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

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

Start Date01 Apr 2025

Sponsor / Collaborator

National Cancer Institute

NCT06577441

/ Not yet recruitingPhase 2IIT

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.

Start Date01 Apr 2025

Sponsor / Collaborator

National Cancer Institute

NCT06756308

/ RecruitingPhase 2IIT

A Phase 2 Study of Enasidenib in IDH2-Mutant Angioimmunoblastic T-Cell Lymphoma

The researchers are doing this study to find out whether enasidenib is a safe treatment for people with angioimmunoblastic T-cell lymphoma (AITL) that has an IDH2 mutation. The researchers will look at the safety of enasidenib when it is given alone or in combination with the drug rituximab.

Start Date24 Dec 2024

Sponsor / Collaborator

Memorial Sloan Kettering Cancer Center

[+2]

100 Clinical Results associated with Enasidenib Mesylate

100 Translational Medicine associated with Enasidenib Mesylate

100 Patents (Medical) associated with Enasidenib Mesylate

352

Literatures (Medical) associated with Enasidenib Mesylate

24 Mar 2025·Journal of biomolecular structure & dynamics

Inhibition of respiratory syncytial virus by Daclatasvir and its derivatives: synthesis of computational derivatives as a new drug development

Article

Author: Mitra, Debanjan ; Abdalla, Mohnad ; Afreen, Shagufta ; Das Mohapatra, Pradeep K.

The most common cause of respiratory tract illness in newborns and young children is the respiratory syncytial virus (RSV). There is no approved vaccination or specific antiviral medication for RSV infections. Here, an attempt has been made to explore the potential of currently marketed drugs as well as their probable derivatives to improve the possibility of developing stronger medications against RSV. From the 100 synthetic drug compounds library, the best drug molecule was identified through drug-likeness properties, toxicity, molecular docking and molecular dynamics simulations. Molecular Mechanics Generalized Born Surface Area (MM-GBSA) was also a method that was applied in this study. Daclatasvir showed the highest binding energy and appeared as the best drug to inhibit matrix protein and a fusion protein of RSV. Based on Daclatasvir, 40 computational derivatives were made. D28, D34 and D40 showed far better results than the actual drug. Changes in lipophilicity character increase the binding energy of derivatives. Molecular dynamic simulations showed their non-deviated, non-fluctuated and stable complex formation with target proteins. The high number of amino acid contacts throughout the trajectory increases the stability and effectiveness of derivatives. The key to producing a novel medicine to eradicate RSV is provided by derivatives. Daclatasvir will be employed as a potential RSV inhibitor up until that point.Communicated by Ramaswamy H. Sarma.

23 Feb 2025·LEUKEMIA & LYMPHOMA

Cost-effectiveness of Enasidenib versus conventional care for older patients with IDH2- mutant refractory/relapsed AML

Article

Author: Zeidan, Amer M. ; Alhajahjeh, Abdulrahman ; Kewan, Tariq ; Stempel, Jessica M. ; Patel, Kishan K. ; Podoltsev, Nikolai A. ; Bewersdorf, Jan Philipp ; Goshua, George ; Mendez, Lourdes ; Stahl, Maximilian ; Shallis, Rory M. ; Huntington, Scott F.

In the randomized phase III IDHENTIFY trial, the IDH2 inhibitor enasidenib (ENA) showed improvement in event-free but not overall survival compared with conventional care regimens (CCR) among patients with relapsed/refractory (R/R), IDH2-mutant AML. We constructed a partitioned survival model to evaluate the cost-effectiveness of enasidenib for the treatment of older patients with R/R, and IDH2-mutant AML. In the base-case scenario, ENA exhibited an incremental effectiveness of 0.234quality-adjusted life-years (QALYs) compared to CCR, and an incremental cost of $126,800, leading to an incremental cost-effectiveness ratio of $540,300/QALY(95% CI: $197,800-$4,777,000/QALY). In probabilistic sensitivity analysis, CCR was favored in 99.8% of simulations. The cost of ENA would need to be decreased by 72% to be cost-effective at a willingness-to-pay threshold of $150,000/QALY. Our findings suggest that ENA is unlikely to be a cost-effective treatment for older patients with IDH2-mutant R/R AML under current pricing.

