泮托拉唑注射液说明书--海南卫康

注射用泮托拉唑钠说明书【药品名称】通用名：注射用泮托拉唑钠曾用名：商品名：英文名：Pantoprazole Sodium for Injection汉语拼音：Zhusheyong pantuolazuona本品主要成分为泮托拉唑钠，其化学名称为：5-二氟甲氧基-2-[ (3, 4-二甲氧基-2-吡啶基 ) 甲基 ] 亚硫酰基-1H-苯骈咪唑钠盐一水合物。

其结构式为：分子式：C16H14F2N3NaO4S · H2O分子量：423.38【性状】本品为白色或类白色疏松块或（和）粉末。

【适应症】适用于十二指肠溃疡、胃溃疡、急性胃粘膜病变，复合性胃溃疡等急性上消化道出血。

【规格】以按泮托拉唑计40mg【用法用量】静脉滴注。

一次一瓶（40mg），每日1～2次，每次用0.9%氯化钠注射液100ml 溶解后，一小时内滴完。

本品不宜用上述之外的液体配制，配制液的ph值应不小于9。

【不良反应】偶见头晕、失眠、嗜睡、恶心、腹泻、便秘、皮疹和肌肉疼痛等症状，但程度较轻。

【禁忌】对本品过敏者或严重肝功能不全者禁用。

【注意事项】①应用本品时应首先排除癌症的可能，因为本品治疗可减轻胃癌症状，从而延误诊断。

②肝、肾功能不全者慎用，根据需要酌情较轻。

【孕妇及哺乳期妇女用药】本品禁用。

【儿童用药】未进行该项实验且我可靠参考文献。

【老年患者用药】老年患者应用泮托拉唑后药代动力学（清除率、半衰期、生物利用度）无明显变化，因此老年人不需要改变剂量。

【药物相互作用】1.在体内较高剂量的泮托拉唑不改变安定的清除率，其血清浓度不受安定的影响，表明安定不影响泮托拉唑的代谢。

2.泮托拉唑与氨茶碱、华法令、避孕药、苯妥英钠、氨基比林、地高辛、双氯芬酸、美托洛尔及抗酸剂等之间无相互作用。

【药物过量】大药剂使用时可出现心律不齐，转氨酶升高，肾功能改变，粒细胞降低等。

【药理毒理】本品通过特异性的作用于胃粘膜壁细胞，降低壁细胞中的H+、K+-ATP酶的活性，从而抑制胃酸的分泌。

商品名称:泮托拉唑肠溶片(潘妥洛克) 通用名称:泮托拉唑肠溶片规格: 40mg×7片/盒,双铝泡罩成份: 潘妥洛克40mg×7片主要成份为泮托拉唑(Pantoprazole)倍半水合钠盐化学名：5-二氟甲氧基-2-[（3，4-二甲氧基-2-吡啶甲基）亚硫酰]-1氢苯并咪唑钠倍半水合物分子式：C16H14F2NaO4S×1.5H2O分子量：432性状: 本品为黄色肠溶衣片，除去包衣后显白色或类白色。

用法用量: 本品若无医师处方，应按下述方法服用，请遵守这些方法，否则可能疗效不佳。

对伴有幽门螺杆菌感染的十二指肠溃疡或胃溃疡须用联合疗法根除感染。

潘妥洛克与抗菌药物的联合使用可采取下述任何一种方案：a、1片潘妥洛克肠溶片×2/日+1000mg阿莫西林×2/日+500mg 克拉霉素×2/日b、1片潘妥洛克肠溶片×2/日+500mg甲硝唑×2/日+500mg克拉霉素×2/日c、1片潘妥洛克肠溶片×2/日+1000mg阿莫西林×2/日+500mg甲硝唑×2/日在联合疗法中，有甲硝唑的方案仅在其他方案不能根除幽门螺杆菌感染的情况下方予使用。

