Fiboflapon Sodium(Fiboflapon Sodium) - 药物靶点：FLAP_专利_临床

概要

基本信息

药物类型

小分子化药

别名

Fiboflapon、Fiboflapon sodium (USAN)、AM 803

+ [4]

靶点

FLAP

作用方式

抑制剂

作用机制

FLAP抑制剂(5-脂氧合酶激活蛋白抑制剂)

治疗领域

免疫系统疾病呼吸系统疾病其他疾病+ [1]

在研适应症-

非在研适应症

哮喘运动诱发哮喘心血管疾病+ [1]

原研机构

Bristol Myers Squibb Co.

在研机构-

非在研机构

Amira Pharmaceuticals, Inc.

GSK Plc

权益机构

Amira Pharmaceuticals, Inc.

GSK Plc

最高研发阶段终止临床2期

首次获批日期-

最高研发阶段(中国)-

特殊审评-

登录后查看时间轴

结构/序列

分子式C38H43N3NaO4S

InChIKeyHBTBYQNCMVSNPE-UHFFFAOYSA-N

CAS号1196070-26-4

关联

18

项与 Fiboflapon Sodium 相关的临床试验

NCT01471665

/ Completed临床2期

A Randomised, Double-blind, Placebo-controlled, Cross-over Study to Evaluate the Effect of Treatment With Repeat Dose GSK2190915 as an add-on to Current Therapy on the Percentage of Neutrophils in Induced Sputum in Asthmatic Patients With Elevated Sputum Neutrophils

The purpose of this study is to investigate the effect on repeat doses of GSK2190915 in asthmatic patients with a high percentage of neutrophils in their sputum. GSK2190915 will be given as an add on to current therapy, and its effects on the percentage of sputum neutrophils in the patients will be assessed.

开始日期2011-06-01

申办/合作机构

GSK Plc

NCT01411111

/ Completed临床1期

An Open Label, Sequential, Single Cohort, Repeat Dose Study to Investigate the Potential Interaction of GSK2190915 on the Pharmacokinetics of Rosuvastatin in Healthy Adult Subjects.

Leukotrienes are potent inflammatory molecules produced mainly by mast cells, eosinophils, monocytes/macrophage and neutrophils in response to allergic or inflammatory stimuli. GSK2190915 is a high affinity 5-lipoxygenase-activating protein (FLAP) inhibitor that attenuates the production of leukotrienes, through the blockage of the first committed step in the leukotriene pathway, 5 lipoxygenase (5-LO) activation.
GSK2190915 has been shown to be an in vitro inhibitor of human organic anion transporting polypeptides 1B1 and 1B3 (OATP1B1 and OATP1B3), hence there is a potential for a pharmacokinetic drug-drug interaction with OATP1/ B1 substrates such as the anti-lipidemic rosuvastatin.
This study will evaluate the effect of repeat oral dosing of GSK2190915 (30milligram (mg) and 100mg) on the steady-state pharmacokinetics (PK) of rosuvastatin (10 mg). In addition, the study will evaluate the safety and tolerability of this combination when co-administered to healthy, adult volunteers in two cohorts.

开始日期2011-01-06

申办/合作机构

GSK Plc

NCT01248975

/ Completed临床2期

A Randomized, Double-Blind, Double-Dummy, Placebo-Controlled, Three-Treatment, Three 6-Week Period Cross-Over, Multi-Center Study to Evaluate the Effect of Adding GSK2190915 300mg as Compared to Adding Montelukast 10mg or Placebo Tablets QD to Fluticasone Propionate/Salmeterol 250/50mcg Diskus BID

The primary objective of this study is to evaluate the efficacy and safety of adding GSK2190915 300mg or placebo tablets administered once daily to fluticasone propionate/salmeterol 250/50mcg inhalation powder administered twice daily in uncontrolled asthmatic subjects > or = 18 years of age over the course of 6 weeks treatment.
The secondary objectives are to undertake an exploratory analysis of the efficacy and safety of adding montelukast 10mg administered once daily to fluticasone propionate/salmeterol 250/50mcg inhalation powder administered twice daily and to investigate the pharmacokinetics and pharmacodynamics of GSK2190915 in uncontrolled asthmatic subjects > or = 18 years of age over the course of 6 weeks treatment.

