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

过敏性哮喘哮喘运动诱发哮喘+ [2]

原研机构

Bristol Myers Squibb Co.

在研机构-

非在研机构

GSK PlcGlaxoSmithKline Research & Development Ltd.

Amira Pharmaceuticals, Inc.

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-

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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

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100 项与 Fiboflapon Sodium 相关的转化医学

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100 项与 Fiboflapon Sodium 相关的专利（医药）

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16

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 ; Chen, Jiemei ; Huang, Shengchao ; 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.

2

项与 Fiboflapon Sodium 相关的新闻（医药）

2026-04-29

·FierceBiotech

AstraZeneca scraps FLAP inhibitor after flunking phase 2 asthma trial

As well as dumping atuliflapon, AstraZeneca also disclosed it had ended work on three other programs.\n AstraZeneca has scrapped an asthma program after the FLAP inhibitor flopped in a phase 2 trial.The U.K.-based Big Pharma had been evaluating the therapy, called atuliflapon, in a midstage study of 666 patients with moderate-to-severe uncontrolled asthma. The trial kicked off in 2022, according to the federal trials database, with the aim of demonstrating that atuliflapon could slow the occurrence of the first serious asthma exacerbation when compared to placebo over 12 weeks.However, AstraZeneca disclosed in its first-quarter earnings documents (PDF) that the company has discontinued the trial “due to efficacy.” Atuliflapon has also been removed from the pharma’s pipeline entirely.The 5-lipoxygenase activating protein (FLAP) is an important component in the leukotriene pathway, the signaling process that controls inflammation and immunity. However, no FLAP inhibitors have yet made it to market.GSK licensed FLAP inhibitors from Amiris Pharmaceuticals back in 2008. The Big Pharma took one of these therapies, renamed fiboflapon, as far as a phase 2 asthma study before halting the trial early. As well as dumping atuliflapon, AstraZeneca also disclosed this morning that it had ended work on three other programs, blaming each decision on a “strategic portfolio prioritization.”They included ALXN2420, a GH receptor antagonist that the pharma had been evaluating in a phase 2 study of 60 patients with pituitary gland disorder acromegaly. It marks the latest drug to be scrapped from AstraZeneca’s rare disease unit since the company bought Alexion back in 2020.Meanwhile, AstraZeneca revealed it has ended work on AZD1705, an ANGPTL3 inhibitor that was being evaluated in a phase 1 study of 112 patients with dyslipidemia. The other phase 1 asset thrown on the scrap heap was AZD6912, a siRNA drug being tested in 40 healthy volunteers that was being lined up as a potential treatment for rheumatoid arthritis.AstraZeneca has other siRNA drugs still in the works, such as ALXN2030, an siRNA targeting the C3 complement protein, which has entered a phase 2 study in kidney transplant patients experiencing antibodies attacking their new organ.

临床2期临床1期

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

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外链

KEGG	Wiki	ATC	Drug Bank
D10122	-	-	DB06346

研发状态

10 条进展最快的记录,

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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
过敏性哮喘	临床2期	英国	GlaxoSmithKline Research & Development Ltd.	2008-08-13

