Sodium sulfate-III

• 分子结构分类: 无机化合物 - 混合金属/非金属化合物 - 碱金属含氧阴离子化合物
• 英文名称: Sodium sulfate-III
• 英文别名: disodium;sulfate
• 化学式: Na2O4S
• 分子量: 142.04
• InChiKey: PMZURENOXWZQFD-UHFFFAOYSA-L

计算性质

• 辛醇/水分配系数(LogP)：
  -7.33
• 重原子数：
  7
• 可旋转键数：
  0
• 环数：
  0.0
• sp3杂化的碳原子比例：
  0.0
• 拓扑面积：
  88.6
• 氢给体数：
  0
• 氢受体数：
  4

ADMET

毒理性

• 毒性总结

鉴定和使用：硫酸钠是一种白色粉末或晶体。它用于标准化染料，在冷冻混合物中，以及用于染料和印刷纺织品。它还用于人类作为泻药和通便剂，以及用于兽医药物。人体研究：可能导致胃肠道刺激和腹泻。动物研究：家禽在饮用含有7500毫克/升硫酸钠的水15天后，死亡率为33%。猪因过量服用导致的中毒爆发特点为抽搐、震颤和惊厥。尸检时最明显的病变是大脑皮层的广泛空泡化和坏死。生态毒性研究：植物受到土壤中4000毫克/升硫酸钠水平的伤害；710毫克/升抑制了根的生长和吸水。在淡水物种中，水蚤和贻贝对硫酸盐的急性敏感性高于摇蚊和胖头鱼，而胖头鱼对硫酸盐的慢性敏感性高于其他三种物种。

IDENTIFICATION AND USE: Sodium sulfate is a white powder, or crystals. It is used for standardizing dyes, in freezing mixtures, and in dying and printing textiles. It is also used as cathartic and purgative in humans and in veterinary medicine. HUMAN STUDIES: It may result in gastrointestinal irritation and diarrhea. ANIMAL STUDIES: Poultry mortality was 33% after drinking water containing 7500 mg/L sodium sulfate for 15 days. Outbreaks of poisoning in pigs due to overdosage were characterized by twitching, tremors and convulsions. The most noticeable lesion at post mortem was widespread vacuolation and necrosis of cerebral cortex. ECOTOXICITY STUDIES: Plants were injured by sodium sulfate levels of 4000 mg/L in soil; 710 mg/L depressed root growth and water absorption. Among aquatic species, the cladoceran and mussel were acutely more sensitive to sulfate than the midge and fathead minnow, whereas the fathead minnow was chronically more sensitive than the other 3 species.

来源:Hazardous Substances Data Bank (HSDB)

毒理性

• 摄入症状

恶心。呕吐。腹痛。腹泻。

Nausea. Vomiting. Abdominal pain. Diarrhoea.

来源:ILO-WHO International Chemical Safety Cards (ICSCs)

毒理性

• 相互作用

农业杀菌剂N-(3,5-二氯苯基)丁二酰亚胺(NDPS)在大鼠体内主要诱导肾毒性。以前的研究表明，NDPS通过氧化丁二酰亚胺环形成N-(3,5-二氯苯基)-2-羟基丁二酰亚胺(NDHS)以及NDHS的水解产物N-(3,5-二氯苯基)-2-羟基丁二酸(2-NDHSA)来诱导肾毒性。我们最近的工作发现，硫酸钠增强了NDPS的肾毒性，这表明NDPS代谢物的硫酸盐结合可能是介导NDPS肾毒性的生物激活步骤。本研究的目的是确定硫酸钠是否也增强了NDPS两种肾毒性代谢物的肾毒性，并进一步观察硫酸钠是否以相同程度增强了NDHS和2-NDHSA的肾毒性。雄性Fischer 344大鼠(每组4-16只)在腹腔注射(非肾毒性剂量0.05 mmol/kg, ip)NDHS或2-NDHSA，或载体(芝麻油中12.5%二甲亚砜)前20分钟接受硫酸钠(10 mg/kg)的腹腔注射。然后在48小时内监测肾功能。硫酸钠预处理增强了NDHS和2-NDHSA非肾毒性剂量对肾脏的影响，导致肾毒性。肾毒性表现为多尿、蛋白尿增加、血尿素氮(BUN)浓度升高、肾脏重量增加和近端肾小管坏死。还观察到硫酸钠对NDHS和2-NDHSA肾毒性增强的差异，因为NDHS的肾毒性增强程度小于2-NDHSA诱导的肾毒性。这些结果支持了一种可能性，即NDPS代谢物的一个或多个硫酸盐结合物有助于NDPS的肾毒性。

