmay potentiate the anticoagulant effect of these agentsresulting in prolongation of the prothrombin time/INR.Frequent monitoring of prothrombin time/INR and dose adjustment of the oral anticoagulant are recommendeduntil the prothrombin time/INR has stabilized in order to prevent bleeding complications [see Warnings andPrecautions (5.3)].7.2 Bile-AcidBindingResinsSince bile-acid binding resins may bind other drugs given concurrently, patients should take FIBRICOR at least 1hour before or 4 to 6 hours after taking another drug.7.3 ImmunosuppressantsImmunosuppressant agents such as cyclosporine andtacrolimus can impair renal function. Whenimmunosuppressants and other potentially nephrotoxicagents are co-administered with FIBRICOR, the lowesteffective dose of FIBRICOR should be employed andrenal function should be monitored. In pregnant rats given oral dietary doses of 15, 75, and 300 mg/kg/day from gestation day 15 through lactation day 21 (weaning), maternal toxicity was observed at an exposure to fenofibric acid that is approximately 50 times that at the MRHD of fenofibric acid [see Nonclinical Toxicology (13.1)].8.3 NursingMothersFIBRICOR should not be used by nursing mothers. A decision should be made whether to discontinue nursing or to discontinue the drug [see Contraindications (4)].8.4 PediatricUseSafety and effectiveness of FIBRICOR in pediatric patients have not been established.8.5 GeriatricUseFIBRICOR is substantially excreted by the kidney as fenofibric acid and fenofibric acid glucuronide, and the risk of adverse reactions to this drug may be greater in patients with impaired renal function. Since elderly patients have a higher incidence of renal impairment, the dose selection for the elderly should be made on the basis of renal function [see Dosage and Administration (2.3) Clinical Pharmacology (12.3)].8 USE IN SPECIFIC POPULATIONS8.1 PregnancyPregnancy Category C: Safety in pregnant women hasnot been established. There are no adequate and wellcontrolled studies of FIBRICOR in pregnant women.FIBRICOR should be used during pregnancy only if thepotential benefit justifies the potential risk to the fetus.In female rats given oral dietary doses of 15, 75, and 300 mg/kg/day of fenofibrate from 15 days prior to matingthrough weaning, maternal toxicity was observed at adose that results in exposure to fenofibric acid that is 50times that at the MRHD of fenofibric acid.In pregnant rats given oral dietary doses of 14, 127, and361 mg/kg/day from gestation day 6–15 during the period of organogenesis, adverse developmental findings werenot observed at 14 mg/kg/day (a dose that results inexposure to fenofibric acid that is approximately twicethat at the MRHD of fenofibric acid). At higher multiples of human doses evidence of maternal toxicity wasobserved.8.6 RenalImpairmentThe use of FIBRICOR should be avoided in patients who have severe renal impairment. Dose reduction is required in patients with mild-to-moderate renal impairment.Monitoring renal function in patients with renalimpairment is recommended. [See Dosage andAdministration (2.3) and Clinical Pharmacology (12.3)].8.7 HepaticImpairmentThe use of FIBRICOR has not been evaluated in patients with hepatic impairment [see Contraindications (4)].10 OVERDOSAGEThere is no specific treatment for overdose withFIBRICOR. General supportive care of the patient isindicated, including monitoring of vital signs andobservation of clinical status, should an overdose occur. If indicated, elimination of unabsorbed