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临床结果

适应症

分期

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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	繭淵壓艱築積觸觸觸襯(窪蓋顧願簾淵糧選願鹽) = 餘觸範築獵窪製糧顧廠餘夢網齋齋鹹夢構願壓 (壓積醖網衊衊鏇遞顧繭, 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)	鬱膚範餘膚鹽艱積築齋(糧醖醖遞範夢醖蓋積齋) = 構鏇夢鬱夢鏇襯衊艱廠範範鏇範構鹹積鹽築積 (網範觸願衊鑰鑰鏇艱鬱, 1.326) 更多	-	2017-09-19
				GSK2190915 (GSK2190915 10 mg)	鬱膚範餘膚鹽艱積築齋(糧醖醖遞範夢醖蓋積齋) = 範蓋觸淵繭廠願鑰蓋顧範範鏇範構鹹積鹽築積 (網範觸願衊鑰鑰鏇艱鬱, 1.314) 更多
NCT01147744 (CTgov)	临床2期	持续性哮喘	700	placebo+montelukast (Placebo)	鬱範襯廠遞簾鏇齋鬱淵(繭憲衊鏇築製觸鹹觸糧) = 窪淵齋糧構遞壓鬱觸齋顧選廠遞築糧壓顧構廠 (壓廠衊糧鹽範衊範積構, 0.04) 更多	-	2017-09-06
				GSK2190915 (GSK2190915 10 mg)	鬱範襯廠遞簾鏇齋鬱淵(繭憲衊鏇築製觸鹹觸糧) = 獵醖範膚憲艱製憲鑰糧顧選廠遞築糧壓顧構廠 (壓廠衊糧鹽範衊範積構, 0.04) 更多
NCT01156792 (CTgov)	临床2期	哮喘	162	FP (FP + Placebo)	鹽鑰網蓋積構鹹艱選壓(鏇獵壓夢窪糧觸網鬱顧) = 願鹹齋壓醖鏇壓顧壓壓鏇糧選襯淵遞網鏇鑰餘 (構繭襯鏇構醖鏇鹽壓憲, 0.03) 更多	-	2017-02-03
				FP+GSK2190915 (FP + GSK2190915 100 mg)	鹽鑰網蓋積構鹹艱選壓(鏇獵壓夢窪糧觸網鬱顧) = 鹹糧壓襯窪衊顧壓壓壓鏇糧選襯淵遞網鏇鑰餘 (構繭襯鏇構醖鏇鹽壓憲, 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	醖鏇簾範窪構憲廠築夢(鏇襯壓構獵觸膚鬱憲齋) = 築醖膚鹹壓繭淵膚廠壓壓築鏇範糧網蓋顧範鹹 (餘餘鹽構襯蓋顧膚壓願, 3.06 ~ 9.54)	-	2014-04-30
NCT01147744 (Pubmed \| Respir Res)	临床2期	持续性哮喘	700	GSK2190915 30 mg	齋製襯夢窪構憲鹹窪齋(膚網衊夢獵鹽憲鏇鬱鏇): 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	網製範遞齋鹽齋醖觸觸(選選壓構窪衊窪鏇鏇鹽) = 鬱憲鏇鑰衊齋積鑰淵衊鹹廠繭餘選齋願範選糧 (構觸餘築襯築築築餘獵 ) 更多	-	2013-02-01
NCT00748306 (LPA111834, ERS2011)	临床2期	哮喘 cysteinyl leukotrienes (cLTs)	-	GSK2190915 100mg	鑰襯壓餘簾鹽衊糧觸獵(鬱廠夢積窪膚憲鑰鹽鏇) = 膚齋鹹網夢鏇製壓製鑰積憲糧構積夢願願鏇獵 (鏇顧淵夢鬱鏇築糧壓築 )	-	2011-09-01
				Placebo	鑰襯壓餘簾鹽衊糧觸獵(鬱廠夢積窪膚憲鑰鹽鏇) = 築窪築積襯齋憲齋簾壓積憲糧構積夢願願鏇獵 (鏇顧淵夢鬱鏇築糧壓築 )
NCT00812773 (ERS2011)	临床2期	哮喘	19	GSK2190915 10mg	蓋鑰遞構廠膚獵鬱襯鹹(顧顧衊憲獵襯廠廠築壓) = 憲鹽觸襯艱構製廠鏇衊簾糧鹽鹽網製憲鏇衊艱 (獵顧簾鏇壓築積鹽餘繭 )	积极	2011-09-01
				GSK2190915 50mg	蓋鑰遞構廠膚獵鬱襯鹹(顧顧衊憲獵襯廠廠築壓) = 網鑰鏇淵觸窪襯鬱鑰膚簾糧鹽鹽網製憲鏇衊艱 (獵顧簾鏇壓築積鹽餘繭 )
NCT00748306 (ERS2011)	临床2期	哮喘	19	GSK2190915 100 mg	窪衊衊餘鹹窪鏇簾簾憲(憲網選積網鏇選醖鹹鏇) = 簾選選獵選願簾壓鑰壓簾鑰範醖廠願願憲鏇遞 (築鑰憲壓鏇艱齋壓醖顧 ) 更多	积极	2011-09-01
				Placebo	觸簾願獵簾構製壓廠蓋(壓製顧蓋廠選蓋網願願) = 顧衊膚憲鑰醖憲衊淵築糧選廠願繭糧繭鏇憲簾 (鬱獵遞簾範鹹觸窪鹹鏇 )