地西他滨/西达尿苷(Decitabine/Cedazuridine) - 药物靶点：CDA x DNMT1_在研适应症：急性髓性白血病，慢性粒单核细胞白血病，骨髓增生异常综合征_专利_临床

概要

基本信息

药物类型

小分子化药

别名

(4R)-2'-Deoxy-2',2'-difluoro-3,4,5,6-tetrahydrouridine、Decitabine/cedazuridine、Decitabine/E7727

+ [6]

靶点

CDA x DNMT1

作用方式

抑制剂

作用机制

CDA抑制剂(胞嘧啶核苷脱氨酶抑制剂)、DNMT1抑制剂(DNA（胞嘧啶-5）-甲基转移酶-1抑制剂)、表观遗传学药物

治疗领域

肿瘤血液及淋巴系统疾病其他疾病+ [3]

在研适应症

急性髓性白血病慢性粒单核细胞白血病骨髓增生异常综合征+ [37]

非在研适应症

急性淋巴细胞白血病难治性贫血难治性贫血伴原始细胞过多+ [8]

原研机构

Astex Pharmaceuticals, Inc.

在研机构

Taiho Oncology, Inc.Thai Otsuka Pharmaceutical Co., Ltd.

National Cancer Institute

+ [8]

非在研机构

Forma Therapeutics, Inc.

Pfizer Inc.

权益机构

National Cancer Institute

The University of Texas MD Anderson Cancer Center

Astex Pharmaceuticals, Inc.

最高研发阶段批准上市

首次获批日期

美国 (2020-07-07),

骨髓增生异常综合征

最高研发阶段(中国)临床1/2期

特殊审评孤儿药 (美国)、孤儿药 (欧盟)、孤儿药 (澳大利亚)

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结构/序列

分子式C9H14F2N2O5

InChIKeyVUDZSIYXZUYWSC-DBRKOABJSA-N

CAS号1141397-80-9

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关联

67

项与地西他滨/西达尿苷相关的临床试验

NCT07437950

/ Not yet recruiting临床2期IIT

A Randomized Phase II Trial of ASTX727 With Standard Duration Versus Shorter Duration of Venetoclax in Genomically Heterogenous AML Among Adults Aged 60 or Older and Less Fit for Intensive Therapy: A MyeloMATCH Substudy

This phase II MyeloMATCH treatment trial compares ASTX727 with standard duration versus shorter duration of venetoclax for the treatment of newly diagnosed acute myeloid leukemia (AML). ASTX727 is a combination of decitabine and cedazuridine. 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. 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. 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. Shorter duration venetoclax may be as effective as standard duration venetoclax when given with ASTX727 for the treatment of newly diagnosed AML.

开始日期2026-10-14

申办/合作机构

National Cancer Institute

NCT07012044

/ Recruiting临床1期IIT

A Phase 1 Study of Oral Cedazuridine and Decitabine Combination (ASTX727, NSC# 820631) and Filgrastim as Maintenance Therapy Post-Hematopoietic Stem Cell Transplant in Children With High-Risk Acute Myeloid Leukemia

This phase I trial tests the safety, side effects, and best dose of ASTX727 and filgrastim for the treatment of children with high risk acute myeloid leukemia that has come back after a period of improvement (recurrent) or that does not respond to treatment (refractory) who have undergone allogenic hematopoietic stem cell transplantation. ASTX727 is a combination of cedazuridine and decitabine. 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. Filgrastim stimulates the production of neutrophils (a type of white blood cell) which can help to prevent infection. Giving ATSX727 and filgrastim may be safe and tolerable in treating children with high risk, recurrent or refractory acute myeloid leukemia who have undergone allogenic hematopoietic stem cell transplantation.