drug should beachieved by emesis or gastric lavage; usual precautionsshould be observed to maintain the airway. BecauseFIBRICOR is highly bound to plasma proteins,hemodialysis should not be considered.In pregnant rabbits given oral gavage doses of 15, 150, and 300 mg/kg/day from gestation day 6–18 during the11 DESCRIPTION FIBRICOR is a lipid regulating agent available as tablets for oral administration. Each tablet contains 35 mg or 105 mg of fenofibric acid. The chemical name for fenofibric acid is 2-[4-(4-chlorobenzoyl)phenoxy]-2methylpropanoic acid with the following structuralformula:Fenofibric acid is a white to almost white crystallinepowder that is stable under ordinary conditions, and has a melting point of 179 – 183°C. Its empirical formula is C 17H 15ClO 4 and molecular weight 318.75. Fenofibric acid is insoluble in water; its solubility increases with pH in buffered media. Inactive Ingredients: Each tablet contains copovidone, crospovidone, magnesium stearate and microcrystalline cellulose. 12 CLINICAL PHARMACOLOGY 12.1 Mechanism of Action The effects of fenofibric acid seen in clinical practice have been explained in vivo in transgenic mice and in vitro in human hepatocyte cultures by the activation of peroxisome proliferator activated receptor α (PPAR α). Through this mechanism, fenofibric acid increases lipolysis and elimination of triglyceride-rich particlesfrom plasma by activating lipoprotein lipase and reducingproduction of apoprotein C-III (an inhibitor of lipoproteinlipase activity). The resulting fall in triglyceridesproduces an alteration in the size and composition of LDLfrom small, dense particles to large buoyant particles.These larger particles have a greater affinity forcholesterol receptors and are catabolized rapidly.Activation of PPAR α also induces an increase in thesynthesis of apoproteins A-I, A-II and HDL-cholesterol.12.2 PharmacodynamicsElevated levels of Total-C, LDL-C, and Apo B, and decreased levels of HDL-C and its transport complex, Apo AI and Apo AII, are risk factors for atherosclerosis.Epidemiologic studies have established thatcardiovascular morbidity and mortality vary directly withthe levels of Total-C, LDL-C, and TG, and inversely with the level of HDL-C. The independent effect of raisingHDL-C or lowering TG on the risk of cardiovascularmorbidity and mortality has not been determined.12.3 Pharmacokinetics The extent and rate of absorption of fenofibric acid after administration of 105 mg FIBRICOR tablets areequivalent to those after administration of 145 mgfenofibrate tablets (TriCor) under fasted conditions.AbsorptionThe absolute bioavailability of FIBRICOR has not beendetermined. Following oral administration of FIBRICORin healthy volunteers, median peak plasma levels offenofibric acid occur by approximately 2.5 hours afteradministration. Exposure after administration of 3 X35 mg FIBRICOR tablets is comparable to 1 X 105 mgFIBRICOR tablets. A food-effect study involving administration ofFIBRICOR to healthy volunteers under fasting conditionsand with a high-fat meal indicated that the C max was decreased by approximately 35% while the AUC remained unchanged. This decrease in exposure is not considered clinically significant, and thereforeFIBRICOR can be taken without regards to meals.Distribution Upon multiple dosing of fenofibrate, fenofibric acid steady state is achieved within 9 days. Plasmaconcentrations of fenofibric acid at steady state areslightly more than double those following a single dose.Serum protein