若患者无联合疗法的指征，如检查幽门螺杆菌阴性，潘妥洛克可按下述剂量单独使用，除非另有医师处方：a、十二指肠溃疡、胃溃疡和反流性食管炎患者一般每日服用1片潘妥洛克肠溶片。

b、个别病例，特别是在其它治疗方法无效的情况下，可将剂量加倍（即每日2片潘妥洛克肠溶片）。

注意:a、肾功能受损和老年患者每日潘妥洛克的剂量一般不应超过40mg，但有些情况例外。

b、为根除幽门螺杆菌感染而使用联合疗法时，老年患者在1周治疗中也使用常规剂量（40mg×2/日）的潘妥洛克。

c、严重肝功能受损衰竭的患者剂量应减少至隔日1片（40mg）潘妥洛克。

功能主治（适应症）: 1.十二指肠溃疡2.胃溃疡3.中重度反流性食管炎4.与下述药物配伍用能够根除幽门螺杆菌感染(1)克拉霉素和阿莫西林(2)克拉霉素和甲硝唑（详见用药方法）以减少该微生物感染所致的十二指肠溃疡与胃溃疡的复发。

亲爱的朋友，很高兴能在此相遇！欢迎您阅读文档潘妥洛克说明书，这篇文档是由我们精心收集整理的新文档。

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潘妥洛克说明书潘妥洛克适用于十二指肠溃疡，胃溃疡，中、重度反流性食管炎。

下面是我们整理的，希望对大家有所帮助。

潘妥洛克商品介绍通用名：泮托拉唑肠溶片生产厂家:德国TakedaGmbH批准文号：注册证号Hxx0162药品规格：40mg*14片【商品名】潘妥洛克【通用名】泮托拉唑肠溶片【汉语拼音】PanTuoLaZuoChangRongPian【英文名】PantoprazoleEnteric-CoatedTablets【主要成分】每片潘妥洛克肠溶片含：45.1mg泮托拉唑钠盐倍半水合物(相当于40mg泮托拉唑)。

【性状】本品为黄色肠溶衣片，除去包衣后显白色或类白色。

【适应症】十二指肠溃疡，胃溃疡，中、重度反流性食管炎，与下述药物配伍用能够根除幽门螺杆菌感染：克拉霉素和阿莫西林，或克拉霉素和甲硝唑，或阿莫西林和甲哨唑(详见用药方法)以减少该微生物感染所致的十二指肠溃疡与胃溃疡的复发。

提示：潘妥洛克不用于治疗病变轻微的胃肠道疾患，如神经性消化不良。

在应用潘妥洛克治疗胃溃疡前，须除外胃与食道的恶性病变，以免因症状缓解而延误诊断。

反流性食管炎的诊断应经内镜检查核实。

【用法用量】本品若无医师处方，应按下述方法服用，请遵守这些方法，否则可能疗效不佳。

对伴有幽门螺杆菌感染的十二指肠溃疡或胃溃疡须用联合疗法根除感染。

潘妥洛克与抗菌药物的联合使用可采取下述任何一种方案：a、1片潘妥洛克肠溶片×2/日+1000mg 阿莫西林×2/日+500mg克拉霉素×2/日;b、1片潘妥洛克肠溶片×2/日+500mg甲硝唑×2/日+500mg克拉霉素×2/日;c、1片潘妥洛克肠溶片×2/日+1000mg阿莫西林×2/日+500mg甲硝唑×2/日。

【通用名】注射用泮托拉唑钠【英文名】PANTOPRAZOLE SODIUM FOR INJECTION【拼音名】ZHUSHEYONG PANTUOLAZUONA【药品类别】抗酸药及抗溃疡病药【化学名】5-二氟甲氧基-2-[(3,4-二甲氧基-2-吡啶基)甲基]亚硫酰基-1H-苯骈咪唑钠盐一水合物【结构式】【分子式】C16H14F2N3NaO4S·H2O【分子量】【性状】本品为白色或类白色疏松块或粉末，专用溶媒为无色的澄明液体。

【药理毒理】本品为胃壁细胞质子泵抑制剂，在中性和弱酸性条件下相对稳定，在强酸性条件下迅速活化，其pH依赖的活化特性，使其对H+、K+-ATP酶的作用具有更好的选择性。

