AMLM22/D4: The International AML Platform Consortium (IAPC) trial – is a randomised, 2-arm trial that will investigate the efficacy of oral Azacitidine combined with an allogeneic dendritic cell vaccine vididencel, compared with oral Azacitidine alone, in maintaining or inducing negativity for measurable residual disease (MRD) in AML patients in first complete remission (CR1) following intensive chemotherapy.

Start Date30 Jun 2025

Sponsor / Collaborator

The Australian Leukaemia & Lymphoma Group

[+1]

NCT06454409 / Not yet recruitingPhase 1IIT

A Phase 1b Study of the Multi-Kinase Inhibitor Regorafenib in Combination With the BCL-2 Inhibitor Venetoclax Plus Azacitidine in Patients With Relapsed/Refractory Acute Myeloid Leukemia

This phase Ib trial tests the safety, side effects, best dose and effectiveness of regorafenib in combination with venetoclax and azacitidine in treating patients with acute myeloid leukemia (AML) that has come back after a period of improvement (relapsed) or that has not responded to previous treatment (refractory). Regorafenib is in a class of medications called kinase inhibitors. It works by blocking the action of an abnormal protein that signals cancer cells to multiply. This helps to slow or stop the spread of cancer cells. 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. Azacitidine is in a class of medications called demethylation agents. It works by helping the bone marrow to produce normal blood cells and by killing abnormal cells. Giving regorafenib in combination with venetoclax and azacitidine may be safe, tolerable and/or effective in treating patients with relapsed or refractory AML.

Start Date20 Mar 2025

Sponsor / Collaborator

City of Hope National Medical Center

[+1]

NCT06597734 / Not yet recruitingPhase 2IIT

A Phase 2 Study Evaluating Olutasidenib in Combination With Hypomethylating Agents in Patients With IDH1-mutated Higher-risk Myelodysplastic Syndromes, Chronic Myelomonocytic Leukemia, or Advanced Myeloproliferative Neoplasm

To learn if olutasidenib, when combined with a drug called a hypomethylating agent (HMA) can help to control MDS, CMML, and/or MPN. The safety of the drug combination will also be studied.

Start Date11 Mar 2025

Sponsor / Collaborator

The University of Texas MD Anderson Cancer Center

[+1]

100 Clinical Results associated with Azacitidine

100 Translational Medicine associated with Azacitidine

100 Patents (Medical) associated with Azacitidine

6,150

Literatures (Medical) associated with Azacitidine

05 Jul 2106·Oncotarget

Luminal STAT5 mediates H2AX promoter activity in distinct population of basal mammary epithelial cells

Article

Author: Barash, Itamar ; Reichenstein, Moshe ; Kisliouk, Tatiana ; Kfir, Shenhav ; Rauner, Gat

Deregulated STAT5 activity in the mammary gland causes parity-dependent tumorigenesis. Epithelial cell cultures transfected with constitutively active STAT5 express higher levels of the histone H2AX than their non-transfected counterparts. Higher H2AX expression may be involved in tumorigenesis. Here, we aimed to link high STAT5 activity to H2AX-GFP expression by looking for distinct types of mammary cells that express these proteins. In vitro and in transgenic mice, only 0.2 and 0.02%, respectively, of the cells expressed the H2AX-GFP hybrid gene. Its expression correlated with that of the endogenous H2AX gene, suggesting that detectable H2AX-GFP expression marks high levels of H2AX transcript. Methylation of the H2AX promoter characterized non-GFP-expressing H2AX-GFP cells and was inversely correlated with promoter activity. Administration of 5-azacytidine increased H2AX promoter activity in an activated STAT5-dependent manner. In transgenic mice, H2AX-GFP expression peaked at pregnancy. The number of H2AX-GFP-expressing cells and GFP expression decreased in a Stat5a-null background and increased in mice expressing the hyperactivated STAT5. Importantly, H2AX-GFP activity was allocated to basal mammary cells lacking stem-cell properties, whereas STAT5 hyperactivity was detected in the adjacent luminal cells. Knockdown of RANKL by siRNA suggested its involvement in signaling between the two layers. These results suggest paracrine activation of H2AX via promoter demethylation in specific populations of basal mammary cells that is induced by a signal from neighboring luminal cells with hyper STAT5 activity. This pathway provides an alternative route for the luminally confined STAT5 to affect basal mammary cell activity.

