A Phase II Study on Trabectedin in Combination With PPARg Agonist Pioglitazone in Patients With Round Cell Myxoid Liposarcomas or Dedifferentiated G1 and G2 Liposarcomas With Stable Disease After a Monotherapy With Trabectedin. (TRABEPIO)

This is a phase 2 study conducted in two sequential stages:
The first stage is an Italian single institution, single arm, pilot study, aimed at exploring the activity of the combination T and P in myxoid liposarcoma patients who achieved a stable disease after a minimum of 4 cycles of T alone. If a minimum required activity will be demonstrated from the first stage, the second stage of the study will be conducted;otherwise, the study will be stopped. The second stage is an Italian open-label, multicenter, randomized, double arm, phase II trial, aimed at evaluating the combination of T and P in myxoid liposarcoma and G1 or G2 dedifferentiated liposarcomas compared to the standard treatment with T alone. Patients will be randomized with a 1:1 ratio to treatments arms as specified below:
Control arm (A): T alone
Experimental arm (B): T in combination with P

开始日期2022-02-02

申办/合作机构

Mario Negri Institute For Pharmacological Research

[+2]

NCT04383119 / Recruiting临床2期IIT

A Randomized Phase II Trial Comparing the Activity of trabectedIn vs Gemcitabine in Patients With Metastatic or Locally Advanced Leiomyosarcoma Pretreated With Conventional Chemotherapy

Study is aimed at evaluating the activity of Trabectedin (arm A) in advanced leiomyosarcomas, having Gemcitabine (arm B) as the comparator.
In addition to the randomized cohort, the study has also an observational prospective cohort which include patients who will refuse the randomization or for whom the investigator will not judge the randomization as an appropriate option.
In order to allow the participation of sites only to the prospective-observational (non randomized) cohort, it was introduced the possibility to participate to the study and receive the ethical approval only to the Observational Prospective Cohort In parallel an optional translational study will be performed, in both cohorts, to identify factors predictive of the activity of Trabectedin or Gemcitabine in this specific histotype.

开始日期2021-10-29

申办/合作机构

Italian Sarcoma Group

[+1]

NCT05597917 / Recruiting临床3期IIT

Phase III Study Comparing Trabectedin (T) Versus T Plus tTF-NGR to Entrap T Inside the Tumor in Patients With Metastatic and/or Refractory Soft Tissue Sarcoma (STS)

In this phase III open label, controlled clinical trial patients with unresectable or metastatic soft-tissue sarcoma after failure of anthracycline-containing first line therapy or with contraindications to these drugs and CD13 positivity in central histology (grade >/= 1+) are treated to evaluate whether tTF-NGR in combination with standard trabectedin chemotherapy prolongs progression-free survival (according to iRECIST), as compared with trabectedin alone. Further objectives are to evaluate the efficacy of tTF-NGR in combination with standard trabectedin chemotherapy with respect to the response rate and overall survival as well as to assess the safety profile of tTF-NGR combined with trabectedin. Before the randomized phase III part of the study, there will be a safety run-in part. The final dose of tTF-NGR established as safe in this safety run-in part will be used for the randomized (parallel 1:1; Arm 1: standard trabectedin, Arm 2: standard trabectedin plus tTF-NGR) phase III part of this trail.

开始日期2021-10-26

申办/合作机构

Universität Stuttgart

[+1]

100 项与曲贝替定相关的临床结果

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100 项与曲贝替定相关的转化医学

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100 项与曲贝替定相关的专利（医药）

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941

项与曲贝替定相关的文献（医药）

2024-02-20·Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

In ovarian cancer maraviroc potentiates the antitumoral activity and further inhibits the formation of a tumor-promoting microenvironment by trabectedin.

