PXS-4728(PXS-4728) - 药物靶点：MAO-B x VAP-1_在研适应症：REM睡眠行为障碍，帕金森病_专利_临床

概要

基本信息

药物类型

小分子化药

别名

+ [4]

靶点

MAO-B x VAP-1

作用机制

MAO-B抑制剂(单胺氧化酶B抑制剂)、VAP-1抑制剂(含铜胺氧化酶抑制剂)

治疗领域

神经系统疾病内分泌与代谢疾病

在研适应症

REM睡眠行为障碍帕金森病

非在研适应症

糖尿病性黄斑水肿非酒精性脂肪性肝炎非增殖性糖尿病视网膜病变

原研机构

Syntara Ltd.

在研机构

Syntara Ltd.

非在研机构

Boehringer Ingelheim GmbH

最高研发阶段临床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C15H21FN2O2

InChIKeyOWNSXNXYELKDSO-DHZHZOJOSA-N

CAS号1478364-40-7

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关联

12

项与 PXS-4728 相关的临床试验

NCT05904717

/ Recruiting临床2期

A Phase 2a, Multi Centre, Double-blind, Randomized, Placebo-controlled, Parallel-group Study to Assess the Effect of 12 Weeks Treatment With Oral PXS-4728A on Microglia Activation, as Measured by Positron Emission Tomography, in Participants With Isolated Rapid Eye Movement Sleep Behavior Disorder

This study is to investigate the safety and efficacy of PXS-4728A as an intervention therapy in participants with iRBD. This study will be conducted in participants aged 50 to 80 years of age and will investigate a single dose level.

开始日期2023-11-08

申办/合作机构

Syntara Ltd.

NCT03979820

/ Terminated临床1期

A Phase I Parallel Group Study in Healthy Subjects to Evaluate the Effect of Multiple Oral Doses of BI 1467335 and Phenelzine as Positive Control on Blood Pressure Response to Oral Tyramine (Double-blind, Randomised, Placebo-controlled Design for BI 1467335 Treatment Groups, Open Label for Phenelzine)

The main objective of the study is investigate the effect of escalating doses of oral tyramine on systolic blood pressure (SBP) at baseline and following an oral treatment with BI 1467335 up to 39 days at a low or high dose once daily compared to placebo and phenelzine (Nardil®) as positive control.

开始日期2019-07-31

申办/合作机构

Boehringer Ingelheim GmbH

NCT03927209

/ Completed临床1期

A Phase I, Open-label, Positron Emission Tomography Study in Healthy Male Subjects to Explore the Inhibition of Monoamine Oxidase B in the Brain After Multiple Oral Doses of BI 1467335 (Non-randomized, Open-label, Parallel-group Study)

The main objective of this trial is to investigate the effect of multiple oral dosing of high dose BI 1467335 over 28 days and multiple oral dosing of low dose BI 1467335 over 42 days on MAO-B occupancy in the brain compared to baseline using [11C]-L-deprenyl-D2 PET tracer in healthy male subjects.

开始日期2019-06-06

申办/合作机构

Boehringer Ingelheim GmbH

100 项与 PXS-4728 相关的临床结果

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100 项与 PXS-4728 相关的转化医学

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100 项与 PXS-4728 相关的专利（医药）

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9

项与 PXS-4728 相关的文献（医药）

2024-07-01·Eye

ROBIN: a randomised, double-masked, placebo-controlled Phase IIa study of the AOC3 inhibitor BI 1467335 in diabetic retinopathy

Article

作者: Dugel, Pravin ; Sivaprasad, Sobha ; Brucker, Alexander ; Jin, Xidong ; Berger, Brian ; Patel, Sunil ; Barranco, Jose Juan Escobar ; Figueira, João ; Silva, Rufino ; Habib, Maged ; Calvo, Pilar ; Bailey, Claire ; Hu, Allen ; Jhaveri, Chirag ; Boyer, David S. ; Ghanchi, Faruque ; Erke, Maja Gran ; Dong Nguyen, Quan ; Bandello, Francesco ; Kunimoto, Derek ; Donate Lopez, Juan ; Talks, James ; Giani, Andrea ; Pagliarini, Sergio ; Varano, Monica ; Menon, Geeta ; Maturi, Raj ; Sen, Harsha ; Rosen, Richard ; Androudi, Sofia ; Ehrlich, Michael S. ; Fawzi, Amani ; Weger, Martin ; Cunningham, Matthew ; Hahn, Paul ; Antoszyk, Andrew ; Manjunatha, Nonavinakere ; Ehlers, Justis P. ; Brown, David

