Evaluation of the Efficacy, Safety and Tolerability of Alisporivir for the Treatment of Hospitalised Patients With Infections Due to SARS-CoV-2 (COVID-19). A Randomised, Open-label, Proof of Concept, Phase 2 Study

COVID-19 is a viral respiratory and systemic disease that has been rapidly spreading globally since the first cases were reported in December 2019 and has now become pandemic. The causative agent of COVID-19 was identified as a novel coronavirus named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2, first designated as 2019-nCoV).
The disease manifestations of COVID-19 can range from mild, self-resolving respiratory disease to severe pneumonia, ARDS, multiorgan failure, and ultimately death. In early reports, the mortality rate among patients admitted to hospital and with confirmed SARS-CoV-2 infection was reported to be between 4 and 15%. Although the disease can afflict all age groups, elderly patients and patients with underlying comorbidities such as high body mass index, hypertension, diabetes, cardiovascular disease, or cerebrovascular disease are at risk of developing severe disease and dying.
There are currently no etiologic treatments for COVID-19, and efforts are underway to identify therapeutics that could be effective in controlling this disease.

开始日期2021-01-08

申办/合作机构

Assistance Publique des Hôpitaux de Paris SA

[+1]

EUCTR2020-002295-13-FR / Unknown status临床2期

Evaluation of the efficacy, safety and tolerability of alisporivir for the treatment of hospitalised patients with infections due to SARS-CoV-2 (COVID-19). A randomised, open-label, proof of concept, Phase 2 study. - CYCLOVID

开始日期2020-10-15

申办/合作机构

Assistance Publique des Hôpitaux de Paris SA

NCT02173574 / Completed临床1期

An Open-label, Two Part Investigation of the Pharmacokinetics, Safety, and Tolerability of Alisporivir and EDP239 When Co-administered to Healthy Adult Subjects

The purpose of Part 1 is to inform dose selection for use of alisporivir and EDP239 in combination and obtain initial safety data for co-administration of alisporivir and EDP239 to support future treatment studies in patients. The purpose of Part 2 is to inform the drug-drug interaction potential of EDP239 more broadly and possibly facilitate the interpretation of lower than expected alisporivir concentrations in Part 1, if observed.

开始日期2014-08-01

申办/合作机构

Enanta Pharmaceuticals, Inc.

100 项与阿拉泊韦相关的临床结果

登录后查看更多信息

100 项与阿拉泊韦相关的转化医学

登录后查看更多信息

100 项与阿拉泊韦相关的专利（医药）

登录后查看更多信息

项与阿拉泊韦相关的文献（医药）

2023-11-01·JHEP reports : innovation in hepatology

The novel cyclophilin inhibitor C105SR reduces hepatic ischaemia–reperfusion injury via mitoprotection

Article

作者: Ahnou, Nazim ; Guichou, Jean-François ; Pawlotsky, Jean-Michel ; Teixeira-Clerc, Fatima ; Morin, Didier ; Pressiat, Claire ; Hulin, Anne ; Ghaleh, Bijan ; Ahmed-Belkacem, Abdelhakim ; Kheyar, Amel

Background & Aims:

Mitochondrial permeability transition pore (mPTP) opening is critical for mediating cell death during hepatic ischaemia-reperfusion injury (IRI). Blocking mPTP opening by inhibiting cyclophilin D (CypD) is a promising pharmacological approach for the treatment of IRI. Here, we show that diastereoisomers of a new class of small-molecule cyclophilin inhibitors (SMCypIs) have properties that make them attractive candidates for the development of therapeutic agents against liver IRI.

Methods:

Derivatives of the parent SMCypI were synthesised and evaluated for their ability to inhibit CypD peptidyl-prolyl cis-trans isomerase (PPIase) activity and for their mitoprotective properties, evaluated by measuring mitochondrial swelling and calcium retention capacity in liver mitochondria. The ability of the selected compounds to inhibit mPTP opening was evaluated in cells subjected to hypoxia/reoxygenation using a calcein/cobalt assay. Their ability to inhibit cell death was evaluated in cells subjected to hypoxia/reoxygenation by measuring lactate dehydrogenase (LDH) release, propidium iodide staining, and cell viability. The compound performing best in vitro was selected for in vivo efficacy evaluation in a mouse model of hepatic IRI.

