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)

治疗领域

肿瘤血液及淋巴系统疾病其他疾病+ [4]

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+ [19]

非在研适应症

造血干细胞移植IDH1突变急性髓性白血病复发性骨髓增生异常综合征+ [1]

原研机构

Astex Pharmaceuticals, Inc.

在研机构

Otsuka Australia Pharmaceutical Pty Ltd.

Astex Pharmaceuticals, Inc.

Otsuka Pharmaceutical Co., Ltd.

+ [9]

非在研机构

FORMA Therapeutics, 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

分子式C9H14F2N2O5

InChIKeyVUDZSIYXZUYWSC-DBRKOABJSA-N

CAS号1141397-80-9

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关联

48

项与地西他滨/西达尿苷相关的临床试验

NCT06661915 / Not yet recruiting临床2期IIT

A Randomized Phase 2 Trial of ASTX727 +/- Iadademstat in Accelerated/Blast-Phase Philadelphia Chromosome-Negative Myeloproliferative Neoplasms (MPNs)

This phase II trial compares the effect of ASTX727 in combination with iadademstat to ASTX727 alone in treating patients with accelerated or blast phase Philadelphia chromosome negative myeloproliferative neoplasms (MPNs). ASTX727 is a combination of two drugs, 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. Iadademstat may stop the growth of tumor cells by blocking some of the enzymes needed for cell growth. Giving ASTX727 in combination with iadademstat may be more effective than ASTX727 alone in treating patients with accelerated or blast phase Philadelphia chromosome negative MPNs.

开始日期2025-01-31

申办/合作机构

National Cancer Institute

NCT06284460 / Withdrawn临床1/2期IIT

Phase I/II Study of a Combination of Decitabine and Cedazuridine (ASTX727) and ASTX029, an ERK Inhibitor, for Patients With RAS Pathway Mutant Myelodysplastic Syndromes and Myelodysplastic/Myeloproliferative Neoplasms

The goal of Part 1 of this clinical research study is to find the highest tolerable dose of ASTX029 that can be given in combination with ASTX727 to participants who have RAS-mutant MDS or MDS/MPN. The goal of Part 2 of this clinical research study is to learn if the dose of ASTX029 found in Part 1 can help to control the disease when used in combination with ASTX727.

开始日期2025-01-31

申办/合作机构

The University of Texas MD Anderson Cancer Center

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

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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30

项与地西他滨/西达尿苷相关的文献（医药）

2024-09-23·BRITISH JOURNAL OF HAEMATOLOGY

Oral decitabine/cedazuridine versus intravenous decitabine for acute myeloid leukaemia: A randomised, crossover, registration, pharmacokinetics study.

Article

作者: Novák, Jan ; Sano, Yuri ; Illes, Arpad ; Santini, Valeria ; Fracchiolla, Nicola Stefano ; Lübbert, Michael ; Lunghi, Monia ; Platzbecker, Uwe ; Rodríguez-Macías, Gabriela ; Metzelder, Stephan K ; Oganesian, Aram ; Arnan, Montserrat ; Mayer, Jiří ; Krauter, Jürgen ; Koristek, Zdenek ; Del Castillo, Teresa Bernal ; Keating, Mary-Margaret ; Geissler, Klaus ; Keer, Harold

This study compared decitabine exposure when administered IV (DEC-IV) at a dose of 20 mg/m² for 5-days with orally administered decitabine with cedazuridine (DEC-C), as well as the clinical efficacy and safety of DEC-C in patients with acute myeloid leukaemia (AML) who were ineligible for intensive induction chemotherapy. In all, 89 patients were randomised 1:1 to DEC-IV or oral DEC-C (days 1-5 in a 28-day treatment cycle), followed by 5 days of the other formulation in the next treatment cycle. All patients received oral DEC-C for subsequent treatment cycles until treatment discontinuation. Equivalent systemic decitabine exposures were demonstrated (5-day area under the curve ratio between the two decitabine formulations of 99.64 [90% confidence interval 91.23%, 108.80%]). Demethylation rates also were similar (≤1.1% difference). Median overall survival (OS), clinical response and safety profile with oral DEC-C were consistent with those previously observed with DEC-IV. Next-generation sequencing was performed to identify molecular abnormalities that impact OS and TP53 mutations were associated with a poor outcome. These findings support the use of oral DEC-C in patients with AML.