binding was approximately 99% in normaland hyperlipidemic subjects. MetabolismFenofibric acid is primarily conjugated with glucuronicacid and then excreted in urine. A small amount of fenofibric acid is reduced at the carbonyl moiety to abenzhydrol metabolite which is, in turn, conjugated withglucuronic acid and excreted in urine.In vitro and in vivo metabolism data indicate thatfenofibric acid does not undergo oxidative metabolism(e.g. cytochrome P450) to a significant extent. The enzymes CYP1A2, CYP2A6, CYP2B6, CYP2C8,CYP2C9, CYP2C19, CYP2D6, CYP2E1, and CYP3A4do not play a role in the metabolism of fenofibric acid.EliminationFenofibric acid is eliminated with a half-life ofapproximately 20 hours, allowing once-daily dosing.Specific Populations Geriatrics: In five elderly volunteers 77 – 87 years of age,the oral clearance of fenofibric acid following a singleoral dose of fenofibrate was 1.2 L/h, which compares to1.1 L/h in young adults. This indicates that an equivalentdose of FIBRICOR can be used in elderly subjects with normal renal function, without increasing accumulation ofthe drug or metabolites [see Use in Specific Populations(8.5)].。
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a rXiv:q uant-ph/99139v22Fe b1999LANL xxx E-print archive No.quant-ph/9901039Fibre bundle formulation of nonrelativistic quantum mechanics IV.Mixed states and evolution transport’s curvature Bozhidar Z.Iliev ∗†‡Short title:Bundle quantum mechanics:IV Basic ideas:→March 1996Began:→May 19,1996Ended:→July 12,1996Revised:→December 1996–January 1997,Revised:→April 1997,September 1998Last update:→October 20,1998Composing/Extracting part IV:→September 27/October 4,1997Updating part IV:→February 14,1999Produced:→February 1,2008LANL xxx archive server E-print No.:quant-ph/9901039HO r TM Subject Classes:Quantum mechanics;Differential geometry1991MSC numbers:81P05,81P99,81Q99,81S99ContentsI.1Introduction1 I.2Evolution of pure quantum states(review)4 I.3Linear transports along paths and Hilbertfibre bundles6 I.4The Hilbert bundle description of quantum mechanics9 I.5The(bundle)evolution transport17 I.6Conclusion18 References19 This article ends at page (20)II.1Introduction1 II.2The bundle equations of motion2 II.3The bundle description of observables8 II.4Conclusion13 References13 This article ends at page (13)III.1Introduction1 III.2Pictures of motion from bundle view-point2 III.2.1Schr¨o dinger picture (2)III.2.2Heisenberg picture (3)III.2.3‘General’picture (8)III.3Integrals of motion11 III.4Conclusion15 References15 This article ends at page (15)1Introduction11Bozhidar Z.Iliev:Bundle quantum mechanics.IV2 2Mixed states22.1Hilbert space description(review) (2)2.2Hilbert bundle description (3)2.3Representations in the different pictures of motion (5)3Curvature of the evolution transport7 4Conclusion9 References9 This article ends at page (10)AbstractWe propose a new systematicfibre bundle formulation of nonrelativistic quantum mechanics.The new form of the theory is equivalent to the usual one but it is in harmony with the modern trends in theoretical physics and potentially admits new generalizations in different directions.In it a pure state of some quantum system is described by a state section(along paths) of a(Hilbert)fibre bundle.It’s evolution is determined through the bundle (analogue of the)Schr¨o dinger equation.Now the dynamical variables and the density operator are described via bundle morphisms(along paths).The mentioned quantities are connected by a number