Results:

The two compounds that showed the strongest inhibition of CypD PPIase activity and mPTP opening, C105 and C110, were selected. Their SR diastereoisomers carried the activity of the racemic mixture and exhibited mitoprotective properties superior to those of the known macrocyclic cyclophilin inhibitors cyclosporin A and alisporivir. C105SR was more potent than C110SR in inhibiting mPTP opening and prevented cell death in a model of hypoxia/reoxygenation. Finally, C105SR substantially protected against hepatic IRI in vivo by reducing hepatocyte necrosis and apoptosis.

Conclusions:

We identified a novel cyclophilin inhibitor with strong mitoprotective properties both in vitro and in vivo that represents a promising candidate for cellular protection in hepatic IRI.

Impact and Implications:

Hepatic ischaemia-reperfusion injury (IRI) is one of the main causes of morbidity and mortality during or after liver surgery. However, no effective therapies are available to prevent or treat this devastating syndrome. An attractive strategy to prevent hepatic IRI aims at reducing cell death by targeting mitochondrial permeability transition pore opening, a phenomenon regulated by cyclophilin D. Here, we identified a new small-molecule cyclophilin inhibitor, and demonstrated the enhanced mitoprotective and hepatoprotective properties of one of its diastereoisomers both in vitro and in vivo, making it an attractive lead compound for subsequent clinical development.

2023-08-01·Nature1区 · 综合性期刊

TRIM5α restricts poxviruses and is antagonized by CypA and the viral protein C6.

1区 · 综合性期刊

Article

作者: Richardson, Samuel ; Smith, Geoffrey L ; Lu, Yongxu ; Zhao, Yiqi ; Albarnaz, Jonas D ; Sreekumar, Meghna

Human tripartite motif protein 5α (TRIM5α) is a well-characterized restriction factor for some RNA viruses, including HIV^1-5; however, reports are limited for DNA viruses^6,7. Here we demonstrate that TRIM5α also restricts orthopoxviruses and, via its SPRY domain, binds to the orthopoxvirus capsid protein L3 to diminish virus replication and activate innate immunity. In response, several orthopoxviruses, including vaccinia, rabbitpox, cowpox, monkeypox, camelpox and variola viruses, deploy countermeasures. First, the protein C6 binds to TRIM5 via the RING domain to induce its proteasome-dependent degradation. Second, cyclophilin A (CypA) is recruited via interaction with the capsid protein L3 to virus factories and virions to antagonize TRIM5α; this interaction is prevented by cyclosporine A (CsA) and the non-immunosuppressive derivatives alisporivir and NIM811. Both the proviral effect of CypA and the antiviral effect of CsA are dependent on TRIM5α. CsA, alisporivir and NIM811 have antiviral activity against orthopoxviruses, and because these drugs target a cellular protein, CypA, the emergence of viral drug resistance is difficult. These results warrant testing of CsA derivatives against orthopoxviruses, including monkeypox and variola.

2022-12-20·Antimicrobial agents and chemotherapy

Targeting Artemisinin-Resistant Malaria by Repurposing the Anti-Hepatitis C Virus Drug Alisporivir

Article

作者: Kaushik, Shikha ; Das, Gobardhan ; Chaurasiya, Ayushi ; Joshi, Nishant ; Garg, Swati ; Kumari, Jyoti ; Kumari, Geeta ; Ranganathan, Anand ; Anam, Zille ; Saini, Savita ; Marothia, Manisha ; Gupta, Kanika ; Singh, Shailja ; Bhattacharjee, Souvik ; Maurya, Mukesh Kumar ; Joshi, Prerna ; Singh, Niharika ; Dubey, Neha ; Shoaib, Rumaisha ; Singhal, Jhalak ; Srivastava, Pallavi ; Kahlon, Amandeep Kaur

The emergence of Plasmodium falciparum resistance raises an urgent need to find new antimalarial drugs. Here, we report the rational repurposing of the anti-hepatitis C virus drug, alisporivir, a nonimmunosuppressive analog of cyclosporin A, against artemisinin-resistant strains of P. falciparum . In silico docking studies and molecular dynamic simulation predicted strong interaction of alisporivir with Pf Cyclophilin 19B, confirmed through biophysical assays with a K d value of 354.3 nM.