2024-09-01·Clinical Lymphoma Myeloma & Leukemia

Oral Decitabine/Cedazuridine Is an Effective Ambulatory Therapy for Patients With Myelofibrosis Refractory to JAK2 Inhibitor Therapy

Article

作者: Dueck, Amylou ; Ginzburg, Yelena ; Handa, Shivani ; Mascarenhas, John O ; Sivakumar, Ganesh ; Tremblay, Douglas ; Hoffman, Ronald ; Kremyanskaya, Marina ; Srisuwananukorn, Andrew

BACKGROUND:

Outcomes are dismal for patients with myelofibrosis (MF) who are no longer responsive to JAK2 inhibitors (JAKi) and/or have increasing blast cell numbers. Although prior reports have suggested the benefits of intravenous decitabine (DAC) combined with ruxolitinib for patients with Myeloproliferative Neoplasm (MPN) accelerated/blast phase (AP/BP), decitabine-cedazuridine (DEC-C), an oral fixed-dose combination providing equivalent pharmacokinetic exposure, has not been evaluated in MF.

METHODS:

We conducted a retrospective analysis of 14 patients with high-risk MF refractory to ruxolitinib or MPN-AP (10-19% blasts) treated with DEC-C +/- JAKi at Mount Sinai Hospital from 2021 to 2024.

RESULTS:

The cohort was elderly (median age,76 years) and almost uniformly possessed high risk mutations with 13 of the 14 patients progressing on JAKi therapy. With a median follow-up of 9.4 months, the median overall survival (OS) was 29 months for the entire cohort. Median OS was 10.8 months for MPN-AP and was not reached for ruxolitinib refractory MF patients. All patients (n = 9) receiving > 4 cycles of DEC-C had clinical benefit exemplified by a reduction in blast cell numbers, spleen size, and lack of progression to MPN-BP (78%). Furthermore, 3/14 patients proceeded to allogeneic stem cell transplant. Myelosuppression was a common adverse event which was managed by reducing the number of days of administration of DEC-C from 5 to 3 per cycle.

CONCLUSIONS:

This report demonstrates the feasibility, tolerability, and clinical benefit of an exclusively ambulatory regimen for high-risk, elderly patients with advanced MF which warrants further evaluation in a prospective clinical trial.

2024-04-01·The Lancet. Haematology

Oral decitabine and cedazuridine plus venetoclax for older or unfit patients with acute myeloid leukaemia: a phase 2 study

Article

作者: Garcia-Manero, Guillermo ; Kadia, Tapan ; Short, Nicholas ; Pierce, Sherry ; Alvarado, Yesid ; Bataller, Alex ; Jain, Nitin ; Masarova, Lucia ; Islam, Rabiul ; Konopleva, Marina ; Kornblau, Steven ; Ravandi, Farhad ; Bazinet, Alexandre ; Montalban-Bravo, Guillermo ; Maiti, Abhishek ; Issa, Ghayas ; Abuasab, Tareq ; Daver, Naval ; DiNardo, Courtney D ; Kantarjian, Hagop ; Yilmaz, Musa ; Huang, Xuelin ; Jabbour, Elias ; Montalbano, Kathryn ; Rausch, Caitlin R

BACKGROUND:

Hypomethylating agents combined with venetoclax are effective regimens in patients with acute myeloid leukaemia who are ineligible for intensive chemotherapy. Decitabine and cedazuridine (ASTX727) is an oral formulation of decitabine that achieves equivalent area-under-curve exposure to intravenous decitabine. We performed a single centre phase 2 study to evaluate the efficacy and safety of ASTX727 plus venetoclax.