开始日期2010-12-01

申办/合作机构

GSK Plc

100 项与 Fiboflapon Sodium 相关的临床结果

登录后查看更多信息

100 项与 Fiboflapon Sodium 相关的转化医学

登录后查看更多信息

100 项与 Fiboflapon Sodium 相关的专利（医药）

登录后查看更多信息

15

项与 Fiboflapon Sodium 相关的文献（医药）

2022-09-01·Gland surgery

Comprehensive analysis reveals potential hub genes and therapeutic drugs in an acquired lymphedema model

Article

作者: Zhang, Yiwen ; Huang, Shengchao ; Chen, Jiemei ; Qiu, Chaoran ; Li, Xiaoping ; Huang, Hui ; Li, Weiwen ; Liao, Chunbang ; Yang, Mei ; Qu, Yuting ; Lin, Zhiquan

Background:

Acquired lymphedema is a common and often severe complication of breast cancer surgery and radiology that seriously affects patients' quality of life. Nevertheless, the pathogenesis for acquired lymphedema is complex and remains unclear. The aim of this study is to find out possible genetic markers and potential drugs for acquired lymphedema.

Methods:

First, the GSE4333 datasets, which include expression data for six female humanized hairless immunocompetent SKH-1 mice (the condition of whom mimics acquired lymphedema), were reanalyzed. According to the criteria of a fold change (FC) ≥1.4 and an adjusted P value <0.05, we identified the differentially expressed genes (DEGs) between a normal group and the lymphedema group. Next, we analyzed the Gene Ontology (GO) terms and enriched signaling pathways associated with these DEGs with an online tool DAVID. We also constructed protein-protein interaction (PPI) networks and selected meaningful gene modules for additional gene-drug interaction research. Finally, the extant drugs targeting these module genes were identified for further study of their therapeutic effects against acquired lymphedema.

Results:

A total of 481 DEGs were identified that were closely associated with the immune system, inflammatory response, and extracellular matrix (ECM) structural constituent terms, among others. Moreover, we identified the top 10 significant genes in the PPI networks and identified one extant drug, fiboflapon, that targets the ALOX5AP gene.

Conclusions:

We ultimately identified 10 hub genes, molecular mechanisms, and one extant drug related to acquired lymphedema. The findings identified targets and a potential drug for further research on acquired lymphedema.

2021-10-01·Prostaglandins & other lipid mediators3区 · 生物学

Intrinsic 5-lipoxygenase activity regulates migration and adherence of mantle cell lymphoma cells

3区 · 生物学

Article

作者: Merrien, Magali ; Xu, Dawei ; Sadeghi, Laia ; Claesson, Hans-Erik ; Björkholm, Magnus ; Sander, Birgitta ; Österborg, Anders ; Xia, Chuanyou ; Wright, Anthony P ; Strååt, Klas

Human B-lymphocytes express 5-lipoxygenase (5-LOX) and 5-LOX activating protein (FLAP) and can convert arachidonic acid to leukotriene B₄. Mantle cell lymphoma (MCL) cells contain similar amounts of 5-LOX as human neutrophils but the function and mechanism of activation of 5-LOX in MCL cells, and in normal B-lymphocytes, are unclear. Here we show that the intrinsic 5-LOX pathway in the MCL cell line JeKo-1 has an essential role in migration and adherence of the cells, which are important pathophysiological characteristics of B-cell lymphoma. Incubation of JeKo-1 with the FLAP inhibitor GSK2190915 or the 5-LOX inhibitor zileuton, at a concentration below 1 μM, prior to stimulation with the chemotactic agent CXCL12, led to a significant reduction of migration. CRISPR/Cas9 mediated deletion of ALOX5 gene in JeKo-1 cells also led to a significantly decreased migration of the cells. Furthermore, 5-LOX and FLAP inhibitors markedly decreased the adherence of JeKo-1 cells to stromal cells. In comparison, these drugs had a similar effect on adherence of JeKo-1 cells as the Bruton tyrosine kinase inhibitor ibrutinib, which has a proven anti-tumour effect. These results indicate that inhibition of 5-LOX may be a novel treatment for MCL and certain other B-cell lymphomas.