of relations derived in this work.The present fourth part of this series is devoted mainly to thefibre bundle description of mixed quantum states.We show that to the conventional density operator there corresponds a unique density morphism(along paths) for which the corresponding equations of motion are derived.It is also investigated the bundle description of mixed quantum states in the different pictures of motion.We calculate the curvature of the evolution transport and prove that it is curvature free iffthe values of the Hamiltonian operator at different moments commute.Bozhidar Z.Iliev:Bundle quantum mechanics.IV 11.IntroductionThis is the fourth part of our series of works considering the application of the theory of fibre bundles to nonrelativistic quantum mechanics.The paper,which is a straightforward continuation of [1,2,3],is orga-nized as follows.The bundle approach to the quantum mechanics of mixed states is in-vestigated in Sect.2.Subsection 2.1is a brief review of the conventional concepts of mixed state(s)and density operator (matrix).Their bundle de-scription is presented in Subsection 2.2.It turns out that to the density operator there corresponds a suitable density morphism along paths .The equations for its time evolution are derived.In Subsection 2.3are studied problems connected with the representations and description of mixed quan-tum states in the different pictures of motion.The equations of motion for density morphisms and operators are derived.Sect.3is devoted to the curvature of the (bundle)evolution transport.The work ends with some remarks in Sect.4.The notation of the present part of the series is identical with the one of the preceding parts for which the reader is referred to [1,2,3].The references to sections,equations,footnotes etc.from the previ-ous three parts of the series,namely [1],[2]and [3],are denoted by the corresponding sequential reference numbers in these parts preceded by the Roman number of the part in which it appears and a dot as a separator.For instance,Sect.I.5and (III.3.16)mean respectively section 5of part I,i.e.of [1],and equation (3.16)(equation 16in Sect.3)of part III,i.e.of [3].Below,for reference purposes,we present a list of some essential equa-tions of [1,2,3]used in this paper.Following the above convention,we retain their original reference numbers.ψ(t )=l γ(t )(Ψγ(t ))∈F ,(I.4.1)l ‡x =l −1x ,(I.4.9)U γ(t,s )=l −1γ(t )◦U (t,s )◦l γ(s ),s,t ∈J,(I.5.10)Γγ(t ):= Γb a (t ;γ) =−1dt C t +[Γγ(t ),C t ]∂t= A H γ,t (t 0),H H γ,t (t 0) ∂t H γ,t(t 0),(III.2.10)A Vγ,t (t 1):=V γ(t 1,t )◦A γ(t )◦V −1γ(t 1,t ):F γ(t 1)→F γ(t 1),(III.2.27)Bozhidar Z.Iliev:Bundle quantum mechanics.IV2i ∂A V t(t1)+i ∂A(t)∂t= A Vγ,t(t1),V H Vγ,t(t1) ∂t Vγ,t(t1).(III.2.41)2.Mixed statesIn the framework of quantum mechanics the most general description of a state of a quantum system is provide via the so-called density(or statistical) matrix(or operator)by means of which is achieved a uniform description of pure and mixed states(see[4,chapter VIII,sect.IV]and[5,§33];for math-ematically rigorous exposition of the problem see[6,chapter IV,sect.8]). This formalism has also a bundle analogue which is described in this section.2.1.Hilbert space description(review)Here we briefly recall the notions of a mixed state and density operator in the conventional Hilbert space description of quantum mechanics[4](see also[7,8]).Consider a quantum system which at a moment t with a probability p i can be found in a state with a state vectorψi(t)∈F.Here i belongs to some set of indexes I and the statistical weights p i are assumed time-independent:0≤p i≤1, i∈I p i=1,∂p iψi(t)|ψi(t)ψ†i(t):F→F.