Study researchers think that a drug called enasidenib may help people with clonal cytopenia of undetermined significance (CCUS) because the drug blocks the mutated IDH2 protein, which may improve blood cell counts. The purpose of this study is to find out whether enasidenib is a safe and effective treatment for CCUS.

Start Date30 Jun 2024

Sponsor / Collaborator

Washington University School of Medicine

[+2]

NCT06176989 / RecruitingPhase 2IIT

Phase II Study of Enasidenib in IDH2-mutated Malignant Sinonasal and Skull Base Tumors

Background:
Cancers of the nasal cavity or skull base are rare. They often are not diagnosed until they are at an advanced stage, and they often spread to other parts of the body. These cancers may have mutations in a gene called IDH2. Researchers want to find out if a drug (enasidenib) that targets the IDH2 mutation can help people with these cancers.
Objective:
To test enasidenib in people with cancers of the nasal cavity or skull base.
Eligibility:
People aged 18 years and older with rare cancers of the nasal cavity or the base of the skull. Their cancer must have an IDH2 gene mutation, and it must have recurred locally or spread to other parts of the body. These cancers can include sinonasal undifferentiated carcinoma; olfactory neuroblastoma; sinonasal large-cell neuroendocrine carcinoma; poorly differentiated sinonasal adenocarcinoma; or chondrosarcoma.
Design:
Participants will be screened. They will have a physical exam with blood and urine tests and tests of their heart function. They will have imaging scans of their brain, skull base, neck, chest, abdomen, and pelvis. A sample of tumor tissue will be collected.
Enasidenib is a tablet taken by mouth with a glass of water. Participants will take the drug once a day, every day, in 28-day cycles. They will not have resting periods between cycles.
Participants will visit the clinic on the first day of each cycle to receive the tablets they will need to take at home until the beginning of the next cycle. They will keep a diary to record the time of each dose they take.
Participants may remain in the study as long as the drug is helping them....

Start Date04 Mar 2024

Sponsor / Collaborator

National Cancer Institute

NCT04203316 / RecruitingPhase 2IIT

An Open-Label Feasibility Study to Assess the Safety and Pharmacokinetics of Enasidenib in Pediatric Patients With Relapsed/Refractory Acute Myeloid Leukemia (R/R-AML) With an Isocitrate Dehydrogenase-2 (IDH2) Mutation

This trial studies the side effects of enasidenib and to see how well it works in treating patients with acute myeloid leukemia that has come back after treatment (relapsed) or has been difficult to treat with chemotherapy (refractory). Patients must also have a specific genetic change, also called a mutation, in a protein called IDH2. Enasidenib may stop the growth of cancer cells by blocking the mutated IDH2 protein, which is needed for cell growth.

Start Date14 Aug 2023

Sponsor / Collaborator

The Children's Oncology Group Foundation, Inc.

[+1]

100 Clinical Results associated with Enasidenib Mesylate

100 Translational Medicine associated with Enasidenib Mesylate

100 Patents (Medical) associated with Enasidenib Mesylate

249

Literatures (Medical) associated with Enasidenib Mesylate

23 Jan 2024·Blood advances

A study to assess the efficacy of enasidenib and risk-adapted addition of azacitidine in newly diagnosed IDH2-mutant AML

Article

Author: Chervin, Jordan ; Dunbar, Andrew J ; Yocum, Ashley O ; Rosenberg, Leonard ; Lance, Jennie R ; Patel, Prapti ; Borate, Uma ; Li, Yan ; Blum, William G ; Lin, Tara ; Vergilio, Jo-Anne ; Baer, Maria R ; Foster, Matthew C ; Heerema, Nyla A ; Collins, Robert H ; Huang, Ying ; Druggan, Franchesca ; Marcus, Sonja ; McNulty, Samantha N ; Stock, Wendy ; Mao, Hsiaoyin Charlene ; Boyiadzis, Michael ; Levine, Ross L ; Shoben, Abigail ; Cai, Sheng F ; Foran, James M ; Litzow, Mark ; Byrd, John C ; Druley, Todd ; Olin, Rebecca L ; Mims, Alice S ; Stefanos, Mona ; Burd, Amy ; Chen, Timothy L ; Stein, Eytan M ; Kovacsovics, Tibor ; Schiller, Gary J ; Druker, Brian J