METHODS:

This study enrolled patients with newly diagnosed (frontline treatment group) acute myeloid leukaemia who were ineligible for intensive chemotherapy (aged ≥75 years, an Eastern Cooperative Oncology Group [ECOG] performance status of 2-3, or major comorbidities) or relapsed or refractory acute myeloid leukaemia. Being aged 18 years or older and having an ECOG performance status of 2 or less were requirements for the relapsed or refractory disease treatment cohort, without any limits in the number of previous lines of therapy. Treatment consisted of ASTX727 (cedazuridine 100 mg and decitabine 35 mg) orally for 5 days and venetoclax 400 mg orally for 21-28 days in 28-day cycles. The primary outcome was overall response rate of ASTX727 plus venetoclax. Living patients who have not completed cycle one were not evaluable for response. Safety was analysed in all patients who started treatment. This study was registered on ClinicalTrials.gov (NCT04746235) and is ongoing. The data cutoff date for this analysis was Sept 22, 2023.

FINDINGS:

Between March 16, 2021, and Sept 18, 2023, 62 patients were enrolled (49 frontline and 13 relapsed or refractory) with a median age of 78 years (IQR 73-82). 36 (58%) were male; 53 (85%) were White, 4 (6%) Black, 2 (3%) Asian and 3 (5%) other or did not answer. 48 (77%) of 62 patients were European LeukemiaNet 2022 adverse risk, 24 (39%) had antecedent myelodysplastic syndromes, 12 (19%) had previously failed a hypomethylating agent, ten (16%) had therapy-related acute myeloid leukaemia, and 11 (18%) had TP53 mutations. The median follow-up time was 18·3 months (IQR 8·8-23·3). The overall response rate was 30 (64%) of 47 patients (95% CI 49-77) in frontline cohort and six (46%) of 13 patients (19-75) in relapsed or refractory cohort. The most common grade 3 or worse treatment-emergent adverse events were febrile neutropenia in 11 (18%) of 62 patients, pneumonia in eight (13%), respiratory failure in five (8%), bacteraemia in four (6%), and sepsis in four (6%). Three deaths occurred in patients in remission (one sepsis, one gastrointestinal haemorrhage, and one respiratory failure) and were potentially treatment related.

INTERPRETATION:

ASTX727 plus venetoclax is an active fully oral regimen and safe in most older or unfit patients with acute myeloid leukaemia. Our findings should be confirmed in larger multicentric studies.

FUNDING:

MD Anderson Cancer Center Support Grant, Myelodysplastic Syndrome/Acute Myeloid Leukaemia Moon Shot, Leukemia SPORE, Taiho Oncology, and Astex Pharmaceuticals.

23

项与地西他滨/西达尿苷相关的新闻（医药）

2024-09-12

·GlobeNewswire-Health Care

Biosplice Therapeutics Announces Initiation of Acute Myeloid Leukemia (AML) and Myelodysplastic Syndromes (MDS) Trial Sponsored by the National Cancer Institute (NCI)