本品能特异性地抑制壁细胞顶端膜构成的分泌性微管和胞浆内的管状泡上的H+、K+-ATP酶，引起该酶不可逆性的抑制，从而有效地抑制胃酸的分泌。

由于H+、K+-ATP 酶是壁细胞泌酸的最后一个过程，故本品抑酸能力强大。

它不仅能非竞争性抑制促胃液素、组胺、胆碱引起的胃酸分泌，而且能抑制不受胆碱或H2受体阻断剂影响的部分基础胃酸分泌。

本品与其它药物伍用时，具有药物间相互作用小的优点。

本品通过肝细胞内的细胞色素P450酶系的第I系统进行代谢，同时也可以通过第II系统进行代谢。

当与其它通过P450酶系代谢的药物伍用时，本品的代谢途径可以通过第II 酶系统进行，从而不易发生药物代谢酶系的竞争性作用，减少体内药物间的相互作用。

无致突变、致癌和致畸作用。

【药代动力学】本品具有较高的生物利用度，首次口服时即可以达到70%～80%，达峰时间1小时，有效抑酸达24小时。

静脉注射与口服给药的生物利用度比值为。

口服40mg 时的tmax为2～4小时，Cmax约为2～3μg/ml，清除半衰期约为小时。

约80%的口服或静注本品的代谢物经尿中排泄，肾功能不全不影响药代动力学，肝功能不全时可延缓清除。

t1/2、清除率和表观分布容积与给药剂量无关。

注射用泮托拉唑钠说明书【药品名称】通用名：注射用泮托拉唑钠曾用名：商品名：英文名：Pantoprazole Sodium for Injection汉语拼音：Zhusheyong pantuolazuona本品主要成分为泮托拉唑钠，其化学名称为：5-二氟甲氧基-2-[ (3, 4-二甲氧基-2-吡啶基 ) 甲基 ] 亚硫酰基-1H-苯骈咪唑钠盐一水合物。

其结构式为：分子式：C16H14F2N3NaO4S · H2O分子量：423.38【性状】本品为白色或类白色疏松块或粉末，专用溶媒为无色的澄明液体。

【药理毒理】本品为胃壁细胞质子泵抑制剂，在中性和弱酸性条件下相对稳定，在强酸性条件下迅速活化，其pH依赖的活化特性，使其对H+、K+-ATP酶的作用具有更好的选择性。

本品能特异性地抑制壁细胞顶端膜构成的分泌性微管和胞浆内的管状泡上的H+、K+-ATP酶，引起该酶不可逆性的抑制，从而有效地抑制胃酸的分泌。

由于H+、K+-ATP酶是壁细胞泌酸的最后一个过程，故本品抑酸能力强大。

它不仅能非竞争性抑制促胃液素、组胺、胆碱引起的胃酸分泌，而且能抑制不受胆碱或H2受体阻断剂影响的部分基础胃酸分泌。

本品与其它药物伍用时，具有药物间相互作用小的优点。

本品通过肝细胞内的细胞色素P450酶系的第I系统进行代谢，同时也可以通过第II系统进行代谢。

当与其它通过P450酶系代谢的药物伍用时，本品的代谢途径可以通过第II 酶系统进行，从而不易发生药物代谢酶系的竞争性作用，减少体内药物间的相互作用。

无致突变、致癌和致畸作用。

【药代动力学】本品具有较高的生物利用度，首次口服时即可以达到70%～80%，达峰时间1小时，有效抑酸达24小时。

静脉注射与口服给药的生物利用度比值为1.2。

口服40mg时的t max为2～4小时，C max约为2～3μg/ml，清除半衰期约为1.1小时。

约80%的口服或静注本品的代谢物经尿中排泄，肾功能不全不影响药代动力学，肝功能不全时可延缓清除。

新产品调研之泮托拉唑---一、概况泮托拉唑钠是在奥美拉唑的基础上基于Me-too药物设计原理，对母体结构进行改造后发现的药效更好的药物，泮托拉唑钠是由德国百克顿有限公司(BydG ulden)首先研制，于1994年在南非首次上市，商品名：潘妥洛克（Pantoloc®），至今已在美国、英国、德国等二十多个国家获准上市,,是继奥美拉唑,兰索拉唑之后全球第三个质子泵抑制剂,主要用于治疗十二指肠和胃溃疡及缓解中至重度的反流性食管炎. 同其它质子泵抑制剂相比,在弱酸条件下稳定,在强酸条件下很快被激活与其它药物相互作用小,其特点是在代谢过程中不易与细胞色素P45 0作用而氧化失效，生物利用度较之奥美拉唑提高7倍，在与其它药物配用时安全性和有效性均高于奥美拉唑和兰索拉唑，在弱酸性环境下也较奥美拉唑和兰索拉唑稳定。