Abstract:

Enasidenib (ENA) is an inhibitor of isocitrate dehydrogenase 2 (IDH2) approved for the treatment of patients with IDH2-mutant relapsed/refractory acute myeloid leukemia (AML). In this phase 2/1b Beat AML substudy, we applied a risk-adapted approach to assess the efficacy of ENA monotherapy for patients aged ≥60 years with newly diagnosed IDH2-mutant AML in whom genomic profiling demonstrated that mutant IDH2 was in the dominant leukemic clone. Patients for whom ENA monotherapy did not induce a complete remission (CR) or CR with incomplete blood count recovery (CRi) enrolled in a phase 1b cohort with the addition of azacitidine. The phase 2 portion assessing the overall response to ENA alone demonstrated efficacy, with a composite complete response (cCR) rate (CR/CRi) of 46% in 60 evaluable patients. Seventeen patients subsequently transitioned to phase 1b combination therapy, with a cCR rate of 41% and 1 dose-limiting toxicity. Correlative studies highlight mechanisms of clonal elimination with differentiation therapy as well as therapeutic resistance. This study demonstrates both efficacy of ENA monotherapy in the upfront setting and feasibility and applicability of a risk-adapted approach to the upfront treatment of IDH2-mutant AML. This trial is registered at www.clinicaltrials.gov as #NCT03013998.

01 Jan 2024·Leukemia research

Corrigendum to “Real-world clinical outcomes with enasidenib in relapsed or refractory acute myeloid leukemia” [Leuk. Res. (2022) 106946]

Author: Marshall, Landon ; Knoth, Russell L ; Hou, Ying ; Copher, Ronda ; McBride, Ali ; Klink, Andrew J ; Gajra, Ajeet

01 Jan 2024·Cell metabolism

Mitochondrial isocitrate dehydrogenase impedes CAR T cell function by restraining antioxidant metabolism and histone acetylation

Article

Author: Si, Xiaohui ; Zhai, Xingyuan ; Gu, Tianning ; Wu, Longyuan ; Wang, Dongrui ; Kong, Delin ; Liu, Lianxuan ; Xiao, Gang ; Jing, Ruirui ; Huang, He ; Wang, Xiujian ; Shao, Mi ; Zhang, Zhaoru ; Guo, Xin ; Cai, Bohan ; Song, Junzhe ; Teng, Xinyi ; Shen, Ying ; Huang, Yue ; Qian, Pengxu ; Wei, Jieping ; Meng, Ye ; Hu, Yongxian

The efficacy of chimeric antigen receptor (CAR) T cell therapy is hampered by relapse in hematologic malignancies and by hyporesponsiveness in solid tumors. Long-lived memory CAR T cells are critical for improving tumor clearance and long-term protection. However, during rapid ex vivo expansion or in vivo tumor eradication, metabolic shifts and inhibitory signals lead to terminal differentiation and exhaustion of CAR T cells. Through a mitochondria-related compound screening, we find that the FDA-approved isocitrate dehydrogenase 2 (IDH2) inhibitor enasidenib enhances memory CAR T cell formation and sustains anti-leukemic cytotoxicity in vivo. Mechanistically, IDH2 impedes metabolic fitness of CAR T cells by restraining glucose utilization via the pentose phosphate pathway, which alleviates oxidative stress, particularly in nutrient-restricted conditions. In addition, IDH2 limits cytosolic acetyl-CoA levels to prevent histone acetylation that promotes memory cell formation. In combination with pharmacological IDH2 inhibition, CAR T cell therapy is demonstrated to have superior efficacy in a pre-clinical model.