开始日期2026-07-26

申办/合作机构

National Cancer Institute

NCT07153497

/ Not yet recruiting临床2期IIT

A Randomized Phase 2 Trial of Olutasidenib-Based Therapies in Patients With Newly Diagnosed IDH1-Mutant Myeloid Malignancies: A MyeloMATCH Substudy

This phase II MyeloMATCH treatment substudy tests the addition of olutasidenib to usual treatment in patients with higher-risk myelodysplastic syndrome (MDS) or patients with acute myeloid leukemia (AML) with a mutation in the IDH1 gene. Olutasidenib blocks the protein made by the mutated IDH1 gene. Blocking this protein may help keep cancer cells from growing. For patients with MDS, olutasidenib will be added to decitabine-cedazuridine (also called ASTX727). Decitabine is in a class of medications called hypomethylating agents and is the standard treatment for MDS. It works by helping the bone marrow produce normal blood cells and by killing abnormal cells in the bone marrow. The cedazuridine makes it possible to take the decitabine by mouth. Adding olutasidenib to the usual treatment for MDS (ASTX727) may increase the likelihood of going into remission. For patients with AML, olutasidenib and ASTX727 will be combined with venetoclax, a class of medications called B-cell lymphoma-2 (BCL-2) inhibitors. Venetoclax may stop the growth of cancer cells by blocking BCL-2, a protein needed for cancer cell survival. Adding olutasidenib to the usual treatment for AML (ASTX727 and venetoclax) may increase the likelihood of going into remission. For low risk MDS, the substudy tests whether giving olutasidenib alone helps improve blood counts.

开始日期2026-05-27

申办/合作机构

National Cancer Institute

100 项与地西他滨/西达尿苷相关的临床结果

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100 项与地西他滨/西达尿苷相关的转化医学

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100 项与地西他滨/西达尿苷相关的专利（医药）

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35

项与地西他滨/西达尿苷相关的文献（医药）

2026-04-15·CANCER

A phase 1 study of ASTX727 plus talazoparib in patients with triple‐negative or hormone resistant/HER2‐negative metastatic breast cancer

Article

作者: Emily Douglas MD ; Erin Conder MS, CCRP ; Kathy D. Miller MD ; Sandra Althouse MS ; Kenneth P. Nephew PhD ; Feyruz V. Rassool PhD ; H. Josh Jang PhD ; Ryan Burgos BS, MBA ; Bryan P. Schneider MD ; Woonbok Chung PhD ; Alexandra Thomas MD ; Tarah Ballinger MD ; Yong Zang PhD ; Katherine Ansley MD ; Jean-Pierre Issa PhD

Abstract:

Background:

Poly(adenosine diphosphate ribose) polymerase (PARP) is recruited to DNA damage sites along with epigenetic factors such as DNA methyltransferase 1 (DNMT1). Inhibitors of DNMT modulate reactive oxygen species (ROS)‐cyclic adenosine monophosphate (cAMP)/Protein Kinase A signaling and induce a “BRCAness phenotype” that further sensitizes cells to PARPi. In preclinical studies, combined DNMTi + PARPi therapy was effective in both triple‐negative (TNBC) and hormone resistant (HRBC) models with intact BRCA.

Methods:

The authors conducted a phase 1 study combining the oral DNMTi ASTX727 with the PARPi talazoparib in patients with previously treated TNBC or HRBC. Patients with deleterious mutations of BRCA were excluded. A classical 3+3 design guided dose escalation/de‐escalation, and 28 days constituted each cycle. Serial peripheral blood mononuclear cells (PBMCs) were analyzed for changes in methylation using the Infinium Methylation EPIC BeadChip and LINE1 sequencing.

Results:

Thirty‐four evaluable patients were enrolled and treated in eight dose cohorts. Myelosuppression was common with grade >3 neutropenia in 42% and grade 3 anemia and thrombocytopenia in 13%. Dose‐limiting toxicity was limited to neutropenia. Efficacy was assessed in 29 patients. There were no objective responses, six patients had stable disease persisting for >4 months in three patients. LINE1 demethylation ranged from ∼2%–10% and immune‐specific CpGs (methylation in immune cells) changed 1%–5% at day 15. Methylation changes were not dose‐dependent.

Conclusions:

ASTX727 plus talazoparib produces significant myelosuppression without other adverse events. Modest methylation changes in PBMCs were detected. There were no objective responses, but some heavily pretreated patients had stable disease for >4 months despite the attenuated doses.