(2.2)Here with a dagger as a superscript we denote the dual Hermitian conjugate vectors and spaces with respect to the inner product ·|· ,i.e.ifψ∈F,then ψ†∈F†is a mapψ†:F→C such thatψ†:χ→ ψ|χ forχ∈F,and a product likeψχ†,ψ,χ∈F is defined as an operatorψχ†:F→F via (ψχ†)(ϕ):=(χ†(ϕ))ψ= χ|ϕ ψforϕ∈F.1The density operator(2.2)is Hermitian,positive definite,trace-class,and of unit trace[4,6].So we have ρ†(t)=ρ(t), ψ(t)|ρ(t)ψ(t) ≥0,Trρ(t)=1,(2.3) where Tr denotes the trace of an operator.Conversely,any such operator is a density operator(in the absence of superselection rules)[6,chapter IV, subsect.8.6].Bozhidar Z.Iliev:Bundle quantum mechanics.IV3 By definition the mean(expectation)value of an observable A isA(t) tρ:=Tr(ρ(t)◦A(t))(2.4) for a system whose state is described by a density operatorρ(t).The time evolution of the density operator is described by postulating the Schr¨o dinger equation for it,called also von Neumann’s or Liouville equation:i dρ(t):=H(t)◦ρ(t)−ρ(t)◦H(t)(2.5)where H(t)is system’s Hamiltonian.Ifρ(t0)is known for some instant of time t0,thenρ(t)=U(t,t0)◦ρ(t0)◦U−1(t,t0),(2.6) where U(t,t0)is the system’s evolution operator(see Sect.I.2).In fact,(2.6) is the general solution of(2.5)with respect toρ(t).2If the sum in(2.2)contains only one term or terms which are proportional up to a phase factor to one of them,the system is said to be in a pure state (described by(one of)the corresponding state vector(s)in(2.2)),otherwise the system’s state is called mixed.A criterion for a state to be pure is ρ2(t)=ρ(t)[4,6].2.2.Hilbert bundle descriptionNow we are ready to apply the bundle approach to systems described via some density operatorρ(t).The easiest way to introduce the bundle ana-logue ofρ(t)is via(2.4).Expressing A from(II.3.1)and substituting the result into(2.4),wefindA(t) tρ= Aγ(t) t Pγ(2.7) whereAγ(t) t Pγ=Tr(Pγ(t)◦Aγ(t))(2.8) is the(bundle)mean value of the morphism A,corresponding to A,in the state characterized by the density morphism along paths P:γ→Pγ:γ(t)→{Pγ(s):s∈J,γ(s)=γ(t)}defined via(cf.(II.3.1))Pγ(t):=l−1γ(t)◦ρ(t)◦lγ(t):Fγ(t)→Fγ(t).(2.9)Bozhidar Z.Iliev:Bundle quantum mechanics.IV4 Meanwhile,equation(2.7)expresses the natural requirement that the expectation value of a dynamical variable A must be independent of the (mathematical)way we calculate it.The bundle density operator has also a representation like(2.2).In fact, substituting(I.4.1)and its Hermitian conjugate,i.eψ†(t)=Ψ‡γ(t)◦lγ(t),(2.10) whereΨ‡x:F x→C is defined byΨ‡x:Φx→ Ψx|Φx x forΨx,Φx∈F x, x∈M,which is a consequence of the unitarity of l x(see(I.4.9)),for the vectorsψi(t)(appearing in(2.2))into(2.2),we get(2.11)ρ(t)=lγ(t)◦Pγ(t)◦l−1γ(t)which is equivalent to(2.9)withPγ(t)= i∈IΨi,γ(t)p i=[H mγ(t),Pγ(t)]dtBozhidar Z.Iliev:Bundle quantum mechanics.IV5 with H mγ(t)being the matrix-bundle Hamiltonian(given by(II.2.12)).This equation is the matrix-bundle analogue of(2.5),to which it is equivalent as it can be proved via the substitution of the matrix form of(2.11)into the one of(2.5)(see also(II.3.10)).Consequently,the results of Sect.II.2show that(2.14)gives the general solution(2.15)with respect to Pγ(t).The matrix equation(2.15)can be written into an invariant form too. To this end we shall use the following result which is a simple corollary of(2.15),(II.2.19),and(II.2.21):IfΨis a section along paths and one of the equations Dγt(Ψγ(t))=0,Dγt[Pγ(t)(Ψγ(t)]=0,or(2.15)is valid,then the remaining two of them are equivalent.From here follows that(2.15)is equivalent to the system(Dγt◦Pγ(t))Ψγ(t)=0,(2.16a)Dγt(Ψγ(t))=0.