AbstractObjectiveTo evaluate the safety and efficacy of BI 1467335 in patients with non-proliferative diabetic retinopathy (NPDR).MethodsROBIN is a Phase IIa, double-masked, randomised, placebo-controlled study (NCT03238963). Patients with NPDR and without centre-involved diabetic macular oedema were included; all had a best corrected visual acuity letter score of ≥70 Early Treatment Diabetic Retinopathy Study letters in the study eye at screening. Patients received oral BI 1467335 10 mg or placebo once daily for 12 weeks. Post-treatment follow-up was 12 weeks. The primary endpoint was the proportion of patients over the 24 weeks with ocular adverse events (AEs). Secondary endpoints were the proportion of patients with ≥2-step improvement from baseline in DRSS severity level at Week 12 and the proportion of patients with non-ocular AEs at 24 weeks.ResultsSeventy-nine patients entered the study (BI 1467335, n = 40; placebo, n = 39). The proportion of patients with ocular AEs over 24 weeks was greater in the BI 1467335 versus the placebo group (35.0% vs 23.1%, respectively). Treatment-related AEs were reported for similar numbers of patients in the placebo and BI 1467335 group (7.7% vs 7.5%, respectively). At Week 12, 5.7% (n = 2) of patients in the BI 1467335 group had a 2-step improvement in DRSS severity level from baseline, compared with 0% in the placebo group.ConclusionsBI 1467335 was well tolerated by patients with NPDR. There was a high variability in DRSS levels for individual patients over time, with no clear efficacy signal.

2020-01-20·Mediators of Inflammation3区 · 医学

Comparison of Inhibitor and Substrate Selectivity between Rodent and Human Vascular Adhesion Protein-1

3区 · 医学

ArticleOA

作者: Henry, Susan H. ; Lieu, Kuo Lee ; Diamond, Christine ; Tulberg, Niklas ; Kubota, Ryo ; Orme, Mark ; Reid, Michael J.

Vascular adhesion protein-1 (VAP-1) is an ectoenzyme that functions as a copper-containing amine oxidase and is involved in leukocyte adhesion at sites of inflammation. Inhibition of VAP-1 oxidative deamination has become an attractive target for anti-inflammatory therapy with demonstrated efficacy in rodent models of inflammation. A previous comparison of purified recombinant VAP-1 from mouse, rat, monkey, and human gene sequences predicted that rodent VAP-1 would have higher affinity for smaller hydrophilic substrates/inhibitors because of its narrower and more hydrophilic active site channel. An optimizedin vitrooxidative deamination fluorescence assay with benzylamine (BA) was used to compare inhibition of five known inhibitors in recombinant mouse, rat, and human VAP-1. Human VAP-1 was more sensitive compared to rat or mouse VAP-1 (lowest IC50concentration) to semicarbazide but was least sensitive to hydralazine and LJP-1207. Hydralazine had a lower IC50in rats compared to humans, although not significant. However, the IC50of hydralazine was significantly higher in the rat compared to mouse VAP-1. The larger hydrophobic compounds from Astellas (compound 35c) and Boehringer Ingelheim (PXS-4728A) were hypothesized to have higher binding affinity for human VAP-1 compared to rodent VAP-1 since the channel in human VAP-1 is larger and more hydrophobic than that in rodent VAP-1. Although the sensitivity of these two inhibitors was the lowest in the mouse enzyme, we found no significant differences between mouse, rat, and human VAP-1. Michaelis-Menten kinetics of the small primary amines phenylethylamine and tyramine were also compared to the common marker substrate BA demonstrating that BA had the highest affinity among the substrates. Rat VAP-1 had the highest affinity for all three substrates and mouse VAP-1 had intermediate affinity for BA and phenylethylamine, but tyramine was not a substrate for mouse VAP-1 under these assay conditions. These results suggest that comparing oxidative deamination in mouse and rat VAP-1 may be important if using these species for preclinical efficacy models.

