A Randomized Phase II Trial of Oral Decitabine and Cedazuridine and Venetoclax Compared With Oral Decitabine and Cedazuridine, Venetoclax, and Enasidenib for Newly Diagnosed Older Adults With IDH2 Mutant Acute Myeloid Leukemia: A MyeloMATCH Treatment Trial

This phase II MyeloMATCH treatment trial studies how well ASTX727 and venetoclax plus enasidenib works compared to ASTX727 and venetoclax alone for the treatment of older patients with newly diagnosed acute myeloid leukemia (AML) or younger patients who are considered unfit for standard treatment, and who have an abnormal change (mutation) in the IDH2 gene. This gene mutation can cause AML to grow and spread. This trial is being done to see if adding enasidenib to the usual treatment can help more patients with the IDH2 gene get rid of AML. Cedazuridine is in a class of medications called cytidine deaminase inhibitors. It prevents the breakdown of decitabine, making it more available in the body so that decitabine will have a greater effect. Decitabine is in a class of medications called hypomethylation agents. It works by helping the bone marrow produce normal blood cells and by killing abnormal cells in the bone marrow. Venetoclax is in a class of medications called B-cell lymphoma-2 (BCL-2) inhibitors. It may stop the growth of cancer cells by blocking Bcl-2, a protein needed for cancer cell survival. Enasidenib works by stopping the growth and spread of tumor cells that have the IDH2 mutation. Giving ASTX727 and venetoclax plus enasidenib may work better in treating AML patients with the IDH2 mutation.

开始日期2025-02-03

申办/合作机构

National Cancer Institute

NCT06577441 / Not yet recruiting临床2期IIT

A Randomized Phase II Trial of Enasidenib-Based Therapies Versus Cedazuridine-Decitabine in Higher-Risk IDH2-Mutated Myelodysplastic Syndrome: A MyeloMATCH Treatment Trial

This phase II MyeloMATCH treatment trial compares the usual treatment of cedazuridine-decitabine (ASTX727) to the combination treatment of ASTX727 and enasidenib in treating patients with higher-risk, IDH2-mutated myelodysplastic syndrome (MDS). ASTX727 is a combination of two drugs, decitabine and cedazuridine. Cedazuridine is in a class of medications called cytidine deaminase inhibitors. It prevents the breakdown of decitabine, making it more available in the body so that decitabine will have a greater effect. Decitabine is in a class of medications called hypomethylation agents. It works by helping the bone marrow produce normal blood cells and by killing abnormal cells in the bone marrow. Enasidenib is an enzyme inhibitor that may stop the growth of cells by blocking some of the enzymes needed for cell growth. Giving ASTX727 in combination with enasidenib may be effective in treating patients with higher-risk IDH2-mutated MDS.

开始日期2025-01-17

申办/合作机构

National Cancer Institute

NCT06240754 / Recruiting临床2期IIT

A Pilot Study of Enasidenib for Patients With Clonal Cytopenia of Undetermined Significance and Mutations in IDH2: A Decentralized Trial

Study researchers think that a drug called enasidenib may help people with clonal cytopenia of undetermined significance (CCUS) because the drug blocks the mutated IDH2 protein, which may improve blood cell counts. The purpose of this study is to find out whether enasidenib is a safe and effective treatment for CCUS.

开始日期2024-10-10

申办/合作机构

Washington University School of Medicine

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100 项与甲磺酸恩西地平相关的临床结果

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100 项与甲磺酸恩西地平相关的转化医学

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100 项与甲磺酸恩西地平相关的专利（医药）

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项与甲磺酸恩西地平相关的文献（医药）

2024-11-01·Expert Opinion on Drug Safety

Safety considerations for drugs newly approved for treating acute myeloid leukemia