The agricultural fungicide N-(3,5-dichlorophenyl)succinimide (NDPS) induces nephrotoxicity as its major toxicity in rats. Previous studies have shown that NDPS induces nephrotoxicity following oxidation of the succinimide ring to form N-(3,5-dichlorophenyl)-2-hydroxysuccinimide (NDHS) and the hydrolysis product of NDHS, N-(3,5-dichlorophenyl)-2-hydroxysuccinamic acid (2-NDHSA). Our recent work found that sodium sulfate potentiated NDPS nephrotoxicity, suggesting that sulfate conjugation of NDPS metabolites might be a bioactivation step mediating NDPS nephrotoxicity. The purpose of this study was to determine if sodium sulfate also potentiated the nephrotoxicity of the two nephrotoxic metabolites of NDPS and further to see if sodium sulfate potentiated NDHS and 2-NDHSA nephrotoxicity to the same degree. Male Fischer 344 rats (4-16 rats/group) received an intraperitoneal (ip) injection of sodium sulfate (10 mg/kg) 20 min before a non-nephrotoxic dose (0.05 mmol/kg, ip) of NDHS or 2-NDHSA, or vehicle (12.5% dimethyl sulfoxide in sesame oil). Renal function was then monitored over 48 hr. Sodium sulfate pretreatment potentiated the renal effects of a non-nephrotoxic dose of NDHS and 2-NDHSA to induce nephrotoxicity. Nephrotoxicity was characterized by diuresis, increased proteinuria, elevated blood urea nitrogen (BUN) concentration, increased kidney weight and proximal tubular necrosis. Differences in the potentiation of NDHS and 2-NDHSA nephrotoxicity by sodium sulfate were also observed as NDHS nephrotoxicity was potentiated to a lesser degree than 2-NDHSA-induced nephrotoxicity. These results support the likelihood that one or more sulfate conjugate(s) of NDPS metabolites contribute to NDPS nephrotoxicity.

来源:Hazardous Substances Data Bank (HSDB)

毒理性

• 相互作用

N-乙酰半胱氨酸（NAC）被认为可以通过两种机制来降低对乙酰氨基酚（AA）的毒性：一是通过增加半胱氨酸的可用性来促进肝脏谷胱甘肽的生物合成；二是通过增加无机硫酸盐的水平，从而增加AA的硫酸化作用及其消除。因为据报道，给予硫酸钠也可以降低AA诱导的毒性，所以我们研究了无机硫酸盐在NAC解毒特性中的作用。同时给予雄性小鼠NAC（4 mmol/kg）和AA（2.5和4 mmol/kg）可以防止AA引起的死亡和肝毒性，而硫酸钠（4 mmol/kg）则不能。NAC或硫酸钠对AA（4.0 mmol/kg）从血液中的半衰期（44分钟）或清除率（9.0 mL/min/kg）没有产生显著变化，尿液中排出的AA-硫酸盐、AA-半胱氨酸或AA-巯基尿酸的量也没有改变。注射硫酸钠或NAC都会增加血清硫酸盐浓度，并防止AA引起的血清硫酸盐减少。AA注射15分钟和30分钟后，肝脏的腺苷3'-磷酸5'-磷酸硫酸盐浓度降低，而注射硫酸钠或NAC可以减轻这种效果。肝脏中谷胱甘肽的浓度在AA之后显著降低。NAC减轻了这种效果，但硫酸钠没有。硫酸钠没有减少由[(3)H]AA衍生出的氚与肝蛋白的结合，而NAC减少了25%的结合。这些发现表明，给予硫酸钠可以增加血清硫酸盐浓度和肝脏腺苷3'-磷酸5'-磷酸硫酸盐水平，但并不能防止对乙酰氨基酚在小鼠中引起的肝毒性。