泮托拉唑钠原料药为白色或类白色疏松块状物或粉末.市场主要是注射用泮托拉唑钠粉针,肠溶片和肠溶胶囊. 。

1、制剂情况2、原料药情况【原料药名称】Pantoprazole Sodium【中文名称】泮托拉唑钠【CAS登记号】138786-67-1【结构式】【化学名称】5-二氟甲氧基-2-[[(3，4-二甲氧基-2-吡啶基)-甲基]亚磺酰基]-1H-苯并咪唑钠一水合物。

【分子式】C16H14F2N3NaO4S·H2O【分子量】423.383、制剂处方资料【性状】本品为白色或类白色疏松块状物或粉末。

辅料为：甘露醇、依地酸二钠。

3.1适应证和用途适用于十二指肠溃疡、胃溃疡、急性胃粘膜病变，复合性胃溃疡等急性上消化道出血。

3.2药理毒理药理作用:泮托拉唑为质子泵抑制剂，通过与胃壁细胞的H+-K+ATP酶系统的两个位点共价结合而抑制胃酸产生的最后步骤。

该作用呈剂量依赖性并使基础和刺激状态下的胃酸分泌均受抑制。

本品与H+-K+ATP酶的结合可导致其抗胃酸分泌作用持续24小时以上。

毒理研究遗传毒性：泮托拉唑的人淋巴细胞染色体畸变试验、中国仓鼠卵巢细胞/HGPRT 正向突变试验及二次小鼠微核试验中的一次结果均为阳性，而大鼠肝脏DNA共价结合试验结果难以判断。

泮托拉唑适应症①十二指肠溃疡po,40mg/d，2和4周后愈合率分别为68%和96%。

国外多中心研究对比发现本品40mg/d与奥美拉唑20mg/d在2及4周的愈合率与症状缓解率均无明显差异。

②胃溃疡对于急性溃疡本品与奥美拉唑疗效无差异，但对于H2受体拮抗剂治疗无效的胃溃疡患者，本品40～80mg/d，8周愈合率为96.7%，12周愈合率达99%。

③反流性食管炎林万隆等总结了国外泮托拉唑对反流性食管炎的疗效，本品40mg/d疗效优于H2受体拮抗剂，与奥美拉唑20mg/d相似，④幽门螺杆菌本品与2种抗菌药物联合应用治疗HP感染，其疗效与其他PPIs与抗菌药物合用的结果相似，HP感染根除率接近或达到90%以上。

药物相互作用与奥美拉唑和兰索拉唑不同，本品在代谢过程中有一个转硫基作用且对细胞色素P450依赖性酶的抑制作用较弱，所以对同时通过该酶代谢的其他合用药物影响较小。

不良反应大多较轻微，发生率约为 2.5%，包括头痛、头晕、嗜睡、恶心、腹泻和便秘、皮疹及肌肉痛。

中文题名泮托拉唑代谢和立体选择性药物动力学研究副题名外文题名论文作者谢智勇著导师钟大放指导学科专业药物分析学研究领域\研究方向学位级别博士学位授予单位沈阳药科大学学位授予日期2005论文页码总数156页关键词泮托拉唑药物分析药物代谢动力学质子泵抑制剂液相色谱－质谱联用(LC/MS)馆藏号B SLW 2008 R975 3【中文摘要】选择性长效质子泵抑制剂泮托拉唑，主要用于治疗胃、十二指肠溃疡和反流性食管炎等胃肠道高分泌疾病，其结构中含有一手性中心硫原子，临床现在以消旋体形式给药。