Review

作者: Góra-Tybor, Joanna ; Gołos, Aleksandra ; Robak, Tadeusz

INTRODUCTIONAcute myeloid leukemia (AML) is typically characterized by a poor prognosis, mainly due to the median age at diagnosis. Until recently, treatment options were limited to intensive chemotherapy (IC) for young patients or hypomethylating agents for those ineligible for IC. Since 2017, nine molecules were registered for newly-diagnosed AML: midostaurin, gilteritinib, quizartinib, enasidenib, ivosidenib, gemtuzumab ozogamicin, CPX-351, glasdegib, and venetoclax.AREAS COVEREDThe review examines the safety profile of these drugs and their interactions with other agents used in supportive care. The PubMed and Google Scholar databases were searched for articles in English concerning new agents in AML from 2017 until 2023. Further relevant publications were obtained by reviewing the prescribing information and Food and Drug Administration (FDA) data.EXPERT OPINIONThe therapeutic spectrum in AML has broadened over several years and can also improve outcomes in older patients. However, in addition to their well-known cytotoxic activity, new molecules cause several unique, off-target toxicities. Also, potential drug-drug interactions (DDI) should be taken into consideration when choosing optimal first-line therapy; this remains a challenge in clinical practice.

2024-10-01·JTO Clinical and Research Reports

Differentiation Syndrome in a Patient With NSCLC Harboring IDH2 Mutation Treated With Enasidenib: Case Report

Article

作者: Sukhadia, Bhoomika ; Oh, Youjin ; Shah, Zunairah ; Tan, Dean ; Chae, Young Kwang

IDH2 gain-of-function mutations cause DNA hypermethylation interfering with cellular differentiation and are linked to poor disease outcomes in NSCLC. IDH2-inhibitor enasidenib is approved for refractory acute myeloid leukemia but has been associated with delayed onset of differentiation syndrome-a potentially fatal inflammatory reaction caused by differentiating agents, namely all-trans retinoic acid and arsenic trioxide. We report the first case of differentiation syndrome in a patient with NSCLC treated with enasidenib, who after 7 weeks experienced bilateral peripheral edema and shortness of breath, with scans exhibiting pericardial effusion and ground-glass opacities suggestive of pneumonitis. Differentiation syndrome should be considered as a differential diagnosis in patients with solid tumors undergoing IDH2-inhibitor targeted therapy.

2024-10-01·JAMA Oncology

A Review

Review

作者: Venugopal, Sangeetha ; Sekeres, Mikkael A.

ImportanceAcute myeloid leukemia (AML) is a clonal hematopoietic cancer that disrupts normal hematopoiesis, ultimately leading to bone marrow failure and death. The annual incidence rate of AML is 4.1 per 100 000 people in the US and is higher in patients older than 65 years. Acute myeloid leukemia includes numerous subgroups with heterogeneous molecular profiles, treatment response, and prognosis. This review discusses the evidence supporting frontline therapies in AML, the major principles that guide therapy, and progress with molecularly targeted therapy.ObservationsAcute myeloid leukemia is a genetically complex, dynamic disease. The most commonly altered genes include FLT3, NPM1, DNMT3A, IDH1, IDH2, TET2, RUNX1, NRAS, and TP53. The incidence of these alterations varies by patient age, history of antecedent hematologic cancer, and previous exposure to chemotherapy and/or radiotherapy for any cancer. Since 2010, molecular data have been incorporated into AML prognostication, gradually leading to incorporation of targeted therapies into the initial treatment approach of induction chemotherapy and subsequent management. The first molecularly targeted inhibitor, midostaurin, was approved to treat patients with AML with FLT3 variants in 2017. Since then, the understanding of the molecular pathogenesis of AML has expanded, allowing the identification of additional potential targets for drug therapy, treatment incorporation of molecularly targeted therapies (midostaurin, gilteritinib, and quizartinib targeting FLT3 variants; ivosidenib and olutasidenib targeting IDH1 variants, and enasidenib targeting IDH2), and identification of rational combination regimens. The approval of hypomethylating agents combined with venetoclax has revolutionized the therapy of AML in older adults, extending survival over monotherapy. Additionally, patients are now referred for hematopoietic cell transplant on a more rational basis.Conclusions and RelevanceIn the era of genomic medicine, AML treatment is customized to the patient’s comorbidities and AML genomic profile.

项与甲磺酸恩西地平相关的新闻（医药）

2024-08-15

·Business Wire

Bicara Therapeutics Expands Board of Directors with Appointments of Mike Powell, Ph.D., and Christopher Bowden, M.D.