项与阿拉泊韦相关的新闻（医药）

2023-08-10

·生物谷

Nature：老药新用抗猴痘，作用更持久，且不易导致耐药性

该研究揭示了细胞蛋白TRIM5α能够抑制包括猴痘病毒（MPXV）在内的多种正痘病毒，而亲环蛋白A （CypA）和病毒蛋白C6则会拮抗TRIM5α。更重要的是，该研究进一步证实了现有的靶向亲环蛋白A 近日，中国疾控中心发布的数据显示，2023年7月份，中国内地（不含港澳台）新增报告491例猴痘确诊病例，这491人均为男性。此前世界卫生组织（WHO）发布的数据显示，几乎全部（98%以上）猴痘确诊病例为男同性恋者。猴痘（monkeypox），是一种人畜共患病，1958年首次在用于研究的猴子中发现，主要在动物中传播。1970年首次在刚果（金）发现人类猴痘病例，此后猴痘一直在非洲的一些国家流行，包括尼日利亚、刚果（金）和中非共和国等。非洲以外地区的猴痘病例通常是因为去非洲旅游所感染。而在2022年上半年，猴痘开始在欧洲和北美地区传播，2022年7月23日，世界卫生组织（WHO）总干事谭德赛宣布，猴痘疫情为“国际关注的突发公共卫生事件”（PHEIC）。天花作为一种疾病，早在1979年就已经被根除，但导致天花的天花病毒，仍然被保存在两个高度安全的实验室里——一个在美国，一个在俄罗斯。天花病毒被用于生物恐怖袭击的威胁导致了一种名为特考韦瑞（Tecovirimat）的药物被批准用于治疗天花，这是一种广谱包膜蛋白抑制剂，对正痘类病毒表现出良好的抗病毒活性。在过去一年里，特考韦瑞被用于治疗严重的猴痘患者，但这也导致了猴痘病毒多种耐药株的出现。因此，急需开发新的猴痘治疗药物。 2023年8月9日，剑桥大学和牛津大学的 Geoffrey Smith 教授团队（赵奕祺博士、陆泳旭博士为共同第一作者）在国际顶尖学术期刊 Nature 上发表了题为：TRIM5α restricts poxviruses and is antagonized by CypA and the viral protein C6 的研究论文。该研究揭示了细胞蛋白TRIM5α能够抑制包括猴痘病毒（MPXV）在内的多种正痘病毒，而亲环蛋白A （CypA）和病毒蛋白C6则会拮抗TRIM5α。更重要的是，该研究进一步证实了现有的靶向亲环蛋白A （CypA）的药物能够有效抑制包括猴痘病毒和天花病毒在内的多种正痘病毒的感染和复制，此外，由于这些药物不直接作用于病毒，这意味着病毒也将更难以进化出耐药性。论文共同通讯作者、剑桥大学 Geoffrey Smith 教授表示，该研究确定的药物比目前用来治疗猴痘的药物作用更持久，预计它也会对一系列其他痘病毒有效，包括天花病毒。痘苗病毒（VACV）是用于根除天花的活疫苗，目前正被用于对猴痘高危人群（男同性恋者）进行免疫接种。痘苗病毒（VACV）、牛痘病毒（CPXV）、猴痘病毒（MPXV）、骆驼痘病毒（CMLV）和天花病毒（VARV）都是正痘病毒，具有免疫交叉保护作用。在根除天花之后，人们还在继续研究痘苗病毒（VACV），将其作为疫苗开发平台。一旦痘病毒感染宿主细胞，这些病毒必须保护自己免受宿主细胞蛋白的攻击，这些细胞蛋白会限制病毒的复制和传播。这项研究开始于一个简单的观察发现——痘苗病毒（VACV）感染会导致人类细胞中TRIM5α水平降低。为了找出背后的原因，研究团队使用CRISPR-Cas9基因编辑技术构建了敲除TRIM5的人类细胞，然后分别过表达TRIM5α、TRIM5γ或TRIM5δ，证实了TRIM5α具有抗病毒活性，TRIM5α通过其SPRY结构域与正痘病毒衣壳蛋白L3结合，减少病毒复制并激活先天免疫。该研究还发现，包括痘苗病毒、兔痘病毒、牛痘病毒、猴痘病毒、骆驼痘病毒和天花病毒在内的几种正痘病毒对TRIM5α的攻击产生了两种防御措施——首先，病毒产生了C6蛋白通过RING结构域与TRIM5结合，诱导其蛋白酶体依赖性降解；其次，亲环蛋白A （CypA）通过与病毒衣壳蛋白L3相互作用被招募到病毒工厂和病毒颗粒中，以拮抗TRIM5α。现在已经有许多以亲环蛋白A（CypA）为靶点的药物，例如CsA，以及CsA的非免疫抑制衍生物Alisporivir和NIM811，实验结果显示，这些药物能够良好的抑制包括猴痘病毒在内的一系列正痘病毒的感染和复制。 CsA是一种已被FDA批准上市免疫抑制剂，用于器官移植、自身免疫疾病的治疗，还具有抗HIV作用，但其存在比较严重的肝肾毒性等副作用。而Alisporivir和NIM811是两款无免疫抑制活性的CsA衍生物，目前至少已进行了2期临床试验。由于这些药物是作用于人体的亲环蛋白A（CypA），而非作用于病毒本身，因此很难导致病毒耐药性的出现。这些结果为使用CsA衍生物对抗正痘病毒（包括猴痘病毒和天花病毒）的试验提供了依据。 Geoffrey Smith 教授表示，这项研究结果完全出乎意料，一开始进行这项研究是为了了解痘病毒是如何逃避宿主防御的，完全没想到这可能会发现治疗猴痘病毒和其它正痘病毒的药物。