31 Dec 2024·Cancer biology & therapy

M6A modification regulates tumor suppressor DIRAS1 expression in cervical cancer cells

Article

Author: Wang, Yu-Yan ; Dai, Ning ; Zhang, Xin ; Gao, Wei-Ran ; Ye, Lian-Hua ; Zhao, An-Qi ; Yin, Yu

DIRAS family GTPase 1 (DIRAS1) has been reported as a potential tumor suppressor in other human cancer. However, its expression pattern and role in cervical cancer remain unknown. Knockdown of DIRAS1 significantly promoted the proliferation, growth, migration, and invasion of C33A and SiHa cells cultured in vitro. Overexpression of DIRAS1 significantly inhibited the viability and motility of C33A and SiHa cells. Compared with normal cervical tissues, DIRAS1 mRNA levels were significantly lower in cervical cancer tissues. DIRAS1 protein expression was also significantly reduced in cervical cancer tissues compared with para-cancerous tissues. In addition, DIRAS1 expression level in tumor tissues was significantly negatively correlated with the pathological grades of cervical cancer patients. DNA methylation inhibitor (5-Azacytidine) and histone deacetylation inhibitor (SAHA) resulted in a significant increase in DIRAS1 mRNA levels in C33A and SiHa cells, but did not affect DIRAS1 protein levels. FTO inhibitor (FB23-2) significantly down-regulated intracellular DIRAS1 mRNA levels, but significantly up-regulated DIRAS1 protein levels. Moreover, the down-regulation of METTL3 and METTL14 expression significantly inhibited DIRAS1 protein expression, whereas the down-regulation of FTO and ALKBH5 expression significantly increased DIRAS1 protein expression. In conclusion, DIRAS1 exerts a significant anti-oncogenic function and its expression is significantly downregulated in cervical cancer cells. The m6A modification may be a key mechanism to regulate DIRAS1 mRNA stability and protein translation efficiency in cervical cancer.

31 Dec 2024·Hematology (Amsterdam, Netherlands)

Combination of venetoclax and azacitidine in relapsed/refractory acute B-cell lymphoblastic leukemia: a case series from a single center

Article

Author: Wang, Li ; Zhang, Yanming ; Fei, Yingying ; Hao, Ziyi ; Yu, Youhuan ; Zhang, Xingxia ; Huang, Sailan ; Wan, Yan ; Lin, Guoqiang ; Yang, Xiaotian ; Zhang, Bing ; Chen, Juan ; Si, Yejun ; Bian, Meiru

OBJECTIVES:

Relapsed/refractory acute B-cell lymphoblastic leukemia (R/R B-ALL) often responds poorly to induction chemotherapy. However, recent research has shown a novel and effective drug treatment for R/R B-ALL.

METHODS:

A total of eight patients with R/R B-ALL were enrolled in the study from November 2021 to August 2022. All patients received chemotherapy based on a combination regimen of venetoclax and azacitidine. The regimen was as follows venetoclax 100 mg d₁, 200 mg d₂, 400 mg d_3-14, azacitidine 75 mg/m² d_1-7.

RESULTS:

Five of eight patients achieved very deep and complete remission (CR) with minimal residual disease (MRD) less than 0.1%. One patient achieved partial remission. Two patients did not achieve remission. There were no serious adverse events and all patients were well tolerated. Three patients were eligible for consolidation chemotherapy and were bridged to CAR-T therapy.

CONCLUSIONS:

The combined regimen of venetoclax and azacitidine may be beneficial for patients with R/R B-ALL.