N-acetylcysteine (NAC) has been proposed to decrease the toxicity of acetaminophen (AA) via two mechanisms: by increasing cysteine availability for hepatic glutathione biosynthesis and by increasing inorganic sulfate levels, which would increase AA sulfation and elimination. Because administration of sodium sulfate also reportedly decreases AA-induced toxicity, we have investigated the role of inorganic sulfate in the antidotal properties of NAC. Simultaneous administration of NAC (4 mmol/kg) and AA (2.5 and 4 mmol/kg) to male mice prevented AA-induced lethality and hepatotoxicity whereas sodium sulfate(4 mmol/kg) did not. Neither NAC nor sodium sulfate produced significant changes in the half-life (44 min) or clearance (9.0 mL/min/kg) of AA (4.0 mmol/kg) from blood nor were the amounts of AA-sulfate, AA-cysteine or AA-mercapturate excreted in urine altered. Injection of either sodium sulfate or NAC increased serum sulfate concentration and prevented the depletion in serum sulfate produced by AA. Hepatic adenosine 3'-phosphate 5'-phosphosulfate concentrations were decreased 15 and 30 min after AA and injection of either sodium sulfate or NAC lessened this effect. The concentration of glutathione in liver was decreased markedly after AA. NAC attenuated this effect but sodium sulfate did not. Sodium sulfate did not decrease covalent binding of tritium derived from [(3)H]AA to liver protein whereas NAC decreased binding by 25%. These findings show that administration of sodium sulfate increases serum sulfate concentration and hepatic adenosine 3'-phosphate 5'-phosphosulfate levels but does not protect against acetaminophen-induced hepatotoxicity in mice.

来源:Hazardous Substances Data Bank (HSDB)

毒理性

• 相互作用

活性炭是扑热息痛吸收的有效抑制剂，而硫酸钠可以防止与扑热息痛硫酸盐形成相关的内源性无机硫酸盐的耗尽。在扑热息痛过量后不久给予活性炭加硫酸钠可能减少扑热息痛的吸收，并通过提供足够的硫酸根离子来促进已吸收扑热息痛的消除，从而加速药物的硫酸化。这项研究的目的是确定硫酸钠是否会改变活性炭对扑热息痛吸收的抑制作用，或者活性炭是否会 影响 硫酸钠的吸收。8名正常成年人在不同时间分别接受了1克扑热息痛、1克扑热息痛和18克硫酸钠（十水合物）、1克扑热息痛和10克活性炭以及1克扑热息痛和10克活性炭和18克硫酸钠的随机顺序给药。收集48小时内的尿液，并检测扑热息痛及其主要代谢物和无机硫酸盐。结果证实，活性炭可以减少扑热息痛的吸收，并表明口服活性炭加硫酸钠不会改变活性炭对扑热息痛吸收的抑制作用或硫酸盐的生物利用度。因此，活性炭和硫酸钠的组合可能对扑热息痛过量的初步管理有用。

Activated charcoal is an effective inhibitor of acetaminophen absorption while sodium sulfate can prevent the depletion of endogenous inorganic sulfate associated with the formation of acetaminophen sulfate. Administration of activated charcoal plus sodium sulfate soon after acetaminophen overdose may reduce acetaminophen absorption and facilitate the elimination of absorbed acetaminophen by providing sufficient sulfate ion for rapid sulfation of the drug. This investigation was designed to determine if sodium sulfate modifies the inhibitory effect of activated charcoal on acetaminophen absorption or if activated charcoal affects the absorption of sodium sulfate. Eight normal adults received, on separate occasions, 1 g acetaminophen, 1 g acetaminophen and 18 g sodium sulfate (decahydrate), 1 g acetaminophen with 10 g activated charcoal and 1 g acetaminophen, with 10 g activated charcoal and 18 g sodium sulfate, in random order. Urine was collected for 48 hours and assayed for acetaminophen and its major metabolites and for inorganic sulfate. The results confirm that activated charcoal can reduce acetaminophen absorption and show that oral administration of activated charcoal with sodium sulfate does not alter the inhibitory effect of activated charcoal on acetaminophen absorption or the bioavailability of the sulfate. A combination of activated charcoal and sodium sulfate may therefore be useful for the initial management of acetaminophen overdose.

来源:Hazardous Substances Data Bank (HSDB)

吸收、分配和排泄

• 吸收

在大鼠吞食硫酸钠后的吸收情况进行了研究。24小时内尿液中排出的35S放射性表明几乎完全从胃肠道吸收。给药后2小时血清中的测定显示硫酸盐浓度增加了3倍，大鼠口服给药后无机硫酸盐的吸收快速且几乎完全。

Absorption of sodium sulfate after ingestion in rats was investigated. 35)S-Radioactivity excreted in urine during 24 hr indicated almost complete absorption from GI tract. Determination in serum 2 hr after admin revealed 3-fold increase in sulfate concentration rapid and almost complete absorption of inorganic sulfate occurs after oral admin in rats.