Article

作者: Naike Casagrande ; Cinzia Borghese ; Giuseppe Corona ; Donatella Aldinucci

Ovarian cancer (OC) is the fifth most frequent cause of cancer-related death in women. Chemotherapy agent trabectedin, affecting cancer cells and tumor microenvironment, has been approved for the treatment of relapsed platinum-sensitive OC patients. CCR5-antagonist maraviroc inhibits tumor growth, metastasis, and enhances the antitumoral activity of DNA-damaging drugs. Here, we found that OC cells expressed CCR5 receptor but did not secret CCR5-ligands. Maraviroc treatment did not affect OC cell viability, but strongly potentiated the antiproliferative activity, apoptosis induction, cell cycle blockage, DNA damage, and ROS formation by trabectedin. In A2780cis cisplatin-resistant cells, the cross-resistance to trabectedin was overcame by the combination with maraviroc. Maraviroc enhanced trabectedin cytotoxicity in OC 3Dimensional spheroids and THP-1-monocytes. Both maraviroc and trabectedin interact with drug efflux pump MDR1/P-gp, overexpressed in recurrent OC patients. Maraviroc increased trabectedin intracellular accumulation and the MDR1-inhibitor verapamil, like maraviroc, increased trabectedin cytotoxicity. In OC tumor xenografts the combination with maraviroc further reduced tumor growth, angiogenesis, and monocyte infiltration by trabectedin. In conclusion, this study offers a preclinical rationale for the use of maraviroc as new option to improve trabectedin activity in relapsed chemoresistant OC patients.

2024-02-15·Nature communications

Trabectedin derails transcription-coupled nucleotide excision repair to induce DNA breaks in highly transcribed genes.

Article

作者: Kook Son ; Vakil Takhaveev ; Visesato Mor ; Hobin Yu ; Emma Dillier ; Nicola Zilio ; Nikolai J L Püllen ; Dmitri Ivanov ; Helle D Ulrich ; Shana J Sturla ; Orlando D Schärer

Most genotoxic anticancer agents fail in tumors with intact DNA repair. Therefore, trabectedin, anagent more toxic to cells with active DNA repair, specifically transcription-coupled nucleotide excision repair (TC-NER), provides therapeutic opportunities. To unlock the potential of trabectedin and inform its application in precision oncology, an understanding of the mechanism of the drug's TC-NER-dependent toxicity is needed. Here, we determine that abortive TC-NER of trabectedin-DNA adducts forms persistent single-strand breaks (SSBs) as the adducts block the second of the two sequential NER incisions. We map the 3'-hydroxyl groups of SSBs originating from the first NER incision at trabectedin lesions, recording TC-NER on a genome-wide scale. Trabectedin-induced SSBs primarily occur in transcribed strands of active genes and peak near transcription start sites. Frequent SSBs are also found outside gene bodies, connecting TC-NER to divergent transcription from promoters. This work advances the use of trabectedin for precision oncology and for studying TC-NER and transcription.

2024-02-08·International journal of molecular sciences

In-Silico Identification of Novel Pharmacological Synergisms: The Trabectedin Case.

Article

作者: Laura Mannarino ; Nicholas Ravasio ; Maurizio D'Incalci ; Sergio Marchini ; Marco Masseroli

The in-silico strategy of identifying novel uses for already existing drugs, known as drug repositioning, has enhanced drug discovery. Previous studies have shown a positive correlation between expression changes induced by the anticancer agent trabectedin and those caused by irinotecan, a topoisomerase I inhibitor. Leveraging the availability of transcriptional datasets, we developed a general in-silico drug-repositioning approach that we applied to investigate novel trabectedin synergisms. We set a workflow allowing the identification of genes selectively modulated by a drug and possible novel drug interactions. To show its effectiveness, we selected trabectedin as a case-study drug. We retrieved eight transcriptional cancer datasets including controls and samples treated with trabectedin or its analog lurbinectedin. We compared gene signature associated with each dataset to the 476,251 signatures from the Connectivity Map database. The most significant connections referred to mitomycin-c, topoisomerase II inhibitors, a PKC inhibitor, a Chk1 inhibitor, an antifungal agent, and an antagonist of the glutamate receptor. Genes coherently modulated by the drugs were involved in cell cycle, PPARalpha, and Rho GTPases pathways. Our in-silico approach for drug synergism identification showed that trabectedin modulates specific pathways that are shared with other drugs, suggesting possible synergisms.