01 Feb 2025·BONE MARROW TRANSPLANTATION

Measurable residual mutated IDH2 before allogeneic transplant for acute myeloid leukemia

Article

Author: Hourigan, Christopher S ; Hegde, Pranay S ; Auletta, Jeffery J. ; Hourigan, Christopher S. ; Saber, Wael ; Chen, Evan C. ; De Lima, Marcos J G ; Chen, Evan C ; Mukherjee, Devdeep ; Page, Kristin M ; Litzow, Mark R. ; Spellman, Stephen R. ; De Lima, Marcos J. G. ; Ravindra, Niveditha ; Wong, Zoë ; Iyer, Sunil G ; Gui, Gege ; Zeger, Scott L. ; Hegde, Pranay S. ; Chen, Yi-Bin ; El Chaer, Firas ; Kebriaei, Partow ; Dillon, Laura W ; Litzow, Mark R ; Iyer, Sunil G. ; Spellman, Stephen R ; Devine, Steven M. ; Devine, Steven M ; Zeger, Scott L ; Jimenez Jimenez, Antonio Martin ; Dillon, Laura W. ; Page, Kristin M. ; Corner, Adam ; Auletta, Jeffery J ; Andrew, Georgia

Abstract:

Routine genetic profiling of acute myeloid leukemia (AML) at initial diagnosis has allowed subgroup specific prognostication, drug development, and clinical management strategies. The optimal approach for treatment response assessment for AML subgroups has not yet however been determined. A nationwide cohort of 257 adult patients in first remission (CR1) from AML associated with an IDH2 mutation (IDH2m) undergoing allogeneic transplant during the period 2013–2019 in the United States had rates of relapse and survival three years after transplantation of 24% and 71%, respectively. Pre-transplant clinical flow cytometry assessment was not useful in stratifying patients based on risk of post-transplant relapse or death. DNA-sequencing was performed on CR1 blood collected within 100 days before transplant. Persistent detection of IDH2m was common (51%) and associated with increased relapse and death compared to testing negative. Co-mutation at initial diagnosis with mutated NPM1 and/or FLT3-ITD was common in this cohort (41%) and use of these validated MRD markers provided superior stratification compared to IDH2m testing. Patients testing negative for IDH2m prior to transplant had low relapse-related death, regardless of conditioning intensity. Post-transplant relapse rates for those with persistently detectable IDH2m in pre-transplant remission were lower after the FDA approval of enasidenib in August 2017.

News (Medical) associated with Enasidenib Mesylate

14 Jan 2025

·www.taihooncology.com

Taiho Oncology Announces Decitabine and Cedazuridine to Be Included in NIH Precision Medicine Trials