570

News (Medical) associated with Azacitidine

26 Sep 2024

·www.globenewswire.com

AB Science provides an update on the microtubule program AB8939 and in particular the ability of AB8939 to generate response on MECOM rearrangement

PRESS RELEASE AB SCIENCE PROVIDES AN UPDATE ON THE MICROTUBULE PROGRAM AB8939 AND IN PARTICULAR THE ABILITY OF AB8939 TO GENERATE RESPONSE ON MECOM REARRANGEMENT Paris, 26 September 2024, 8.30am CET AB Science SA (Euronext - FR0010557264 - AB) today provides an update on the microtubule program AB8939 and in particular the ability of AB8939 to generate response on MECOM rearrangement. AB8939 is a novel microtubule destabilizer currently evaluated in phase 1 clinical trial (study AB18001, NCT05211570) in patients with refractory and relapsed acute myeloid leukemia (AML). The phase 1 clinical trial of AB8939 completed its first step, consisting in determining the maximum tolerated dose following 3 consecutive days of AB8939 treatment, and was authorized to proceed with the next step, consisting in determining the maximum tolerated dose following 14 consecutive days of AB8939 treatment. The phase 1 clinical trial continues to determine MTD and the study is now at the last cycle of the 14 days evaluation. The next step will be to determine the MTD in the combination of AB8939 with Vidaza® (azacitidine). AB Science previously reported [1] a case of complete bone marrow response in an AML patient in failure to prior treatment with azacitidine and presenting with a MECOM gene rearrangement, which consists of chromosomic aberrations of EVI1 oncogene, leading to one of the worst prognostics in AML and is associated with lack of response and resistance to conventional chemotherapy. New data confirm that there is a signal of activity against MECOM, with AB8939 generating a complete response in combination with Vidaza, as evidenced by a synergistic effect in a patient-derived xenograft (PDX) mouse model bearing the MECOM rearrangement. PDX are cell lines coming from patients that are grafted to immune deficient mice to mimic as closely as possible the human disease. AB8939 was able to generate 50% response when used as a single agent on MECOM cell lines ex vivo in a non-clinical setting.In the phase 1 trial, 4 patients bore the MECOM rearrangement and 50% responded to AB8939 when used as a single agent.In phase 1, so far, AB8939 does not appear to be toxic to bone marrow, avoiding severe neutropenia and suggesting the possibility to use the drug for long-term treatment. These data taken together confirm the opportunity to develop AB8939 in phase 2 clinical trial in MECOM as a single agent or in combination with Vidaza. The advantage is that a small study could be sufficient to comply with FDA guideline on accelerated approval. Professor Olivier Hermine, President of the AB Science Scientific Committee and member of the French Academy of Sciences and Head of haematology Department at Necker Hospital commented: “AB8939 can be developed in the other patients suffering from AML, but MECOM represents a real opportunity to use the accelerated approval pathway, since it lacks treatment, patients are unresponsive to existing therapy and survival is usually inferior to 6 months. A phase 2 with a limited sample size, non-controlled, and showing a 30% response rate at month 3, with a survival potential at 6 months would probably be convincing enough for an accelerated approval. This will be discussed with FDA in future regulatory milestone. This study could be implemented in 2025. Moreover, MECOM extends beyond AML and are present in high-risk myelodysplasia (MDS) and ovarian cancer.” Two patents have been filed protecting AB8939 in AML, one global composition of matter (granted) and a second one protecting the use of AB8939 in cancers displaying MECOM rearrangement (pending), with protection until 2036 and 2044 respectively. About MECOM AML represents a heterogeneous group of diseases with different responses to treatment, which can be separated by genetic abnormalities. Overexpression of MECOM occurs in approximately 10% of AML patients and is associated with a poor prognosis, in part due to its important role in the maintenance of leukemic stem cells (LSCs) [2]. Because of their quiescent (inactive) state, LSCs are not targeted by any antimitotic chemotherapy and can therefore re-establish the disease after therapy. About AB8939 AB8939 is a new synthetic microtubule-destabilizing drug. Preclinical data show that AB8939 has broad anticancer activity [3-5], with a notable advantage over standard chemotherapies that target microtubules of being able to overcome P-glycoprotein (Pgp) and myeloperoxidase (MPO) mediated drug resistance. Development of drug resistance often restricts the clinical efficacy of microtubule-targeting chemotherapy drugs (for example, taxanes and vinca alkaloids); thus, AB8939 has strong potential to be developed in numerous oncology indications. AB8939 was granted orphan drug designation for AML from the U.S. Food and Drug Administration (FDA). AB8939 was entirely discovered by the laboratories of AB Science, which retains full ownership of intellectual rights, and is an example of AB Science’s focus on innovative drug development focused on improving patients’ lives. The first indication AB8939 is being developed for is acute myeloid leukemia (AML). Cytarabine (Ara-C) and azacytidine are standard chemotherapies