A Multicentre, Open Label, Randomised, Controlled, Basket, Pragmatic, Phase II, Clinical and Translational Study to Determine the Efficacy and Safety of Plitidepsin Versus Control in Immunocompromised Adult Patients With Symptomatic COVID-19 Requiring Hospital Care

The primary objective of this study is to evaluate efficacy of plitidepsin in pre-specified groups of immunocompromised patients with symptomatic COVID-19 requiring hospital care versus control in terms of mortality.

开始日期2023-04-19

申办/合作机构

Pharma Mar SA

EUCTR2022-002489-34-ES / Not yet recruiting临床2期

A Multicentre, Open label, Randomised, Controlled, Basket, Pragmatic, Phase II, Clinical and Translational Study to Determine the Efficacy and Safety of Plitidepsin versus Control in Immunocompromised Adult Patients with Symptomatic COVID-19 requiring Hospital Care (NEREIDA)

开始日期2023-02-09

申办/合作机构

Pharma Mar SA

EUCTR2022-002489-34-PL / Not yet recruiting临床2期

开始日期2023-01-16

申办/合作机构

Pharma Mar SA

100 项与 Plitidepsin 相关的临床结果

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100 项与 Plitidepsin 相关的转化医学

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100 项与 Plitidepsin 相关的专利（医药）

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331

项与 Plitidepsin 相关的文献（医药）

2024-03-01·Journal of Hazardous Materials

A low-cost TICT-based staining agent for identification of microplastics: Theoretical studies and simple, cost-effective smartphone-based fluorescence microscope application

Article

作者: Kim, Cheal ; Lee, Jae Jun ; Kang, Jiyun

A novel staining agent, (5-(4-(diethylamino)benzylidene)- 1,3-dimethylpyrimidine-2,4,6(1 H,3 H,5 H)-trione) (DDB) was developed for the effective detection of environmentally harmful microplastics. DDB has competitive cost advantages, namely its facile synthesis and high yield, over Nile Red (NR), which is commonly used for microplastic staining. The unique photophysical properties of DDB, including emissive twisted intramolecular charge transfer (TICT) and aggregation-induced emission (AIE), were corroborated via spectroscopic investigations and density functional theory (DFT) calculations. Notably, DDB demonstrated superior selectivity for staining microplastics (polyethylene (PE), polyurethane (PU), polypropylene (PP), polyvinyl chloride (PVC), polystyrene (PS), and polyethylene terephthalate (PET)) over non-plastic materials in water. Furthermore, modulation of the solvent environment during the staining process yielded distinct fluorescence in both the green and red channels for specific types of plastic with the interplay between locally excited (LE) and TICT states. Treatment with 5% ethanol results in the selective staining of PE and PET with the emission of red fluorescence, whereas treatment with 30% ethanol facilitates the selective staining of PU, PVC, and PET with the emission of green fluorescence. Additionally, DDB could selectively stain microplastics in spiked soil and river water samples. Furthermore, a smartphone-based fluorescence microscope was developed at a cost below $100, validating the effective detection of microplastics stained with the newly synthesized DDB. The outcomes of this research demonstrate the potential of DDB as an economical and efficient agent for selective microplastic detection.

2024-02-10·British Journal of Cancer

EEF1A2 promotes HIF1A mediated breast cancer angiogenesis in normoxia and participates in a positive feedback loop with HIF1A in hypoxia

Article

作者: Balan, Poornima ; Naik, Monali ; Dixit, Manjusha ; Patel, Saket Awadhesbhai ; Mohapatra, Nachiketa ; Hassan, Md Khurshidul ; Korrapati, Purna Sai

BACKGROUND:

The eukaryotic elongation factor, EEF1A2, has been identified as an oncogene in various solid tumors. Here, we have identified a novel function of EEF1A2 in angiogenesis.

METHODS:

Chick chorioallantoic membrane, tubulogenesis, aortic ring, Matrigel plug, and skin wound healing assays established EEF1A2's role in angiogenesis.