(2.16b) (Note:γis not a summation index here and bellow!)If we denote by˜Pγ(t)the restriction of Pγ(t):Fγ(t)→Fγ(t)on the set of (state)sections alongγwhich are(linearly)transported alongγby means of the evolution transport,i.e the ones satisfying(2.16b),then(2.16)is equivalent to˜Dγ(˜Pγ(t))=0(2.17)twhere˜D is the defined by(II.3.25)differentiation along paths of bundle morphisms(along paths in the present case).The above discussion shows the equivalence of(2.17)and(2.15),a fact which is also an evident corollary of(II.3.27)and(II.2.21).The equation(2.17)can be called a(bundle) Schr¨o dinger equation for the density morphism.A simple verification proves that the linear map Pγ(t0)→Pγ(t),defined by(2.14),satisfies(I.3.2)and(I.3.3).So,freely speaking,we may say that this is a‘transport-like’map by means of which Pγis‘transported’along γ.This is something like‘representation’of the evolution transport in the space of morphisms alongγ.The rigorous study of this problem(see the end of subsection III.2.1and[9,sect.3])reviles that the pointed map is a linear transport alongγin thefibre bundle of bundle morphisms(along paths)of(F,π,M).With respect to this transport along paths the density morphism(alongγ)is a linearly transported section(alongγ)of the bundle of morphisms(alongγ)of(F,π,M).2.3.Representations in the different pictures of motionLet us turn now our attention to the description of mixed states in the different pictures of motion(see Sect.III.2).In the Schr¨o dinger picture of the Hilbert bundle(resp.space)description of quantum mechanics,which,in fact,was investigated until now in this sec-tion,the motion of a quantum system is described by pairs like(Pγ(t),Aγ(t))Bozhidar Z.Iliev:Bundle quantum mechanics.IV6 (resp.(ργ(t),Aγ(t)))of generally time-depending morphisms along paths of (F,π,M)(resp.operators acting on F)representing the density morphism (resp.operator)and some dynamical variable A.The transition to the Heisenberg picture is achieved via the general for-mulae(III.2.4)and(III.2.7)for bundle morphisms along paths in(F,π,M) and operators in F,respectively.In particular,for the density morphism P and operatorρthey,respectively,give:P Hγ,t(t0):=U−1γ(t,t0)◦Pγ(t)◦Uγ(t,t0)=Pγ(t0):Fγ(t0)→Fγ(t0),(2.18)ρH t(t0):=U−1(t,t0)◦ρ(t)◦U(t,t0)=ργ(t0):F→F(2.19) where(2.14)and(2.6)were used.Consequently in the Heisenberg pic-ture the Hilbert bundle and Hilbert space descriptions are by means of pairs like P Hγ,t(t0),A Hγ,t(t0) = Pγ(t0),A Hγ,t(t0) and ρH t(t0),A H t(t0) = ρ(t0),A H t(t0) ,respectively,in which the time dependence is entirely shifted from the density morphisms and operators to the observables.So,in this picture the density morphisms and operators are constant(s of motion),do not evolve in time,while the observer’s evolution is governed by the Heisen-berg equation of motion for them(see(III.2.10),or(III.2.8),or(III.2.24)).Of course,in the Heisenberg picture the mean values remain unchanged:A Hγ,t(t0) t0P Hγ,t = A H t(t0) t0ρH t= Aγ(t) t Pγ= A(t) tρ,(2.20)whereA Hγ,t(t0) t0P Hγ,t:=Tr Pγ(t0)◦A Hγ,t(t0) , A H t(t0) t0ρH t:=Tr ρ(t0)◦A H t(t0) .(2.21)The chain equation(2.20)is a corollary of the invariance of the trace of a product(composition)of operators with respect to a cyclic permutation of the multipliers.The shift from the Schr¨o dinger to‘general’picture is done by the general equations(III.2.27)and(III.2.30).Hence,in the V-picture of motion the density morphism P and operatorρ,respectively,areP Vγ,t(t1)=Vγ(t1,t)◦Pγ(t)◦V−1γ(t1,t):Fγ(t1)→Fγ(t1),(2.22)ρV t(t1)=Vγ(t1,t)◦ργ(t)◦V−1(t1,t):F→F.