前期对泮托拉唑代谢和动力学的研究表明，泮托拉唑经肝药酶进行广泛代谢，代谢途径包括亚砜氧化为砜或还原为硫醚、O-去甲基化、芳... >> 详细【外文摘要】Pantoprazole, a chiral benzimidazole sulfoxide derivative, is an irreversible proton pump inhibitor which is used clinically as racemate in the treatment of reflux esophagitis,Zoliinger-Ellison syndrome, peptic ulcers, and other acid-related, hypersecretory gastrointestinal disorders. In previous studies on the metabolism and pharmacokinetics of pantoprazole, it is extensively metabolized in the liver through the cytochrome P450 system and also exhibits polymorphic metabolism in humans. Pantoprazole undergoes metabolic pathways including sulfoxide oxidation and reduction (cataly zed mainly by CYP3A4),O-demethylation and aromatic hydroxylation (catalyzed by CYP2C19 and CYP3A4). The demethylated and hydroxylated metabolites then undergo phase II metabolism (glucuronidation or sulfation). In the EMs, the AUC of l-pantoprazole was slightly higher than that of d-pantoprazole. However, significant differences in the AUC (approximately 3 times greater for the d-pantoprazole than that for the l-pantoprazole) were observed in the PMs. It is important for complete understanding of the absorption, distribution, metabolism,and excretion of pantoprazole enantiomers, and for development of pantoprazole enantiomer, to gain further understanding of pantoprazole metabolism and stereoselective pharmacokinetics and its mechanism.The thesis aimed to isolate and identify metabolites of pantoprazole, to investigate pantoprazole metabolism in microbial model and in mammals. The stereoselective pharmacokinetics of pantoprazole was studied by assays for simultaneous determination of pantoprazole and its metabolites in different biological matrices and its mechanism was also revealed. It would offer some references and inspirations for the development of chiral drugs.1. Isolation and identification of pantoprazole metabolites A total of fifteen metabolites of pantoprazole were isolated from the biotransformed culture sample of pantoprazole by Cunninghamella blakesleeana AS 3.153 and urine sample of rat after multi-dose oral administration of pantoprazole and identified by NMR and ESI-MS. They were 8 phase I metabolites, 4 glucuronides, 2 N-acetylcysteine metabolites, and one glucoside, which could be used as reference substances in the studies on metabolism and stereoselective pharmacokinetics of pantoprazole. Using multi-stage ion trap mass spectrometric analysis, the characteristic fragment ions of pantoprazole and its metabolites were obtained. The collision-induced dissociation of protonated pantoprazole and its metabolites proceeds mainly via the following well-defined fragmentation pathways: The MS²spectra of glucuronides, N-acetylcysteine metabolites,and glucosides were dominated by an abundant loss of 176 (glucuronic acid - H₂O), 129 (CH₂=C(COOH)NHCOCH₃), and 162 Da (glucose - H₂O), respectively. After this dominating dissociation, the protonated phase I metabolites were formed. If it was a sulfone derivative, there was one characteristic fragment ion formed by the loss of 64 Da (SO₂). If it was a sulfine derivative, there were two characteristic fragment ions formed by the losses of 33 (·SH) and 34 Da (H₂S). When the sulfoxide functionality has not been changed, The MS²spectrum of the protonated metablite only provided one characteristic fragment ion, which was formed by the cleavage of C₂-S bond of the benzimidazole. Sometimes, there were some fragment ions formed by the losses of 20 (HF), 40 (2×HF), and 68 Da (HOCHF₂).2. The metabolism of pantoprazole in the microbial model and in mammals and their comparison Metabolites of pantoprazole in the microbial model of C. blakesleeana AS3.153 and in mammals (rat, dog, and human) were investigated by LC/MS〒method. A total of 37 metabolites were found andidentified by comparisons of their chromatographic behaviors,ESI-MS, and MS/MS spectra to those of pantoprazole, pantoprazole sulfone, pantoprazole thioether, and 15 isolated standards. These metabolites included 4'-O-demethyl-pantoprazole (RM8), 6-hydroxy-pantoprazole (RM13), conjugated metabolites of RM13 with glucuronic acid and sulphuric acid (RM16-RM19),5'-hydroxy-pantoprazole (RM14), rearranged metabolites (RM26), conjugated metabolites of pantoprazole sulfone with glucuronic acid (RM20 and RM21),4'-O-demethyl-pantoprazole sulfone (RM1), 6-hydroxy-pantoprazole sulfone (RM22), 1'-N-oxidic-pantoprazole sulfone (RM23), conjugated metabolites of RM22 with glucuronic acid and sulphuric acid (RM24 and RM25), conjugated metabolites of pantoprazole thioether with glucose (MM5 and MM6), 4'-O-demethyl-pantoprazole thioether (RM11), conjugated metabolites of RM11 with glucuronic acid (RM12), 6-hydroxy-pantoprazole thioether (RM2),conjugated