Biosplice expands its clinical candidate, cirtuvivint, as standalone treatment and combination therapy in patients with AML and MDS, representing next step in ongoing collaboration with the NCISAN DIEGO, Sept. 12, 2024 (GLOBE NEWSWIRE) -- Biosplice Therapeutics, Inc. (“Biosplice”), a clinical-stage biotechnology company pioneering advancements in small molecule inhibition of CDC-like kinases (CLK) and Dual-specificity tyrosine phosphorylation-regulated (DYRK) kinases, is pleased to announce that the U.S. Food and Drug Administration (FDA) has cleared the NCI-sponsored Investigational New Drug (IND) application for cirtuvivint. This small molecule inhibitor of CLK and DYRK kinases is in development for the treatment of hematological malignancies and solid tumors. This clearance allows for the initiation of a new clinical trial of cirtuvivint, both as a standalone treatment for patients with relapsed/refractory AML and MDS as well as in combination with ASTX727 for patients with frontline high-risk MDS. The clinical study (NCI protocol 10674, NCT06484062) will be sponsored by the NCI, part of the National Institutes of Health, with Dr. Maximilian Stahl from the Dana-Farber Cancer Institute serving as principal investigator. This trial will be conducted in participating centers of the NCI’s Experimental Therapeutics Clinical Trials Network including Dana-Farber Cancer Institute and Memorial Sloan Kettering Cancer Center. The study aims to enroll up to 52 patients and will be conducted under the Cooperative Research and Development Agreement (CRADA) executed between Biosplice and the NCI. “We are thrilled that the NCI has received FDA clearance to launch this groundbreaking new Phase 1 trial of cirtuvivint in liquid tumors, both as monotherapy and in combination with ASTX727,” stated Dr. Yusuf Yazici, Chief Medical Officer of Biosplice. “This milestone is a major step forward in our efforts to advance innovative treatments targeting CLKs and DYRKs. Given that dysregulated alternative splicing is commonly implicated in AML and MDS, cirtuvivint’s ability to regulate alternative splicing via CLK and DYRK inhibition may provide a promising new therapeutic pathway for patients. Based on compelling anti-tumor activity across both solid and liquid tumors in in vitro and in vivo models, as well as data from two prior Phase 1 trials in solid tumors, cirtuvivint promises to greatly improve outcomes for patients in these critical and underserved areas.” This milestone highlights the ongoing collaboration between Biosplice and the NCI’s Cancer Therapy Evaluation Program (CTEP) through the NCI Experimental Therapeutics (NCI-NExT) program. After extensive evaluation, cirtuvivint was chosen for inclusion by NCI in the NExT programs following a competitive review. NCI-NExT partners with external researchers and leading scientific experts to accelerate the development of the most promising and innovative therapies, guiding them from early-stage research through to regulatory approval. About Biosplice:Biosplice stands at the forefront of research concentrating on the study and regulation of Cdc2-like kinases (CLKs) and dual-specificity tyrosine-regulated kinases (DYRKs). These kinases play pivotal roles in cell cycle regulation, splicing, and neurodevelopment, marking them as critical targets for therapeutic intervention in a range of diseases, including osteoarthritis, cancer, neurological disorders, and diabetes. With a robust chemical platform for kinase inhibition and a deep understanding of kinase signaling pathways, Biosplice leverages cutting-edge technologies to discover and develop highly selective kinase inhibitors. Biosplice’s drugs in clinical development include lorecivivint for osteoarthritis (completed Phase 3) and cirtuvivint for numerous cancers, with a broad preclinical pipeline that encompasses Alzheimer’s disease, diabetes and other degenerative conditions. About Cirtuvivint:Cirtuvivint is a small molecule inhibitor of CLK and DYRK kinases, which are increasingly recognized as key drivers of various cancers. By targeting these kinases, cirtuvivint modulates alternative pre-mRNA splicing, which may reduce the expression of genes vital for tumor growth, survival, and drug resistance. The compound has shown broad anti-tumor activity across a range of solid and liquid tumors in extensive preclinical studies. Cirtuvivint has also been investigated for the treatment of advanced solid tumors in two clinical trials. The first, SM08502-ONC-01 (NCT03355066), was a first-in-human dose escalation study designed to evaluate safety, tolerability, pharmacokinetics, and pharmacodynamics in patients with advanced solid tumors. The second, SM08502-ONC-03 (NCT05084859), was a Phase 1b trial assessing the efficacy of cirtuvivint in combination with standard treatments for patients with advanced castration-resistant prostate cancer, advanced non-small cell lung cancer, and advanced colorectal cancer. Learn more at https://www.biosplice.com

临床1期临床申请临床3期

2024-06-20

·PRNewswire

Escend Announces Poster Presentation at the Annual Meeting of the European Hematology Association (EHS) from an Investigator-Initiated Phase I/II study evaluating ES-3000 in Myelodysplastic Syndrome (MDS)