(2.23) Since in the V-picture the Hilbert bundle(resp.space)description is via pairs like P Vγ,t(t1),A Vγ,t(t1) resp. ρV t(t1),A V t(t1) ,the mean values of the observables remain unchanged,as in the Heisenberg picture:A Vγ,t(t1) t1P Vγ,t = A V t(t1) t1ρV t= Aγ(t) t Pγ= A(t) tρ,(2.24)Bozhidar Z.Iliev:Bundle quantum mechanics.IV7whereA Vγ,t(t1) t1P Vγ,t:=Tr P Vγ,t(t1)◦A Vγ,t(t1) ,A V t(t1) t1ρV t:=Tr ρV t(t1)◦A V t(t1) .(2.25) In the V-picture the density morphisms,operators,and observables gen-erally change in time.For all of them this change is governed by the equa-tions(III.2.41)and(III.2.39),but for the density morphisms and operators they can be written in a more concrete form.For this purpose we have to calculate the last terms in the r.h.s.of(III.2.41)and(III.2.39).Using(III.2.27)and(2.5),we obtain∂ρ(t)∂t◦V−1(t1,t)=1. Analogously,applying(III.2.33)and the just get equation,wefind∂ρ(t)∂t Vt (t1)◦lγ(t1)=1.At last,substituting the above two equations into(III.2.41)and(III.2.39), we,respectively,geti ∂P Vγ,t(t1),(2.26)i ∂ρV t(t1)(2.27)where(III.2.37)and(III.2.42)were taken into account.These are the equa-tions of motion for the density morphism and operator in the V-picture.If the evolution transport and operator are known(in the V-picture), then combining,from one hand,(2.22),(2.14)and(III.2.48)and,from the other hand,(2.23),(2.6),and(III.2.47),we get the general solution of(2.26) and(2.27),respectively,in the formP Vγ,t(t1)=U Vγ(t,t1,t0)◦Pγ,t(t1)◦ U Vγ(t,t1,t0) −1,(2.28)ρV t(t1)=U V(t,t1,t0)◦ρt(t1)◦ U V(t,t1,t0) −1.(2.29) As one can expect,in the case of Heisenberg picture,due to(III.2.49), these formulae reproduce(2.18)and(2.19)respectively.3.Curvature of the evolution transportLetη:J×J′→M with J and J′being R-intervals.According to[10, Sect.3]the curvature of the(bundle)evolution transport U is R:η→Rη,Bozhidar Z.Iliev:Bundle quantum mechanics.IV8 with Rη:(s,t)→Rη(s,t),(s,t)∈J×J′,whereRη(s,t):=Dη(·,t)s ◦Dη(s,·)t−Dη(s,·)t◦Dη(·,t)s:Sec2(F,π,M)→π−1(η(s,t))(3.1)Here D is the differentiation along paths assigned to U by(II.2.18).In a localfield of bases the local components of the curvature are[10, equation3.3](Rη(s,t))a b=∂∂t[Γa b(s;η(·,t))]+Γa c(s;η(·,t))Γc b(t;η(s,·))−Γa c(t;η(s,·))Γc b(s;η(·,t)).(3.2) Physically we interpretη(s,·):t→η(s,t)andη(·,t):s→η(s,t)as world lines(trajectories)of observers with proper times t and s respectively. So,using the fundamental relation(II.2.21)we can explicitly calculate the curvature.The easiest way to do this is to choose the bases{e a(x)}and {f a(t)}such that l x(t)=[δa b]=11(see remark II.2.1).Then E(t)=0and H mγ(t)=H(t)=H(t).Hence,now(3.2)reduces toRη(s,t)=1,(3.3)where we have assumed,as usual,that H(s)is independent of the observers trajectoryγ.(This equality is valid only in the special basis in which it is derived!)From here it follows that the evolution transport is curvature free if and only if the values of the Hamiltonian operator at different moments commute, viz.Rη=0⇐⇒[H(s),H(t)]=0.(3.5) for some(and hence any)pathγ:J→M.Here r,s,t∈J and˘Hγ,t(r)is(the transported by means of lγs→t Hamiltonian which is)calculated via(II.3.20).Consider now a curvature free evolution transport on W=η(J,J′), i.e.Rη(s,t)≡0for every(s,t)∈J×J′.From[10,proposition3.3]we know that in this case there exists afield of base{e i}over W in which the transport’s coefficients vanish along any pathγin W.In it,due to(II.2.14) and(II.2.21),we haveUγ(t,t0)=11, Γγ(t)=0, H mγ(t)=0for everyγ.