项与曲贝替定相关的新闻（医药）

2024-03-12

·Science Daily

How a natural compound from sea squirts combats cancer

Trabectedin, a promising drug derived from the sea squirt Ecteinascidia turbinata, has shown potential in combating cancers resistant to conventional treatments. However, its precise mechanism of action has remained elusive -- until now. Numerous anti-cancer drugs function by targeting the DNA within cancerous cells, halting their proliferation. Yet, cancer cells occasionally develop mechanisms to repair the damage inflicted by these drugs, diminishing their effectiveness. Consequently, physicians are increasingly embracing a novel approach to cancer treatment known as precision medicine. This method involves selecting medications that precisely align with the unique attributes of an individual's cancer. Precision medicine proves particularly beneficial in addressing cancers that have evolved to evade conventional treatments. Trabectedin, a promising drug derived from the sea squirt Ecteinascidia turbinata, has shown potential in combating cancers resistant to conventional treatments. However, its precise mechanism of action has remained elusive -- until now. A collaborative effort led by Dr. SON Kook and Professor Orlando D. SCHÄRER from the Center for Genomic Integrity within the Institute for Basic Science in South Korea, along with Dr. Vakil TAKHAVEEV and Professor Shana STURLA from ETH Zurich, Switzerland, has illuminated the inner workings of this mysterious compound. Using highly sensitive high throughput COMET Chip assays to detect breaks formed in the genomes of cells, IBS researchers revealed trabectedin induces persistent breaks in the DNA of cancer cells. The researchers showed that these DNA breaks are only formed in cells with high levels of DNA repair, specifically those that operate a pathway called transcription-coupled nucleotide excision repair (TC-NER). TC-NER is a vital mechanism that identifies DNA damage during transcription, initiating repair processes involving two endonucleases ERCC1-XPF and XPG. Trabectedin's DNA damage disrupts this process by allowing the initial incision by ERCC1-XPF but blocking the subsequent action by XPG, halting the TC-NER process. This disruption of the repair process leads to long-lasting DNA breaks that ultimately kill cancer cells. Analysis of the DNA break patterns induced by trabectedin revealed that breaks are formed throughout the genome, but only at sites where active transcription and with it, TC-NER occurs. Using this new insight into the mechanism of how DNA breaks are accumulated, the researchers sought to determine where in the genome these breaks occur. This led to the development of a new method called TRABI-Seq (for TRABectedin-Induced break sequencing), which allows for the precise identification of trabectedin's action sites within tumor cell DNA. "This incision by ERCC1-XPF creates a markable free hydroxyl group in the DNA, enabling us to sequence DNA and locate these breaks," explains Dr. Son. TRABI-Seq is being tested on various cancer cells to determine trabectedin's efficacy in targeting tumors with advanced DNA repair capabilities, often associated with elevated transcription levels due to oncogene activation. It is hoped that these findings will help position trabectedin as both a predictive marker to identify vulnerable cancers and a therapeutic option for precision treatment. With its ability to target tumors resistant to conventional therapies, trabectedin may provide further hope in the fight against drug-resistant cancer with highly active DNA repair capabilities.