2020-09-01·Chemical biology & drug design4区 · 医学

Fingerprint‐based computational models of 5‐lipo‐oxygenase activating protein inhibitors: Activity prediction and structure clustering

4区 · 医学

Article

作者: Zhang, Shengde ; Qin, Zijian ; Yan, Aixia ; Huo, Donghui ; Tu, Guiping

Abstract:

Inflammatory diseases can be treated by inhibiting 5‐lipo‐oxygenase activating protein (FLAP). In this study, a data set containing 2,112 FLAP inhibitors was collected. A total of 25 classification models were built by five machine learning algorithms with five different types of fingerprints. The best model, which was built by support vector machine algorithm with ECFP_4 fingerprint had an accuracy and a Matthews correlation coefficient of 0.862 and 0.722 on the test set, respectively. The predicted results were further evaluated by the application domain dSTD‐PRO (a distance between one compound to models). Each compound had a dSTD‐PRO value, which was calculated by the predicted probabilities obtained from all 25 models. The application domain results suggested that the reliability of predicted results depended mainly on the compounds themselves rather than algorithms or fingerprints. A group of customized 10‐bit fingerprint was manually defined for clustering the molecular structures of 2,112 FLAP inhibitors into eight subsets by K‐Means. According to the clustering results, most of inhibitors in two subsets (subsets 2 and 4) were highly active inhibitors. We found that aryl oxadiazole/oxazole alkanes, biaryl amino‐heteroarenes, two aromatic rings (often N‐containing) linked by a cyclobutene group, and 1,2,4‐triazole group were typical fragments in highly active inhibitors.