疫苗临床研究诊断试剂

2021-06-17

·学术经纬

前沿 - 无关β淀粉样蛋白！科学家们找到了阿尔茨海默病治疗新方向

▎药明康德内容团队编辑日前，《自然》子刊Nature Aging发表了一篇关于阿尔茨海默病的重要论文。研究人员们针对阿尔茨海默病的最大风险基因，探明了其在小鼠中的作用机理，并有望带来全新的治疗方法。值得一提的是，这个潜在疗法与流行理论中的β淀粉样蛋白无关，可谓拓展了全新的道路！众所周知，APOE4等位基因是阿尔茨海默病最大的遗传风险因素。相比携带两条APOE3等位基因的低风险人群，如果普通人携带一条APOE4基因，就能将阿尔茨海默病风险提高4倍。倘若携带两条APOE4基因，风险更是要猛增15倍！ APOE4基因究竟有何能耐，可以对阿尔茨海默病造成如何巨大的影响呢？去年4月，南加州大学Berislav Zlokovic教授团队在《自然》杂志发文，揭开了背后的奥秘：原来这个基因能让大脑的毛细血管周细胞（capillary pericytes）发生退行性病变，加速血脑屏障的破坏。 ▲去年4月的一项研究奠定了本文的基础（图片来源：《自然》官网截图）这让血液里的有毒物质更容易进入大脑，损害脑细胞，从而影响认知功能。而且无论患者有没有出现β淀粉样蛋白，都会出现记忆上的问题。基于这些发现，Zlokovic教授团队再接再厉，在这项新研究中进一步探明了APOE4基因破坏周细胞的机理。研究人员们发现，随着周细胞的破坏，阿尔茨海默病患者血管中的“亲环蛋白A”水平会有所上升，而它恰恰是一种促炎症的蛋白。考虑到最近兴起的阿尔茨海默病“炎症假说”，亲环蛋白A也得到了科学家们的特别关注。 ▲在大脑周细胞里激活的亲环蛋白A（上图红色）会激活MMP9（下图红色），影响到毛细血管（蓝色）（图片来源：参考资料[2]；Credit：Angeliki Nikolakopoulou, PhD）在携带APOE4的小鼠模型中，研究人员们指出亲环蛋白A能激活一种叫做“基质金属蛋白酶A 9”（matrix metalloproteinase 9，缩写MMP9）的酶。这种酶会破坏血脑屏障中的血管，从而破坏血脑屏障。有趣的是，在携带APOE3的小鼠中，研究人员们并没有观察到这个现象。这也能够解释为何APOE4才是阿尔茨海默病的遗传风险因子。考虑到亲环蛋白A在周细胞中起到了调控血管完整性的作用，这篇论文的作者们顺理成章地想到，如果能抑制亲环蛋白A，是否就能避免激活MMP9，从而保护血脑屏障的完整性？ ▲亲环蛋白抑制剂能改善APOE4小鼠的病情（图片来源：参考资料[1]）为了测试这个想法，科学家们在携带APOE4的小鼠中使用了一种亲环蛋白A抑制剂，而结果恰如他们预料！在抑制剂的作用下，即便携带APOE4基因，小鼠的血脑屏障完整性也能有所改善。更重要的是，这种抑制剂还能预防神经元的损失，也能预防小鼠行为上出现问题！综合来看，本研究表明针对亲环蛋白A - MMP9通路的药物有望减缓APOE4基因带来的血管异常与神经退行性症状。这个发现如果能在人体中得到重复，影响是巨大的。 “目前为止，晚期阿尔茨海默病患者还几乎没有任何（治疗）希望，这对患者和他们所爱的人来说是很艰难的一件事，”本研究负责人Zlokovic教授点评道，“我们可能将干预方法集中在血脑屏障修复和血管的强度上，而与淀粉样蛋白病理无关。