寡核苷酸

2024-02-27

·药融圈

现场深度解读：AI+自动化赋能新药研发

会议主题丨第七届成都生物医药创新者峰会举办时间丨2024年3月7日-8日主办方丨药融圈☞点击获取最新会议日程PART/1 演讲预告 2024年3月8日，智化科技CEO夏宁博士受邀参加“小分子创新者先锋论坛”，并将于14:00 – 14:30发表以“AI+自动化赋能新药研发”为主题的演讲。PART/2 公司介绍智化科技成立于2018年，专注于AI赋能化学创新的研发，致力于重塑化学未来，并利用人工智能和化学大数据，通过化学合成的智能化、自动化，大幅度提高化学合成效率。智化科技以化学大数据为驱动，自主研发多种算法模型，配合人工智能技术和机器人，为生物医药、化工、新材料等领域客户提供领先的产品服务及解决方案。PART/3 产品介绍 ChemAIRS - AI辅助逆合成路线设计平台基于化学大数据挖掘与深度学习算法，ChemAIRS只需要输入目标分子便能够在数分钟内对该分子设计出多条合成路线，并充分考虑原料可及性、反应可行性、官能团兼容性、手性合成策略等因素，为化学家提供多样可行合成思路。ChemAIOS - 实验室智能化管理系统ChemAIOS是智化科技自主研发的AI赋能数字化全流程实验室管理系统，帮助您规范实验流程，实现数据闭环，提升研发效率，打造未来实验室数据生态。ChemAIoT - 化学实验室人工智能自动化解决方案AI（人工智能）+IoT（物联网）+ Automation（自动化）结合，基于丰富的化学信息学经验沉淀，自研的人工智能算法赋能复合机器人，通过连接各类仪器设备、非标定制模块，为化学、检验检测、生物、医疗等领域提供综合解决方案，实现实验室全流程智动化。ChemAILAB - 自动化化学合成服务ChemAILAB结合智化科技自主研发的ChemAIRS和ChemAIoT，并通过ChemAIOS实现人员、设备、物料的协同，进行实验项目及数据的管理，打造人机协作的自动化、数智化的化学实验室，旨在提高化学合成服务效率，为客户提供更高效、更专业的化学合成服务。实验室超3000m²，配置16间现代化有机合成实验室，含2间公斤级实验室，并拥有超100名专业化学素养的科学家，均来自行业头部的企业及院校，化学合成经验平均在五年以上。PART/4 ADC团队基于AI赋能的自动化设备和路线设计平台，智化科技为合作伙伴提供ADC Linker-Payload的结构设计、合成路线设计和优化、Payload结构改造、衍生物合成路线设计以及CRO特异化定制服务。受益于ChemAIRS强大的合成路线设计能力，ChemAILAB能高效合成创新Payload分子，加速创新药物的开发。AI算法推荐更优的纯化方案，即使是含有脂肪族长链的Linker-Payload也能被快速有效地分离。同时，基于AI赋能的自动化实验室确保了高效、精准、批量的自动化投料，提高了Payload合成成功率，并有效地避免了高活性物质对研究人员的伤害。ChemAILAB团队已经成功交付近400个Linker-Payload分子，包括PEG类、肽链、VC、VA、VK等系列，并完成了依喜替康类、MMAE类、曲贝替定类等不同类型的Payload设计和合成。凭借团队丰富的合成经验、成熟的CMC技术以及独特的人工智能算法，智化科技将持续为ADC药物的创新和研发提供赋能，并不断推动ADC领域的前沿技术和创新。PART/5 偶遇我们 2024年3月7日—8日，智化科技期待与您相聚B11号展台，共同探讨人工智能赋能药物研发的经验和前景，建立合作关系，并共同推动医药领域的进步和创新。↓↓展位号：B11号PART/6 联系智化邮箱：bd@chemical.ai pr@chemical.ai网站：https://www.chemical.ai电话：021-58213013PART/7 会议联系 13625705846关于药融圈药融圈PRHub旨在帮助生物医药科技型企业进行品牌推广及商务拓展服务，针对客户的真实需求制定系统化解决方案，通过“翻译-降维-场景化”将客户的品牌信息以直白易懂的方式被公众知悉，同时在流量渠道覆盖100万+垂直用户基础上实现合作目的，帮助合作伙伴完成从品牌开始到商务为终的闭环营销服务。我们已经完成了数十场线下1000人规模的生物医药研发类会议，涵盖小分子新药，大分子新药，改良型新药，BD跨境交易等领域，品牌会议包括中国国际生物及化学制药产业大会(6000人以上)，仿制药峰会（600人以上），新药创新者系列峰会（1200人以上），服务了百余家上市/独角兽/生物技术/制药企业。点击阅读原文查看会议详情