来源:DrugBank

吸收、分配和排泄

• 消除途径

如果直肠排出物未被吸收的硫酸盐；尿液（吸收的硫酸盐的主要排出途径）

Rectal effluent if unabsorbed sulfates ; urine (predominant route for absorbed sulfates )

来源:DrugBank

吸收、分配和排泄

硫酸根浓度在调节3'-磷酸腺苷5'-磷酸硫酸酯（PAPS）合成中的重要性尚不清楚。因此，本研究旨在确定无机硫酸根增加可用性对各种组织稳态PAPS浓度的影响。为了增加组织硫酸根浓度，将2-16 mmol/kg的硫酸钠和含硫氨基酸（半胱氨酸或甲硫氨酸）静脉输注2小时到戊巴比妥麻醉的大鼠体内。在输注过程中定期取血样并分析硫酸根浓度。输注2小时后，取出肝脏、肾脏和大脑以量化组织中的PAPS和硫酸根浓度。输注硫酸钠、半胱氨酸和甲硫氨酸以剂量和时间依赖性方式增加了血清和组织中的硫酸根浓度。在输注硫酸钠期间，血清硫酸根浓度从0.8增加到14 mM，而输注半胱氨酸和甲硫氨酸分别将血清硫酸根浓度增加到4.8和2.0 mM。在硫酸根输注期间，组织中的硫酸根浓度也增加了。肝脏硫酸根浓度从0.8增加到4.8 mM，肾脏浓度从0.6增加到31 mM，大脑浓度从0.1增加到0.6 mM。与血清硫酸根浓度相似，硫酸根输注在增加组织硫酸根浓度方面最有效，半胱氨酸效果居中，甲硫氨酸效果最差。尽管肝脏、肾脏和大脑的硫酸根浓度分别通过输注硫酸根增加了6倍、50倍和6倍，但组织的PAPS水平并没有明显改变。只有在输注较高剂量（8或16 mmol/kg/2小时）的硫酸钠时，肝脏的PAPS浓度才会显著增加（30-35%）。

The importance of tissue sulfate concentrations in regulating 3'-phosphoadenosine 5'-phosphosulfate (PAPS) synthesis is not known. Therefore, this study was conducted to determine the influence of increased availability of inorganic sulfate on steady-state PAPS concentrations in various tissues. To increase tissue sulfate concentrations, 2-16 mmol/kg of sodium sulfate and sulfur-containing amino acids (cysteine or methionine) were infused intravenously for 2 hr into pentobarbital-anesthetized rats. Serial blood samples were taken during the infusion and analyzed for sulfate concentrations. After 2 hr of infusion, liver, kidney, and brain were removed for quantification of tissue PAPS and sulfate concentrations. Infusion of sodium sulfate, cysteine, and methionine increased serum and tissue sulfate concentrations in a dose- and time-dependent manner. Serum sulfate concentrations increased from 0.8 to 14 mM during the infusion of sodium sulfate, whereas infusions of cysteine and methionine increased serum sulfate concentrations to 4.8 and 2.0 mM, respectively. Tissue sulfate concentrations also increased during sulfate infusion. Liver sulfate concentration increased from 0.8 to 4.8 mM, kidney concentration increased from 0.6 to 31 mM, and brain concentration increased from 0.1 to 0.6 mM. Similar to the serum sulfate concentrations, sulfate infusion was the most effective in increasing tissue sulfate concentrations, cysteine was intermediate, and methionine the least effective. Although sulfate concentrations in liver, kidney, and brain increased 6-, 50-, and 6-fold by infusing sulfate, respectively; tissue PAPS levels were not altered markedly. Hepatic PAPS concentrations increased significantly (30-35%) only when infused with the higher doses (8 or 16 mmol/kg/2 hr) of sodium sulfate.