这有望在晚期阿尔茨海默病中放缓、乃至终止神经退行和认知能力的衰退。能研究这一潜在疗法，我们倍感振奋。” ▲本研究的通讯作者Berislav Zlokovic教授（图片来源：南加州大学；Credit：Richard Carrasco）值得一提的是，本研究中使用的亲环蛋白A抑制剂叫做Debio-025（alisporivir），本身是一种丙肝疗法。未来，人们也将评估它在阿尔茨海默病治疗中的全新潜力。本文题图：123RF 参考资料： [1] Montagne, A., Nikolakopoulou, A.M., Huuskonen, M.T. et al. APOE4 accelerates advanced-stage vascular and neurodegenerative disorder in old Alzheimer’s mice via cyclophilin A independently of amyloid-β. Nat Aging 1, 506–520 (2021). https://doi-org.libproxy1.nus.edu.sg/10.1038/s43587-021-00073-z APOE4 [1] Montagne, A., Nikolakopoulou, A.M., Huuskonen, M.T. et al. APOE4 accelerates advanced-stage vascular and neurodegenerative disorder in old Alzheimer’s mice via cyclophilin A independently of amyloid-β. Nat Aging 1, 506–520 (2021). https://doi-org.libproxy1.nus.edu.sg/10.1038/s43587-021-00073-z [2] USC study reveals potential new treatment target for Alzheimer's disease, Retrieved June 14, 2021, from https://www.eurekalert.org/pub_releases/2021-06/ksom-usr061121.php 本文来自药明康德内容微信团队，欢迎转发到朋友圈，谢绝转载到其他平台。如有开设白名单需求，请在“学术经纬”公众号主页回复“转载”获取转载须知。其他合作需求，请联系wuxi_media@wuxiapptec.com。新冠病毒专题癌症突破智慧之光大脑逻辑 | 母爱 | 脑细胞 | 阿兹海默病血检 | 孤独 | 可乐 | 生酮饮食 | 阿尔茨海默病病毒假说 | 大脑抗衰老 | 麦克阿瑟天才奖 | APP蛋白 | 畅游大脑 | 细菌感染假说 | 睡眠与心血管疾病 | 电击提高记忆力 | 明星抗抑郁药 | 重新定义生死 | 脑机接口 | 分子蓝图 | 不睡会死 | 突破血脑屏障 | 清除困意热门前沿

合作

2021-01-18

·BioSpace

Phase II Research Against Covid-19 Launched in France With Debiopharm's Antiviral Alisporivir