metabolites of RM2 with glucuronic acid and sulphuric acid (RM3-RM5),6-hydroxy-4'-O-demethyl-pantoprazole thioether (RM6), conjugated metabolites of RM6 with glucuronic acid and sulphuric acid (RM9 and RM10), benzimidazole-related metabolites (RM27, RM30, RM34, and RM35), and pyridine-related metabolites (RM28,RM29, RM31-RM33). The major metabolic pathways of pantoprazole in the microbial model and in mammals were oxidation and reduction of the sulfoxide functionality,4'-O-demethylation, 6-hydroxylation, 5'-hydroxylation, 1'-N-oxidation, rearrangement and conjugation with glucuronic acid, sulphuric acid, glucose, and glutathione. Secondary metabolism via these pathways was also evidenced. Two new metabolic pathways (conjugation with glucose and glutathione) were found in this study.Pantoprazole was extensively metabolized both in the microbial model and in mammals (rat, dog, and human) to produce 6 and 35 metabolites, respectively. Except for that metabolites of RM2, RM7, RM11, and RM15 were the phase I metabolites of pantoprazole in the microbial model and in mammals, there were some differences in phase II metabolic reactions of pantoprazole between the microbial model and mammals.Only two glucosides were present in the microbial model, whereas the phase II metabolites of pantoprazole were found to be glucuronides (9 metabolites), sulfates (5 metabolites), and two N-acetylcysteine metabolites in mammals.3. Studies on the stereoselective pharmacokinetics and its mechanism of pantoprazole Using the assay for simultaneous determination of pantoprazole enantiomers and its two metabolites (pantoprazole sulfone and pantoprazole thioether) in plasma, the chiral inversion of pantoprazole enantiomers (d-pantoprazole in human and pantoprazole enantiomers in dog and rats) and the stereoselective pharmacokinetics of pantoprazole in rats have been studied. The stereoselective distribution of pantoprazole enantiomers after multi-dose oral administration of pantoprazole enantiomers to rat at 25 ㎎/㎏has been investigated by the LC/MS/MS method for simultaneous determination of parent drug and its four metabolites (pantoprazole thioether, pantoprazole sulfone, 4'-O-demethyl -pantoprazole thioether, 6-hydroxy-pantoprazole thioether) in tissues. Moreover, the stereoselective metabolism of pantoprazole enantiomers in rats liver microsomes has also been studied by another LC/MS/MS method of simultaneous determination of its three metabolites (pantoprazole sulfone, 4'-O-demethyl-pantoprazole thioether, 6-hydroxy-pantoprazole).These results indicated that the chiral inversion of pantoprazole enantiomers could not occur in mammals (human, dog, and rat), and pantoprazole has an enantioselective pharmacokinetics profile in Wistar rats. The concentrations of l-pantoprazole in plasma and tissues (liver, stomach, duodenum, small intestine intestine content, large intestine, and cecum) were higher than those of d-pantoprazole. The in situ absorption study showed no evidence of enantioselective absorption of the two enantiomers fromthe intestine and the protein binding of pantoprazole enantiomers may not influence the enantioselective disposition of pantoprazole after oral administration. Whereas, the metabolism of pantoprazole enantiomers in rat liver microsomes were enantioselective, which was mainly contributed to the different pharmacokinetics of pantoprazole enantiomers. These metabolic pathways included 4'-O-demethylation and 6-hydroxylation (catalyzed by CYP2C19), and oxidation of the sulfoxide functionality (catalyzed by CYP3A4).4. Pharmacokinetics of l-pantoprazole The studies of stereoselective pharmacodynamics ofpantoprazole enantiomers have proved the eudomer was l-pantoprazole. In order to develop a single optical isomer, the pharmacokinetics of l-pantoprazole has been studied in this investigation.l-Pantoprazole is rapidly absorbed after oral administration, with T〒approximately 23 and 16 min in dog and rats, respectively. l-Pantoprazole is subjected to low first-pass hepatic extraction, as reflected in an estimated absolute oral bioavailability of 63.9% and 88.9% in dog and rats,respectively.l-Pantoprazole and its two metabolites (pantoprazole sulfone and pantoprazole thioether) are mainly distributed to gastrointestines (stomach, small intestine,large intestine, and cecum), which are useful to its therapy of hypersecretory gastrointestinal disorders.In the present study, a total of fifteen metabolites of pantoprazole were isolated and identified by NMR and ESI-MS, moreover, a total of 37 metabolites were observed in microbial model and in mammals by the analysis of LC/MS〒. Two new metabolic pathways,conjugation with glucose and glutathione, were found. 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