2018-07-01·Translational Research2区 · 医学

Inhibition of semicarbazide-sensitive amine oxidase reduces atherosclerosis in apolipoprotein E-deficient mice

2区 · 医学

Article

作者: Wang, Shu-Huei ; Kao, Hsien-Li ; Unzeta, Mercedes ; Weston, Chris J ; Solé, Montse ; Yu, Tse-Ya ; Li, Hung-Yuan ; Chen, Yuh-Lien ; Chuang, Lee-Ming ; Tsai, Feng-Chiao ; Lin, Mao-Shin ; Hung, Chi-Sheng ; Li, Yu-I

Inflammation, oxidative stress, and formation of advanced glycated end products (AGEs) and advanced lipoxidation end products (ALEs) are important for atherosclerosis. Vascular adhesion protein-1 (VAP-1) participates in inflammation and has semicarbazide-sensitive amine oxidase (SSAO) activity, which catalyzes oxidative deamination to produce hydrogen peroxide and aldehydes, leading to generation of AGEs and ALEs. However, the effect of VAP-1/SSAO inhibition on atherosclerosis remains controversial, and no studies used coronary angiography to evaluate if plasma VAP-1/SSAO is a biomarker for coronary artery disease (CAD). Here, we examined if plasma VAP-1/SSAO is a biomarker for CAD diagnosed by coronary angiography in humans and investigated the effect of VAP-1/SSAO inhibition by a specific inhibitor PXS-4728A on atherosclerosis in cell and animal models. In the study, VAP-1/SSAO expression was increased in plaques in humans and in apolipoprotein E (ApoE)-deficient mice, and colocalized with vascular endothelial cells and smooth muscle cells (SMCs). Patients with CAD had higher plasma VAP-1/SSAO than those without CAD. Plasma VAP-1/SSAO was positively associated with the extent of CAD. In ApoE-deficient mice, VAP-1/SSAO inhibition reduced atheroma and decreased oxidative stress. VAP-1/SSAO inhibition attenuated the expression of adhesion molecules, chemoattractant proteins, and proinflammatory cytokines in the aorta, and suppressed monocyte adhesion and transmigration across human umbilical vein endothelial cells. Consequently, the expression of markers for macrophage recruitment and activation in plaques was decreased by VAP-1/SSAO inhibition. Besides, VAP-1/SSAO inhibition suppressed proliferation and migration of A7r5 SMC. Our data suggest that plasma VAP-1/SSAO is a novel biomarker for the presence and the extent of CAD in humans. VAP-1/SSAO inhibition by PXS-4728A is a potential treatment for atherosclerosis.

4

项与 PXS-4728 相关的新闻（医药）

2023-10-18

·SYNAPSE

Pharmaxis finalises sale of MBU to Arna Pharma; shifts focus to blood-related cancer treatments