for AML treatment, however, drug resistance is a major limitation to successful therapy. In vivo data from a highly resistant Ara-C patient derived xenograft (PDX) mouse model showed that AB8939, administered alone or in combination with Ara-C, increased survival relative to single agent Ara-C, with an accompanying significant reduction of blasts in blood and decrease in tumor growth. Further evidence of therapeutic potential was demonstrated using an azacytidine resistant PDX model with AB8939, administered alone or in combination with azacytidine, showing a significant reduction of blasts relative to single agent azacytidine. Moreover, while azacytidine was associated with strong treatment related hematotoxicity, AB8939 did not induce hematotoxicity throughout its 4-week treatment period. About acute myeloid leukemia (AML) Acute myeloid leukemia (AML) is a serious, life-threating condition and the most common cause of leukemia-related mortality, with a majority of patients facing a highly unsatisfactory prognosis. As such, AML represents an unmet medical need, with limited therapeutic options for patients who are refractory or too frail to benefit from potentially curative but highly toxic treatment, or for those patients that have relapsed following a first complete response. The prevalence of AML in western countries is around 1 per 5,000 persons, corresponding to around 100,000 cases in Europe and 60,000 in the USA. Among AML patients, it is estimated that approximately 50% of the patients will not have stem cell transplantation and will relapse. Therefore, the estimated targeted population of AB8938 in AML is around 80,000 people in Europe and the US. References [1] AB Science press release dated 13 March 2023 [2] Paubelle E, Plesa A, Hayette S, et al. Efficacy of All-Trans-Retinoic Acid in High-Risk Acute Myeloid Leukemia with Overexpression of EVI1. Oncol Ther. 2019;7(2):121-130. Doi:10.1007/s40487-019-0095-9 [3] Goubard A, Humbert M, Mansfield C, Hermine O, Dubreuil P, et al. In Vivo Assessment of the Next Generation Microtubule-Destabilizing Agent AB8939 in Patient-derived Xenograft Models of Acute Myeloid Leukemia. Blood (2019) 134 (Supplement_1): 5142. doi.org/10.1182/blood-2019-127143 [4] Goubard A, Humbert M, Mansfield C, Hermine O, Dubreuil P, et al. AB8939, a Microtubule-Destabilizing Agent with Potential to Overcome Multidrug Resistance, is Active Across the Range (M0–M7) of Acute Myeloid Leukemia Subtypes. Blood (2019) 134 (Supplement_1): 5154. doi.org/10.1182/blood-2019-127021 [5] Humbert M, Goubard A, Mansfield C, Hermine O, Dubreuil P, et al. Anticancer Activity of a Highly Potent Small Molecule Tubulin Polymerization Inhibitor, AB8939. Blood (2019) 134 (Supplement_1): 2075. doi.org/10.1182/blood-2019-122540 About AB ScienceFounded in 2001, AB Science is a pharmaceutical company specializing in the research, development and commercialization of protein kinase inhibitors (PKIs), a class of targeted proteins whose action are key in signaling pathways within cells. Our programs target only diseases with high unmet medical needs, often lethal with short term survival or rare or refractory to previous line of treatment. AB Science has developed a proprietary portfolio of molecules and the Company’s lead compound, masitinib, has already been registered for veterinary medicine and is developed in human medicine in oncology, neurological diseases, inflammatory diseases and viral diseases. The company is headquartered in Paris, France, and listed on Euronext Paris (ticker: AB). Further information is available on AB Science’s website: www.ab-science.com. Forward-looking Statements - AB ScienceThis press release contains forward-looking statements. These statements are not historical facts. These statements include projections and estimates as well as the assumptions on which they are based, statements based on projects, objectives, intentions and expectations regarding financial results, events, operations, future services, product development and their potential or future performance. These forward-looking statements can often be identified by the words "expect", "anticipate", "believe", "intend", "estimate" or "plan" as well as other similar terms. While AB Science believes these forward-looking statements are reasonable, investors are cautioned that these forward-looking statements are subject to numerous risks and uncertainties that are difficult to predict and generally beyond the control of AB Science and which may imply that results and actual events significantly differ from those expressed, induced or anticipated in the forward-looking information and statements. These risks and uncertainties include the uncertainties related to product development of the Company which may not be successful or to the marketing authorizations granted by competent authorities or, more generally, any factors that may affect marketing capacity of the products developed by AB Science, as well as those developed or identified in the public documents published by AB Science. AB Science disclaims any obligation or undertaking to update the forward-looking information and statements, subject to the applicable regulations, in particular articles 223-1 et seq. of the AMF General Regulations. For additional information, please contact: AB ScienceFinancial Communication & Media Relations investors@ab-science.com Attachment CP AB8939 Update. VENG VF

