甲磺酸恩西地平(Enasidenib Mesylate) - 药物靶点：IDH2_在研适应症：急性髓性白血病，意义不明的克隆性血细胞减少症，IDH2突变急性髓系白血病_专利_临床

概要

基本信息

药物类型

小分子化药

别名

2-Methyl-1-(4-(6-(trifluoromethyl)pyridin-2-yl)-6-(2-(trifluoromethyl)pyridin-4-ylamino)-1,3,5-triazin-2-ylamino)propan-2-ol、Enasidenib、IDHIFA

+ [6]

靶点

IDH2

作用机制

IDH2抑制剂(线粒体异柠檬酸脱氢酶[NADP]抑制剂)

治疗领域

肿瘤血液及淋巴系统疾病其他疾病

在研适应症

急性髓性白血病意义不明的克隆性血细胞减少症IDH2突变急性髓系白血病+ [9]

非在研适应症

晚期恶性实体瘤软骨肉瘤胶质瘤+ [3]

原研机构

Celgene Corp.

在研机构

Celgene Corp.

The University of Texas MD Anderson Cancer Center新基医药咨询（上海）有限公司

+ [3]

非在研机构-

最高研发阶段批准上市

首次获批日期

美国 (2017-08-01),

急性髓性白血病

最高研发阶段(中国)临床3期

特殊审评快速通道 (美国)、孤儿药 (美国)、孤儿药 (澳大利亚)、临床急需境外新药 (中国)

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结构

分子式C20H21F6N7O4S

InChIKeyORZHZQZYWXEDDL-UHFFFAOYSA-N

CAS号1650550-25-6

关联

47

项与甲磺酸恩西地平相关的临床试验

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2024-10-28

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

[+2]

NCT05564390 / Recruiting临床2期IIT

Master Screening and Reassessment Protocol (MSRP) for the NCI MyeloMATCH Clinical Trials

This MyeloMATCH Master Screening and Reassessment Protocol (MSRP) evaluates the use of a screening tool and specific laboratory tests to help improve participants' ability to register to clinical trials throughout the course of their myeloid cancer (acute myeloid leukemia or myelodysplastic syndrome) treatment. This study involves testing patients' bone marrow and blood for certain biomarkers. A biomarker (sometimes called a marker) is any molecule in the body that can be measured. Doctors look at markers to learn what is happening in the body. Knowing about certain markers can give doctors more information about what is driving the cancer and how to treat it. Testing patients' bone marrow and blood will show doctors if patients have markers that specific drugs can target. The marker testing in this study will let doctors know if they can match patients with a treatment study (myeloMATCH clinical trial) that tests treatment for the type of cancer they have or continue standard of care treatment with their doctor on the Tier Advancement Pathway (TAP).

开始日期2024-06-18

申办/合作机构

National Cancer Institute

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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270

项与甲磺酸恩西地平相关的文献（医药）

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 ; Shah, Zunairah ; Tan, Dean ; Chae, Young Kwang ; Oh, Youjin

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

Contemporary Management of Acute Myeloid Leukemia

Review

作者: Sekeres, Mikkael A. ; Venugopal, Sangeetha

Importance:

Acute 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.

Observations:

Acute 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 Relevance:

In the era of genomic medicine, AML treatment is customized to the patient’s comorbidities and AML genomic profile.

2024-09-19·Blood Cancer Journal

Current status and research directions in acute myeloid leukemia.

Review

作者: Yilmaz, Musa ; Daver, Naval ; Kadia, Tapan ; Kantarjian, Hagop ; Sasaki, Koji ; Ravandi, Farhad ; Short, Nicholas J ; Borthakur, Gautam ; Issa, Ghayas ; Jabbour, Elias ; DiNardo, Courtney D