RESULT:

Higher EEF1A2 levels in breast cancer cells enhanced cell growth, movement, blood vessel function, and tubule formation in HUVECs, as confirmed by ex-ovo and in-vivo tests. The overexpression of EEF1A2 could be counteracted by Plitidepsin. Under normoxic conditions, EEF1A2 triggered HIF1A expression via ERK-Myc and mTOR signaling in TNBC and ER/PR positive cells. Hypoxia induced the expression of EEF1A2, leading to a positive feedback loop between EEF1A2 and HIF1A. Luciferase assay and EMSA confirmed HIF1A binding on the EEF1A2 promoter, which induced its transcription. RT-PCR and polysome profiling validated that EEF1A2 affected VEGF transcription and translation positively. This led to increased VEGF release from breast cancer cells, activating ERK and PI3K-AKT signaling in endothelial cells. Breast cancer tissues with elevated EEF1A2 showed higher microvessel density.

CONCLUSION:

EEF1A2 exhibits angiogenic potential in both normoxic and hypoxic conditions, underscoring its dual role in promoting EMT and angiogenesis, rendering it a promising target for cancer therapy.

2024-03-01·Journal of Biological Chemistry

Elongation factor 1A1 regulates metabolic substrate preference in mammalian cells

Article

作者: Hatam Tehrani, Helia ; Cumming, Robert C ; Borrelli, Matthew J ; Twumasi-Ankrah, Jessica S ; Betts, Dean H ; Kozlov, Alexandra M ; Maini, Siddhant ; Wilson, Rachel B ; Sawyez, Cynthia G ; Shepherd, Trevor G ; Borradaile, Nica M ; Chen, Yun Jin

Eukaryotic elongation factor 1A1 (EEF1A1) is canonically involved in protein synthesis but also has noncanonical functions in diverse cellular processes. Previously, we identified EEF1A1 as a mediator of lipotoxicity and demonstrated that chemical inhibition of EEF1A1 activity reduced mouse liver lipid accumulation. These findings suggested a link between EEF1A1 and metabolism. Therefore, we investigated its role in regulating metabolic substrate preference. EEF1A1-deficient Chinese hamster ovary (2E2) cells displayed reduced media lactate accumulation. These effects were also observed with EEF1A1 knockdown in human hepatocyte-like HepG2 cells and in WT Chinese hamster ovary and HepG2 cells treated with selective EEF1A inhibitors, didemnin B, or plitidepsin. Extracellular flux analyses revealed decreased glycolytic ATP production and increased mitochondrial-to-glycolytic ATP production ratio in 2E2 cells, suggesting a more oxidative metabolic phenotype. Correspondingly, fatty acid oxidation was increased in 2E2 cells. Both 2E2 cells and HepG2 cells treated with didemnin B exhibited increased neutral lipid content, which may be required to support elevated oxidative metabolism. RNA-seq revealed a >90-fold downregulation of a rate-limiting glycolytic enzyme, hexokinase 2, which we confirmed through immunoblotting and enzyme activity assays. Pathway enrichment analysis identified downregulations in TNFA signaling via NFKB and MYC targets. Correspondingly, nuclear abundances of RELB and MYC were reduced in 2E2 cells. Thus, EEF1A1 deficiency may perturb glycolysis by limiting NFKB- and MYC-mediated gene expression, leading to decreased hexokinase expression and activity. This is the first evidence of a role for a translation elongation factor, EEF1A1, in regulating metabolic substrate utilization in mammalian cells.

项与 Plitidepsin 相关的新闻（医药）

2023-09-21

·FierceBiotech

Different roads, same destination: Study shows COVID variants evolve to suppress immunity