Drug combination part of next-generation trials targeting specific genetic mutations in patients with myelodysplastic syndromes and acute myeloid leukemia PRINCETON, New Jersey, January 14, 2025 — Taiho Oncology, Inc., a company developing and commercializing novel treatments for hematologic malignancies and solid tumors, announced today that oral decitabine and cedazuridine will be included in next-generation clinical trials for precision medicine treatments initiated by the National Cancer Institute (NCI), part of the National Institutes of Health (NIH). Announced by the NIH on Oct. 23, 2024, the Myeloid Malignancies Molecular Analysis for Therapy Choice, or myeloMATCH, trials will be sponsored by NCI and conducted by the NCI-funded National Clinical Trials Network. The myeloMATCH program is comprised of trials evaluating new treatment combinations that target cancer-driving genetic mutations in myelodysplastic syndromes (MDS) or acute myeloid leukemia (AML). Across the myeloMATCH program, patients will undergo rapid genetic testing of their tumors and then be matched to trials involving oral decitabine and cedazuridine, other studies within myeloMATCH or, if there are no other myeloMATCH targeted combination options for their cancer types, standard treatment. “The myeloMATCH program is designed to ensure patients with aggressive malignancies of the blood and bone marrow receive therapy directed at specific, identified abnormalities in a timely manner,” said Harold Keer, MD, PhD, Chief Medical Officer, Taiho Oncology. “We are excited to have oral decitabine and cedazuridine included in this innovative clinical trial program. The inclusion of all oral regimens in the setting of myeloid malignancies has the potential to produce practice-changing data and reduce the treatment burden that patients and their loved ones face.” Oral decitabine and cedazuridine will be included in two trials within the myeloMATCH program: A Phase 2 trial (ClinicalTrials.gov, NCT06577441) will compare oral decitabine and cedazuridine to the combination treatment of oral decitabine and cedazuridine and enasidenib in treating patients with higher-risk, IDH2-mutated MDS. The trial will compare the complete remission (CR) rate between the two study groups and assess other endpoints, including safety. A Phase 2 trial (ClinicalTrials.gov, NCT06672146) will compare oral decitabine and cedazuridine and venetoclax plus enasidenib compared to oral decitabine and cedazuridine and venetoclax alone for the treatment of older patients with newly diagnosed AML or younger patients who are unable to receive standard treatment, and who have a mutation in the IDH2 gene. The trial will evaluate safety and compare the rate of measurable residual disease (MRD) negative complete remission (CR), as well as other secondary endpoints. For more information about myeloMATCH and the sub-studies that are currently open, click here. About Taiho Oncology, Inc. The mission of Taiho Oncology, Inc. is to improve the lives of patients with cancer, their families and their caregivers. The company specializes in the development and commercialization of orally administered anti-cancer agents for various tumor types. Taiho Oncology has a robust pipeline of small molecule clinical candidates targeting solid tumor and hematological malignancies, with additional candidates in pre-clinical development. Taiho Oncology is a subsidiary of Taiho Pharmaceutical Co., Ltd. which is part of Otsuka Holdings Co., Ltd. Taiho Oncology is headquartered in Princeton, New Jersey and oversees its parent company’s European and Canadian operations, which are located in Baar, Switzerland and Oakville, Ontario, Canada. For more information, visit https://www.taihooncology.com/, and follow us on LinkedIn and X. Taiho Oncology Contact: Leigh Labrie (609) 664-9878 llabrie@taihooncology.com

Phase 2

15 Aug 2024

·www.businesswire.com

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.

Executive ChangeImmunotherapyDrug Approval

06 Aug 2024

·www.fiercepharma.com

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.

Clinical ResultDrug ApprovalPhase 3Acquisition

100 Deals associated with Enasidenib Mesylate

External Link

KEGG	Wiki	ATC	Drug Bank
-	Enasidenib Mesylate	L01XX59	DB13874

R&D Status

Approved

10 top approved records.

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Indication	Country/Location	Organization	Date
Acute Myeloid Leukemia	US	Bristol Myers Squibb Co.	01 Aug 2017

Developing

10 top R&D records.

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Indication	Highest Phase	Country/Location	Organization	Date
IDH2 mutation Acute Myeloblastic Leukemia	Phase 3	US	Celgene Corp.	30 Dec 2015
IDH2 mutation Acute Myeloblastic Leukemia	Phase 3	CN	Celgene Corp.	30 Dec 2015
IDH2 mutation Acute Myeloblastic Leukemia	Phase 3	AU	Celgene Corp.	30 Dec 2015
IDH2 mutation Acute Myeloblastic Leukemia	Phase 3	AT	Celgene Corp.	30 Dec 2015
IDH2 mutation Acute Myeloblastic Leukemia	Phase 3	BE	Celgene Corp.	30 Dec 2015
IDH2 mutation Acute Myeloblastic Leukemia	Phase 3	BR	Celgene Corp.	30 Dec 2015
IDH2 mutation Acute Myeloblastic Leukemia	Phase 3	CA	Celgene Corp.	30 Dec 2015
IDH2 mutation Acute Myeloblastic Leukemia	Phase 3	CZ	Celgene Corp.	30 Dec 2015
IDH2 mutation Acute Myeloblastic Leukemia	Phase 3	DK	Celgene Corp.	30 Dec 2015
IDH2 mutation Acute Myeloblastic Leukemia	Phase 3	FR	Celgene Corp.	30 Dec 2015