2026-03-10·Blood Advances

Venetoclax/FluBu2 RIC transplant followed by all-oral venetoclax/decitabine maintenance for poor-risk MDS/AML

Article

作者: Stone, Richard M. ; Fiorilla, Jade ; DeAngelo, Daniel J. ; Auriemma, Elise ; Murdock, H. Moses ; Fell, Geoffrey ; Kelkar, Amar H. ; Panaro, Kevin M. ; Garcia, Jacqueline S. ; Lindsley, R. Coleman ; Antin, Joseph H. ; Cutler, Corey S. ; Ryan, Jeremy ; Soiffer, Robert J. ; Shapiro, Roman ; Gooptu, Mahasweta ; Lim, Felicia ; Brock, Jennifer ; Bosch-Vilaseca, Anna ; Bat-Erdene, Denbaa ; Ritz, Jerome ; Abel, Gregory A. ; Kim, Haesook T. ; Letai, Anthony ; Ho, Vincent T.

Abstract:

To improve the tolerability of posttransplant maintenance and outcomes despite poor-risk disease genetics, we conducted a phase 1 study of venetoclax (Ven) with FluBu2 (fludarabine/busulfan) reduced-intensity chemotherapy transplantation using tacrolimus/methotrexate graft-versus-host disease (GVHD) prophylaxis, followed by all-oral Ven/decitabine-cedazuridine (Ven/Dec-c) maintenance in patients with poor-risk MDS/AML (myelodysplastic syndrome/acute myeloid leukemia; N = 30). Overall, 58% had previous Ven exposure and 63% had TP53 mutation; 15/19 had TP53 multihit state. At a median of +55 days, prophylactic maintenance therapy with Ven (400 mg on days 1-14) and Dec-c (35 mg decitabine and 100 mg cedazuridine tablet on days 1, 3, and 5, or days 1, 2, and 3) was initiated for 8 cycles of 42 days each in 26 of 30 patients (87%; of the remaining patients, 3 relapsed early and 1 withdrew). On maintenance, grade 3/4 neutropenia (96%) occurred although infections were rare (n = 2). No dose-limiting toxicities occurred. The 6-month acute GVHD grade 2 to 4 rate was 13%. The 1-year moderate/severe chronic GVHD rate was 31%. At a median follow-up of 25.1 months (range, 15-33), median overall survival (OS) and progression-free survival (PFS) were not reached. On maintenance, 2-year OS was 77%, PFS was 62%, nonrelapse mortality was 0%, and cumulative incidence of relapse was 38%. Exploratory studies identified 96% of patients had pretransplant next-generation sequencing molecular residual disease (MRD) positivity, favorable survival in those with non-TP53 MRD positivity, and delayed conversion on maintenance in 11 of 18 (61%) with TP53-MRD positivity. Patient-reported outcomes assessed in the first 6 months of maintenance were stable except for emotional function, which significantly improved. This trial was registered at www.ClinicalTrials.gov as NCT03613532.

2026-02-10·Blood Advances

Decitabine-cedazuridine in patients with MDS and TP53 mutations

Article

作者: Griffiths, Elizabeth A. ; Urrutia, Samuel ; Garcia-Manero, Guillermo ; Sano, Yuri ; Savona, Michael ; Bataller, Alex ; McCloskey, James ; Sasaki, Koji ; Keer, Harold N. ; Oganesian, Aram ; Montalban-Bravo, Guillermo ; Zeidan, Amer ; Kantarjian, Hagop ; Yee, Karen