1

项与 Fiboflapon Sodium 相关的新闻（医药）

2023-09-10

·CPHI制药在线

5-脂氧合酶及其抑制剂研究进展

关注并星标CPHI制药在线脂氧合酶是一类非血红素含铁双加氧酶，存在于动、植物的组织和细胞中，可催化花生四烯（AA）、二十二碳六烯酸和各种多不饱和脂肪酸(polyunsaturated fatty acid，PUFA)的氧化反应。脂氧合酶主要分为1、3、5、8、12、15-脂氧合酶6种亚型。其中5-脂氧合酶(5-lipoxygenase，5-LOX)是脂氧合酶同工酶中最常见的、研究较为深入的非血红素铁蛋白氧化代谢酶，是许多高活性氧化脂质生物合成中的关键酶。5-LOX作用于AA氧化通过两步完成：第一步使5-LOX氧化成5-羟过氧化二十碳四烯酸（5-HPETE）再转化为5-羟基二十碳四烯酸（5-HETE）。第二步催化5-HPETE生成白三烯A4(leukotriene A4，LTA 4 )。LTA 4既可转化为致炎物白三烯B4(leukotriene B4，LTB4)，也可生成白三烯C4(leukotriene C4，LTC4)进而生成白三烯D4(leukotriene D4，LTD4)、白三烯E4(leukotrieneE4，LTE4)等导致过敏反应的反应物质。白三烯物质（LT）是哮喘、慢性阻塞性肺疾病、炎症性肠病、关节炎、动脉粥样硬化、皮炎和癌症等多种慢性炎症性疾病相关的促炎性脂质介质，通过进一步的双加氧作用和对外源化学物的协同氧化作用，在炎症、哮喘、脑缺血、部分恶性肿瘤及阿尔茨海默症等疾病的发生和发展中具有极其重要的作用。5-LOX抑制剂通过阻断LT的产生，抑制AA转变为LT，从而减少炎症的产生。因此，开发有效的5-LOX抑制剂对治疗上述疾病至关重要。根据抑制剂的作用机制可将5-LOX抑制剂分为直接抑制剂和间接抑制剂。直接抑制剂直接抑制剂主要针对5-LOX分子结构特点进行研发，比如干扰5-LOX C-端催化结构域中Fe2+与Fe3+正常的转换，或者是与铁离子络合来抑制5-LOX的活性。直接抑制剂包括氧化还原抑制剂、非氧化还原抑制剂、铁离子配体抑制剂。间接抑制剂主要是围绕FLAP进行设计，在5-LOX途径中需要FLAP的参与，抑制了FLAP 就能阻断 5-LOX 途径。 1、氧化还原抑制剂氧化还原抑制剂一般是亲脂性的小分子芳香族化合物，例如酚类化合物和醌类化合物。1,4-苯醌AA-861是第一批氧化还原型5-LOX抑制剂，经多项研究证实其在体内可产生抗炎作用，并已经通过了预防季节性过敏性鼻炎的临床试验。苯醌衍生物在人类单核细胞、中性粒细胞和整个人类血液中可作为5-LOX的有效活性抑制剂，对两种LT相关炎症标准化动物模型的实验研究表明，新型1,4-苯醌RF-Id能够通过抑制LT的产生，在体内抑制导致抗炎反应的5-LOX。此外，氧化还原抑制剂还包括去甲二氢愈创木酸 (NDGA)、香豆素、黄酮类化合物等几类物质，它们均在体外实验证实具有高效的5-LOX 抑制作用。氧化还原抑制剂能把Fe3+还原为Fe2+，从而干扰了铁离子的正常催化循环，阻止5-LOX 的激活，导致5-LOX途径不能正常进行。此外，黄酮类的某些化合物，例如槲皮素、芦丁由于B环上具有邻位的酚羟基，他们还能与Fe3+络合，从而加大了对 5-LOX 的抑制作用。另外，研究人员用荧光法测定了氧化还原抑制剂的氧化还原电势，并揭示了氧化还原抑制剂的作用机制，当氧化还原抑制剂存在时，它降低了Fe2+与Fe3+之间的转换，抑制了酶催化反应，从而需要更多的脂质过氧化物去氧化Fe2+转变成 Fe3+，因此，在酶催化反应过程中，真正参与催化反应的脂质过氧化物的量是很少的，酶催化反应即被抑制。 2、非氧化还原抑制剂非氧化还原抑制剂属于竞争型抑制剂，它能与底物AA竞争结合到5-LOX 的活性中心，导致5-LOX途径受阻，相对于其他抑制剂具有更高的选择性，但是磷酸化作用和Ca2+会干扰这些抑制剂。ZD2138 和ZM230487属于非氧化还原抑制剂中的两个代表。