Clinical Result

Indication

Phase

Evaluation

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT04281498 (MPN-RC 119, CTgov)	Phase 2	Primary Myelofibrosis	6	Enasidenib+Ruxolitinib	zdudxleqww(kmkkdaxlzr) = chubttlxtf xqdnlxlwqt (geabqhsewr, atrqhfmgnx - ogonibidor) View more	-	18 Dec 2024
NCT05010772 (4277, ASH2024)	Phase 1	Acute Myeloid Leukemia complex cytogenetics \| antecedent MDS/MPN \| therapy-related AML ... View more	31	ASTX727 alone	tfrpsrzugb(kgjhgkgazb) = shlgpssetd dokvjomgty (reamybwudk ) View more	Positive	09 Dec 2024
				ASTX727 plus venetoclax	tfrpsrzugb(kgjhgkgazb) = vrygwkhcvz dokvjomgty (reamybwudk ) View more
ASH2024	Not Applicable	Myelodysplastic Syndromes	-	Enasidenib 100 mg PO QD	kbatezdanf(ybjhmjcxsx) = None of the 87 severe AE (SAE) were related to ENA in these two cohorts. Differentiation syndromes were manageable and reported in 5/58 (8.6%) patients. gnregycmwh (wfwyeavkfz ) View more	-	07 Dec 2024
				Azacitidine (AZA, 75 mg/m2/d x 7 days, SC)
NCT01915498 \| NCT02677922 \| NCT02577406 \| NCT02632708 (Pubmed \| Blood Adv) Manual	Not Applicable	Acute Myeloid Leukemia IDH2 Mutation	643	enasidenib ± azacitidine or chemotherapy	qgedkmysfb(quacsqlhmz) = yjimnrxndu bngedsxxua (essiruzwhq ) View more	Positive	20 Mar 2024
				Enasidenib plazacitidineine	qgedkmysfb(quacsqlhmz) = ndffkxemon bngedsxxua (essiruzwhq )
NCT03728335 (Tandem Meetings ASTCT and CIBMTR2024) Manual	Phase 1	IDH2 mutation Acute Myeloblastic Leukemia Maintenance IDH2 Mutation	15	Enasidenib 100 mg/day	erfiwyzsqs(vmpnbjfxgj) = hqzthykrji ztizoqdfpv (xfphtffgah ) View more	Positive	01 Feb 2024
NCT03013998 (Pubmed) Manual	Phase 1/2	Acute Myeloid Leukemia First line IDH2 Mutation	60	Enasidenib monotherapy	sqmqbaascn(wnaytkbkjs) = fhjkenvscf onfodwtmly (fzrldfhmxv ) View more	Positive	23 Jan 2024
				Enasidenib + azacitidine combination therapy	sqmqbaascn(wnaytkbkjs) = biuycprlnl onfodwtmly (fzrldfhmxv ) View more
NCT05010772 (ASH2023)	Phase 1	Acute Myeloid Leukemia Maintenance	23	ASTX727 35/100 mg	uuesgnvovw(nciuajcgkh) = wwzvflgyqo veawwdbayt (aobgdajzpv ) View more	-	10 Dec 2023
				ASTX727 35/100 mg + Venetoclax 400 mg	uuesgnvovw(nciuajcgkh) = owhyhbrnsf veawwdbayt (aobgdajzpv ) View more
NCT04092179 (Phase Ib/II Study, ASH2023)	Phase 1/2	Myeloid Tumor	27	Enasidenib + Venetoclax	cnpcyrqban(cyvxmydrtz) = iknukupsfk nwndeflcie (rtvyjuadjf, 8.2 - NR) View more	-	09 Dec 2023
INNV-07 (SNO2023)	Not Applicable	Adjuvant	1	Enasidenib	kaewpeevba(nnsivmqfij) = cijvjzmafo tibgummymp (bocpdfktez )	Positive	10 Nov 2023

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