News (Medical) associated with Enasidenib Mesylate

01 Aug 2023

·www.globenewswire.com

Auron Establishes Premier Scientific Advisory Board to Support the Advancement of its AI-Powered Platform and Pipeline Targeting Cellular Plasticity in Cancer

Advisory Board includes recognized physicians, clinicians and scientists with deep expertise spanning multi-omic platforms, translational biology, drug discovery and clinical developmentNEWTON, Mass., Aug. 01, 2023 (GLOBE NEWSWIRE) -- Auron Therapeutics, a platform-based, product-driven biotechnology company focused on developing novel cancer therapies that target cellular plasticity, today announced the members of its scientific advisory board (SAB), comprised of distinguished physician-scientists, clinical investigators, and research & development veterans from world-leading cancer centers and biopharmaceutical companies. The most recent addition, Charles M. Rudin M.D., Ph.D., is the Chief of the Thoracic Oncology Service at Memorial Sloan Kettering Cancer Center (MSK). The SAB collaborates with Auron’s leadership to provide strategic guidance, as the company advances its proprietary platform and its research programs for both solid tumors and hematologic malignancies. “Our scientific advisors are some of the most renowned international minds in oncology drug discovery and development, which speaks to the importance of our unique approach to cancer drug discovery and development,” said Kate Yen, Ph.D., founder and chief executive officer of Auron. “Together, they have an incredible wealth of knowledge and expertise that we can apply to maximize the power of our multi-omic platform and enable the potential of therapies targeting cellular plasticity in a range of cancers. This is an exciting time at Auron. We are honored to benefit from their expansive contributions to the field of oncology and appreciate their guidance as we advance our efforts to deliver transformational therapies for patients in need.” Auron’s proprietary platform is a multi-omic, AI-powered platform that combines computational and translational biology to understand the drivers of two hallmarks of cancer: cellular plasticity and dysregulated differentiation in cancer cells. Leveraging its platform, Auron aims to identify novel targets paired with patient selection and efficacy biomarkers, and ultimately, small molecule product candidates that target the drivers of altered cellular plasticity. “We have seen tremendous innovation in oncology over the last decade, including the advent of personalized targeted therapies and immunotherapy. However, we continue to struggle with acquired resistance to these therapies,” said Dr. Rudin, Chief of the Thoracic Oncology Service, Co-Director of the Druckenmiller Center for Lung Cancer Research, and Sylvia Hassenfeld Chair in Lung Cancer Research at MSK. “I am impressed by the sophistication of Auron’s platform, analyzing the plasticity of cancer cells as a key resistance mechanism. Auron is taking a distinct approach that is defining promising targets not previously identified or addressed. I am delighted to partner with the SAB, Kate and the Auron team, to maximize the full potential of this platform, with the ultimate goal of bringing forward more durably effective treatment options for our patients.” Auron’s Scientific Advisory Board Members Stéphane de Botton, M.D.Dr. de Botton is a physician, clinical investigator and head of drug development in acute leukemias in the Department of Hematology at Gustave Roussy Cancer Center in Villejuif, France. He also belongs to the research unit UMR 1170 for novel preclinical research. He is a member of the executive board of the Acute Leukemia French Association (ALFA) that focuses on the clinical and translational research in adult acute myeloid leukemia. Richard Chesworth, Ph.D.Dr. Chesworth is an entrepreneur in residence at Third Rock Ventures, focused on building new drug discovery and development companies. He has contributed to the research and development of thirteen different compounds entering clinical trials, resulting in two FDA-approved new molecular entities, including TAZVERIK® for the treatment of both epithelioid sarcoma and relapsed/refractory follicular lymphoma. Dr. Chesworth previously served as chief scientific officer at Kymera Therapeutics, head of chemistry and senior vice president of research at Epizyme, head of chemistry at EnVivo, and principal scientist at Surface Logix and Pfizer. Ross L. Levine, M.D., Co-founder Dr. Levine is a member of the Human Oncology and Pathogenesis Program and an attending physician on the Leukemia Service, Department of Medicine, the Laurence Joseph Dineen Chair in Leukemia Research with Special Emphasis on Leukemia in Children and Young People, Deputy Physician-In-Chief, Translational Research at MSK, and a professor of Medicine at Weill Cornell Medical College. His laboratory has identified myeloproliferative neoplasm (MPN) predisposition alleles and characterized somatic genetic and epigenetic alterations in MPN and acute myeloid leukemia (AML) patients, which has led to new mechanism-based therapies. In 2011, Dr. Levine was elected to the American Society of Clinical Investigation and in 2018 to the Association of American Physicians. Dr. Levine is the recipient of numerous awards, including the Dameshek Prize from the American Society for Hematology, a Scholar Award from the Leukemia and Lymphoma Society, the Boyer Award for clinical investigation from Memorial Sloan Kettering Cancer Center, and an NCI Outstanding Investigator Award. Charles M. Rudin, M.D., Ph.D.Dr. Rudin is a medical oncologist at MSK specializing in the care of patients with lung cancer. He is the Chief of the Thoracic Oncology Service, Co-Director of the Druckenmiller Center for Lung Cancer Research, and Sylvia Hassenfeld Professor and Chair in Lung Cancer Research at MSK. Dr. Rudin also