Patients with myelodysplastic syndromes (MDS) harboring TP53 mutations have poor outcomes. The objective of this study is to evaluate patients with TP53 mutations treated in the phase 2/3 studies of decitabine-cedazuridine (DEC-C) in MDS. We divided patients into three groups: TP53wt, TP53single-hit, and TP53multi-hit. We then performed propensity matching of patients who were treated with DEC-C vs a cohort of patients treated with parenteral hypomethylating agents (HMA). 180 patients were analyzed of which 73 (40.5%) had TP53 mutations, 23 (12%) with TP53multi-hit. Patients with TP53multi-hit more frequently had complex cytogenetics (69.5%), and had fewer median number of co-mutations (2.5, IQR 2-3) compared to TP53single-hit(3, IQR 1-5), or TP53wt (4, IQR 3-6) (p=0.002). Patients with TP53multi-hit had a higher chance of lack of response with 39.1% vs 28.1% for TP53single-hit (p=0.2). Patients with TP53mult-hit lost response earlier at 8.2 months, vs 13.2 months for TP53single-hit, and 15.1 months for TP53wt (p=0.1). Median overall survival (mOS) was 11.5 months (95% CI: 8.6 - 19.1) for TP53mult-hit, 22.1 months (95% CI: 14.6 - 35.9) for TP53single-hit, and 31.7 months (95% CI: 19.5 - 51.1) for TP53wt (log-rank, p < 0.005). Propensity scores matched 47 TP53mutpatients treated with DEC-C and 47 TP53mut patients treated with single agent parenteral HMA. Median survival was 13.1 months (95% CI: 8.4 - 21.3) for DEC-C vs 8.0 months (95% CI: 5.2 - 13.0) for single agent parenteral HMA (log-rank, p=0.047). In patients with MDS harboring TP53mut, DEC-C may improve overall survival compared to parenteral HMA.

73

项与地西他滨/西达尿苷相关的新闻（医药）

2026-05-15

·EndPoints

Aardvark's next move after clinical hold; Alumis' verdict on Acelyrin asset

Plus, news about Tenaya’s TN-401 and Taiho’s Inqovi. 📉 Aardvark to unblind rare disease trial following clinical hold: The FDA has placed a full clinical hold on the company’s candidate for Prader-Willi syndrome, called ARD-101. Aardvark plans to unblind all studies of the drug, including the Phase 3 HERO trial, and assess data before deciding on next steps. The company previously paused enrollment in the late-stage study voluntarily. Aardvark’s share price $AARD was down about 25% when the market opened Friday. — Ayisha Sharma 🥫 Alumis finally makes decision on Acelyrin asset: A year after merging with Acelyrin, Alumis has decided to can a thyroid eye disease asset from the California biotech. Alumis will look for “strategic alternatives” for lonigutamab following a review that lasted about a year. The ValenzaBio-derived candidate had mixed Phase 2 data at the beginning of 2025, a month before Acelyrin and Alumis announced their marriage . — Kyle LaHucik ❤️‍🩹 Tenaya’s early-stage gene therapy data: The California biotech said its treatment, called TN-401, produced “dramatic” improvements in electrical stability in a rare heart condition. Six patients with arrhythmogenic right ventricular cardiomyopathy enrolled across two dose cohorts saw reductions in premature ventricular contractions ranging from 31% to 84%, Tenaya reported. — Ayisha Sharma 🟢 FDA approves Taiho’s Inqovi for certain AML patients: The agency greenlit a combination of Inqovi plus AbbVie and Roche’s Venclexta for newly-diagnosed patients with acute myeloid leukemia who are 75 years or older, or ineligible for intensive induction chemotherapy. Inqovi is already approved for certain patients with myelodysplastic syndromes and chronic myelomonocytic leukemia. — Ayisha Sharma