来源:Hazardous Substances Data Bank (HSDB)

吸收、分配和排泄

在大鼠口服Na235SO4后，对无机硫酸盐的吸收进行了研究。在口服Na235SO4后，35S放射性在血浆中已经在15分钟内可测量，其血浆浓度在大约1.5-2小时后达到峰值。在大鼠口服Na235SO4以及不同量的未标记Na2SO4（每只大鼠0.25-5.0毫摩尔Na2SO4）后24小时内尿液中排出的35S放射性表明，无机硫酸盐几乎完全从胃肠道吸收。在大鼠口服5.0毫摩尔Na2SO4后2小时测定血清中无机硫酸盐的浓度，结果显示血清硫酸盐浓度增加了三倍。这些数据表明，在大鼠口服给药后，无机硫酸盐的吸收迅速且几乎完全。文章还讨论了这与药物硫酸盐结合中硫酸盐可用性的重要性。

The absorption of inorganic sulfate after ingestion was investigated in rats. After oral administration of Na235SO4, 35S radioactivity was measurable in plasma already after 15 min and its plasma concentration reached a peak after about 1.5-2 hr. The 35S-radioactivity excreted in urine during 24 hr after ingestion of Na235SO4 together with varying amounts of unlabelled Na2SO4 (0.25-5.0 mmol Na2SO4 per rat) indicated an almost complete absorption of inorganic sulfate from the gastrointestinal tract. Determination of the inorganic sulfate concentration in rat serum 2 hr after oral administration of 5.0 mmol Na2SO4 revealed a three-fold increase in serum sulfate concentration. The data suggest a rapid and almost complete absorption of inorganic sulfate after oral administration in the rat. Its importance in relation to the sulfate availability for sulfate conjugation of drugs is discussed.

来源:Hazardous Substances Data Bank (HSDB)

吸收、分配和排泄

硫酸钠可以用来增强酚类药物与硫酸盐的结合，并用于治疗高钙血症。人们认为硫酸盐在消化道的吸收缓慢且不完全。这次调查的目的是确定大量硫酸钠（18.1克作为十水合物，相当于8.0克无水盐）的吸收情况，并比较在正常受试者单次给药和分四次等量每小时给药的生物利用度。单次给药和分次给药后72小时尿液中自由硫酸盐的回收率分别为53.4 +/- 15.8%和61.8 +/- 7.8%（平均值 +/- 标准差，n=5，p > 0.2）。单次给药产生严重腹泻，而分次给药只引起轻微或没有腹泻。因此，大量硫酸钠在3小时内分次口服给药时，耐受性良好，吸收程度显著。口服硫酸钠可能有助于治疗对乙酰氨基酚过量的早期治疗。

Sodium sulfate can be used to enhance the conjugation of phenolic drugs with sulfate and to treat hypercalcemia. It is thought that sulfate in is absorbed slowly and incompletely from the digestive tract. The purposes of this investigation were to determine the absorption of large amount of sodium sulfate(18.1 g as the decahydrate, equivalent to 8.0 g of the anhydrous salt) and to compare the bioavailability when this amount is administered orally to normal subjects as a single dose and as four equally divided hourly doses. The 72-hr urinary recovery of free sulfate following single and divided doses was 53.4 +/- 15.8 and 61.8 +/- 7.8%, respectively (mean +/- SD, n=5, p > 0.2). The single dose produced severe diarrhea while the divided doses caused only mild or no diarrhea. Thus, a large amount of sodium sulfate, when administered orally in divided doses over 3 hr, is well tolerated and is absorbed to a significant extent. Orally administered sodium sulfate may be useful for the early treatment of acetaminophen overdose.

来源:Hazardous Substances Data Bank (HSDB)

反应信息

• 作为反应物：
  描述：

  Sodium sulfate-III 以12%的产率得到
  参考文献：
  名称：

  PECULEA, MARIUS;POPESCU, VASILE;BECA, TITUS;BALINT, EUGEN;MIHAI, MIRCEA

  摘要：

  DOI：
• 作为产物：
  描述：

  disodium;carbonate 生成 Sodium sulfate-III
  参考文献：
  名称：

  SOKOLOVA, G. M.;KOMAROV, V. I.;BEREZINA, M. I.;DOBIN, E. YA.;DMITRIEVA, S+, ISSLED. V OBL. TEXNOL. FOSFORSODERZH. PRODUKTOV I SULFIT. SOLEJ, L.,(1988+

  摘要：

  DOI：
• 作为试剂：
  描述：

  3,4-dimethoxy-10-hydroxy-5,6,7,8,13,14-hexahydrodibenz[c,g]azecine 、 3-溴丙烯 、 碳酸氢钠 在 氩 、 二氯甲烷 、 水 、 Sodium sulfate-III 、 苯 作用下， 以 水 为溶剂， 反应 2.0h， 以affords 106 mg of 6-allyl-3,4-dimethoxy-10-hydroxy-5,6,7,8,13,14-hexahydrodibenz[c,g]azecine as a colorless oily material的产率得到6-allyl-3,4-dimethoxy-10-hydroxy-5,6,7,8,13,14-hexahydrodibenz[c,g]azecine
  参考文献：
  名称：