Pharmaxis Ltd (ASX:PXS, OTC:PMXSF) has completed the sale of its mannitol respiratory business (MBU) to Arna Pharma Pty Ltd. On October 3, 2023, PXS announced it would sell MBU as part of a major company restructure to focus on developing drugs to treat blood-related cancers. The restructure involves the creation of clinical stage drug development company, Syntara as well as the sale of MBU, along with changes to the company’s board of directors. Pharmaxis CEO Gary Phillips said at the time: “Over the last few years Pharmaxis has built a commanding position in lysyl oxidase biology and chemistry research. “We have collaborated with leading clinicians and scientists worldwide and forged through the early-stage studies that have given us a clinical pipeline with great potential and resulted in multiple Nature publications. “Building on this heritage and the proven capability of our discovery and development teams, the restructure announced today and the creation of Syntara enables us to focus and accelerate our clinical development programs.” Arna Pharma, an Australian pharmaceutical company involved in a global healthcare alliance, has taken charge of the day-to-day operations of the Medical Business Unit (MBU), which includes Bronchitol® and Aridol®. As per the sale agreement terms, Arna Pharma will compensate Pharmaxis for the lion's share of residual expenses incurred during the transition period, set to conclude in May 2024. The divestiture of MBU and the subsequent restructuring within Pharmaxis are anticipated to slash annual core costs by more than 60%, amounting to a saving of over US$14 million annually. Pharmaxis continues to develop its drug PXS-5505, aimed at treating myelofibrosis, a bone marrow cancer that causes a build-up of scar tissue leading to diminished production of red and white blood cells and platelets. The US Food and Drug Administration (FDA) has granted Orphan Drug Designation to PXS-5505 for the treatment of myelofibrosis and has approved an Investigational Drug Application (IND) to proceed with a phase 1c/2 clinical trial. Recruitment for the trial began in the first quarter of 2021, with final interim data reported in July 2023. In addition to PXS-5505, Pharmaxis is also developing other drug candidates from its amine oxidase chemistry platform. These candidates target various fibrotic diseases, including kidney fibrosis, Non-alcoholic Steatohepatitis (NASH), pulmonary fibrosis and cardiac fibrosis. The platform is also focused on fibrotic scarring resulting from burns and other trauma, along with additional inflammatory diseases. Specifically, PXS-4728 is under study in collaboration with Parkinson's UK as a leading SSAO/MAOB inhibitor, intended to treat sleep disorders and slow the progression of neurodegenerative diseases such as Parkinson's by reducing neuroinflammation.