The understanding of the molecular pathobiology of acute myeloid leukemia (AML) has spurred the identification of therapeutic targets and the development of corresponding novel targeted therapies. Since 2017, twelve agents have been approved for the treatment of AML subsets: the BCL2 inhibitor venetoclax; the CD33 antibody drug conjugate gemtuzumab ozogamicin; three FLT3 inhibitors (midostaurin, gilteritinib, quizartinib); three IDH inhibitors (ivosidenib and olutasidenib targeting IDH1 mutations; enasidenib targeting IDH2 mutations); two oral hypomethylating agents (oral poorly absorbable azacitidine; fully absorbable decitabine-cedazuridine [latter approved as an alternative to parenteral hypomethylating agents in myelodysplastic syndrome and chronic myelomonocytic leukemia but commonly used in AML]); and CPX-351 (encapsulated liposomal 5:1 molar ratio of cytarabine and daunorubicin), and glasdegib (hedgehog inhibitor). Other targeted therapies (menin inhibitors, CD123 antibody-drug conjugates) are showing promising results. To achieve optimal results in such a rare and heterogeneous entity as AML requires expertise, familiarity with this rare cancer, and the access to, and delivery of disparate therapies under rigorous supportive care conditions. In this review, we update the standard-of-care and investigational therapies and outline promising current and future research directions.

32

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

10 条进展最快的记录,

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适应症	最高研发状态	国家/地区	公司	日期
意义不明的克隆性血细胞减少症	临床2期	美国	Bristol Myers Squibb Co.	2024-10-10
贫血	临床2期	美国	Celgene Corp.	2022-01-12
单核细胞白血病	临床2期	美国	Celgene Corp.	2022-01-12
IDH2突变急性髓系白血病	临床2期	德国	Celgene Corp.	2020-08-27
骨髓增生异常综合征	临床2期	德国	Celgene Corp.	2020-08-27
难治性急性髓细胞白血病	临床2期	美国	Celgene Corp.	2019-12-02
复发性急性髓细胞白血病	临床2期	美国	Celgene Corp.	2019-12-02
慢性粒单核细胞白血病	临床2期	美国	Celgene Corp.	2018-01-17
高危骨髓增生异常综合征	临床2期	美国	Celgene Corp.	2018-01-17
晚期恶性实体瘤	临床2期	美国	Celgene Corp.	2014-12-08

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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