has chaired the National Cancer Institute (NCI) Small Cell Lung Cancer Research Consortium since its inception in 2015. He directs a broad program of therapeutic research, including preclinical and clinical investigations to identify and test novel therapeutic approaches to small cell and non-small cell lung cancer. Dr. Rudin is the recipient of numerous awards and honors, including an NCI Outstanding Investigator Award, the NCI Director’s Service Award, and the Paul Bunn Lifetime Achievement Award from the International Association for the Study of Lung Cancer. Mikhail (Misha) Roshal, M.D., Ph.D.Dr. Roshal is a practicing hematopathologist, associate attending physician, and Director of the Clinical Flow Cytometry Laboratory in the Department of Pathology at MSK. His major clinical expertise is in development of robust flow cytometry-based assays for assessment of treatment response of hematologic neoplasms. Dr. Roshal’s research interests are in molecular genetic characterization of treatment resistant and rare disease populations and in defining molecular genetic triggers of lineage infidelity and unusual differentiation pathways in acute leukemia. Kimberly Stegmaier, M.D.Dr. Stegmaier is a professor of Pediatrics at Harvard Medical School and the Ted Williams Chair at Dana-Farber Cancer Institute and has advanced the application of genomics to drug and protein target discovery for pediatric malignancies. She is the Vice Chair for Pediatric Oncology Research, Co-director of the Pediatric Hematologic Malignancy Program, and an attending physician providing clinical care in Pediatric Oncology at the Dana-Farber Cancer Institute and Boston Children’s Hospital. Dr. Stegmaier is also an Institute Member of the Broad Institute of Harvard and MIT. She has served as a Council Member with the Society for Pediatric Research and as the Chair for the American Association for Cancer Research (AACR) Pediatric Cancer Working Group. Dr. Stegmaier is the recipient of numerous awards, including the Joanne Levy, MD, Memorial Award for Outstanding Achievement from the American Society of Hematology. Eytan M. Stein, M.D., Co-founderDr. Stein is the Chief of Leukemia Service in the Division of Hematologic Malignancies, associate attending physician, clinical investigator and Director of the Program for Drug Development in Leukemia at MSK. He conducts novel Phase 1 clinical trials of compounds that target the genetic and epigenetic basis of myeloid malignancies and serves as the lead investigator at MSK for the BEAT AML master clinical trial. Dr. Stein led the clinical trials of IDHIFA® and TIBSOVO®, isocitrate dehydrogenase (IDH) inhibitors, in patients with relapsed and refractory AML that led to their FDA approvals. Shin-San Michael Su, Ph.D.Dr. Michael Su is a pioneering biotech leader with deep expertise in drug discovery and translational medicine. He served as Chief Scientific Officer of Volastra Therapeutics and as Chief Scientific Officer of Decibel Therapeutics. Before that, Dr. Su was a Co-founder and Senior Vice President of Research and Development at Agios Pharmaceuticals, where he led the team responsible for identifying the oncogenic cause of IDH mutants in cancer and the discovery of IDHIFA® and TIBSOVO®, FDA-approved treatments for AML with IDH mutations. He served as General Director and Vice President of the Biomedical Engineering Research Laboratory at ITRI in Taiwan and spent 14 years in scientific leadership roles at Vertex Pharmaceuticals, concluding his tenure as Program Executive and Vice President of the Novartis-Vertex kinase collaboration. George Thomas, M.D.Dr. Thomas is a professor of Pathology at the Knight Cancer Institute, Oregon Health & Science University in Portland, Oregon, and Associate Medical Director of the Knight Diagnostics Laboratory. His clinical area of expertise is in precision oncology of prostate and kidney cancers. Dr. Thomas directs a translational research program that studies treatment induced metabolic reprogramming in these cancers, with the goal of developing new combination therapies. Matthew Vander Heiden, M.D., Ph.D., Co-founderDr. Vander Heiden is a professor in the Department of Biology at the Massachusetts Institute of Technology, and Director of the Koch Institute for Integrative Cancer Research. He is also an Institute Member of the Broad Institute of Harvard and MIT, and an Instructor in Medicine at the Dana-Farber Cancer Institute and Harvard Medical School. Using a combination of biochemistry, molecular biology and mouse models, the aim of the Vander Heiden laboratory is to understand how metabolism influences different stages of tumor biology with a goal to improve cancer treatment in the clinic. Paresh Vyas, MRCP FRCP FRCPathDr. Vyas is a professor of Hematology at Oxford University, and a research-consulting Hematologist with a clinical practice in myeloid disorders (MDS, AML and MPD) and allogeneic stem cell transplant at the MRC Molecular Haematology Unit, Weatherall Institute of Molecular Medicine, University of Oxford. He is Co-lead of the Oxford BRC Hematology and Stem Cells Theme, is on the Board of NHSBT, Vice-chair of the MRC Clinical Training Panel and Translational Lead for the UK Therapy Acceleration Program. About Auron Therapeutics Auron Therapeutics is a platform-based, product-driven biotechnology company focused on developing therapies that target cellular plasticity for solid tumor cancers and hematological malignancies. Auron has built a proprietary AI-powered platform that integrates large, multi-omic datasets to rapidly compare tumor tissue to normal tissues and enable a systems-biology understanding of the pathways that are associated with tumor plasticity, dysregulated differentiation, and treatment resistance. For more information, please visit www.aurontx.com. Contact: Monique AllaireTHRUST Strategic Communicationsmonique@thrustsc.com