它们属于甲氧基四氢吡喃衍生物，临床研究表明，ZD2138 能够有效抑制关节炎和哮喘病。实验研究表明，一些天然产物和ZD2138 的杂交体 L-697198，以及通过对L-697198结构进行优化而得到的L-708780和L-739010，表现出良好的生物利用度。但后续动物实验发现，该种抑制剂有多种毒性，限制了它的临床使用。此外，L-739,010、CJ-13,610和PF-419183也是非氧化还原型5-LOX抑制剂，在细胞测定中显示IC50的低纳摩尔范围。L-739,010可以减少LT介导的炎症反应，且其抗痛觉亢进活性与炎症大脑中LT水平降低有关，在急性卡拉胶模型和慢性炎症模型中表现出优异的药效和药代动力学，但难以形成共价蛋白结合代谢物。CJ-13,610在大鼠内侧半月板横切面模型上对骨关节炎疼痛有抑制作用，口服CJ-13,610可逆转该动物模型的两种疼痛模式，包括触觉异位痛和负重差异。通过大鼠气囊模型证明了PF-4191834对LTB4产生的抑制作用，PF-4191834也完成了哮喘的Ⅱ期临床试验，但其用于膝骨关节炎的Ⅱ期临床试验因出现晕厥、急性肝炎和胃溃疡出血等严重不良事件而被终止。 3、铁离子配体抑制剂铁离子配体抑制剂大体包括两种，异羟基肟酸类和羟基脲类，羟肟酸衍生物BWA4C和羟基脲衍生物Zileuton是有效的口服5-LOX抑制剂。BWA4C是溃疡性结肠炎患结肠组织中LTB4合成的有效选择性抑制剂，以BWA4C为代表的乙酰异羟肟酸5-脂氧合酶抑制剂有助于评价LTB4在溃疡性结肠炎中的临床意义，并为该病的治疗提供新的途径。Zileuton使急性和慢性气道功能得到了改善，也减少了β受体激动剂或糖皮质激素的需求，并在美国被批准用于治疗哮喘，但是对于变应性鼻炎、类风湿关节炎和炎症性肠病的治疗潜力较低，并且它有许多缺点，如肝毒性和不良药代动力学特征等。以Zileuton结构为基础设计出了一种新型抑制剂VIA-2291，可以在支气管痉挛动物模型中表现出比Zileuton高5倍的效力，口服半衰期16 h，对哮喘患者的运动性支气管收缩有一定的疗效。VIA-2291已成功完成动脉粥样硬化和心血管疾病的Ⅱ期临床试验，成为临床开发中领先的5-LOX抑制剂之一。RBX-7796是一种具有十二烷基链的尿素衍生物，可抑制大鼠血液中LTB4的体外合成，并对各种炎症和支气管收缩动物模型有活性。间接抑制剂间接抑制剂不直接抑制5-LOX的活性。FLAP是5-LOX 激活蛋白，它能结合底物 AA 并且把它转移给5-LOX。在细胞中，5-LOX 与 FLAP 是共同表达的。当给予足够的底物 AA，如果缺少FLAP，细胞也不能合成白三烯等物质。MK886 是研发出来的第一代间接抑制剂，同时也是第一个用于临床的间接抑制剂。它能与AA竞争FLAP 上的结合位点，导致5-LOX 无法与FLAP 相互结合，5-LOX 途径因此受阻。此外，抑制剂AM803正在进行临床实验，并已经完成了对哮喘病人的二期阶段试验，它的衍生物AM103也成功通过了一期临床实验。不过研发的某些抑制剂也存在问题，如NGDA和MK0591 等也存在两方面的缺陷，一是不能特异性针对5-LOX，对人体正常的代谢也有一定的干扰，从而限制了临床应用；二是稳定性不够，直接影响抑制剂的抑制效力。参考资料 [1]李丹凤,范涛,鹿欣雨.5-脂氧合酶抑制剂的研究进展[J].生命的化学,2023,43(05):666-673. [2]黄凯,蒋世云,陈柳军.5-脂氧合酶及其抑制剂[J].中国生物化学与分子生物学报,2014,30(12):1190-1196. 作者简介：小泥沙，食品科技工作者，食品科学硕士，现就职于国内某大型药物研发公司，从事营养食品的开发与研究。智药研习社近期课程报名来源：CPHI制药在线声明：本文仅代表作者观点，并不代表制药在线立场。本网站内容仅出于传递更多信息之目的。如需转载，请务必注明文章来源和作者。投稿邮箱：Kelly.Xiao@imsinoexpo.com▼更多制药资讯，请关注CPHI制药在线▼点击阅读原文，进入智药研习社~