2026-05-15

·四两同学

0515-衰老第一次能“验尿追踪”：Nature Aging 新技术公布

一、尿液一测，就能知道体内衰老细胞多不多 5月13日 Nature Aging 发表 Technical Report，Hartono et al. 开发了一种注射用纳米探针，注射后通过尿液比色读数，即可追踪体内衰老细胞的变化。技术路径：探针注入血液后，被一种叫 MMP-7 的蛋白酶（衰老细胞特异性分泌）切割，释放出金纳米颗粒，经肾脏进入尿液，再用比色法读取信号。检测限比旧方法提升 250 倍，小鼠尿液信号与肿瘤组织中 p21 阳性细胞比例高度吻合（AUC=0.933）。已在 8 例肺癌/肺纤维化患者活检组织中验证了 MMP-7 的特异性。临床场景：化疗后想判断体内衰老细胞是否在减少，不用抽血，直接验尿。Senolytic 药物（清除衰老细胞的药）治疗后，尿液信号应声下降，提示疗效可实时追踪。 Q：这项技术普通人什么时候能用上？ A：目前是 Technical Report，即技术方法验证，尚未进入临床试验审批流程。探针本身需要 GMP 生产、人体安全性验证、III 期临床验证——每步都需要时间。但路径是清晰的，离实际应用比大多数实验室研究更近。 Q：MMP-7 只在肺癌里验证过，其他癌症可以用吗？ A：研究团队同时测试了黑色素瘤、前列腺癌、乳腺癌等多个癌细胞系，MMP-7 分泌存在差异。这个探针的优势在于可以通过更换底物肽链来适配不同的 SASP 蛋白酶，属于模块化平台——但目前 MMP-7 场景仅限肺癌和肺纤维化。当前限制：技术验证阶段，人体临床数据待补充；MMP-7 特异性需在更多癌种中验证。| Nature Aging，2026-05-13（doi:10.1038/s43587-026-01116-z）二、肌肉干细胞为什么老了就跑不动了 5月14日 Nature Aging 发表 Article，David E. Lee et al.（杜克大学）揭示了一条此前未被充分认识的肌肉干细胞激活通路——谷氨酰胺驱动的还原 TCA 循环。机制：肌肉干细胞激活时需要大量脂肪酸来构建细胞膜，这个过程叫"从头合成脂肪"。年轻干细胞靠谷氨酰胺进入还原 TCA 循环，源源不断供给脂肪合成原料；老年干细胞丢掉了这条通路，激活信号来了也跑不动。这是肌肉衰减（sarcopenia）的直接代谢根源。干预可能：同位素稳定追踪实验确认，补充谷氨酰胺或直接激活 reductive TCA 循环，可以在老年小鼠中恢复肌肉干细胞的激活能力。 Q：吃谷氨The, the, the酰胺能改善肌肉吗？ A：不能直接画等号。这是小鼠干细胞层面的代谢发现，从食物到肌肉干细胞内的代谢通量，中间差着好几步。但这个发现给 sarcopenia 药物研发提供了一个新靶点——真正能用的药还需要几年。 Q：和之前雷帕霉素试验（0513）有什么关联？ A：PEARL 试验（0513）证明低剂量雷帕霉素在健康人身上安全；这个研究从机制上解释了 mTOR 抑制和肌肉维持之间的代谢逻辑——两条线是互补的，mTOR 抑制是上游事件，谷氨酰胺代谢是下游执行路径。当前限制：全程小鼠实验，无人体数据；从代谢发现到药物干预还有距离。| Nature Aging，2026-05-14（doi:10.1038/s43587-026-01120-3）三、肠道变老，会直接让你的脑子记不住东西肠道和大脑之间有一条高速公路，叫肠-脑轴。Stanford 医学院与 Arc Institute 在 Nature 发表研究，阐明了衰老肠道如何通过这条路直接影响记忆功能。机制：随着肠道老化，肠道上皮细胞产生一类特定的代谢物（3-吲哚丙酸是其中之一），这些物质通过血液循环进入大脑，抑制海马区神经前体细胞的增殖——新神经元长不出来，记忆自然跟不上。实验中，给老年小鼠补充 3-吲哚丙酸，神经前体细胞活性恢复，记忆测试表现回升。 Q：3-吲哚丙酸吃什么能补？ A：3-吲哚丙酸是肠道菌群分解色氨酸的产物，十字花科蔬菜（西兰花、芥蓝）有助于维持产生这类代谢物的菌群丰度。但食物补充和研究中使用的剂量差距很大，目前无法做到"吃够量"。研究方向是开发稳定剂型，这比单纯食补更现实。当前限制：动物实验，人体数据计划中；食物来源不足以达到研究剂量。| Nature，2026-03（Stanford/Arc Institute）今日速递 • FDA 批准 Inqovi：急性髓系白血病迎来口服复方制剂。5月13日获批，口服 decitabine + cedazuridine 复方，联合 venetoclax 用于无法耐受强化化疗的 AML 患者，老年/合并症患者直接获益。（FDA，2026-05-13） • FDA 加速批准 Beqalzi（sonrotoclax）：套细胞淋巴瘤新 BCL-2 抑制剂。5月13日加速批准，既往至少两线治疗（含 BTK 抑制剂）后复发的套细胞淋巴瘤患者适用。BCL-2 通路是淋巴瘤细胞存活的关键，抑制后诱导凋亡。（FDA，2026-05-13） • 818号令施行满两周，细胞治疗进入法治化阶段。5月1日起《生物医学新技术临床研究和临床转化应用管理条例》正式实施，首部针对细胞治疗、基因编辑的全链条监管法规落地，野蛮生长时代结束。（国务院令第818号）今日健康Tips 关注尿液颜色，是一个不花钱的信号今天的头条研究说明一件事：体内衰老细胞多不多，理论上有办法追踪了。在技术还没成熟之前，有一个更简单的信号可以关注——尿的颜色和气味。长期深色尿、泡沫多、有异味，可能提示水分摄入不足、蛋白负荷过重或泌尿系统问题。最简单的行动：每天观察晨尿（起床后第一次），淡黄色透明为佳；如果持续深黄且多泡，连续三天记录后找医生聊一次。不需要仪器，不需要试剂盒。 *参考资料* • ALBANC Nanoprobe: Hartono et al., Nature Aging, 2026-05-13 • Muscle Stem Cell Glutamine: Lee et al., Nature Aging, 2026-05-14 • Gut-Brain Memory: Stanford/Arc Institute, Nature, 2026-03 • FDA Approvals: FDA.gov, 2026-05-13