Clinical ResultPhase 1Orphan DrugPhase 2

23 Sep 2024

·www.prnewswire.com

Curis Announces the 3rd Annual Symposium on IRAK4 in Cancer

Symposium hosted by Eric S. Winer, MD, and Grzegorz S. Nowakowski, MD Updated data for 10 evaluable patients in Curis's PCNSL study Experts will present at the virtual meeting, free and open to the public, on September 26, 2024 LEXINGTON, Mass., Sept. 23, 2024 /PRNewswire/ -- Curis, Inc. (NASDAQ: CRIS), a biotechnology company focused on the development of emavusertib (CA-4948), an orally available, small molecule IRAK4 inhibitor, today announced the 3rd Annual Symposium on IRAK4 in Cancer taking place virtually on September 26, 9:00 AM-1:00 PM E.T. Hosted by Dr. Eric S. Winer (Dana-Farber Cancer Institute) and Dr. Grzegorz S. Nowakowski (Mayo Clinic Comprehensive Cancer Center), this symposium will focus on IRAK4, an emerging target in the treatment of hematologic malignancies and solid tumors. Experts will discuss the promise of IRAK4 inhibition in cancer, including current clinical studies of emavusertib and opportunities for future development. Symposium presentations will include updated data for 10 evaluable R/R PCNSL patients as of the July 10, 2024 cutoff date. The Company continues to enroll patients in the PCNSL study and is on track to enroll 15-20 patients by year-end. "As the leader in IRAK4 inhibition in oncology with emavusertib, we are honored to provide a forum for discussing the biology of the IRAK4 pathway and IRAK4 inhibition in the research and development of therapies to benefit patients living with cancer," said James Dentzer, President, and Chief Executive Officer of Curis. Symposium co-chairs: Eric Winer, MD, Clinical Director and Adult Leukemia Institute Physician, Dana-Farber Cancer Institute; Assistant Professor of Medicine, Harvard Medical School Grzegorz Nowakowski, MD, Professor of Oncology and Medicine, Division of Hematology, Deputy Director of Mayo Clinic Comprehensive Cancer Center for Clinical Research and Vice-Chair of Division of Hematology Joining our hosts will be the following speakers and participants: Bently Doonan, MD, Assistant Professor, Division of Hematology and Oncology, University of Florida College of Medicine Andrés Ferreri, MD, Contract Professor of Oncology, University Vita-Salute San Raffaele; Head of the Lymphoma Unit, I.R.C.C.S. Ospedale San Raffaele Klaus Metzeler, MD, Professional of Translational Hematology, University of Leipzig Guillermo Garcia-Manero, MD, Professor, Chief of Section of Myelodysplastic Syndromes, Deputy Chair of Translational Research and Fellowship Program Director Department of Leukemia, Division of Cancer Medicine, The University of Texas MD Anderson Cancer Center Marina Konopleva, MD, PhD, Professor of the Department of Oncology, Professor of the Department of Molecular Pharmacology, and Miriam Mandel Faculty Scholar in Cancer Research, Albert Einstein College of Medicine Kian Lim, MD, PhD, Associate Professor, Department of Medicine, Division of Oncology, Washington University School of Medicine in St. Louis Lakshmi Nayak, MD, Director of the Center for CNS Lymphoma Dana‑Farber Cancer Institute; Associate Professor of Neurology, Harvard Medical School Han Tun, MD, Hematologist, Internist, Oncologist, Departments of Hematology and Mayo Clinic Comprehensive Cancer Center To learn more about this free-to-attend symposium and register, please visit About Curis, Inc. Curis is a biotechnology company focused on the development of emavusertib, an orally available, small molecule IRAK4 inhibitor. Emavusertib is currently undergoing testing in the Phase 1/2 TakeAim Lymphoma study (CA-4948-101) in patients with relapsed/refractory primary central nervous system lymphoma (PCNSL) in combination with the BTK inhibitor ibrutinib, as a monotherapy in the Phase 1/2 TakeAim Leukemia study (CA-4948-102) in patients with relapsed/refractory acute myeloid leukemia (AML) and relapsed/refractory high risk myelodysplastic syndrome (hrMDS) with either a FLT3 mutation or a splicing factor mutation (U2AF1 or SF3B2), and as a frontline combination therapy with azacitidine and venetoclax in patents with AML (CA-4948-104). Emavusertib has received Orphan Drug Designation from the U.S. Food and Drug Administration for the treatment of AML and MDS and from the European Commission for the treatment of PCNSL. Curis, through its 2015 collaboration with Aurigene, has the exclusive license to emavusertib (CA-4948). Curis licensed its rights to Erivedge® to Genentech, a member of the Roche Group, under which they are commercializing Erivedge® for the treatment of advanced basal cell carcinoma. For more information, visit Curis's website at . SOURCE Curis, Inc. WANT YOUR COMPANY'S NEWS FEATURED ON PRNEWSWIRE.COM? 440k+ Newsrooms & Influencers 9k+ Digital Media Outlets 270k+ Journalists Opted In GET STARTED