  Dibenzazecines

  摘要：

  通式为：##SPC1## 的二苯并氮杂环化合物（其中R.sup.1和R.sup.2相同或不同，分别表示氢原子、羟基、低碳基氧基、芳基烷氧基或羟甲基基团；或者相邻并结合在一起时，它们可以是一个烷二氧基基团；R.sup.3、R.sup.4和R.sup.5相同或不同，分别表示氢原子、羟基或低碳基氧基，或者当相邻并结合在一起时，它们可以是一个烷二氧基基团；而R.sup.6表示氢原子、烷基、烯基、芳基烷基或环烷基）或其酸加成盐，表现出中枢神经系统抑制作用，如镇痛作用、镇静作用等；可以从二苯并喹啉中制备。

  公开号：

  US03932384A1

文献信息

• INDOLES
  申请人：GlaxoSmithKline LLC

  公开号：US20130345200A1

  公开（公告）日：2013-12-26

  Herein are disclosed indoles of formula (I) where the various groups are defined herein, and which are useful for treating cancer.

  本文公开了式(I)中各个基团的定义，并且这些化合物对于治疗癌症是有用的。
• AZAADAMANTANE DERIVATIVES AND METHODS OF USE
  申请人：AbbVie Inc.

  公开号：US20150158867A1

  公开（公告）日：2015-06-11

  The invention relates to compounds that are azaadamantane derivatives, particularly ether- or amine-substituted azaadamantane derivatives and salts and prodrugs thereof, compositions comprising such compounds, methods of using such compounds and compositions, processes for preparing such compounds, and intermediates obtained during such processes.

  本发明涉及的化合物是氮杂金刚烷衍生物，特别是醚或胺基取代的氮杂金刚烷衍生物及其盐和前药，包括这种化合物的组合物，使用这种化合物和组合物的方法，制备这种化合物的过程以及在这种过程中获得的中间体。
• INDOLE AND INDAZOLE COMPOUNDS THAT ACTIVATE AMPK
  申请人：PFIZER INC.

  公开号：US20130267493A1

  公开（公告）日：2013-10-10

  The present invention relates to indole and indazole compounds of Formula (I) that activate 5′ adenosine monophosphate-activated protein kinase (AMPK). The invention also encompasses pharmaceutical compositions containing these compounds and methods for treating or preventing diseases, conditions, or disorders ameliorated by activation of AMPK.

  本发明涉及式（I）的吲哚和吲唑化合物，其激活5'-腺苷酸单磷酸激活蛋白激酶（AMPK）。该发明还包括含有这些化合物的药物组合物以及通过激活AMPK来治疗或预防由其改善的疾病，病况或障碍的方法。
• 5-SUBSTITUTED INDAZOLE-3-CARBOXAMIDES AND PREPARATION AND USE THEREOF
  申请人：Samumed, LLC

  公开号：US20150266825A1

  公开（公告）日：2015-09-24

  Indazole compounds for treating various diseases and pathologies are disclosed. More particularly, the present disclosure concerns the use of an indazole compound or analogs thereof, in the treatment of disorders characterized by the activation of Wnt pathway signaling (e.g., cancer, abnormal cellular proliferation, angiogenesis, Alzheimer's disease, lung disease, fibrotic disorders, cartilage (chondral) defects, and osteoarthritis), the modulation of cellular events mediated by Wnt pathway signaling, and neurological conditions/disorders/diseases linked to overexpression of DYRK1A.

  本发明揭示了用于治疗各种疾病和病理的吲唑化合物。更具体地，本发明涉及使用吲唑化合物或其类似物治疗以Wnt通路信号激活为特征的紊乱（例如癌症、异常细胞增殖、血管生成、阿尔茨海默病、肺病、纤维性疾病、软骨（软骨）缺陷和骨关节炎），调节由Wnt通路信号介导的细胞事件，以及与DYRK1A过度表达相关的神经系统状况/紊乱/疾病。
• Antibacterial agents
  申请人：Axten MICHAEL Jeffrey

  公开号：US20060041123A1

  公开（公告）日：2006-02-23

  Quinoline and naphthyridine derivatives useful in the treatment of bacterial infections in mammals, particularly humans.

  喹啉和萘啶衍生物可用于治疗哺乳动物（尤其是人类）的细菌感染。

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