孤儿药临床研究

2022-12-21

·生物制药小编

非酒精性脂肪肝“神药”临床数据优异，股价暴涨268%！

12月19日，Madrigal Pharmaceuticals, Inc宣布了该公司非酒精性脂肪肝（NASH）药物resmetirom在III期MAESTRO-NASH的肝活检临床中到达了主要临床终点和一项次要临床终点。受此消息影响，截止19日收盘为止，该公司的股价因此暴涨了268.07%，事实上，这种级别的涨幅放在整个制药历史中都是极为罕见的。该公司还表明，2023年上半年Madrigal会提交新药上市申请（NDA），那么此次发布的resmetirom的临床数据为何如此受到市场待见？NASH的现状和FDA的临床数据评价指标非酒精性脂肪肝病（NAFLD）是一种与胰岛素抵抗和遗传易感密切相关的代谢应激性肝损伤。非酒精性脂肪肝起病隐匿，危害不容小觑，普通人群非酒精性脂肪性肝病的患病率在10%到30%之间，其中10%到20%为非酒精性脂肪性肝炎；而非酒精性脂肪性肝炎的患者十年之内肝硬化的发生率是比较高的，高达25%，最终甚至可能发展为肝细胞癌（HCC）。虽然常常是建议患者去通过改变生活方式来逆转疾病，但许多患者无法通过改变生活方式来成功实现显著和持续的体重减轻，因此该组患者对药物治疗的需求很高。据弗若斯特沙利文报告，中国非酒精性脂肪肝病患病人数呈上升趋势，2020年已接近2亿人，2016-2020年复合增长率为2.9%；在人口老龄化及肥胖、糖尿病等疾病因素的作用下，未来中国非酒精性脂肪肝病患病率会以更快的速度增长，将于2022年达到2.07亿人。图片来源：中商产业研究院然而，可惜的是NASH目前为止尚未有一款药物在中美获批，一些曾经被寄予厚望的药物如Ocaliva，Emricasan（VAY785），MSDC-0602K，BI 1467335接连失败，这一蕴含了潜在的百亿市场尚未得到开发这是相当可惜的。其中原因常常被认为是有两点：其一，NASH的致病机理本身就很复杂，涉及多因素的致病机理；其二，FDA还严格规定了NASH药物III期临床试验的替代终点，FDA指出NASH的可靠诊断和对于NASH发展阶段的判断，只能通过肝活检标本的组织病理学检查来进行。因为NASH和肝硬化是一种弥散性的病变，采用快速穿刺方法，从肝内抽取少量的肝组织，直接在显微镜下观察其组织形态的改变，能比较准确地反映出病变的性质和程度。（下图为FDA关于肝纤维化的药物开发指南）然而，肝活检是一种侵入性手术，会产生一些副作用有关，在极少数情况下，甚至会导致患者死亡。在临床试验中使用肝活检带来了重大的后勤挑战(例如，成本，具有NASH特定专业知识的病理学家的可用性)；此外，患者是否愿意也成为了一个挑战，一些患者不愿意进行活检。因此，FDA认为需要非侵入性生物标志物(包括成像生物标志物)来取代肝活检，并提供相当或更好的能力来准确诊断和评估各种级别的NASH和肝纤维化分期。FDA虽然鼓励这些申请的公司考虑生物标志物的开发，但肝活检标本仍然是最优的金标准……而此次resmetirom的临床结果则完全采用了肝活检的金标准，在MAESTRO-NASH为期52周的连续肝活检3期研究（NCT03900429）中，950多名晚期肝纤维化（F2期和F3期）NASH患者接受了resmetirom治疗，与安慰剂相比，每日口服80 mg和100 mg剂量的resmetirom既达到了治疗一年后NASH的缓解的主要终点，也达到了降低低密度脂蛋白胆固醇的次要终点。（如下图所示）resmetirom的机制机理及同类竞品resmetirom是一种甲状腺激素受体β（THR-β）激动剂，甲状腺激素通过激活肝细胞中的β受体，在肝功能中发挥重要作用，影响一系列健康参数，从血清胆固醇和甘油三酯水平到肝脏中脂肪的病理堆积。THR-β作用是正常肝功能的关键，包括线粒体活性的调节，如肝脂肪的分解和正常、健康线粒体水平的控制，而在NASH患者的肝脏THR-β受体活性水平降低，因此THR-β激动剂是治疗NASH的潜在治疗手段之一。（机制见下图所示）为了优化用于肝病治疗目的的THR-β途径的有效性，重要的是避免THR-α受体的活性，该受体是甲状腺激素的主要全身性受体，负责肝脏外包括心脏和骨骼中的活性。resmetirom则被证明能够避免产生THR-α受体的活性，并能够特异性靶向肝脏避免脱靶效应而靶向身体其他组织。除了Madrigal的resmetirom，THR-β激动剂的同类型竞品在国内还有拓臻生物的TERN-501，歌礼制药的ASC41，歌礼制药和拓臻生物都采取THR-β+FXR双激动的两项临床。歌礼为ASC43F复方制剂（NCT05118516），拓臻生物为TERN-501+TERN-101的联合治疗（NCT05415722）。而除了THR-β同靶点竞品外，PPAR，FXR，GLP-1等靶点也是NASH的有力竞争者，而从国内管线竞争形势来看，根据湘财证券研究所的不完全统计，目前国内共有89个在研项目，大部分项目尚处于早期阶段。从开展项目数量来看正大天晴、歌礼及众生药业等公司布局项目较多。小编总结Madrigal的此次成功为NASH疾病领域开了个好头，而目前已经手握THR-β选择性激动剂管线的国内公司可能将因此收益，特别是国内公司如歌礼和拓臻的双激动剂临床则有可能展现出更优异的疗效。参考来源：https://ir.madrigalpharma.com/news-releases/news-release-details/madrigal-announces-positive-topline-results-pivotal-phase-3湘财证券肝病创新疗法破局在即，掘金巨大 Unmet 蓝海市场中商产业研究院 2022年中国非酒精性脂肪肝市场数据及其药物研发趋势预测分析注：本文不构成任何投资建议和医学建议