Phase 1Executive Change

05 Jun 2023

·www.fiercebiotech.com

Foghorn finally has clear route back to clinic after FDA lifts yearlong hold on blood cancer drug

An independent committee concluded that a patient's death was not caused by differentiation syndrome. Foghorn Therapeutics has been sitting in dock for over a year due to an FDA clinical hold placed on its blood cancer drug in the wake of a patient death. Now, the biotech can set sail once again. A phase 1 trial of FHD-286 in multiple acute myelogenous leukemia (AML) and myelodysplastic syndrome (MDS) was initially placed on partial hold in May 2022 following the death of a patient with potential differentiation syndrome. The syndrome is associated with AML and MDS drugs that promote differentiation of myeloblasts into mature cells. The partial hold was upgraded to a full hold in August last year. Since then, Foghorn has amended the trial, and CEO Adrian Gottschalk said in a release Monday morning that the company had worked with the FDA to resolve the regulator's issues “with a focus on patient safety.” “Clinical data suggest FHD-286 is a potent, broad-based differentiation therapeutic, and we believe it has significant combination potential as a treatment in AML,” added Gottschalk, who expects a new phase 1 study to launch in the third quarter of the year. In response to the hold, Foghorn established an independent adjudication committee of leading AML experts, which concluded the rate of differentiation syndrome in the paused study had been 15%. While one of these cases was the patient who died, the committee decided that the syndrome did not contribute to the death. FHD-286 is an enzymatic inhibitor of BRG1 and BRM, two proteins that promote cancer cell growth. The upcoming study will see the drug tested in combination with the chemotherapies Dacogen or cytarabine in relapsed and/or refractory AML patients. Foghorn isn’t the only drug developer to have seen differentiation syndrome when treating AML and MDS. The FDA put a phase 1b clinical trial of Kura Oncology’s menin inhibitor KO-539 on hold in 2021 after a death potentially linked to differentiation syndrome. Further back, Agios Pharmaceuticals had cases in recipients of enasidenib and ivosidenib, inhibitors of isocitrate dehydrogenase. In all cases, the holds were eventually lifted, with the latter drugs now marketed in the U.S. by Bristol Myers Squibb and Servier, respectively.