(3.6)Bozhidar Z.Iliev:Bundle quantum mechanics.IV9 Notice,equation(III.2.3)is valid for arbitrary evolution transports along any fixed path in appropriate bases along it,while(3.6)holds only for curvature free evolution transports in a suitably chosenfield of bases in a whole set W.The connection of the special bases in which(3.6)is true with the Heisenberg picture is the same as discussed in Subsect III.2.2for the bases in which(III.2.3)are satisfied.We want to emphasize on the fact that according to(II.2.12)the lo-cal vanishment of the matrix-bundle Hamiltonian does not imply the same property for the Hamiltonian as an operator or morphism.4.ConclusionIn the present work we have seen that the bundle formulation of quantum mechanics admits natural description of mixed states.We have derived different versions of the equation of motion for the density morphism along paths,which now replaces the conventional density operator.The mixed states were considered from the view-point of different bundle pictures of motion.Here we have calculated the curvature of the evolution transport. It turns to be curvature free iffthe values of the Hamiltonian at different moments commute.This paper ends the introduction of general formalism of Hilbert bundle description of nonrelativistic quantum mechanics.The interpretation of this description and its possible further developments will be given elsewhere. AcknowledgmentsThis work was partially supported by the National Foundation for Scientific Research of Bulgaria under Grant No.F642.References[1]Bozhidar Z.Iliev.Fibre bundle formulation of nonrelativistic quan-tum mechanics.I.Introduction.The evolution transport.(LANL xxx archive server,E-print No.quant-ph/9803084)Submitted to J.Physics A:Math.&Gen.,March1998.[2]Bozhidar Z.Iliev.Fibre bundle formulation of nonrelativistic quan-tum mechanics.II.Equations of motion and observables.(LANL xxx archive server,E-print No.quant-ph/9804062)Submitted to J.Physics A:Math.&Gen.,April1998.[3]Bozhidar Z.Iliev.Fibre bundle formulation of nonrelativistic quan-tum mechanics.III.Pictures and integrals of motion.(LANL xxxBozhidar Z.Iliev:Bundle quantum mechanics.IV10 archive server,E-print No.quant-ph/9806046)Submitted to J.Physics A:Math.&Gen.,October1998.[4]A.M.L.Messiah.Quantum mechanics.Interscience,New York,1958.(Vol.I and vol.II.).[5]P.A.M.Dirac.The principles of quantum mechanics.Oxford at theClarendon Press,Oxford,fourth edition,1958.[6]E.Prugoveˇc ki.Quantum mechanics in Hilbert space,volume92of Pureand applied mathematics.Academic Press,New York-London,second edition,1981.[7]A.Uhlmann.A gaugefield governing parallel transport along mixedstates.Lett.Math.Phys.,21(3):229–236,March1991.[8]J.Anandan.A geometric view of quantum mechanics.In Anan-dan J.S.,editor,Quantum coherence,Proceedings of the Conference on Fundamental Aspects of Quantum theory,Columbia,South Carolina, 14–16December1989.World Scientific,Singapore,1990.(See also Preprint MPI-PAE/PTh77/90,1990and Found.Phys.,21(11):1265–1284,1991).[9]Bozhidar Z.Iliev.Transports along paths infibre bundles.III.Consis-tency with bundle morphisms.JINR Communication E5-94-41,Dubna, 1994.(LANL xxx archive server,E-print No.dg-ga/9704004).[10]Bozhidar Z.Iliev.Linear transports along paths in vector bundles.III.Curvature and torsion.JINR Communication E5-93-261,Dubna, 1993.。