LAUSANNE, Switzerland, Jan. 18, 2021 /PRNewswire/ -- Debiopharm ( ), a Swiss biopharmaceutical company, announced today the first patient dosed in an investigator-initiated, randomized phase II, open-label clinical trial for its antiviral alisporivir (Debio 025). The study will be conducted by the AP-HP to assess the efficacy and safety of the cyclophilin inhibitor in the treatment of early stage, hospitalized COVID-19 patients not requiring medical ventilation nor exhibiting signs of acute respiratory distress syndrome. The primary objective of this "proof-of-concept" trial is to evaluate the reduction in COVID-19 viral load in alisporivir treated patients. The secondary objective involves the analysis of clinical & radiological efficacy, safety and tolerability of the compound plus Standard of Care (SOC) compared to SOC alone. Patients in the investigational arm will receive alisporivir either orally or via a nasogastric tube, at the dose of 600mg twice daily for 14 days during the trial led by Prof. Jean-Michel Pawlotsky, virologist, Head of the Biology and Pathology Department of the Henri Mondor Hospital Group, Greater Paris University Hospitals. The trial, supported by both the hospital group and Debiopharm, will be carried out in multiple centers in France including the Henri Mondor Hospital Group. Medical observations have shown that viral infections such as COVID-19 can be life-threatening due to an overreaction of the body's immune defense system. Part of the cyclophilin inhibitor class of antivirals, this macrocyclic cyclophilin inhibitor could prove to be a valuable additional therapy to SOC due to its non-immunosuppressive nature. "New evidence generated by our research group suggests that alisporivir's antiviral activity could work by decreasing the viral load in the cells and reducing the risk of pulmonary damage caused by an excessive immune response from infected patients. The treatment is expected to be most effective in the early stages of infection by inhibiting the virus' capacity to replicate and multiply, potentially due to the drug's capacity to accumulate in the lungs and strong distribution throughout the body overall," explained Prof. Jean-Michel Pawlotsky, Head of the Biology and Pathology Department at the Henri Mondor Hospital Group. "The preliminary evidence provide a scientific rational for this Phase II trial, with hopes that treatment will help patients to avoid advancing to more life-threatening phase of the COVID-19 infection. We are thrilled that this compound will be tested for its ability to fight this pandemic and save lives," expressed Bertrand Ducrey, CEO, Debiopharm. Involved in anti-viral research for over 20 years, Debiopharm has maintained its commitment to fighting cancer and infectious diseases. In addition to its anti-infective alisporivir, the company focuses on developing novel antibiotics to help battle highly-resistant "super-bugs" fueling the growing crisis in antibiotic resistance. Despite the substantial financial responsibility that this COVID-19 trial represents – expected to reach several millions in clinical research and product supply costs - the company has committed to donating all potential commercial revenue to fund research against infectious diseases. If phase II results show the results required to advance to phase III, Debiopharm will seek to partner with a larger global pharmaceutical company or public healthcare organization for rapid patient access. Debiopharm's commitment to patients Debiopharm, awarded the Swiss Biotech Success Story 2020, develops innovative therapies targeting high unmet medical needs in oncology and infectious diseases. Bridging the gap between disruptive discovery products and real-world patient reach, we identify high-potential compounds and technologies for in-licensing, clinically demonstrate their safety and efficacy and then select large pharmaceutical commercialization partners to maximize patient access globally. Visit us Follow us @DebiopharmNews at Debiopharm Contact Dawn Haughton - Communication Manager 289393@email4pr.com Tel: +41 (0)21 321 01 11 1. Softic L et al. Inhibition of SARS-CoV-2 infection by the non-immunosuppressive macrocyclic cyclophilin inhibitor Alisporivir (Debio025); Antimicrob Agents Chemother. 2020 Jul; 64(7): e00876-20.

100 项与阿拉泊韦相关的药物交易

登录后查看更多信息

外链

KEGG	Wiki	ATC	Drug Bank
D10087	阿拉泊韦	-	DB12139

研发状态

10 条进展最快的记录,

后查看更多信息

适应症	最高研发状态	国家/地区	公司	日期
慢性丙型肝炎	临床3期	美国	Debiopharm International SA	2011-12-01
慢性丙型肝炎	临床3期	加拿大	Debiopharm International SA	2011-12-01
慢性丙型肝炎	临床3期	法国	Debiopharm International SA	2011-12-01
慢性丙型肝炎	临床3期	德国	Debiopharm International SA	2011-12-01
慢性丙型肝炎	临床3期	印度	Debiopharm International SA	2011-12-01
慢性丙型肝炎	临床3期	意大利	Debiopharm International SA	2011-12-01
慢性丙型肝炎	临床3期	西班牙	Debiopharm International SA	2011-12-01
慢性丙型肝炎	临床3期	土耳其	Debiopharm International SA	2011-12-01
慢性丙型肝炎	临床3期	英国	Debiopharm International SA	2011-12-01
慢性丙型肝炎基因型 1	临床3期	美国	Debiopharm International SA	2011-03-01