License out/inOrphan DrugASH

19 Sep 2024

·www.businesswire.com

InnoCare Announces Approval of Clinical Trial of BCL2 Inhibitor ICP-248 for Acute Myeloid Leukemia in China

BEIJING--( BUSINESS WIRE )--InnoCare Pharma (HKEX: 09969; SSE: 688428), a leading biopharmaceutical company focusing on the treatment of cancer and autoimmune diseases, announced today the approval of the Investigational New Drug (IND) to conduct the clinical trial of B-cell lymphoma-2 (BCL2) inhibitor ICP-248 in combination with azacitidine for acute myeloid leukemia (AML) in China. Acute myeloid leukemia (AML) is a malignant hematological disease originating from hematopoietic stem/progenitor cells, accounting for about 80% of acute leukemia in adults. The risk of developing AML increases with age and is more common in middle-aged and elderly people. AML is also not uncommon in individuals under 18 years old, representing about 15-20% of pediatric leukemia and 80% of leukemia in neonates and infants 1 . BCL2 is an important regulatory protein of apoptosis pathway, and its abnormal expression is related to the development of various hematologic malignancies. ICP-248 is a novel, orally bioavailable BCL2-selective inhibitor. It has anti-tumor effect by selectively inhibiting BCL2 and restoring the mechanism of programmed cell death. Dr. Jasmine Cui, the co-founder, chairwoman and CEO of InnoCare, said, "With strong pipeline in hemato-oncology, InnoCare is dedicated to developing therapeutics with diverse mechanisms of action (MoA) to achieve comprehensive coverage of blood tumor indications. ICP-248 is an important global asset of our company in the field of hematology. We will accelerate clinical development and look forward to bringing greater benefits to patients with hematological malignancies early." About InnoCare InnoCare is a commercial stage biopharmaceutical company committed to discovering, developing, and commercializing first-in-class and/or best-in-class drugs for the treatment of cancer and autoimmune diseases with unmet medical needs in China and worldwide. InnoCare has branches in Beijing, Nanjing, Shanghai, Guangzhou, Hong Kong, and United States. InnoCare Forward-looking Statements This report contains the disclosure of some forward-looking statements. Except for statements of facts, all other statements can be regarded as forward-looking statements, that is, about our or our management's intentions, plans, beliefs, or expectations that will or may occur in the future. Such statements are assumptions and estimates made by our management based on its experience and knowledge of historical trends, current conditions, expected future development and other related factors. This forward-looking statement does not guarantee future performance, and actual results, development and business decisions may not match the expectations of the forward-looking statement. Our forward-looking statements are also subject to a large number of risks and uncertainties, which may affect our short-term and long-term performance. ____________________ 1 Guiding Principles for Clinical Research and Development of New Drugs for Acute Myeloid Leukemia