2026-05-15

·PMLiVE

US FDA approves Taiho’s Inqovi for older adults with acute myeloid leukaemia

The US FDA has approved Taiho’s Inqovi plus venetoclax as a treatment for adults with newly diagnosed acute myeloid leukaemia (AML). The approval is for patients who are 75 years or older or who are ineligible for intensive induction chemotherapy. Inqovi (decitabine and cedazuridine) in combination with venetoclax is the first and only all-oral combination treatment regimen approved for this patient population, offering an alternative to parenteral hypomethylating agent–based regimens that require frequent clinic visits. The approval was supported by results from the phase 2 ASCERTAIN-V study of INQOVI plus venetoclax in adult patients with newly diagnosed AML who were ineligible for intensive induction chemotherapy. Inqovi is an orally administered hypomethylating regimen previously approved in the U.S. and Canada for the treatment of adults with myelodysplastic syndromes (MDS) and chronic myelomonocytic leukemia (CMML). Peter Melnyk, President and Chief Executive Officer of Taiho Oncology, said: “This FDA approval represents a significant milestone for patients with newly diagnosed acute myeloid leukaemia who are not candidates for intensive induction chemotherapy. “With the approval of an all-oral regimen, Inqovi in combination with venetoclax brings a new treatment option to this patient population and underscores our commitment to advancing innovative, patient-focused therapies in haematologic malignancies.” In 2026, an estimated 22,720 people in the U.S. will be diagnosed with AML, a cancer of the blood and bone marrow. More than half of those patients are likely to be ineligible for intensive induction chemotherapy due to advanced age or health concerns. Harold Keer, Chief Medical Officer of Taiho Oncology, said: “This approval marks an important step forward in expanding how treatment can be delivered for this patient population, offering an all-oral option that can potentially reduce the overall treatment burden associated with receiving treatment in hospitals or infusion centers. We believe this approach has the potential to make a meaningful impact for patients and caregivers.”