BOSTON--( BUSINESS WIRE )--Bicara Therapeutics, a clinical-stage biotechnology company developing transformative bifunctional therapies for patients with solid tumors, today announced the appointments of Mike Powell, Ph.D., and Christopher Bowden, M.D., to the company’s board of directors. Dr. Powell currently serves as executive partner of Omega Funds and will serve as Bicara’s chairman of the board. Dr. Bowden is the former chief medical officer of Agios Pharmaceuticals and current chief medical officer of Remix Therapeutics and will serve as an independent director. “ Mike and Chris are distinguished biopharma industry leaders that have contributed to the approvals of multiple innovative oncology medicines. We are thrilled to welcome them to our board of directors,” said Claire Mazumdar, Ph.D., MBA, chief executive officer of Bicara Therapeutics. “ The combination of Mike’s four decades of pharmaceutical clinical development experience and Chris’ strategic medical and corporate expertise will be critical as we continue to advance ficerafusp alfa (BCA101) into late-stage development for recurrent/metastatic head and neck squamous cell carcinoma as well as other indications.” About Mike Powell, Ph.D. Dr. Mike Powell joined Omega Funds as executive partner in 2021 from Sofinnova Investments, where he served as managing general partner since 1997. Previously, Dr. Powell was Group Leader at Genentech from 1990 to 1997, where his focus was on drug delivery, CMC, and formulation of both small molecule and protein drug entities. Before this, he served as the director of product development for Cytel Corp, an immunology biotech company. Prior to this, he was senior scientist and project team leader at Syntex Research (Roche). Dr. Powell was the first person in the biotech industry to become a fellow of the American Association of Pharmaceutical Scientists (AAPS). He was previously board president of the AIDS Vaccine Advocacy Coalition, an advisor to the Institute for One World Health, IAVI, and the Bill and Melinda Gates Foundation, and an adjunct associate professor in the Department of Pharmaceutical Chemistry at the University of Kansas. Dr. Powell holds a Ph.D. in physical chemistry from the University of Toronto, and a postdoc in bio-organic chemistry at the University of California. About Christopher Bowden, M.D. Dr. Chris Bowden currently serves as the chief medical officer of Remix Therapeutics. Prior to Remix, Dr. Bowden served as a strategic advisor and chief medical officer of Agios Pharmaceuticals from 2014-2022. As chief medical officer at Agios, he oversaw clinical development that led to U.S. approvals for the IDH inhibitors IDHIFA™ and TIBSOVO™ in acute myeloid leukemia (AML), for TIBSOVO™ in cholangiocarcinoma and for PYRUKYND™ for adults with pyruvate kinase deficiency. Prior to joining Agios, Dr. Bowden was vice president of product development in oncology, franchise lead (signaling group) at Genentech, Inc. where he was responsible for the successful development of several novel targeted oncology medicines, including Zelboraf™ and Tarceva™. Dr. Bowden received his M.D. from Hahnemann University School of Medicine in Philadelphia after which he completed his internal medicine training at Roger Williams Medical Center and the Providence VA Medical Center, Rhode Island. He conducted his medical oncology fellowship at the National Cancer Institute Medicine Branch. Dr. Bowden is board certified in internal medicine and medical oncology. About Ficerafusp Alfa (BCA101) Ficerafusp alfa is a bifunctional antibody designed to inhibit the epidermal growth factor receptor (EGFR) and disable transforming growth factor beta (TGF-β) directly at the tumor site. This approach is designed with the intent to allow ficerafusp alfa to inhibit tumor proliferation, while restoring the cytolytic activity of the local immune cells. Ficerafusp alfa is currently being evaluated in a dose expansion phase of an open-label Phase 1/1b study in combination with pembrolizumab in HPV-negative patients with R/M HNSCC, advanced squamous non-small cell lung cancer (SqNSCLC), or squamous cancer of the anal canal (SCAC) and as a monotherapy for cutaneous squamous cell carcinoma (cSCC). About Bicara Therapeutics Bicara Therapeutics is a clinical-stage biotechnology company developing bifunctional therapies engineered to combine the precision of well validated, tumor-targeting antibodies with the power of tumor microenvironment modulators. The Company’s bifunctional antibodies are designed to deliver an immunomodulatory payload directly to the tumor microenvironment to ramp up immune cell activity, offering the potential for synergistic therapeutic impact at the site of the tumor. Bicara’s lead product candidate, ficerafusp alfa, is a EGFR/TGF-β-trap bifunctional antibody in clinical development for multiple tumor types. For more information, please visit www.bicara.com or follow us on LinkedIn or X.