Phase 1

05 Jun 2023

·www.fiercebiotech.com

ASCO: At long last, Servier finds a survival benefit in difficult brain cancer

Servier picked up vorasidenib in the $1.8 billion acquisition of Agios Pharmaceuticals’ cancer unit in 2020. Servier promised in March that interim data from a phase 3 study would “shift the treatment paradigm” for a type of brain cancer that has long been stagnant in clinical research. Now, we’ve got the goods. Vorasidenib resulted in an “unprecedented” median 27.7 months of progression free survival (PFS) in patients with residual or recurrent grade 2 glioma with a certain mutation. Patients treated also had a significant improvement in time to next intervention, which was a key secondary endpoint of the study. Servier trumpeted the results from the phase 3 INDIGO trial Sunday at the American Society of Clinical Oncology conference in Chicago. The company had previously teased in March that vorasidenib had beaten placebo on the primary endpoint at an interim analysis, but the specifics were kept under wraps. INDIGO is a registration-enabling late-stage trial featuring patients with residual or recurrent grade 2 glioma, who have an isocitrate dehydrogenase 1/2 (IDH1/2) mutation and have undergone surgery as their only treatment. Gliomas are a common tumor that grow within the brain or spinal cord in the glial or precursor cells of the central nervous system. Patients with this type of cancer have a particularly poor prognosis, and available treatment options have high toxicities. There’s been little progress in finding more advanced treatments over the past few decades. There are several different types of glioma. The 331-patient study had 172 people with oligodendroglioma and 159 with astrocytoma. Vorasidenib met the primary endpoint of PFS and the key secondary endpoint of time to next intervention at the prespecified second interim analysis. On the PFS measure, the therapy hit 27.7 months compared to 11.1 on placebo. On the secondary measure, Servier said that the median time to next intervention was not reached for vorasidenib but was 17.8 months for placebo. Servier said the PFS result was statistically significant and clinically meaningful, which a p-value of 0.000000067. The data cutoff was Sept. 6, 2022. The INDIGO results demonstrate the impact of targeting these glioma mutations early, according to Servier’s Susan Pandya, M.D., vice president of clinical development and head of cancer metabolism global development for oncology and immuno-oncology. Servier said the safety profile was “well tolerated” and consistent with previous phase 1 testing. The most common grade 3 adverse events were liver enzyme elevations, which can indicate liver damage and seizures. The rate of seizures was 4.2% for vorasidenib and 2.5% for placebo. The FDA granted a fast-track designation to vorasidenib in March. The company will now work to establish a timeline for submission of an application for approval to the agency. Servier picked up the therapy in the $1.8 billion acquisition of Agios Pharmaceuticals’ cancer unit in 2020. Vorasidenib was the jewel of the buyout, which also included two approved drugs, Idhifa and Tibsovo.

Clinical ResultPhase 3AcquisitionASCOFast Track

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.

to view more data

Indication	Highest Phase	Country/Location	Organization	Date
CCUS Clonal Cytopenia of Undetermined Significance	Phase 2	US	Bristol Myers Squibb Co.	30 Jun 2024
Anemia	Phase 2	US	Celgene Corp.	12 Jan 2022
Monocytic leukemia	Phase 2	US	Celgene Corp.	12 Jan 2022
Chronic Myelomonocytic Leukemia	Phase 2	DE	Celgene Corp.	27 Aug 2020
IDH2 mutation Acute Myeloblastic Leukemia	Phase 2	DE	Celgene Corp.	27 Aug 2020
Myelodysplastic Syndromes	Phase 2	DE	Celgene Corp.	27 Aug 2020
Advanced Malignant Solid Neoplasm	Phase 2	US	Celgene Corp.	08 Dec 2014
Advanced Malignant Solid Neoplasm	Phase 2	FR	Celgene Corp.	08 Dec 2014
Chondrosarcoma	Phase 2	US	Celgene Corp.	08 Dec 2014
Chondrosarcoma	Phase 2	FR	Celgene Corp.	08 Dec 2014