抗体药物偶联物引进/卖出医药出海

2023-10-02

·BioSpace

Boundless Bio Appoints New Board Members and Establishes Clinical Advisory Board

James Christensen, Ph.D., and Nancy Whiting, Pharm.D., join Board of Directors George Demetri, M.D., to serve as first member of Clinical Advisory Board SAN DIEGO--(BUSINESS WIRE)-- Boundless Bio, a clinical stage, next-generation precision oncology company interrogating extrachromosomal DNA (ecDNA) biology to deliver transformative therapies to patients with previously intractable oncogene amplified cancers, today announced the appointment of two new members to its Board of Directors and the establishment of its Clinical Advisory Board. Industry veterans James (“Jamie”) Christensen, Ph.D., Chief Scientific Officer of Mirati Therapeutics, and Nancy Whiting, Pharm.D., Chief Executive Officer of Recludix Pharma, will join Boundless Bio’s Board of Directors. George Demetri, M.D., Director of the Sarcoma Center at the Dana-Farber Cancer Institute, will serve as the first member of the company’s Clinical Advisory Board. “We are thrilled to welcome these highly accomplished professionals who bring deep oncology drug development experience to Boundless Bio,” said Zachary Hornby, President and Chief Executive Officer of Boundless Bio. “Jamie and Nancy are incredibly valuable additions to our Board of Directors, having each led the discovery, development, and regulatory approvals of multiple approved cancer medicines. George is a world-renowned leader in the clinical translation of innovative treatment strategies for cancer, and his appointment establishes our Clinical Advisory Board. Together, their involvement and experience will prove invaluable as we continue to advance the Phase 1/2 clinical trial of BBI-355, progress additional ecDNA-directed therapeutic candidates (ecDTx) into the clinic, and initiate drug discovery programs arising from our Spyglass platform for identifying novel ecDNA targets." Appointment of Jamie Christensen, Ph.D., and Nancy Whiting, Pharm.D., to Board of Directors Dr. Jamie Christensen has served as the Chief Scientific Officer of Mirati Therapeutics, a publicly traded precision oncology company, since 2013 and is responsible for drug discovery, translational research, drug manufacturing, and companion diagnostics research. At Mirati, Dr. Christensen leads activities related to the discovery and advancement of the company’s clinical and preclinical programs, including Mirati’s first approved product, Krazati®(adagrasib). Prior to Mirati, Dr. Christensen was the Head of Oncology Precision Medicine and a member of the executive leadership team in the Oncology Research Unit at Pfizer. He joined Pfizer in 2003, where his responsibilities included leading oncology nonclinical research and translational sciences for programs including Sutent® (sunitinib malate) and Xalkori® (crizotinib). Prior to Pfizer, Dr. Christensen held positions at SUGEN/Pharmacia as a group leader in preclinical research and exploratory development. He began his career in the pharmaceutical industry at Warner Lambert/Parke-Davis. Dr. Christensen has authored or co-authored over 150 peer-reviewed research articles in scientific journals including Science, Nature, Cancer Cell, Cancer Discovery, New England Journal of Medicine, and many others. He received his Ph.D. at North Carolina State University and his B.S. in biology from Northern Illinois University. Dr. Nancy Whiting is the Chief Executive Officer of Recludix Pharma, a private company developing novel treatments for inflammatory disease and cancer, and has an established track record in all phases of oncology drug development. Prior to Recludix, Dr. Whiting was a 15-year veteran of Seagen where she served most recently as Executive Vice President of Corporate Strategy, Alliances, and Communication. Prior to this role at Seagen, Dr. Whiting served as Executive Vice President of Development, Senior Vice President of Clinical Development and Medical Affairs, and Head of Experimental Medicine. During her tenure at Seagen, Dr. Whiting played a central role in the development and regulatory approvals of cancer medicines Adcetris® (brentuximab vedotin), Padcev® (enfortumab vedotin-ejfv), Tukysa® (tucatinib) and Tivdak® (tisotumab vedotin). Prior to her career in the pharmaceutical industry, Dr. Whiting practiced as a clinical oncology pharmacist at the Seattle Cancer Care Alliance. Dr. Whiting serves on the Board of Directors of Caribou Biosciences. She received her Pharm.D. from the University of Washington and completed her undergraduate degree at the University of British Columbia. Appointment of George Demetri, M.D., to Clinical Advisory Board Dr. George Demetri currently serves as the Quick Family Chair in Medical Oncology and Director of the Sarcoma Center at Dana-Farber Cancer Institute, as well as Professor of Medicine at Harvard Medical School and Co-Director of the Ludwig Center at Harvard. He has dedicated his career to translational and clinical research aimed at developing clinical therapeutics from scientific mechanisms to treat life-threatening cancers. Dr. Demetri is a pioneer in the development of multiple targeted cancer therapies, and research from his collaborative efforts has resulted in FDA and worldwide regulatory approvals of several cancer therapies, including Gleevec® (imatinib), Sutent® (sunitinib), Stivarga® (regorafenib), Votrient® (pazopanib), Yondelis® (trabectedin), and Tazverik® (tazemetostat). Dr. Demetri received his undergraduate degree in biochemistry from Harvard College and M.D. from Stanford University School of Medicine, after which he completed his internal medicine residency and chief residency at the University of Washington Hospitals in Seattle and subsequently trained in medical oncology at the Dana-Farber Cancer Institute and Harvard Medical School. He is also a member of the Science Policy and Government Affairs Committee of the American Association for Cancer Research, for which he served as the immediate past chair. About Boundless Bio Boundless Bio is a clinical-stage precision oncology company dedicated to unlocking a new paradigm in cancer therapeutics to address the significant unmet need in patients with oncogene amplified tumors by targeting extrachromosomal DNA (ecDNA), a root cause of oncogene amplification observed in more than 14% of cancer patients. Boundless Bio is developing the first ecDNA-directed therapy (ecDTx), BBI-355, which is being evaluated in a Phase 1/2 clinical trial, and has multiple other pipeline programs advancing in preclinical development and discovery. To date, Boundless Bio has raised more than $250 million from leading life sciences investors. For more information, visit . Follow us on LinkedIn and Twitter.