MENLO PARK, Calif., June 20, 2024 /PRNewswire/ -- Escend Pharmaceuticals, Inc., a privately held oncology company, announced today a poster presentation with initial data from the Australasian Leukaemia and Lymphoma Group's (ALLG) investigator-initiated Phase I/II platform study (MYDAS-T MDS05 domain 1) evaluating ES-3000 alone and in combination with ASTX727 at European Hematology Association (EHS) in Madrid, Spain. The poster is entitled, 'Combining oral Wnt/β catenin/inflammasome pathway inhibitor, a bis-benzylisoquinoline alkaloid (ES-3000) with oral decitabine/cedazuridine (ASTX727)* as a treatment strategy for myelodysplasia'. The primary objectives of the initial phase of the trial are to assess the safety profile of ES-3000 and determine the recommended phase 2 dose and dosing schedule of ES-3000 in combination with fixed-dose decitabine/cedazuridine (ASTX727). The results indicate a response in 40% of evaluable patients who received ES-3000 as a single agent. The dose-limiting toxicities as per BION modeling allowed the study to dose escalate. A copy of the poster is available at Escend Pharmaceuticals' website About ES-3000 ES-3000 is a small molecule, oral investigational product that reduces leukemic stem cells by β-catenin and Calmodulin protein-dependent kinase II gamma (CamKIIγ). ES-3000 is being developed for the treatment of myeloid malignancies including acute myeloid leukemia (AML), chronic myeloid leukemia (CML), and myelodysplastic syndrome (MDS). About Escend Escend's development strategy is to select drug candidates with established clinical safety that have not yet achieved US marketing approval and develop them for oncology based on new mechanism of action details, where their effects on specific cellular pathways can be leveraged for the development of novel therapeutics. About Australasian Leukaemia and Lymphoma Group's (ALLG) The Australasian Leukaemia and Lymphoma Group (ALLG) is Australia's and New Zealand's only collaborative clinical trial organisation that sponsors local investigator-initiated clinical trials. Established in 1973, the ALLG's membership of over 1,300 blood cancer health professionals at 94 networked sites includes haematologists, clinician researchers, scientists and nurses treating leukaemia, lymphoma, myeloma, myelodysplastic syndromes and other haematological malignancies. The ALLG plans, designs, conducts, monitors and publishes investigator initiated clinical trials to create better treatments and better lives for patients with blood cancers. For further information about this press release, please contact Saira Bates ([email protected]) or visit *Astex Pharmaceuticals study drug SOURCE Escend Pharmaceuticals, Inc.

临床研究临床结果

2024-04-01

·FierceBiotech

'One-two punch' of epigenetic cancer drugs could knock out colorectal cancer cells

An upcoming trial in patients with colorectal cancer will be the first to test an DNMT inhibitor and an EZH2 inhibitor together in any type of cancer. A pair of epigenetic cancer drugs packs a “one-two punch” against colorectal tumors to knock them out more effectively than either medication alone, a new study in cells suggests. In a journal article published March 27 in Science Advances, a team of researchers led by scientists from the Van Andel Institute in Grand Rapids, Michigan showed that a low dose of the DNA methyltransferase (DNMT) inhibitor decitabine combined with Tithe EZH2 inhibitor tazemetostat successfully induced changes that would make cancer cells more vulnerable to destruction by the immune system. The chemotherapy decitabine is commercialized by Eisai as Inqovi; tazemetostat is commercialized by Ipsen as Tazverik. Neither company was involved in the study. While agents in both classes of drugs are FDA approved to treat blood cancer, they haven't had much success in solid tumors such as colorectal cancer, Scott Rothbart, Ph.D., the study’s corresponding author, said in a press release. “Our findings highlight the promise of combination cancer therapies by revealing how these two medications interact, with the DNMT inhibitor priming cancer cells in a way that makes the EZH2 inhibitor more effective.” “Epigenetic” is a term that refers to typically reversible modifications made to genes that do not directly alter the genes themselves, but rather affect their expression. Cancer progression involves many epigenetic changes both to the cancer cells themselves and to the immune cells that would otherwise destroy them. Scientists have attempted to destroy cancer by countering these changes pharmacologically and restoring the expression of anti-cancer genes. The most established means of doing so is with histone deacetylase inhibitors, or HDAC inhibitors, such as Merck’s Zolinza (vorinostat) for lymphoma and Acrotech Biopharma’s Beleodaq (belinostat) for myeloma. The only other FDA-approved DNMT inhibitor besides Inquovi is Celgene’s acute myeloid leukemia drug Vidaza (azacitidine). Tazverik is the sole EZH2 inhibitor with FDA approval. Earlier work by Van Andel Institute researchers showed that DNMT inhibitors cause cancer cells to act as though they’ve been infected by a virus, making them more vulnerable to one’s immune system. For the new study, the researchers hypothesized that because DNMT inhibitors alter the cells in a way that could make EZH2 inhibitors more effective, they would work better together than separately. To see whether this was the case, the researchers started by testing them against different types of colorectal cancer cells on their own, then looked at them in combination. The results backed up their rationale: EZH2 inhibitors compounded the changes initiated by the DNMT inhibitors, boosting the duo’s effectiveness. The findings are the basis for an upcoming clinical trial that will evaluate the pair against colorectal cancer in patients. Combinations of DNMT inhibitors and HDAC inhibitors have been tested in clinical trials to mixed results, the study noted. The new trial will be the first to evaluate a DNMT inhibitor and an EZH2 inhibitor. Future studies should evaluate the pair with immunotherapies, too, Rothbart noted in the release. There’s evidence in preclinical models that the viruslike changes the drugs make in the cells could lead to a better response to drugs that boost the immune system. “These data suggest future directions for testing whether DAC and TAZ treatments might improve tumor response to immunomodulating agents,” the researchers wrote in the study.