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


NCT02094443 (CTgov)	临床2期	慢性丙型肝炎基因型 3	52	Alisporivir+Ribavirin (Alisporivir 300 mg BID)	壓積廠積衊餘廠製製簾(構襯糧蓋衊網簾鹽艱鹹) = 窪鬱憲鬱衊獵網夢遞廠遞獵簾膚糧餘觸顧願餘 (淵齋鹽窪網蓋遞衊積構, 膚餘網壓壓衊艱網窪積 ~ 範獵窪艱餘膚顧網鹹顧) 更多	-	2016-10-13
				Alisporivir+Ribavirin (Alisporivir 400 mg BID)	壓積廠積衊餘廠製製簾(構襯糧蓋衊網簾鹽艱鹹) = 範憲築簾願淵網獵簾顧遞獵簾膚糧餘觸顧願餘 (淵齋鹽窪網蓋遞衊積構, 繭蓋壓鏇選廠衊簾醖淵 ~ 製積遞範築鏇鑰網範選) 更多
NCT01318694 (CTgov)	临床3期	慢性丙型肝炎基因型 1	1,081	Peginterferon alfa-2a+Alisporivir+Ribavirin (Treatment Arm A)	鏇積繭構構艱構蓋繭鑰(窪醖糧顧糧顧鬱襯獵糧) = 繭範餘製壓選膚艱醖遞齋窪築製網壓鬱網製構 (醖壓壓壓積選夢範艱齋, 鏇齋鏇積築網鹽窪廠淵 ~ 範膚憲齋鏇遞鏇壓壓簾) 更多	-	2016-09-30
				Peginterferon alfa-2a+Alisporivir+Ribavirin (Treatment Arm B)	鏇積繭構構艱構蓋繭鑰(窪醖糧顧糧顧鬱襯獵糧) = 廠夢構觸醖蓋網鏇觸簾齋窪築製網壓鬱網製構 (醖壓壓壓積選夢範艱齋, 鬱夢網艱選築製觸壓顧 ~ 繭廠窪鑰願選鹹繭餘鹽) 更多
NCT02753699 (CTgov)	临床3期	慢性丙型肝炎	723	Alisporivir (From Study 2210)	獵齋獵蓋選繭築膚糧鏇(憲憲選顧鬱簾衊築醖窪) = 簾鏇鹹淵廠遞蓋鏇觸願鏇鹹顧獵鑰鏇襯鏇鑰鏇 (構艱齋醖壓蓋願鹹糧鹹, 膚襯網艱齋鬱淵築繭獵 ~ 糧願積願鏇憲壓築壓鏇) 更多	-	2016-08-26
				Alisporivir (From Study 2301)	獵齋獵蓋選繭築膚糧鏇(憲憲選顧鬱簾衊築醖窪) = 築鬱齋繭繭糧築鏇鏇醖鏇鹹顧獵鑰鏇襯鏇鑰鏇 (構艱齋醖壓蓋願鹹糧鹹, 鏇製積製鹽鹽構積壓鬱 ~ 構遞積衊顧簾積構簾鏇) 更多
NCT01500772 (CTgov)	临床3期	慢性丙型肝炎基因型 1	6	Peginterferon alfa-2a+Alisporivir+Ribavirin	糧蓋鏇膚鑰醖構獵鏇窪(廠網窪艱繭艱遞簾膚餘) = 網選簾窪範鏇製窪鏇築襯觸衊觸餘觸製窪獵淵 (鹹鹹顧範網廠鏇憲繭選, 廠遞獵積鏇壓鹽鏇憲憲 ~ 糧餘衊構夢網鏇積壓積) 更多	-	2016-06-27
NCT00537407 (CTgov)	临床2期	慢性丙型肝炎基因型 1	50	Debio 025+Peg-IFNα2a+Ribavirin (Treatment Arm A)	膚構積構繭廠鏇積網鹹(蓋壓餘鬱憲構齋襯壓醖) = 構顧繭繭鑰糧壓糧壓願簾鹽窪齋選窪艱簾鑰蓋 (壓膚襯鏇醖製獵遞願鏇, 衊顧製獵襯選網鏇膚構 ~ 淵鑰衊蓋淵蓋繭網選範) 更多	-	2015-05-07
				Debio 025+Peg-IFNα2a+Ribavirin (Treatment Arm D)	膚構積構繭廠鏇積網鹹(蓋壓餘鬱憲構齋襯壓醖) = 壓範築範齋憲願願繭齋簾鹽窪齋選窪艱簾鑰蓋 (壓膚襯鏇醖製獵遞願鏇, 衊範鏇顧齋鏇醖遞觸窪 ~ 鹽餘襯艱壓築窪鹹獵齋) 更多