高管变更免疫疗法上市批准

2024-08-06

·FiercePharma

Servier snags FDA approval for Voranigo, the first targeted therapy for a common type of brain tumor

This marks the first FDA approval of a systemic therapy for patients with grade 2, IDH-mutant gliomas. Servier has expanded its IDH drug armamentarium with the FDA approval for an IDH1/2 dual inhibitor. The approval represents the first major treatment advance in low-grade brain cancer in more than two decades.The new FDA approval is for Servier’s Voranigo, or vorasidenib, for adult and children ages 12 and older with low-grade glioma with a susceptible IDH1 or IDH2 mutation. As the FDA noted in its press release, this marks the first approval of a systemic therapy for this type of grade 2 IDH-mutant brain cancer, which includes oligodendrogliomas and astrocytomas.Servier obtained Voranigo through its $2 billion acquisition of Agios Pharmaceuticals’ oncology business in 2021. Royalty Pharma, which earlier this year acquired a stake in Agios’ royalty payments for Voranigo, has projected the drug could reach more than $1 billion in annual peak sales in the U.S.Gliomas are the most common primary malignant brain tumors in adults, and IDH1 or IDH2 mutations are present in nearly all grade 2 diffuse gliomas in adults. By Royalty’s estimates, there are around 1,500 new diagnoses for these two IDH-mutant gliomas each year in the U.S.Current therapeutic interventions for these patients are more than 20 years old and are all used off label, Islam Hassan, M.D., senior medical director at Servier, noted in an interview with Fierce Pharma ahead of Tuesday’s FDA decision.Before Voranigo, Servier already has the IDH1 inhibitor Tibsovo and the IDH2 inhibitor Idhifa. Although doctors have been using the two meds off-label because of the lack of treatment options, neither was approved for brain cancer.Voranigo, for its part, was designed to penetrate the blood-brain barrier to be effective against brain tumors, Hassan explained. In a phase 3 trial coded INDIGO, Voranigo significantly reduced the risk of tumor progression or death by 61% compared with placebo among patients with residual or recurrent grade 2 IDH-mutant glioma. These patients had undergone no previous treatment other than surgery.In addition, Voranigo also showed a statistically significant benefit in delaying the need for the next treatment, slashing the risk for further treatment by 74% in the study.The trial is ongoing to gather overall survival data. Still, Hassan argued that the progression-free survival data are just as important, because these tumors will continue to grow and penetrate the brain and may develop into high-grade disease.Besides the Voranigo monotherapy regimen, Servier has been evaluating the IDH inhibitor alongside Merck’s immunotherapy Keytruda in recurrent or progressive IDH1-mutant gliomas. While anti-PD-1 antibody drugs like Keytruda have been largely unsuccessful in brain tumors, Hassan pointed to a previous study in which patients received Voranigo and Keytruda before surgery. In tissues collected from surgery, Servier noticed some changes in the immune microenvironment that Hassan said warrant further development of this combination.Servier is also testing Voranigo alongside the chemotherapy temozolomide in high-grade IDH-mutant glioma. As Hassan noted, these patients with grade 4 gliomas are typically excluded from other clinical trials.The FDA approval triggers a $200 million milestone payment from Servier to Agios, plus a $905 million payment from Royalty to Agios in exchange for a 15% royalty on U.S. net sales of up to $1 billion for the therapy.