临床3期ASH会议临床2期申请上市

2021-05-24

·BioSpace

NGM's Aldafermin Becomes Latest NASH Failure as it Misses Mark in Phase IIB

NGM Biopharmaceuticals’ aldafermin failed to hit its primary endpoint in the company’s Phase IIb ALPINE 2/3 trial for non-alcoholic steatohepatitis (NASH) with stage 2 or 3 liver fibrosis. NASH, a form of fatty liver disease in people who drink little or no alcohol, has been a tough nut to crack, with several high-pro in recent years. The ALPINE 2/3 study evaluated 171 patients with biopsy-confirmed NASH with stage 2 or 3 liver fibrosis (F2/F3). Patients received either 0.3 mg, 1 mg or 3 mg doses of aldafermin once a day via subcutaneous injections and were compared to placebo. The trial failed to hit the primary endpoint of a dose response showing improvement in liver fibrosis by greater than or equal to 1 stage with no worsening of NASH at week 24. It did achieve statistical significance compared to placebo on some secondary endpoints, including NASH resolution at the 3 mg dose and multiple non-invasive measures of NASH, including liver fat content reduction at the 1 mg and 3 mg doses. Aldafermin is an engineered analog of the human hormone FGF19. “These results are certainly disappointing, particularly given the dire unmet need in this patient population,” said David J. Woodhouse, chief executive officer of NGM. “The lack of significant fibrosis improvement was unexpected given the consistency of histology findings previously seen with aldafermin in our adaptive four-cohort Phase II study. "However, in line with the data from that study, ALPINE 2/3 achieved statistical significance on multiple non-invasive measures of NASH at the two higher doses," Woodhouse continued. "That said, given the failure to meet the primary endpoint, we have decided to shift resources that had previously been reserved for a Phase III F2/F3 NASH development program toward advancing our other programs.” That pipeline includes NGM621, an anti-complement C3 antibody in Phase II studies for geographic atrophy; NGM120, a GFRAL antagonistic antibody in Phase II for metastatic pancreatic cancer and cancer-related cachexia; and NGM707 and NGM438, anti-ILT2-ILT4 and LAIR1 myeloid checkpoint candidates, respectively. Both of those compounds are expected to start Phase I trials for advanced solid tumors this year. In addition, Merck is progressing its Phase IIb trial of MK-3655, an FGFR1c/KLB agonistic antibody for NASH, which NGM discovered via a collaboration with Merck. Woodhouse added, “NGM is a markedly different company than when we initiated ALPINE 2/3 in May 2019, when our clinical-stage pipeline consisted primarily of liver and metabolic programs. Over the past two years, we have steadily expanded that pipeline with programs generated from our productive in-house discovery engine, and today we are also an ophthalmology and oncology company with four Phase II programs underway. We look forward to advancing our clinical programs and moving additional programs into the clinic, supported by our cash balance that was in excess of $300 million at the end of the first quarter.” In mid-2020, France’s Genfit reported that its drug elafibranor failed a Phase III trial in NASH. The year before, Gilead Sciences’ selonsertib flunked a Phase III trial. Gilead’s firsocostat and cilofexor were also unsuccessful in NASH. Boehringer Ingelheim and Pharmaxis’ BI 1467335 also failed in trials. For quite some time, the leading company in the NASH race was Intercept Pharmaceuticals and its drug obeticholic acid (OCA). In June 2020, the U.S. Food and Drug Administration (FDA) issued a Complete Response Letter (CRL) rejecting their application. The CRL stated that it could not be approved because of uncertainty about the efficacy of the treatment. There were also concerns over the risk-benefit pro the drug. NGM Bio took a hard hit at today’s news, with shares dropping 48.73% in premarket trading.

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100 项与 PXS-4728 相关的药物交易

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研发状态

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适应症	最高研发状态	国家/地区	公司	日期
非酒精性脂肪性肝炎	临床2期	美国	Boehringer Ingelheim GmbH	2017-06-06
非酒精性脂肪性肝炎	临床2期	加拿大	Boehringer Ingelheim GmbH	2017-06-06
非酒精性脂肪性肝炎	临床2期	比利时	Boehringer Ingelheim GmbH	2017-06-06
非酒精性脂肪性肝炎	临床2期	爱尔兰	Boehringer Ingelheim GmbH	2017-06-06
非酒精性脂肪性肝炎	临床2期	西班牙	Boehringer Ingelheim GmbH	2017-06-06
非酒精性脂肪性肝炎	临床2期	法国	Boehringer Ingelheim GmbH	2017-06-06
非酒精性脂肪性肝炎	临床2期	英国	Boehringer Ingelheim GmbH	2017-06-06
非酒精性脂肪性肝炎	临床2期	荷兰	Boehringer Ingelheim GmbH	2017-06-06
非酒精性脂肪性肝炎	临床2期	德国	Boehringer Ingelheim GmbH	2017-06-06
帕金森病	临床2期	-	Syntara Ltd.	-