Now that the researchers have a clear idea of the proteins at play in the virus's evolution, the next step will be to try to develop new treatments that target them from multiple angles. The spike protein on the surface of SARS-CoV-2, the virus that causes COVID-19, has basked in the spotlight since the pandemic began. And for good reason: After all, that spike is what enables it to enter human cells. But despite its notoriety, the protein is just one of several that make SARS-CoV-2 a tricky foe, as scientists from the University of California, San Francisco’s Quantitative Biosciences Institute (QBI), Icahn School of Medicine at Mount Sinai and University College London show in an article published online Sept. 21 in Cell. The findings shed light on how the virus is evolving and support a combination approach that tackles the proteins that help it suppress the immune system, study lead and QBI founder Nevan Krogan, Ph.D., told Fierce Biotech Research. “We’ve figured out how this virus is going to behave as it goes forward, or at least a big part of it,” he said. “And what we need to do, just like we do with HIV, is fight it with a cocktail of therapies.” The new findings build on the 50-plus studies published over the course of the pandemic by the QBI Coronavirus Research Group, a network of scientists founded by Krogan that has been tracking COVID’s evolution and identifying potential therapies since the virus emerged in 2020. Besides a plethora of papers, the collaboration has also led to two clinical trials, including one with Spanish pharma PharmaMar assessing the use of cancer drug plitidepsin as a treatment for immunocompromised patients with COVID. “We now have a deep mechanistic understanding of how this virus works,” Krogan said. That now includes an explanation for the convergent evolution of different strains of the virus—that is, the way it mutates via different mechanisms but seemingly ends with the same result: suppression of the innate immune response. “It’s converging on the same kind of final output, but it’s doing so through different kinds of evolutionary trajectories through different mutations,” Krogan said. “It’s almost like if you try to force it to go one way, it’ll go another way and do what it wants.” To map this out, the researchers took healthy lung cells and cultured sets of them with major strains of the virus, from alpha through omicron BA.1. Then they used various computational tools to examine how protein and gene expression changed between strains as well as how the virus affected genes within the host cells. While the way the virus evolved to outsmart the immune system changed depending on the strain, as expected, there was a common mechanism involving a handful of select proteins. One of them, ORF9b, stood out as being especially complicit in enabling pre-omicron variants of the virus to suppress the innate immune response, the body’s first line of defense against pathogens, and invade cells. Interestingly, the original strain of omicron was less effective than alpha or delta in getting around that defense system, the researchers noted—potential evidence for the theory that it arose from a chronically ill, immunocompromised patient. Future offshoots, including BA.5, made up for that by expressing higher levels of another protein, ORF6, which once again bumped up the virus’s ability to suppress innate immunity. (The researchers went into more detail on ORF6 in a second paper, also published Sept. 18, in Cell Host & Microbe.) Now that the researchers have a clear idea of the proteins at play, the next step will be to try to develop new treatments that target them from multiple angles. Work is ongoing now to develop therapies that would target the SARS-CoV-2 proteins that manipulate the immune response. “Ultimately, these drugs could effectively be used in a ‘cocktail’ with therapies that target viral entry involving the spike protein,” Krogan said in an email. Meanwhile, his COVID research efforts will be helped along by a $200,000 award he received Sept. 20 as the first-ever recipient of Research!America’s Discovery | Innovation | Health prize, sponsored by Pfizer.