临床结果上市批准临床3期并购

2024-07-25

·药明康德

《科学》：意想不到的抗癌机制找到了！把癌细胞当作病毒击杀，一箭双雕治疗多种癌症

▎药明康德内容团队编辑对于多种癌症，异柠檬酸脱氢酶（IDH）突变是一种常见的致癌突变。例如，在极其凶险的肝内胆管癌中，有27%的病例都有IDH突变；此外，超过80%的低级别胶质瘤、12%的急性髓系白血病、40%的软骨肉瘤也都与这种突变存在关联。正常状态下，IDH生成的代谢产物α-酮戊二酸可以为细胞代谢提供能量。然而一旦发生突变，情况就截然不同了。突变的IDH会产生一种名为2-羟基戊二酸（2HG）的致癌代谢产物。2HG不会参与主要的代谢途径，而是在细胞中不断堆积。随着浓度的升高，2HG会让很多参与表观遗传和代谢调控的酶（例如去甲基化酶）活性下降，导致一系列生理过程的失调，促进肿瘤生长。对于这些由IDH突变导致的癌症，科学家们已经找到了应对策略。通过阻断IDH（具体来说，包括IDH1和IDH2两种酶），可以阻止2HG的产生，恢复去甲基化酶的活性。自首款IDH2抑制剂（Idhifa）和首款IDH1抑制剂（Tibsovo）分别于2017、2018年获批上市，用于治疗复发性/难治性急性髓系白血病以来，近年来陆续有IDH抑制剂及联合疗法问世或提出上市申请，为白血病、肝内胆管癌、神经胶质瘤等癌症患者带来治疗希望。此外，多款正在临床试验阶段的IDH1抑制剂也在文末呈现。图片来源：123RF 不过，虽然药物已经投入使用，但IDH类抑制剂阻止肿瘤生长的具体机制却仍不清楚，这也限制了对这些药物更加有效的使用与进一步研发。最近，一项发表于《科学》的研究揭开了IDH1抑制剂抗癌的真相。来自马萨诸塞州总医院、博德研究所等机构的研究团队发现，IDH1抑制剂使用了“病毒模拟”的巧妙“骗术”，让机体在面对癌细胞时，就像是遭受病毒感染一样激活免疫反应，从而避开了癌细胞的免疫逃逸。研究团队指出，这项研究揭示了一种出乎意料的IDH1抑制剂作用机制。 IDH1突变型肿瘤有着典型的免疫逃逸特征，它们可以将细胞毒性（CD8+）T细胞排斥在肿瘤微环境之外，并且削弱这些“癌症杀手”的杀伤能力。因此，要改善IDH1靶向治疗的效果，首先就要了解IDH1突变如何改变免疫监督、如何通过抑制这一途径来促进T细胞募集。在这项研究中，研究团队设计了IDH1突变肝癌小鼠模型。结果，免疫正常的小鼠在使用了IDH1抑制剂后，肿瘤细胞中的DNA迅速去甲基化，CD8+ T细胞向肿瘤微环境浸润，肿瘤细胞的增殖也开始减缓。相反，IDH1抑制剂对免疫缺陷小鼠的作用很有限。接下来的转录分析，找到了IDH1抑制剂影响肿瘤免疫反应的线索：此时，肿瘤细胞内应答病毒的基因表达上调。明明面对的是肿瘤，为什么机体会产生类似抗病毒的反应呢？这件事要从内源性逆转录病毒（Endogenous Retrovirus，ERV）说起。千百万年前，逆转录病毒在感染了我们的灵长类祖先后，将自己的RNA逆转录为DNA，整合到人类祖先的遗传物质中。如今，我们的基因序列中，仍有一部分来自远古病毒的遗迹，这就是ERV转座子。通常情况下，体内的这些ERV元件处于表观遗传沉默状态。但当IDH1抑制剂存在时，正如前文提到的DNA去甲基化，ERV和其他转座子也在这个过程中被激活、得到重新表达。一系列连锁反应也就此开启。 ▲研究机制示意图（图片来源：参考资料[1]） ERV转座子的活化会引起双链DNA的积累，而作为双链DNA的传感器，原本在高甲基化时被沉默的cGAS（环鸟苷酸-腺苷酸合酶），此时也得到了重新激活。得到激活后，cGAS在感知到双链DNA时会进一步激活干扰素基因刺激因子（STING）信号，从而开启抗病毒I型干扰素。这时，以为遭遇了病毒感染的免疫系统启动免疫监督程序，最终将CD8+ T细胞募集到至肿瘤微环境。这个过程就是病毒模拟应答（viral mimicry）。值得一提的是，IDH1抑制剂对抗肿瘤的方式还不止病毒模拟这一条，它还能增强肿瘤细胞对干扰素γ的敏感性，因此实现“双管齐下”的抗癌策略。综上，这项研究表明，通过利用病毒模拟应答，有望进一步提升IDH1抑制剂治疗癌症的效果，并且这一机制也可能应用于具有类似代谢或表观遗传改变的其他癌症类型，实现更广阔的临床治疗场景。参考资料： [1] Meng-Ju Wu et al, Mutant IDH1 inhibition induces dsDNA sensing to activate tumor immunity, Science (2024). DOI: 10.1126/science.adl6173 [2] Jason R. Pitarresi and Katherine A. Fitzgerald. Unmasking immune suppression, Science (2024). DOI: 10.1126/science.adq5196 [3] Targeted drug treatment leads tumor cells to imitate viral infection, researchers discover (2024, July 12) retrieved 22 July 2024 from https://medicalxpress.com/news/2024-07-drug-treatment-tumor-cells-imitate.html 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。免责声明：药明康德内容团队专注介绍全球生物医药健康研究进展。本文仅作信息交流之目的，文中观点不代表药明康德立场，亦不代表药明康德支持或反对文中观点。本文也不是治疗方案推荐。如需获得治疗方案指导，请前往正规医院就诊。