INDClinical Study

100 Deals associated with Azacitidine

External Link

KEGG	Wiki	ATC	Drug Bank
D03021	Azacitidine	L01BC07	DB00928

R&D Status

Approved

10 top approved records.

to view more data

Indication	Country/Location	Organization	Date
Juvenile Myelomonocytic Leukemia	US	Bristol Myers Squibb Co.	20 May 2022
Philadelphia chromosome positive chronic myelogenous leukemia	CN	Bristol-Myers Squibb Pharma EEIG	24 Apr 2017
High Risk Myelodysplastic Syndrome	AU	Celgene Pty Ltd.	30 Nov 2009
Acute Myeloid Leukemia	EU	Bristol-Myers Squibb Pharma EEIG	17 Dec 2008
Acute Myeloid Leukemia	IS	Bristol-Myers Squibb Pharma EEIG	17 Dec 2008
Acute Myeloid Leukemia	LI	Bristol-Myers Squibb Pharma EEIG	17 Dec 2008
Acute Myeloid Leukemia	NO	Bristol-Myers Squibb Pharma EEIG	17 Dec 2008
Chronic Myelomonocytic Leukemia	EU	Bristol-Myers Squibb Pharma EEIG	17 Dec 2008
Chronic Myelomonocytic Leukemia	IS	Bristol-Myers Squibb Pharma EEIG	17 Dec 2008
Chronic Myelomonocytic Leukemia	LI	Bristol-Myers Squibb Pharma EEIG	17 Dec 2008
Chronic Myelomonocytic Leukemia	NO	Bristol-Myers Squibb Pharma EEIG	17 Dec 2008
Myeloproliferative Disorders	EU	Bristol-Myers Squibb Pharma EEIG	17 Dec 2008
Myeloproliferative Disorders	IS	Bristol-Myers Squibb Pharma EEIG	17 Dec 2008
Myeloproliferative Disorders	LI	Bristol-Myers Squibb Pharma EEIG	17 Dec 2008
Myeloproliferative Disorders	NO	Bristol-Myers Squibb Pharma EEIG	17 Dec 2008
Myelodysplastic Syndromes	US	Bristol Myers Squibb Co.	19 May 2004

Developing

10 top R&D records.

to view more data

Indication	Highest Phase	Country/Location	Organization	Date
Immunoblastic Lymphadenopathy	Phase 3	JP	Celgene Corp.	06 Nov 2018
Thrombocytopenia	Phase 3	US	Celgene Corp.	26 Apr 2013
Thrombocytopenia	Phase 3	AU	Celgene Corp.	26 Apr 2013
Thrombocytopenia	Phase 3	BE	Celgene Corp.	26 Apr 2013
Thrombocytopenia	Phase 3	BR	Celgene Corp.	26 Apr 2013
Thrombocytopenia	Phase 3	CA	Celgene Corp.	26 Apr 2013
Thrombocytopenia	Phase 3	CZ	Celgene Corp.	26 Apr 2013
Thrombocytopenia	Phase 3	DK	Celgene Corp.	26 Apr 2013
Thrombocytopenia	Phase 3	FI	Celgene Corp.	26 Apr 2013
Thrombocytopenia	Phase 3	FR	Celgene Corp.	26 Apr 2013