临床研究

2023-07-31

·PRNewswire

GLOBAL SARCOMA THERAPY NOW LISTED ON PHARMACEUTICAL BENEFITS SCHEME

YONDELIS® (trabectedin) now PBS listed for Australian patients Listing described as "wonderful news" for patients living with rare lipo and leiomyo sarcomas YONDELISÒ (trabectedin) demonstrates 45% reduction in risk of disease progression or death versus dacarbazine1 SINGAPORE, July 31, 2023 /PRNewswire/ -- AUSTRALIAN cancer patients who have been diagnosed with rare soft tissue sarcomas will now have affordable access to a global therapy shown to improve survival, following its listing on the Pharmaceutical Benefits Scheme (PBS). The therapy YONDELIS (trabectedin) is a novel anti-tumour agent originally derived from the sea squirt and will be available to eligible patients on the PBS from August 1. It is used extensively around the world and has been shown to improve progression-free survival for patients with liposarcoma and leiomyosarcoma when used after anthracycline-based therapy.1 Until today, some patients have paid up to $50,000 to access YONDELIS treatment. News of the PBS listing is being welcomed by oncologists and the Australian sarcoma community, who say it will alleviate cost of treatment pressures for those patients whose disease has progressed. Medical oncologist and Scientific Advisory Committee member and Lead of the ANZSA National Sarcoma Database Dr Susie Bae, said YONDELIS has been available in Europe since 2007 for patients with advanced soft tissue sarcoma, and Australian patients had waited many years for reimbursed access. "This milestone means patients don't need to worry about not being able to afford or miss out on an active drug that can potentially buy precious time with their loved ones, by providing disease control and keeping symptoms at bay for longer," Dr Bae said. Melbourne patient advocate and mother of two Karen Lurati – herself diagnosed with liposarcoma six years ago – said this listing provided new hope for other patients. "A PBS listing for YONDELIS is so exciting for those people who may not have been able to afford the treatment before," she said. "Rare cancers don't often get (Government) funding or attention. To now have this therapy on the PBS is great progress. "Patients often feel that they have to go overseas and spend enormous amounts of money on treatments that may not be available in Australia. This can be frustrating and financially crippling. So, for patients to have access to a global therapy in their own country is wonderful news." And Rare Cancers Australia (RCA) Chief Executive Richard Vines said he was "delighted with this outcome", describing the listing as "great news" for patients living with an L-sarcoma. "For too long, sarcoma patients have been unable to access all therapies which may provide benefit," he said. Today's announcement means they can access a PBS funded medicine instead of having to try and find tens of thousands of dollars – if not more – to self-fund a treatment that may give them more time." YONDELIS is marketed in Australia by independent pharmaceutical company Specialised Therapeutics, under an exclusive license arrangement with international partner PharmaMar. ST Chief Executive Officer Carlo Montagner said the PBS listing was a significant milestone for the company. He commented: "We acquired the YONDELIS rights in 2019 following requests from key oncology groups and doctors, who had been importing the product at great cost and with complex logistics for those patients diagnosed with these rare cancers. "This PBS listing is the culmination of a substantive effort by our team together with the oncology community to achieve full regulatory approval and a PBS listing. "We look forward to continuing our work with the sarcoma community." Ends. About Specialised Therapeutics Asia Headquartered in Singapore, Specialised Therapeutics (ST) is an international biopharmaceutical company established to commercialise new therapies and technologies to patients in Australia, New Zealand and across South-East Asia. ST and its regional affiliates collaborate with leading global pharmaceutical and diagnostic companies to bring novel, innovative and life-changing healthcare solutions