上市批准临床研究

100 项与甲磺酸恩西地平相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
-	甲磺酸恩西地平	L01XX59	DB13874

研发状态

批准上市

10 条最早获批的记录,

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适应症	国家/地区	公司	日期
急性髓性白血病	美国	Bristol Myers Squibb Co.	2017-08-01

未上市

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适应症	最高研发状态	国家/地区	公司	日期
晚期恶性实体瘤	临床3期	法国	Celgene Corp.	2014-12-08
晚期恶性实体瘤	临床3期	美国	Celgene Corp.	2014-12-08
胶质瘤	临床3期	美国	Celgene Corp.	2014-12-08
免疫母细胞性淋巴结病	临床3期	美国	Celgene Corp.	2014-12-08
免疫母细胞性淋巴结病	临床3期	法国	Celgene Corp.	2014-12-08
血液肿瘤	临床2期	美国	Agios Pharmaceuticals, Inc.	2013-08-27
血液肿瘤	临床2期	法国	Agios Pharmaceuticals, Inc.	2013-08-27

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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


NCT05010772 (4277, ASH2024)	临床1期	急性髓性白血病 complex cytogenetics \| antecedent MDS/MPN \| therapy-related AML ... 更多	31	ASTX727 alone	(壓憲壓繭繭鹹醖艱憲壓) = 淵壓蓋壓簾簾齋襯膚積顧糧憲遞鑰範選廠糧願 (憲獵憲廠網餘窪鹹夢齋 ) 更多	积极	2024-12-09
				ASTX727 plus venetoclax	(壓憲壓繭繭鹹醖艱憲壓) = 鹽壓範簾網鬱選製襯艱顧糧憲遞鑰範選廠糧願 (憲獵憲廠網餘窪鹹夢齋 ) 更多
NCT01915498 \| NCT02677922 \| NCT02577406 \| NCT02632708 (Pubmed \| Blood Adv) 人工标引	N/A	急性髓性白血病	643	enasidenib ± azacitidine or chemotherapy	鑰願積糧遞夢範鬱壓襯(製夢製獵網窪夢網製遞) = 鑰壓築窪顧衊淵艱築襯襯願壓鏇繭糧繭獵淵鬱 (簾鏇選願窪憲糧範鑰餘 ) 更多	积极	2024-03-20
				Enasidenib + azacitidine	鑰願積糧遞夢範鬱壓襯(製夢製獵網窪夢網製遞) = 夢簾積憲鹽膚簾夢蓋構襯願壓鏇繭糧繭獵淵鬱 (簾鏇選願窪憲糧範鑰餘 )
NCT03728335 (Tandem Meetings ASTCT and CIBMTR2024) 人工标引	临床1期	IDH2突变急性髓系白血病维持	15	Enasidenib	(餘蓋構憲遞憲壓窪簾窪) = 壓廠網糧廠艱窪製獵齋窪構夢膚鬱鹽鹹獵網構 (製廠獵壓襯衊選艱願遞 ) 更多	积极	2024-02-01