上市批准临床结果临床2期

100 项与地西他滨/西达尿苷相关的药物交易

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外链

KEGG	Wiki	ATC	Drug Bank
-	地西他滨/西达尿苷	L01XY	DB15694

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	欧盟	Otsuka Pharmaceutical Netherlands B.V.	2023-09-15
急性髓性白血病	冰岛	Otsuka Pharmaceutical Netherlands B.V.	2023-09-15
急性髓性白血病	列支敦士登	Otsuka Pharmaceutical Netherlands B.V.	2023-09-15
急性髓性白血病	挪威	Otsuka Pharmaceutical Netherlands B.V.	2023-09-15
慢性粒单核细胞白血病	澳大利亚	Otsuka Australia Pharmaceutical Pty Ltd.	2020-10-29
骨髓增生异常综合征	美国	Taiho Oncology, Inc.	2020-07-07

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适应症	最高研发状态	国家/地区	公司	日期
难治性贫血	临床3期	美国	Astex Pharmaceuticals, Inc.	2018-02-15
难治性贫血	临床3期	奥地利	Astex Pharmaceuticals, Inc.	2018-02-15
难治性贫血	临床3期	加拿大	Astex Pharmaceuticals, Inc.	2018-02-15
难治性贫血	临床3期	捷克	Astex Pharmaceuticals, Inc.	2018-02-15
难治性贫血	临床3期	法国	Astex Pharmaceuticals, Inc.	2018-02-15
难治性贫血	临床3期	德国	Astex Pharmaceuticals, Inc.	2018-02-15
难治性贫血	临床3期	匈牙利	Astex Pharmaceuticals, Inc.	2018-02-15
难治性贫血	临床3期	意大利	Astex Pharmaceuticals, Inc.	2018-02-15
难治性贫血	临床3期	西班牙	Astex Pharmaceuticals, Inc.	2018-02-15
难治性贫血	临床3期	英国	Astex Pharmaceuticals, Inc.	2018-02-15

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临床结果

适应症

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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