to patients affected by a range of diseases. Our mission is to provide therapies that would otherwise not be available to communities in our regions. The company's broad therapeutic portfolio currently includes novel agents in oncology, haematology, neurology, ophthalmology and supportive care. Additional information can be found at About YONDELIS® (trabectedin) YONDELIS® (trabectedin) is a novel, multimodal, synthetically produced antitumor agent, originally derived from the sea squirt, Ecteinascidia turbinata. The anti-cancer medicine works by preventing tumor cells from multiplying and is approved in 76 countries in North America, Europe, South America and Asia for the treatment of advanced soft-tissue sarcomas as a single-agent, and in 69 countries for relapsed ovarian in combination with doxorubicin HCl liposome injection. The approval was based on the results of a pivotal phase 3, randomised, open-label controlled study which evaluated YONDELIS versus dacarbazine in over 500 patients with unresectable or metastatic liposarcoma (LPS) or leiomyosarcoma (LMS) previously treated with an anthracycline and at least one additional chemotherapy regimen. LPS and LMS are subtypes of soft tissue sarcoma (STS) and represent more than 35% of all STS cases.3 The median progression-free survival (PFS) among the YONDELIS treatment group was 4.2 months compared to 1.5 months in the dacarbazine treatment group, representing a 45% reduction in the risk of disease progression or death with YONDELIS (HR=0.55; 95% CI: 0.44 - 0.70; p<0.001).1 Among the 340 patients who received YONDELIS and were included in the safety analysis in the randomised trial, the most common (≥20%) adverse reactions were nausea (73%), fatigue (67%), vomiting (44%), constipation (36%), decreased appetite (34%), diarrhoea (34%), dyspnoea (25%), peripheral oedema (24%) and headache (23%). The most common (≥20%) laboratory abnormalities were neutropenia (49%), increased alanine transaminase (ALT) (45%), anaemia (39%), increased aspartate aminotransferase (AST) (35%), thrombocytopaenia (30%) and increased blood alkaline phosphatase (20%).1 About Soft Tissue Sarcoma Soft tissue sarcoma is a rare type of cancer that forms as a painless lump (tumour) in any one of the soft tissues connecting all the organs and body structures – including fat, muscle, nerves, deep skin tissue, blood vessels and the tissue surrounding joints (synovial tissue). Soft tissue sarcomas commonly develop in the thigh, shoulder and pelvis and may sometimes develop in the abdomen or chest.6 Metastatic or locally advanced STS is generally considered incurable, with the mainstay of treatment being systemic chemotherapy. For some patients with limited disease burden however, long-term remission can be achieved through a multimodality approach involving medical, surgical and radiation therapy.4 About PharmaMar PharmaMar is a biopharmaceutical company focused on the research and development of new oncology treatments, whose mission is to improve the healthcare outcomes of patients afflicted by serious diseases with our innovative medicines. The Company is inspired by the sea, driven by science, and motivated by patients with serious diseases to improve their lives by delivering novel medicines to them. PharmaMar intends to continue to be the world leader in marine medicinal discovery, development and innovation. PharmaMar has developed and now commercializes Yondelis® in Europe by itself, as well as Zepzelca® (lurbinectedin), in the US; and Aplidin® (plitidepsin), in Australia, with different partners. In addition, it has a pipeline of drug candidates and a robust R&D oncology program. PharmaMar has other clinical-stage programs under development for several types of solid cancers: lurbinectedin, ecubectedin, PM534 and PM54. It also has a preclinical and clinical program in virology. Headquartered in Madrid (Spain), PharmaMar has subsidiaries in Germany, France, Italy, Belgium, Austria, Switzerland and The United States. PharmaMar also wholly owns Sylentis, a company dedicated to researching therapeutic applications of gene silencing (RNAi). To learn more about PharmaMar, please visit us at . SOURCE Specialised Therapeutics