高管变更临床研究

100 项与曲贝替定相关的药物交易

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KEGG	Wiki	ATC	Drug Bank
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研发状态

适应症	最高研发状态	国家/地区	公司
脂肪肉瘤	批准上市	澳大利亚更多	Specialised Therapeutics 更多
平滑肌肉瘤	批准上市	美国更多	Janssen Products LP 更多
铂敏感性卵巢癌	批准上市	澳大利亚更多	Specialised Therapeutics 更多
肉瘤	批准上市	新西兰更多	Specialised Therapeutics Australia Pty Ltd. 更多
软组织肿瘤	批准上市	日本更多	Taiho Pharmaceutical Co., Ltd. 更多

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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


NCT02367924 (YonSar, ESMO2022) 人工标引	临床4期	局部晚期软组织肉瘤	130	Trabectedin	(壓鬱網製顧憲蓋廠鏇鹹) = 廠製夢鏇艱窪醖醖範糧願夢築顧觸觸憲觸觸簾 (範餘遞廠積鑰築構窪繭, 51.5 ~ 68.8) 更多	积极	2022-09-10
NCT04067115 (U01CA236220 \| SARC037, ASCO2023) 人工标引	临床1期	尤文肉瘤	20	Trabectedin+Irinotecan	(壓齋齋鏇製糧蓋繭艱鏇) = T=1.0 mg/m2, I=25 mg/m2 簾選襯醖獵齋淵鏇製醖 (壓鹹窪鹹壓蓋觸鏇齋網 ) 更多	积极	2023-05-31
EUCTR2017-001755-31-DE \| NCT03127215 (ESMO2022) 人工标引	临床2期	实体瘤 harboring DNA repair deficiencies	85	trabectedin+olaparib	(觸蓋鹽淵願餘願窪積齋) = 鏇築獵選鏇築繭餘艱網製觸艱廠遞製衊膚製願 (顧簾壓獵淵鑰醖壓鏇憲 )	积极	2022-09-10
EUCTR2017-001755-31-DE \| NCT03127215 (ESMO2022) 人工标引	临床2期	实体瘤 harboring DNA repair deficiencies	85	physician’s choice	(觸蓋鹽淵願餘願窪積齋) = 艱遞鹹遞鑰鑰製蓋淵鹽製觸艱廠遞製衊膚製願 (顧簾壓獵淵鑰醖壓鏇憲 ) 更多	积极	2022-09-10
NCT02805725 (TARMIC, ESMO2023) 人工标引	临床1/2期	软组织肉瘤	30	Trabectedin+cyclophosphamide	(鹽鑰觸顧獵網鹹膚糧鹹) = 壓鹹襯鬱顧構網觸構遞觸構網顧艱鑰蓋鹹網顧 (築蓋鬱膚廠廠製憲醖淵, 2.7; 32.4) 更多	积极	2023-10-23