Clinical Result

Indication

Phase

Evaluation

View All Results

Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT01998035 (phase 2 study, CTgov)	Phase 1/2	Hodgkin's Lymphoma \| Non-Hodgkin Lymphoma	58	romidepsin+5-azacitidine (Phase I)	xbwzjhjcwh(bhxnwwkmcx) = agkupbclgp zgnawdophl (rcnfkjwacq, amepzjpnsg - jfdmmlyobl) View more	-	22 Aug 2024
NCT01998035 (phase 2 study, CTgov)	Phase 1/2	Hodgkin's Lymphoma \| Non-Hodgkin Lymphoma	58	5azacytidine+romidepsin+5-azacytidine (Phase II)	vjjyelhdot(tdrzsjtgcu) = rlckddasit iwzpbupiuv (rbdwiimvyr, crvbqawoiv - ixduqjppfg)	-	22 Aug 2024
NCT03703375 (CTgov)	Phase 3	Immunoblastic Lymphadenopathy	93	Azacitidine (Oral Azacitidine)	utzjvnmxis(xtaetbmknl) = humdlqtzxv dafvpjlphf (ebcekrzpen, djgnfuwrsd - kaaggdllys) View more	-	08 Jul 2024
NCT03703375 (CTgov)	Phase 3	Immunoblastic Lymphadenopathy	93	Romidepsin+Bendamustine+Gemcitabine (Investigators Choice Therapy Combined (Romidepsin, Bendamustine, Gemcitabine))	utzjvnmxis(xtaetbmknl) = xakdwtqwux dafvpjlphf (ebcekrzpen, kccnkknjkl - wdchrhctkt) View more	-	08 Jul 2024
NCT04493138 (Pubmed) Manual	Phase 1	Myeloproliferative Disorders \| Myelodysplastic Syndromes CBL Mutation \| FLT3 Mutation	12	Azacitidine + Quizartinib (30-60mg)	tgexfszhhq(jxrgnjmskz) = thrombocytopenia (n=5, 42 %), anemia (n=4, 33 %), lung infection (n=2, 17 %), skin infection (n=2, 17 %), hyponatremia (n=2, 17 %) and sepsis (n=2, 17 %). ucioodpygc (pixfeziaqv ) View more	Positive	01 Jul 2024
NCT02828358 (AALL15P1, Pubmed)	Phase 2	DNA hypermethylation	31	Azacitidine	thnwjndffz(prmtfrwtxj) = tdmrodqrhb pumunludgc (bzmlivrimy )	Negative	13 Jun 2024
EULAR2024	Not Applicable	Crouzon Syndrome With Acanthosis Nigricans UBA1 gene	57	Azacitidine	fizezgpvwv(maydmggalo) = bnvhucvick wztjsmxadz (xqidlbvmaa )	Positive	05 Jun 2024
EULAR2024	Not Applicable	Crouzon Syndrome With Acanthosis Nigricans	-	Azacitidine	aauzvkxzia(acansnuaok) = Following a cycle of azacitidine, the patient experienced fluctuating delirium, gradually improving over several months gtsarxihze (nodyorckqj )	-	05 Jun 2024
NCT05469737 (ASTREON, ASCO2024) Manual	Phase 2	Myelodysplastic Syndromes	47	Oral-AZA 200 mg	ntpdrdyotn(tvowybfhmd) = nhxszynxah fyvtbydvpp (uodwfmvkkl ) View more	Positive	24 May 2024
NCT05469737 (ASTREON, ASCO2024) Manual	Phase 2	Myelodysplastic Syndromes	47	Oral-AZA 300 mg	ntpdrdyotn(tvowybfhmd) = ofqqtrrcva fyvtbydvpp (uodwfmvkkl ) View more	Positive	24 May 2024
NCT01757535 (QUAZAR AML-001, ASCO2024) Manual	Phase 3	Acute Myeloid Leukemia with Myelodysplasia-Related Changes Maintenance	101	Oral-AZA 300 mg	oqzwzwexkb(jewtiihnsn) = lociqgnxlx gpbhsmhhbi (szigvggeje, 14.59 - 31.97) View more	Positive	24 May 2024
NCT01757535 (QUAZAR AML-001, ASCO2024) Manual	Phase 3		101	Placebo	oqzwzwexkb(jewtiihnsn) = ttpvwwljwc gpbhsmhhbi (szigvggeje, 10.05 - 19.65) View more	Positive	24 May 2024
NCT01995578 (CTgov)	Phase 2	Acute Myeloid Leukemia \| Myelodysplastic Syndromes	32	low dose 5'-azacitidine	gophvafhve(gzmvkxonzp) = bbpmvhchxc neylcwctcm (aptiqnnygf, qtzkrjtvlq - cwsxieufaq) View more	-	22 May 2024
NCT04722601 (CTgov)	Phase 1/2	Follicular Lymphoma	2	Venetoclax+Obinutuzumab+CC-486	fyeustyvtg(ozbprhgjpr) = anxtafmoxx uqviiglava (ycofgzynwq, bmgoipsxjp - qukyszrqbv) View more	-	16 May 2024

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