临床结果引进/卖出临床3期上市批准

2023-06-06

·美通社

绿叶制药进口药品注射用芦比替定上市申请获国家药品监督管理局受理用于治疗复发性小细胞肺癌

上海 2023年6月6日 /美通社/ -- 绿叶制药集团（2186.HK）宣布，国家药品监督管理局已受理其抗肿瘤进口药品注射用芦比替定的上市申请，用于治疗含铂化疗中或化疗后疾病进展的转移性小细胞肺癌（SCLC）成人患者。此前，该产品已被纳入优先审评品种名单。芦比替定为一种选择性的致癌基因转录抑制剂，独特的双重作用机制使其在抑制肿瘤基因转录、导致肿瘤细胞凋亡的同时，还可调节肿瘤微环境，从而进一步发挥抗肿瘤作用。该药物于2020年获得美国食品药品监督管理局（FDA）的附条件批准，用于治疗上述适应症。此次上市申请基于芦比替定在中国开展的单臂、包含剂量递增及扩展的临床研究，旨在评估该药物在包括复发性SCLC在内的晚期实体瘤中国患者中的安全性、耐受性、PK特征和初步疗效。临床结果显示：芦比替定（3.2 mg/m 2 ）二线治疗中国SCLC患者具有显著的抗肿瘤疗效及可控的安全性。其在复发性SCLC受试者中，由独立评估委员会评估的总有效率（ORR）达到45.5%。中国肺癌的发病率及死亡率高居癌症之首，2020年新发患者约81.5万人，死亡约71.4万人 [1] ，其中SCLC占肺癌的13~17% [2] 。SCLC患者确诊时多为晚期，预后极差，五年生存率仅7%，广泛期SCLC的五年生存率仅3% [3] 。尽管SCLC对于初始治疗非常敏感，但大多数患者在初始治疗后出现耐药及复发；据统计，约75%的局部晚期患者和超过90%的转移性患者在治疗2年内复发 [4] 。SCLC的高复发率为其治疗带来巨大挑战，临床亟需创新治疗方案。芦比替定是近26年来唯一一个获得美国FDA批准的用于治疗复发性SCLC的新分子实体。其获批主要基于芦比替定的一项单药治疗105例接受铂类药物化疗后出现疾病进展的SCLC成年患者（包括铂类敏感和耐药患者）的开放、多中心、单臂、II期篮子试验。主要研究结果显示：接受芦比替定治疗的患者ORR达到35%，中位缓解持续时间（DoR）为5.3个月。在中国开展的临床试验首次在中国人群中探索芦比替定的疗效和安全性。研究结果提示，芦比替定在一线含铂化疗出现进展的中国复发性SCLC人群中的疗效与国外II期临床试验SCLC队列的疗效结果有可比性，并倾向于获得更好的有效率。此项临床研究的初步结果也在2022 ASCO（美国临床肿瘤学会）年会、以及第25届全国临床肿瘤学大会暨2022年CSCO（中国临床肿瘤学会）年会上发布，获得海内外专家学者的广泛关注。除了在中国内地以外，芦比替定还在中国香港处于上市审评阶段。此外，该产品已作为临床急需药品落地海南博鳌乐城国际医疗旅游先行区特定医疗机构、并通过在香港地区的"指定患者药物使用计划"服务于中国患者。绿叶制药集团总裁杨荣兵表示："小细胞肺癌是一种治疗相对困难的肺癌亚型，具有恶性程度高、预后差、复发性高的特点。该疾病复发后缺乏新的药物治疗选择是当下临床应用中所面临的主要挑战。我们很高兴地看到芦比替定的上市申请已获得国家药品监督管理局受理，并期待这一创新治疗方案尽快惠及更多有需要的患者，改善他们的生存获益。" 芦比替定最初由绿叶制药的合作伙伴PharmaMar进行开发。绿叶制药获得该药物在中国开发及商业化的独家权利。关于芦比替定芦比替定是从海鞘 Ecteinacidia turbinata 中分离出的海洋化合物ET-736的衍生物，ET-736中的氢原子被甲氧基取代。芦比替定能够选择性地抑制多种肿瘤所依赖的致癌基因转录。除了其对癌细胞的直接作用，芦比替定还能够抑制肿瘤相关巨噬细胞的转录过程，以及下调对肿瘤生长至关重要的细胞因子的产生。继在美国获得附条件批准用于治疗转移性小细胞肺癌后，芦比替定还在9个国家获批上市，并已获得ESMO小细胞肺癌指南（2021版）、NCCN小细胞肺癌指南（2022版）和2023年中国临床肿瘤学会（CSCO）小细胞肺癌指南推荐。绿叶制药集团拥有芦比替定的中国权益。关于绿叶制药集团绿叶制药集团是致力于创新药物的研发、生产和销售的国际化制药公司。绿叶制药在中国、美国和欧洲设有研发中心，拥有超过30个中国在研药物和10多个海外在研药物。绿叶制药在微球、脂质体、透皮释药等先进药物递送技术领域达到国际先进水平，在新分子实体、生物抗体领域收获多项创新成果，并在细胞治疗、基因治疗等领域进行了积极布局和开发。绿叶制药深度布局全球供应链体系，已在全球建有8大生产基地，超过30条生产线，并建立了与国际接轨的GMP质量管理和控制体系。公司现有30余个上市产品，产品覆盖肿瘤、中枢神经系统、心血管、消化与代谢等治疗领域；业务遍及全球80多个国家和地区，其中包括中国、美国、欧洲、日本等全球主要医药市场，以及高速增长的各地新兴市场。关于 PharmaMar PharmaMar是一家专注于研究和开发创新肿瘤治疗方案的生物制药公司，其使命是让创新药物惠及重大疾病患者，帮助其提升临床获益。PharmaMar以海洋为源，以科学为驱动力，以患者为导向，通过提供创新药物以改善重大疾病患者的生活质量，并致力于持续成为海洋药物发现、开发和创新的全球领导者。 PharmaMar已自主开发并在欧洲地区商业化Yondelis ®、在美国及中国与合作伙伴合作开发并商业化Zepzelca ®（芦比替定），及在澳大利亚与合作伙伴合作商业化Aplidin ®(Plitidepsin)。此外，PharmaMar拥有一系列候选药物、强大的肿瘤研发项目，及针对多种实体瘤的临床在研项目，包括：芦比替定和Ecubectedin。PharmaMar总部位于西班牙马德里，并在德国、法国、意大利、比利时、奥地利、瑞士和美国设有子公司。致力于研究基因沉默(RNAi)疗法应用的公司Sylentis为其全资子公司。参考文献： [1]. International Agency for Research on Cancer – Population Fact Sheets – China. Available at https:\/\/gco.iarc.fr\/today\/data\/factsheets\/populations\/160-china-fact-sheets.pdf. Accessed in June 2023. [2]. 中国临床肿瘤学会指南工作委员会. 中国临床肿瘤学会（CSCO）小细胞肺癌诊疗指南2022. 人民卫生出版社. 2022 [3]. Cancer.Net. Lung Cancer - Small Cell. Available at https:\/\/www.cancer.net\/cancer-types\/33776\/view-all. Accessed in June 2023. [4]. Rudin CM, et al. Nat Rev Dis Primers. 2021 Jan 14;7(1):3.