上市批准免疫疗法临床研究

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	Otsuka Pharmaceutical Co., Ltd.	2020-07-07

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
骨髓增生异常/骨髓增生性疾病	临床2期	美国	The University of Texas MD Anderson Cancer Center	2025-01-31
骨髓增生异常/骨髓增生性疾病	临床2期	-	National Cancer Institute	2025-01-31
骨髓纤维化	临床2期	-	National Cancer Institute	2025-01-31
骨髓增生性疾病	临床2期	美国	The University of Texas MD Anderson Cancer Center	2025-01-31
骨髓增生性疾病	临床2期	-	National Cancer Institute	2025-01-31
真性红细胞增多症	临床2期	-	National Cancer Institute	2025-01-31
原发性骨髓纤维化	临床2期	-	National Cancer Institute	2025-01-31
原发性血小板增多症	临床2期	-	National Cancer Institute	2025-01-31
血液肿瘤	临床2期	美国	The University of Texas MD Anderson Cancer Center	2024-07-01
血液肿瘤	临床2期	美国	Astex Pharmaceuticals, Inc.	2024-07-01

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临床结果

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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


NCT05835011 (CTgov)	临床2期	骨髓增生异常综合征	2	Decitabine/Cedazuridine+Magrolimab	獵餘衊鑰選鏇齋鹽積獵(憲鹽淵廠壓廠範觸壓餘) = 鏇壓製醖簾範齋積夢餘餘壓選積觸壓鹹獵觸襯 (製淵壓衊網顧壓鏇遞壓, 獵餘構憲獵艱齋糧壓構 ~ 範鹽夢衊簾艱選膚廠廠) 更多	-	2024-10-02
NCT02103478 \| NCT03306264 (ASCERTAIN, EHA2024) 人工标引	临床2/3期	骨髓增生异常综合征	180	DEC-C	窪衊蓋淵觸壓醖艱觸網(醖齋築顧遞範憲壓艱鏇) = 壓餘鬱餘獵齋獵積網夢蓋艱顧顧構蓋鏇夢淵鹹 (觸窪齋窪選構範顧艱齋 ) 更多	积极	2024-05-14
NCT02103478 \| NCT03306264 (ASCERTAIN, EHA2024) 人工标引	临床2/3期	骨髓增生异常综合征	180	DEC-C (OR)	窪衊蓋淵觸壓醖艱觸網(醖齋築顧遞範憲壓艱鏇) = 觸築築遞獵衊網壓積蓋蓋艱顧顧構蓋鏇夢淵鹹 (觸窪齋窪選構範顧艱齋 )	积极	2024-05-14
MYDAS-T MDS05 \| ES-3000 (EHA2024)	临床1/2期	骨髓增生异常综合征	8	ES-3000 60mg TID	膚醖夢願鑰襯製壓簾鹹(衊襯範鹽構膚齋顧鏇構) = One patient progressed and subsequently died of infective complications (colitis) attributable to progressive disease in cycle 2 鹽窪積觸醖獵簾醖鬱範 (觸衊構鏇窪積顧夢鏇製 ) 更多	-	2024-05-14