临床1期核酸药物

100 项与 Fiboflapon Sodium 相关的药物交易

登录后查看更多信息

外链

KEGG	Wiki	ATC	Drug Bank
D10122	-	-	DB06346

研发状态

10 条进展最快的记录,

登录

后查看更多信息

适应症	最高研发状态	国家/地区	公司	日期
持续性哮喘	临床2期	美国	GSK Plc	2010-06-28
持续性哮喘	临床2期	日本	GSK Plc	2010-06-28
持续性哮喘	临床2期	保加利亚	GSK Plc	2010-06-28
持续性哮喘	临床2期	波兰	GSK Plc	2010-06-28
持续性哮喘	临床2期	罗马尼亚	GSK Plc	2010-06-28
持续性哮喘	临床2期	乌克兰	GSK Plc	2010-06-28
哮喘	临床2期	荷兰	GSK Plc	2008-12-01
哮喘	临床2期	英国	GSK Plc	2008-12-01
运动诱发哮喘	临床2期	美国	GSK Plc	2008-12-01
心血管疾病	临床1期	欧洲	Amira Pharmaceuticals, Inc.	-

登录后查看更多信息

临床结果

适应症

分期

评价

查看全部结果

研究	分期	人群特征	评价人数	分组	结果	评价	发布日期


NCT00850642 (CTgov)	临床2期	哮喘	7	Placebo	壓鹹糧願鏇積鏇觸憲築(鹽襯觸積積範觸鏇衊鏇) = 積窪糧選觸簾醖築窪壓範夢構艱醖簾鏇鏇壓廠 (鏇衊夢膚顧艱齋鬱獵壓, 2.8415) 更多	-	2018-03-01
NCT00812929 (GSK Clinical Study LPA112025, CTgov)	临床2期	哮喘 \| 运动诱发哮喘	47	Placebo (Placebo)	鏇獵夢衊顧窪鏇簾觸顧(鏇餘鏇構構觸鑰觸艱網) = 築壓簾觸廠壓糧繭襯願憲鑰淵遞範願鑰淵憲齋 (選鑰構淵鑰鏇築積鬱壓, 1.326) 更多	-	2017-09-19
				GSK2190915 (GSK2190915 10 mg)	鏇獵夢衊顧窪鏇簾觸顧(鏇餘鏇構構觸鑰觸艱網) = 憲膚艱積簾積醖壓蓋築憲鑰淵遞範願鑰淵憲齋 (選鑰構淵鑰鏇築積鬱壓, 1.314) 更多
NCT01147744 (CTgov)	临床2期	持续性哮喘	700	placebo+montelukast (Placebo)	糧鏇艱憲積齋顧壓淵積(蓋願窪觸顧艱糧夢醖餘) = 窪觸淵遞醖鹹願鹹鬱夢醖淵壓顧觸窪鹽簾糧網 (顧選窪積構網糧艱鏇衊, 0.04) 更多	-	2017-09-06
				GSK2190915 (GSK2190915 10 mg)	糧鏇艱憲積齋顧壓淵積(蓋願窪觸顧艱糧夢醖餘) = 蓋齋簾廠糧鏇鑰構構遞醖淵壓顧觸窪鹽簾糧網 (顧選窪積構網糧艱鏇衊, 0.04) 更多
NCT01156792 (CTgov)	临床2期	哮喘	162	FP (FP + Placebo)	網製鬱選遞獵製糧鑰範(築積網願願範繭艱鏇夢) = 積齋鹹繭醖衊網壓蓋網醖淵蓋齋鹽膚廠夢鏇鹽 (獵網鹹積蓋糧遞選窪壓, 0.03) 更多	-	2017-02-03
				FP+GSK2190915 (FP + GSK2190915 100 mg)	網製鬱選遞獵製糧鑰範(築積網願願範繭艱鏇夢) = 顧鑰遞壓艱築膚壓衊獵醖淵蓋齋鹽膚廠夢鏇鹽 (獵網鹹積蓋糧遞選窪壓, 0.03) 更多
NCT00812929 (GSK Clinical Study LPA112025, Pubmed \| Allergy Asthma Proc)	临床2期	运动诱发哮喘	47	GSK2190915 200 mg	憲淵簾糧顧觸獵構齋醖(壓窪築範獵糧築獵選蓋) = 築範獵簾築淵積鹽築襯鏇齋鹹選構襯糧繭範壓 (顧範鹽鑰築醖遞範窪齋, 3.06 ~ 9.54)	-	2014-04-30
NCT01147744 (Pubmed \| Respir Res)	临床2期	持续性哮喘	700	GSK2190915 30 mg	顧願獵觸範壓艱簾鏇鬱(獵膚餘繭獵簾範鬱糧壓): mean difference = 0.115, P-Value = 0.044	-	2013-05-17
				Placebo
NCT00748306 (Pubmed \| Clin Exp Allergy)	临床2期	轻度哮喘	19	GSK2190915 100 mg	糧鹽鑰廠簾淵遞網壓製(繭願鏇膚觸淵廠襯膚艱) = 窪醖憲鑰襯艱衊醖夢鏇願衊憲構顧醖築齋夢鹹 (顧構繭蓋築積積餘夢鑰 ) 更多	-	2013-02-01
NCT00748306 (ERS2011)	临床2期	哮喘	19	GSK2190915 100 mg	顧構觸膚壓鑰憲憲壓獵(壓鹽積鹹衊醖觸醖遞夢) = 憲網積繭憲襯積鹽鬱衊糧膚網膚繭範衊積齋蓋 (齋襯鹹廠觸齋觸鏇願製 ) 更多	积极	2011-09-01
				Placebo	積鏇壓襯衊憲網範鹽選(蓋積餘網餘夢網壓衊築) = 鑰窪繭憲蓋選簾觸構膚艱積鑰遞憲鑰壓鏇窪鏇 (構鏇醖糧鹽齋築顧範遞 )
NCT00748306 (LPA111834, ERS2011)	临床2期	哮喘 cysteinyl leukotrienes (cLTs)	-	GSK2190915 100mg	窪築衊鏇蓋遞餘獵顧窪(鏇製網艱鏇鹹鹽壓夢積) = 鬱憲鑰壓夢衊顧鏇鏇選願製構衊餘獵醖襯積構 (襯膚築獵鬱鑰醖蓋鹽鏇 )	-	2011-09-01
				Placebo	窪築衊鏇蓋遞餘獵顧窪(鏇製網艱鏇鹹鹽壓夢積) = 簾構鑰窪觸壓憲壓憲網願製構衊餘獵醖襯積構 (襯膚築獵鬱鑰醖蓋鹽鏇 )
NCT00812773 (ERS2011)	临床2期	哮喘	19	GSK2190915 10mg	壓膚餘淵醖築願憲窪鬱(窪鬱餘鬱齋築製蓋簾簾) = 糧製選衊膚範積齋顧醖鬱蓋醖築積範淵遞窪鹽 (憲壓簾糧蓋襯齋鏇鏇衊 )	积极	2011-09-01
				GSK2190915 50mg	壓膚餘淵醖築願憲窪鬱(窪鬱餘鬱齋築製蓋簾簾) = 鏇積製餘製憲淵選衊顧鬱蓋醖築積範淵遞窪鹽 (憲壓簾糧蓋襯齋鏇鏇衊 )