ASCO会议优先审批临床结果CSCO会议临床2期

100 项与 Plitidepsin 相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
D11032	Plitidepsin	L01XX57	DB04977

研发状态

适应症	最高研发状态	国家/地区	公司
新型冠状病毒感染	终止	墨西哥更多	Pharma Mar SA 更多
难治性侵袭性非霍奇金淋巴瘤	无进展	瑞士更多	Pharma Mar SA 更多
复发性多发性骨髓瘤	无进展	捷克更多	Pharma Mar SA 更多
浆细胞骨髓瘤难治	无进展	美国更多	Pharma Mar SA 更多
白血病	无进展	西班牙更多	Pharma Mar SA 更多

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临床结果

适应症

分期

评价

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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


NCT04382066 (CTgov)	临床1期	新型冠状病毒感染	46	Plitidepsin 1.5 mg/day (Experimental 1)	糧願觸餘膚憲簾鏇顧鬱(網衊構齋鑰餘顧遞遞憲) = 廠淵糧憲襯夢餘窪簾鬱觸蓋遞鏇獵遞夢衊積齋 (獵鬱襯繭網廠蓋鹽壓齋, 鹹願窪獵艱網顧鏇廠獵 ~ 壓艱醖遞鏇鹽繭獵網鏇) 更多	-	2021-09-24
NCT04382066 (CTgov)	临床1期	新型冠状病毒感染	46	Plitidepsin 2.0 mg/day (Experimental 2)	糧願觸餘膚憲簾鏇顧鬱(網衊構齋鑰餘顧遞遞憲) = 蓋餘衊廠醖鏇獵鏇顧廠觸蓋遞鏇獵遞夢衊積齋 (獵鬱襯繭網廠蓋鹽壓齋, 鬱壓願遞壓製鑰選齋鑰 ~ 積積遞壓衊膚遞膚壓餘) 更多	-	2021-09-24
NCT03117361 (CTgov)	临床2期	多发性骨髓瘤	10	bortezomib+Dexamethasone+plitidepsin	淵襯願壓廠醖夢範壓廠(範築構蓋構選積積廠餘) = 製築範淵網積襯蓋網範鬱獵簾夢蓋範醖鹹窪鏇 (網範膚鹽艱鹽窪鏇網淵, 鑰淵製齋願鹽製壓糧糧 ~ 憲網鏇選網艱製鹹積願) 更多	-	2020-12-02
NCT00780975 (CTgov)	临床2期	去势抵抗性前列腺癌 \| 晚期前列腺癌	8	Aplidin	憲糧壓蓋構鑰積廠鑰窪(齋鹹選鑰蓋顧鏇壓觸衊) = 鹽簾鹽鬱積鏇觸鬱製鹽簾膚衊製鹹觸壓壓觸製 (鏇齋遞範憲鹽選網膚鬱, 鹹憲壓衊簾網夢積醖壓 ~ 範鏇襯獵鹹壓鏇製觸鏇) 更多	-	2020-11-24
NCT01102426 (CTgov)	临床3期	复发性多发性骨髓瘤 \| 浆细胞骨髓瘤难治	255	Dexamethasone+Plitidepsin (Plitidepsin+Dexamethasone)	積繭觸獵壓簾醖範壓窪(鹹鹹獵衊齋網鑰築醖願) = 餘鹽鏇網壓願築網蓋蓋顧製選築夢醖糧觸獵繭 (衊鏇艱鑰夢淵選觸襯觸, 構餘鏇糧壓繭構膚製襯 ~ 選願壓夢齋襯願鑰鑰蓋) 更多	-	2020-10-22