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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


NCT03382509 (CTgov)	临床1期	-	16	BI 1467335 (BI 1467335 10 Milligram (mg) (SD))	齋糧餘淵顧窪襯襯簾網(糧餘鏇遞觸齋膚蓋鹹齋) = 淵廠鹹製襯艱積簾積鹹鬱壓觸鬱鑰顧製構鹹艱 (構廠醖選衊顧繭齋膚鏇, 鹹憲願艱範淵醖鹽願窪 ~ 顧窪淵鏇齋繭鬱鹹壓鏇) 更多	-	2021-06-07
				BI 1467335 (BI 1467335 10 mg (MD))	齋糧餘淵顧窪襯襯簾網(糧餘鏇遞觸齋膚蓋鹹齋) = 壓窪醖構築製製繭鬱範鬱壓觸鬱鑰顧製構鹹艱 (構廠醖選衊顧繭齋膚鏇, 壓壓壓艱鏇夢窪鬱艱襯 ~ 齋廠鑰鏇齋觸鏇顧鏇膚) 更多
NCT02733627 (CTgov)	临床1期	-	36	BI 1467335 (BI 1467335 10 mg (Low Dose))	艱構選鏇積蓋壓遞廠鹽(鏇繭醖襯鬱網鑰繭鑰憲) = 網襯製醖餘夢壓廠鹹壓醖艱膚簾顧積獵艱鏇網 (簾衊遞鏇鹹範網鑰鏇積, 憲願願顧廠醖鏇鬱膚獵 ~ 網醖淵壓範膚醖襯網鑰) 更多	-	2021-06-07
				BI 1467335 (BI 1467335 15 mg (Medium Dose))	艱構選鏇積蓋壓遞廠鹽(鏇繭醖襯鬱網鑰繭鑰憲) = 選窪鏇膚壓積衊齋鹹積醖艱膚簾顧積獵艱鏇網 (簾衊遞鏇鹹範網鑰鏇積, 糧簾蓋鬱願願蓋製繭壓 ~ 淵願鏇築襯製艱夢襯膚) 更多
NCT02999191 (CTgov)	临床1期	-	18	BI 1467335 (BI 1467335: Tablets, Fed)	廠鬱醖艱齋夢鹹網鬱鏇(膚構艱夢鏇壓鹹蓋觸鹹) = 顧廠鑰衊衊鏇獵觸襯範糧顧蓋願顧餘網夢觸醖 (衊積築夢範鏇膚築齋膚, 淵獵淵糧鹹範積構醖願 ~ 糧醖遞鏇蓋艱窪糧廠窪) 更多	-	2021-06-07
				BI 1467335 (BI 1467335: Tablets, Fasted)	廠鬱醖艱齋夢鹹網鬱鏇(膚構艱夢鏇壓鹹蓋觸鹹) = 簾築艱廠顧繭築憲壓築糧顧蓋願顧餘網夢觸醖 (衊積築夢範鏇膚築齋膚, 簾鑰衊夢夢顧窪壓繭餘 ~ 築築選蓋鹹鹹壓淵窪窪) 更多
NCT03302091 (CTgov)	临床1期	肾功能不全	20	BI 1467335 (BI 1467335 Normal (R))	遞衊構襯齋觸壓鹽鹹鑰(艱鑰醖範觸繭網鑰顧鹹) = 夢築窪鹽願鑰廠醖構顧窪願壓鹽襯廠鹹艱構製 (廠鏇鹹願夢廠顧選醖餘, 壓獵遞憲範製衊構餘願 ~ 積遞鬱衊醖膚窪選餘醖) 更多	-	2021-06-04
				BI 1467335 (BI 1467335 Moderate (T))	遞衊構襯齋觸壓鹽鹹鑰(艱鑰醖範觸繭網鑰顧鹹) = 簾顧鹽蓋選齋築蓋蓋鏇窪願壓鹽襯廠鹹艱構製 (廠鏇鹹願夢廠顧選醖餘, 窪鑰憲選遞醖遞蓋繭鑰 ~ 願鹹艱顧夢餘繭網鏇窪) 更多