NCT03023124 (ASCO2023) 人工标引	临床2期	孤立性纤维瘤	23	Trabectedin	(窪夢夢鬱憲膚積壓憲範) = 0% 廠衊鬱襯觸顧積齋餘廠 (選網壓襯觸鹹衊艱獵蓋 )	不佳	2023-05-26
NCT03023124 (ASCO2023) 人工标引	临床2期	孤立性纤维瘤	23	Adriamycin+Dacarbazine	(窪夢夢鬱憲膚積壓憲範) = 0% 廠衊鬱襯觸顧積齋餘廠 (選網壓襯觸鹹衊艱獵蓋 )	不佳	2023-05-26
NCT02993705 (MITO 26, Pubmed) 人工标引	临床2期	子宫癌肉瘤 \| 卵巢癌肉瘤	45	Trabectedin	(窪鹹醖築選築鏇顧鑰觸) = 顧膚鹹窪壓齋簾鬱獵齋衊築鹹觸窪蓋積窪夢觸 (蓋鏇鬱淵獵鹽鹽簾構鬱, 6 ~ 23) 更多	不佳	2022-10-08
NCT05131386 (SYNERGIAS, ESMO2023) 人工标引	临床2期	晚期肉瘤	33	Trabectedin 1.5mg/m2 + Radiotherapy	(糧網簾淵醖艱鏇齋鏇網) = 衊範蓋蓋遞鹹範積觸餘窪鏇糧選蓋鏇顧顧製憲 (壓網壓願壓遞蓋構襯鑰 ) 更多	积极	2023-10-23
NCT03590210 (NitraSarc, ASCO2023) 人工标引	临床2期	肉瘤二线	92	Nivolumab+Trabectedin (patients with advanced lipo- or leiomyosarcomas + GA)	(築蓋顧鏇襯觸壓鬱觸築) = 顧餘鑰獵簾遞築鬱觸齋鹹衊簾鏇鹽築壓積膚積 (夢選廠糧觸選構襯鑰鏇 ) 更多	积极	2023-05-26
NCT03590210 (NitraSarc, ASCO2023) 人工标引	临床2期	肉瘤二线	92	Nivolumab+Trabectedin (patients with non-L-sarcomas + GB)	(築蓋顧鏇襯觸壓鬱觸築) = 觸選齋襯製襯窪鑰膚繭鹹衊簾鏇鹽築壓積膚積 (夢選廠糧觸選構襯鑰鏇 ) 更多	积极	2023-05-26
NCT03138161 (SAINT, ESMO2022) 人工标引	临床1/2期	平滑肌肉瘤一线	26	trabectedin+ipilimumab+nivolumab	(觸蓋製襯窪鑰艱顧網廠) = The MTD for trabectedin (T) was 1.2 mg/m^2 艱蓋淵鏇繭鏇築顧構願 (襯窪餘糧鹽衊衊積蓋壓 ) 更多	积极	2022-09-10
NCT03886311 (ASCO2023) 人工标引	临床2期	平滑肌肉瘤末线	15	Nivolumab+Trabectedin+Talimogene laherparepvec (mITT patients who had completed at least one treatment cycle and had a follow-up CT scan)	(廠壓範壓鑰齋遞糧觸網) = 繭製齋遞襯遞窪製遞鹹選獵鹹淵夢鑰網遞糧簾 (窪壓選糧網築簾製鬱構, 3 ~ 18) 更多	积极	2023-05-26