NCT01102426 (CTgov)	临床3期	复发性多发性骨髓瘤 \| 浆细胞骨髓瘤难治	255	Dexamethasone (Dexamethasone)	積繭觸獵壓簾醖範壓窪(鹹鹹獵衊齋網鑰築醖願) = 齋衊製鹹膚艱製鬱齋壓顧製選築夢醖糧觸獵繭 (衊鏇艱鑰夢淵選觸襯觸, 壓襯獵壓廠鬱艱鹹醖廠 ~ 夢築糧顧顧糧鹽願製顧) 更多	-	2020-10-22
NCT03070964 (CTgov)	临床2期	免疫母细胞性淋巴结病 \| 淋巴瘤	14	plitidepsin	鏇膚鬱顧餘壓膚襯築構(憲鏇蓋襯膚鹹蓋醖淵齋) = 膚範鬱蓋齋夢淵範廠繭衊餘構鬱遞膚鏇憲蓋願 (襯鬱壓艱鹽鹽醖願願糧, 簾鑰鏇築淵餘構齋壓鬱 ~ 衊醖鏇廠鹽遞廠艱醖範) 更多	-	2020-10-14
NCT01149681 (CTgov)	临床2期	骨髓纤维化 \| 原发性血小板增多症 \| 真性红细胞增多症后骨髓纤维化 ... 更多	12	APLIDIN (plitidepsin)	醖製憲顧糧構獵觸繭壓(願鑰衊鏇鬱糧觸築築餘) = 遞遞鏇觸製鹹築壓廠廠糧選觸衊淵願鏇築窪觸 (衊衊遞遞窪憲遞獵憲構, 壓憲顧築壓憲鏇廠鏇遞 ~ 壓築網鹽餘範鏇衊鹹夢) 更多	-	2020-10-12
NCT02100657 (CTgov)	临床1期	浆细胞骨髓瘤难治 \| 复发性多发性骨髓瘤	39	BTZ+DXM+plitidepsin (All Participants)	襯膚簾淵淵壓壓繭廠選(廠窪壓築齋醖鹹齋簾積) = 築簾鹽壓齋衊顧膚繭鏇鬱構醖願網鹹繭簾膚淵 (襯製鹽鹽鹽繭鏇膚構範, 鹹網齋餘壓廠憲繭窪鹽 ~ 願鏇簾獵衊積構艱憲鑰) 更多	-	2020-10-12
NCT02100657 (CTgov)	临床1期	浆细胞骨髓瘤难治 \| 复发性多发性骨髓瘤	39	BTZ+DXM+Plitidepsin (Plitidepsin (4 mg/m2)+BTZ (1 mg/m2)+DXM (40 mg))	醖壓願憲齋範顧糧膚選(衊願範獵襯網願淵鑰鬱) = 蓋鹽範觸構網遞夢蓋觸積鹽蓋鑰製鬱醖簾網簾 (築顧製齋淵窪憲壓艱醖, 顧衊夢鏇壓鏇衊遞糧製 ~ 鹽餘觸窪願網網襯鏇淵) 更多	-	2020-10-12
NCT01876043 (CTgov)	临床2期	脂肪肉瘤	24	Plitidepsin	膚襯獵膚願願遞範膚積(網鑰鏇製鬱願範夢鹹鹹) = 衊範遞淵願齋網襯鬱鏇夢鏇膚鏇網鹹構願簾製 (夢蓋壓積簾積鏇窪繭構, 構簾繭廠願鬱築齋範顧 ~ 壓範衊範網憲顧夢觸淵) 更多	-	2019-11-12
NCT01102426 (ADMYRE, Pubmed \| Ann Hematol) 人工标引	临床3期	复发性多发性骨髓瘤末线	255	dexamethasone+plitidepsin	鹽憲憲願壓醖窪積願網(餘觸淵繭選積願簾範廠) = 範製願膚願憲範衊鬱憲製壓簾範襯鏇簾膚繭鏇 (築廠膚築構淵簾齋襯艱 ) 更多	优效	2019-09-01
NCT01102426 (ADMYRE, Pubmed \| Ann Hematol) 人工标引	临床3期	复发性多发性骨髓瘤末线	255	dexamethasone	鹽憲憲願壓醖窪積願網(餘觸淵繭選積願簾範廠) = 淵醖構憲積醖積範鬱繭製壓簾範襯鏇簾膚繭鏇 (築廠膚築構淵簾齋襯艱 ) 更多	优效	2019-09-01
NCT00780143 (CTgov)	临床1/2期	难治性白血病	3	Aplidin	觸選願襯選顧簾選夢齋(獵艱鹹鹽願範遞簾鹹觸) = 鹹願醖蓋糧觸膚構糧網網顧膚糧積夢艱選夢壓 (壓夢簾壓獵衊網繭願夢, 選膚廠獵廠壓蓋醖夢網 ~ 鏇製簾憲餘鬱顧餘齋膚) 更多	-	2018-11-09