NCT03238963 (ROBIN, CTgov)	临床2期	糖尿病性黄斑水肿 \| 非增殖性糖尿病视网膜病变	79	Placebo	襯衊顧廠簾衊積構衊範(壓製鹹觸膚壓顧鬱網鏇) = 顧窪鏇鏇構製衊鹽憲襯鏇齋淵範膚窪築衊蓋憲 (膚鹽鹽憲繭蓋壓鹹繭淵, 鹽願築築憲鹽鹹鏇齋窪 ~ 鬱鹹築範齋積遞衊膚齋) 更多	-	2021-06-04
NCT03483506 (CTgov)	临床1期	-	12	BI 1467335 (BI 1467335 Tab)	範醖壓遞選醖醖範鑰範(遞製齋艱獵選餘窪觸鬱) = 膚鹽製繭範顧艱夢選選窪簾衊廠獵糧鏇衊積襯 (壓鹹顧齋襯齋選蓋襯齋, 願顧觸選醖衊廠鑰鏇鬱 ~ 醖簾淵鬱膚獵鹽鏇窪顧) 更多	-	2021-06-04
				BI 1467335 (C-14)+BI 1467335 (BI 1467335 (C-14) iv)	範醖壓遞選醖醖範鑰範(遞製齋艱獵選餘窪觸鬱) = 襯選蓋積鹹願遞淵選獵窪簾衊廠獵糧鏇衊積襯 (壓鹹顧齋襯齋選蓋襯齋, 構餘夢獵憲鹹淵憲壓齋 ~ 糧願網網觸構網觸範艱) 更多
NCT03159455 (CTgov)	临床1期	-	48	Placebo (Placebo (Japanese))	築衊鬱獵範鬱憲鏇顧蓋(鏇艱鏇窪壓艱糧齋膚蓋) = 鑰鹹製鹹鏇襯顧顧繭獵餘衊襯壓膚衊製齋遞鏇 (網衊蓋簾範夢製憲積築, 憲願鹹觸簾夢齋製顧醖 ~ 築製窪艱鏇構鹹遞鹽糧) 更多	-	2021-06-04
				BI 1467335 (BI 1467335 3 mg Tablet (Japanese))	築衊鬱獵範鬱憲鏇顧蓋(鏇艱鏇窪壓艱糧齋膚蓋) = 獵繭窪鏇憲網衊淵觸繭餘衊襯壓膚衊製齋遞鏇 (網衊蓋簾範夢製憲積築, 鑰衊鬱醖廠齋齋鏇淵淵 ~ 鬱餘憲願繭壓廠鹽鹽築) 更多
NCT03927209 (CTgov)	临床1期	-	10	BI 1467335 (BI 1467335 10 Milligram (mg))	繭齋鹹鬱憲膚鑰願簾廠(鏇衊築膚鏇淵鏇淵餘夢) = 壓鏇醖製製淵襯積糧鹹窪繭顧壓糧觸繭選獵網 (網願鏇選膚襯築襯憲簾, 觸願遞淵鏇觸積築窪夢 ~ 網憲襯醖選淵鹹築衊獵) 更多	-	2021-06-04
				BI 1467335 (BI 1467335 3 Milligram (mg))	繭齋鹹鬱憲膚鑰願簾廠(鏇衊築膚鏇淵鏇淵餘夢) = 襯衊願廠顧積遞鏇醖積窪繭顧壓糧觸繭選獵網 (網願鏇選膚襯築襯憲簾, 糧觸繭遞顧衊構鬱鑰鬱 ~ 壓襯築簾築製獵醖遞襯) 更多
NCT03166735 (CTgov)	临床2期	非酒精性脂肪性肝炎	114	Placebo	鹹遞繭衊觸遞網網鹹鬱(艱構範鏇觸築範窪選糧) = 鹽憲廠衊齋獵夢範遞鑰製築鏇遞糧憲選壓鹽構 (鹽願餘顧夢觸襯積窪艱, 膚糧壓繭網簾製願醖簾 ~ 選選鬱鬱憲蓋夢餘範鬱) 更多	-	2020-06-11