NIBIT-ML1 (AACR2026)	临床2期	转移性黑色素瘤	42	ASTX727 plus I+N	製憲襯遞廠構壓廠選醖(衊窪遞獵構積醖醖衊鹽) = 顧願壓獵繭餘製蓋窪觸淵淵網齋淵願範蓋壓壓 (製顧網餘構膚網醖壓廠, 5.0 ~ 13.8) 更多	积极	2026-04-21
				I+N	製憲襯遞廠構壓廠選醖(衊窪遞獵構積醖醖衊鹽) = 蓋夢鑰顧網網選醖鏇簾淵淵網齋淵願範蓋壓壓 (製顧網餘構膚網醖壓廠, 5.0 ~ 6.6) 更多
NCT06802146 (ASH2025)	临床1期	意义不明的克隆性血细胞减少症	138	DEC/CED	餘願簾夢構壓壓鏇簾製(壓觸鏇築範壓壓製簾遞) = 襯網餘餘糧觸蓋膚餘糧顧築夢糧簾淵鬱構膚選 (衊齋簾製鹽衊獵鹽鏇鏇 ) 更多	积极	2025-12-06
NCT06661915 (ASH2025)	临床2期	骨髓增生性疾病	50	ASTX727 + iadademstat	夢製顧夢壓獵製窪製積(範繭觸範繭鏇夢窪顧遞) = 餘餘衊窪鏇襯齋窪鏇醖鏇遞壓鏇衊觸構範選蓋 (鹹艱範壓鏇壓觸廠鹹糧 )	积极	2025-12-06
				ASTX727	夢製顧夢壓獵製窪製積(範繭觸範繭鏇夢窪顧遞) = 鑰壓鹹鏇壓醖積鑰顧簾鏇遞壓鏇衊觸構範選蓋 (鹹艱範壓鏇壓觸廠鹹糧 )
NCT05010772 (ASH2025)	临床1期	急性髓性白血病维持	35	ASTX727 35/100 mg PO	築繭範製衊鏇範網壓鏇(襯壓艱蓋鹽網鏇壓窪鬱) = 衊憲選遞窪鏇夢網廠壓糧鑰壓積築糧遞網遞蓋 (製窪獵蓋廠獵鬱蓋淵網 ) 更多	积极	2025-12-06
				ASTX727 35/100 mg PO + venetoclax 400 mg (azole adjusted) PO	築繭範製衊鏇範網壓鏇(襯壓艱蓋鹽網鏇壓窪鬱) = 範餘簾醖壓範糧顧廠獵糧鑰壓積築糧遞網遞蓋 (製窪獵蓋廠獵鬱蓋淵網 ) 更多
ISRCTN30808508 (AMMO, ASH2025)	临床2期	骨髓增生性疾病	77	ASTX727	糧糧餘鬱齋醖襯鬱鑰繭(構窪衊衊齋糧壓齋糧觸) = 齋範蓋蓋範願網網範廠積憲選夢壓鹽積簾積淵 (餘夢淵蓋築夢膚夢糧鬱, 39.3 ~ 66.3) 更多	积极	2025-12-06
				Hydroxycarbamide/Best Supportive Care	糧糧餘鬱齋醖襯鬱鑰繭(構窪衊衊齋糧壓齋糧觸) = 範廠選願淵鑰壓鑰獵築積憲選夢壓鹽積簾積淵 (餘夢淵蓋築夢膚夢糧鬱, 14.9 ~ 49.4) 更多
NCT04655755 (ASH2025)	临床1/2期	高危骨髓增生异常综合征 \| 慢性粒单核细胞白血病一线	69	Oral decitabine/cedazuridine + venetoclax	糧夢鹹鹽醖餘窪鹽衊醖(鏇製憲壓廠遞蓋廠願憲) = Patients with ASXL1mut had a median OS not reached (vs 18 months in patients with ASXL1wt, P=0.008) 衊艱鹹糧遞遞糧觸鹹範 (繭艱鑰繭餘襯憲廠鏇範 ) 更多	积极	2025-12-06
NCT05360160 (SAVE, ASH2025)	临床2期	急性髓性白血病 NPM1 mutation \| KMT2A rearrangement	17	Decitabine/cedazuridine + venetoclax + revumenib	獵壓選鬱艱繭壓膚獵齋(鹽築艱窪鏇簾網衊醖網) = QTc prolongation occurred in 8 (47%) pts; 3 were grade 2 (18%), the rest were grade 1 (29%) 觸鹽鹹鹽艱網鏇鬱鬱範 (衊壓製齋選鹽鑰蓋糧繭 ) 更多	积极	2025-12-06
NCT04340843 (ETCTN/NCI 10330, CTgov)	临床2期	软骨肉瘤 \| 中枢神经系统肿瘤 \| 脑转移瘤	19	ASTX727+Belinostat (Treatment (Belinostat, ASTX727))	壓夢構鑰簾鹹艱鹹積簾 = 構壓憲壓壓積襯觸選壓廠構艱製鬱觸選膚蓋糧 (鹹構艱顧鑰築觸憲積範, 構廠醖積繭鹽選範糧鬱 ~ 窪築築築獵鹽膚鏇餘繭) 更多	-	2025-09-16
				SGI-110+Belinostat (Treatment (Belinostat, SGI-110))	觸積鬱淵簾糧艱壓鏇衊 = 齋獵夢膚鏇願網襯願餘廠簾繭網衊鹽構壓鏇簾 (壓壓鑰廠遞遞鬱製襯壓, 夢選衊遞鹽齋餘製繭構 ~ 糧選鑰獵憲憲網糧膚鏇) 更多
NCT04657081 (ASCO2025) 人工标引	临床2期	急性髓性白血病一线	101	decitabine-cedazuridine (DEC-C)+venetoclax	齋膚齋鹹範淵繭鹽憲廠(醖範觸構蓋艱窪衊積襯) = 製範遞選鬱積構構糧衊製廠淵鹹網繭願醖獵鹹 (艱繭鏇鹹築齋獵膚顧顧, 36.5 ~ 56.7) 更多	积极	2025-05-23
NCT04657081 (S135, EHA2025)	临床1/2期	急性髓性白血病	189	DECITABINE-CEDAZURIDINE (DEC-C) (DEC-C + VEN)	衊繭糧齋鹹顧鹽蓋淵顧(顧蓋積積廠築蓋鹹艱願) = 膚遞簾衊遞願憲獵齋繭獵廠餘鏇簾廠鑰觸鹽窪 (夢觸鹽蓋顧餘簾襯糧構, 36.5 ~ 56.7) 更多	积极	2025-05-14