NCT01915498 \| NCT02677922 \| NCT02577406 \| NCT02632708 (Pubmed) 人工标引	N/A	急性髓性白血病 IDH2 Mutation	643	enasidenib ± azacitidine or chemotherapy	窪糧網廠襯鑰製繭餘製(糧齋壓鹽鏇網鬱醖顧鹹) = 構艱範獵餘廠築夢獵獵夢蓋艱膚膚獵鬱憲鑰鬱 (鬱簾網襯觸遞鹹蓋膚窪 ) 更多	积极	2024-03-20
				Enasidenib + azacitidine	窪糧網廠襯鑰製繭餘製(糧齋壓鹽鏇網鬱醖顧鹹) = 廠繭網選淵醖憲醖淵觸夢蓋艱膚膚獵鬱憲鑰鬱 (鬱簾網襯觸遞鹹蓋膚窪 )
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 IDH2 Mutation	15	Enasidenib	簾襯窪觸選餘艱繭衊齋(夢膚製繭觸壓憲鏇簾廠) = 鹹構齋範餘膚構壓夢窪鑰窪願鏇獵鹽憲齋鏇顧 (餘範膚衊積觸淵構鑰顧 ) 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 IDH2 Mutation	60	Enasidenib	蓋壓鹹構範糧鬱醖觸醖(衊觸簾窪窪繭構遞製壓) = 膚製獵製積鹽獵鹽積鹹廠蓋顧艱壓繭顧醖艱簾 (襯選願築遞齋餘鏇製窪 ) 更多	积极	2024-01-23
				Enasidenib + azacitidine	蓋壓鹹構範糧鬱醖觸醖(衊觸簾窪窪繭構遞製壓) = 醖廠壓鑰鹹鏇衊觸遞窪廠蓋顧艱壓繭顧醖艱簾 (襯選願築遞齋餘鏇製窪 ) 更多
NCT04092179 (Phase Ib/II Study, ASH2023)	临床1/2期	髓系肿瘤	27	Enasidenib + Venetoclax	膚顧積選築鑰構構繭鏇(襯醖獵觸衊構鬱壓夢鏇) = 齋鑰艱遞襯觸糧積鬱顧蓋醖願積糧構鏇簾製網 (鹽繭餘繭衊壓膚築鬱餘, 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)	餘淵窪醖構衊鹹選淵遞(範網鏇鏇窪簾鏇範襯範) = 簾獵餘窪壓網廠窪醖膚築糧範醖餘鑰獵鬱築鹹 (壓鹹醖構夢繭獵窪簾夢, 簾鹽鬱糧餘觸夢鏇觸衊 ~ 鹹襯壓餘糧憲築積範製) 更多	-	2022-11-22
				AZA+AG-221 (Phase 1b Dose-finding Stage: AG-221 (200mg) + AZA)	餘淵窪醖構衊鹹選淵遞(範網鏇鏇窪簾鏇範襯範) = 簾窪構糧壓鹽積廠製醖築糧範醖餘鑰獵鬱築鹹 (壓鹹醖構夢繭獵窪簾夢, 繭艱壓廠襯鬱憲鹹齋齋 ~ 鹽鹽艱鑰願選構醖簾網) 更多
NCT03728335 (ASH2022) 人工标引	临床1期	急性髓性白血病维持 IDH2 Mutation	15	Enasidenib	蓋夢築齋艱簾鹽淵淵範(齋廠積蓋遞顧夢憲衊鹹) = 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) 憲糧範願獵繭齋製遞餘 (衊艱齋壓齋膚網艱積遞 ) 更多	积极	2022-11-15
NCT04281498 (ASH2022) 人工标引	临床2期	骨髓增生性疾病 IDH2 Mutation	6	Ruxolitinib Phosphate+Enasidenib Mesylate	繭積廠網築獵網鏇築鬱(艱廠顧廠獵鹽觸壓壓網) = 窪鹽遞鹽襯艱憲築窪築鏇襯糧夢窪築網簾鹹夢 (壓製壓衊鬱鏇醖構繭鹽 ) 更多	积极	2022-11-15
NCT03515512 (Pubmed) 人工标引	临床1期	IDH2突变急性髓系白血病 IDH2 Mutation	19	Enasidenib	膚簾積憲願繭窪艱壓鏇(選齋窪齋膚憲蓋襯選壓) = 艱構壓鑰積窪構醖獵廠齋齋廠簾壓觸襯齋願齋 (襯膚壓鹽簾廠顧網廠獵 ) 更多	积极	2022-09-23
NCT02577406 (IDHENTIFY, CTgov)	临床3期	急性髓性白血病	319	AG-221 (AG-221)	遞醖廠鹹選鏇齋廠遞繭(範願構繭範觸繭遞積顧) = 遞網獵遞鏇衊鬱構醖鑰築願範觸醖積繭積顧襯 (襯製鹽範淵構衊夢鹹衊, 夢憲憲艱築積構鬱觸醖 ~ 膚鹽積襯獵艱醖選鬱鹽) 更多	-	2022-09-10
				IDAC+hydroxyurea+LDAC+azacitidine (Conventional Care Regimens (CCRs))	遞醖廠鹹選鏇齋廠遞繭(範願構繭範觸繭遞積顧) = 製鹹鬱構餘衊築夢蓋夢築願範觸醖積繭積顧襯 (襯製鹽範淵構衊夢鹹衊, 鬱遞獵範獵襯廠網鹽鏇 ~ 遞餘醖願觸淵簾糧鹹構) 更多
NCT03383575 (Pubmed) 人工标引	临床2期	骨髓增生异常综合征一线 IDH2 Mutation	50	azacitidine+enasidenib	鏇獵廠網網繭廠築網鹽(鏇遞廠願觸艱遞廠願壓) = The most common adverse events were neutropenia (40%), nausea (36%), constipation (32%), and fatigue (26%). Hyperbilirubinemia from off-target UGT1A1 inhibition occurred in 14% of patients (8%; grades 3 and 4), and IDH-inhibitor-associated differentiation syndrome (IDH-DS) in 8 patients (16%). 夢鬱鏇範夢觸窪願衊衊 (衊膚顧襯襯願繭築鬱範 )	积极	2022-08-16
				enasidenib