NCT03013998 (Pubmed) 人工标引	临床1/2期	急性髓性白血病一线	60	Enasidenib	(衊繭網鹹製積獵蓋鹹簾) = 製艱鹽構壓衊鑰選壓網襯醖餘鹹壓鹽鏇鑰糧憲 (窪窪鹽繭範顧餘壓鬱糧 ) 更多	积极	2024-01-23
				Enasidenib + azacitidine	(衊繭網鹹製積獵蓋鹹簾) = 蓋鹽繭築蓋築顧襯積遞襯醖餘鹹壓鹽鏇鑰糧憲 (窪窪鹽繭範顧餘壓鬱糧 ) 更多
NCT04092179 (Phase Ib/II Study, ASH2023)	临床1/2期	髓系肿瘤	27	Enasidenib + Venetoclax	(願襯觸衊蓋壓鹹築膚簾) = 願範顧獵築糧鹹齋艱壓築鑰衊範淵鬱齋遞壓範 (築積膚鏇獵衊鹽壓鹽構, 8.2 ~ NR) 更多	-	2023-12-09
NCT02677922 (AG-221-AML-005 \| AG221-AML-005, CTgov)	临床1/2期	急性髓性白血病	130	AZA+AG-221 (Phase 1b Dose-finding Stage: AG-221 (100mg) + AZA)	糧醖鹹淵壓糧夢願繭網(獵製構醖簾鏇選製淵鑰) = 窪鏇鑰夢鏇衊遞築齋鑰鬱觸顧淵餘願範築簾獵 (獵糧範鬱顧窪範鑰願選, 網鏇糧製簾鹽窪繭衊衊 ~ 窪範鏇鏇簾廠選蓋餘鹹) 更多	-	2022-11-22
				AZA+AG-221 (Phase 1b Dose-finding Stage: AG-221 (200mg) + AZA)	糧醖鹹淵壓糧夢願繭網(獵製構醖簾鏇選製淵鑰) = 廠簾憲齋窪鑰鹹積製膚鬱觸顧淵餘願範築簾獵 (獵糧範鬱顧窪範鑰願選, 選鏇顧築鏇衊淵繭窪餘 ~ 選艱夢窪夢鹹簾鹽齋糧) 更多
NCT04281498 (ASH2022) 人工标引	临床2期	骨髓增生性疾病 IDH2 Mutation	6	Ruxolitinib Phosphate+Enasidenib Mesylate	(醖願壓製鏇願繭鏇淵繭) = 鹹壓餘糧壓築鬱襯鹹淵齋願醖膚夢衊繭鹹獵壓 (觸顧鏇衊構簾憲醖網淵 ) 更多	积极	2022-11-15
NCT03728335 (ASH2022) 人工标引	临床1期	急性髓性白血病维持 IDH2 Mutation	15	Enasidenib	(獵餘膚齋鹽膚蓋糧蓋遞) = grade ≥3 AEs were mainly due to hematologic toxicity including: lymphopenia (26%; n=4), anemia (20%; n=3), neutropenia (13%; n=2), and thrombocytopenia (6%; n=1) 壓遞顧積網膚淵選艱鹹 (繭衊顧觸範窪淵窪簾網 ) 更多	积极	2022-11-15
ASH2022 人工标引	临床1/2期	IDH1突变急性髓性白血病 IDH Mutation	27	ASTX727+Venetoclax+ivosidenib	(壓憲願遞顧範餘遞繭選) = 衊膚構鑰膚鹹膚鑰鏇齋窪醖淵願餘蓋襯網構廠 (齋餘壓簾遞顧顧範膚網 ) 更多	积极	2022-11-15
				ASTX727+Venetoclax+enasidenib	(壓憲願遞顧範餘遞繭選) = 膚繭餘願觸窪製顧構積窪醖淵願餘蓋襯網構廠 (齋餘壓簾遞顧顧範膚網 ) 更多
NCT03515512 (Pubmed) 人工标引	临床1期	IDH2突变急性髓系白血病 IDH2 Mutation	19	Enasidenib	(繭願鹽夢製築壓繭遞糧) = 願願憲製廠願選簾簾憲範鏇範醖構獵選醖憲夢 (廠簾顧鹹鑰顧夢繭餘窪 ) 更多	积极	2022-09-23