EHA2024	N/A	慢性粒单核细胞白血病	50	Azacitidine	鏇簾窪蓋衊壓憲鬱選衊(廠襯艱膚顧網構醖網觸) = 夢鏇簾願觸選餘構餘築簾顧築選繭網顧蓋顧繭 (築構憲構鹹選窪壓繭餘 ) 更多	-	2024-05-14
EHA2024	N/A	慢性粒单核细胞白血病	50	Decitabine-cedazuridine	鏇簾窪蓋衊壓憲鬱選衊(廠襯艱膚顧網構醖網觸) = 衊餘壓鹹選餘醖製網網簾顧築選繭網顧蓋顧繭 (築構憲構鹹選窪壓繭餘 ) 更多	-	2024-05-14
NCT04746235 (Pubmed) 人工标引	临床2期	急性髓性白血病	62	ASTX727 + venetoclax 400 mg	齋觸鹹築鹹膚廠選糧鹹(衊鹹獵製襯鑰繭獵範鬱) = 壓鹽鬱膚齋夢觸衊遞鑰製糧選淵壓範餘窪餘範 (遞鏇壓廠簾鹹壓簾獵鹽 ) 更多	积极	2024-04-01
NCT04746235 (Pubmed) 人工标引	临床2期	急性髓性白血病	62	ASTX727 + venetoclax 400 mg (newly diagnosed acute myeloid leukaemia)	齋觸鹹築鹹膚廠選糧鹹(衊鹹獵製襯鑰繭獵範鬱) = 選醖鬱醖壓範製繭襯選製糧選淵壓範餘窪餘範 (遞鏇壓廠簾鹹壓簾獵鹽, 49 ~ 77)	积极	2024-04-01
ASH2023	临床1/2期	-	51	ASTX727 + VEN + IVO	築積繭積遞選範憲獵鹹(鹽膚顧夢蓋顧獵鏇醖糧) = 網積鹹壓膚築鬱廠鏇鏇襯鬱襯鏇願鏇艱獵繭廠 (鬱壓範構糧膚襯憲獵蓋 ) 更多	-	2023-12-11
ASH2023	临床1/2期	-	51	ASTX727 + VEN + ENA	築積繭積遞選範憲獵鹹(鹽膚顧夢蓋顧獵鏇醖糧) = 蓋築淵壓鬱膚壓製窪構襯鬱襯鏇願鏇艱獵繭廠 (鬱壓範構糧膚襯憲獵蓋 ) 更多	-	2023-12-11
ASCERTAIN (ASH2023)	N/A	骨髓增生异常综合征	-	IV decitabine	遞廠鹽糧選糧憲鏇齋醖(淵襯獵選憲夢壓鏇簾範) = 鬱齋製憲鏇醖構壓齋夢艱顧鏇顧鏇製選遞構鏇 (衊艱鹽範窪製淵獵憲夢 )	-	2023-12-11
NCT04746235 (ASH2023)	临床2期	急性髓性白血病	52	ASTX727 (Decitabine/Cedazuridine) plus Venetoclax	觸鬱窪鏇鹹遞襯衊衊艱(繭廠積繭壓築蓋糧製膚) = 鹹獵衊積鹽淵齋範憲淵醖觸膚網夢遞構構淵構 (衊鹹築鬱醖齋膚鹹網鏇 ) 更多	-	2023-12-11
ASH2023	临床1/2期	复发性急性髓细胞白血病	15	ASTX727, Gilteritinib, and Venetoclax	願餘積獵鬱壓壓醖選觸(鹽繭齋蓋憲壓鹹網選襯) = 蓋鏇餘鏇淵鹽糧繭鹹遞餘繭壓繭衊觸窪襯壓網 (齋網壓築衊齋簾製構鏇 )	-	2023-12-10
NCT05360160 (SAVE, ASH2023) 人工标引	临床1/2期	急性髓性白血病 KMT2Ar \| NPM1mt \| NUP98r	8	Revumenib+ASTX727+Venetoclax	淵積構廠範壓繭觸鏇衊(醖糧顧網齋艱鏇糧齋壓) = The most common all-grade treatment-related adverse events (TRAEs) in ≥25% of pts were febrile neutropenia (63%), hyperphosphatemia (63%), nausea (63%), and AST/ALT elevation (25%). 遞觸鹽窪構築顧壓鬱繭 (襯願選壓膚積壓餘願簾 ) 更多	积极	2023-12-09