Clinical Result

Indication

Phase

Evaluation

View All Results

Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT03013998 (Pubmed)	Phase 1/2	Acute Myeloid Leukemia IDH2-mutant	-	Enasidenib monotherapy	ihdyuurlut(zenyjmfiki) = yqigqvsosq rwqxickwpy (xqbnuqnhwq )	-	23 Jan 2024
				Enasidenib + Azacitidine combination therapy	ihdyuurlut(zenyjmfiki) = ipgggjfyoj rwqxickwpy (xqbnuqnhwq )
NCT04092179 (Phase Ib/II Study, ASH2023)	Phase 1/2	Myeloid Tumor	27	Enasidenib + Venetoclax	fhjdbbnoqv(idhdtuxpzy) = bxqochjjyt jquqwyvdoe (mvkccvcwkm, 8.2 - NR) View more	-	09 Dec 2023
NCT02677922 (AG-221-AML-005 \| AG221-AML-005, CTgov)	Phase 1/2	Acute Myeloid Leukemia	130	AZA+AG-221 (Phase 1b Dose-finding Stage: AG-221 (100mg) + AZA)	jelpoxfroh(snelrlppwo) = sohbwhkktu mbqbxoaojr (mkqinyebru, nzsmrbifrf - fpxbjucbuk) View more	-	22 Nov 2022
				AZA+AG-221 (Phase 1b Dose-finding Stage: AG-221 (200mg) + AZA)	jelpoxfroh(snelrlppwo) = hgovgrwdit mbqbxoaojr (mkqinyebru, nzbbwkhmav - whuafbazqe) View more
NCT03728335 (ASH2022) Manual	Phase 1	Acute Myeloid Leukemia Maintenance IDH2 Mutation	15	Enasidenib	igclkjpqut(bfvzuilbmt) = grade ≥3 AEs were mainly due to hematologic toxicity including: lymphopenia (26%; n=4), anemia (20%; n=3), neutropenia (13%; n=2), and thrombocytopenia (6%; n=1) qgughvpkyl (kcmwhxjjmz ) View more	Positive	15 Nov 2022
NCT04281498 (ASH2022) Manual	Phase 2	Myeloproliferative Disorders IDH2 Mutation	6	Ruxolitinib Phosphate+Enasidenib Mesylate	bxkzrhblad(rqsphvqxer) = qtnsnnzknq ozwponvrgr (ceioxjpijb ) View more	Positive	15 Nov 2022
NCT03515512 (Pubmed) Manual	Phase 1	IDH2 mutation Acute Myeloblastic Leukemia IDH2 Mutation	19	Enasidenib	gmqbqnqnfx(zdhtnpcuac) = qzrmrmrewp jajibesqwb (dxobtfsvgt ) View more	Positive	23 Sep 2022
NCT02577406 (CTgov)	Phase 3	Acute Myeloid Leukemia	319	AG-221 (AG-221)	hjylixmzik(ogztxvdyzd) = qwnaqoitki gobpuqbwts (quxeesizkm, yjrptrcxiv - jgivqypzxg) View more	-	10 Sep 2022
				IDAC+hydroxyurea+LDAC+azacitidine (Conventional Care Regimens (CCRs))	hjylixmzik(ogztxvdyzd) = jynknncjvz gobpuqbwts (quxeesizkm, mnbmhovbdw - kribcpcidw) View more
NCT03383575 (Pubmed) Manual	Phase 2	Myelodysplastic Syndromes First line IDH2 Mutation	50	azacitidine+enasidenib	uujowjntnc(dicoopqnem) = The most common adverse events were neutropenia (40%), nausea (36%), constipation (32%), and fatigue (26%). Hyperbilirubinemia from off-target UGT1A1 inhibition occurred in 14% of patients (8%; grades 3 and 4), and IDH-inhibitor-associated differentiation syndrome (IDH-DS) in 8 patients (16%). kgfobdijcq (uxgjimvkcu )	Positive	16 Aug 2022
				enasidenib
NCT02577406 (IDHENTIFY, Pubmed) Manual	Phase 3	IDH2 mutation Acute Myeloblastic Leukemia IDH2 Mutation	319	Enasidenib	wmcmxoshdi(alqcmbumew) = ncibsdkszv ooxafsiywq (hzgwseqgma ) View more	Similar	17 Jun 2022
				conventional care	wmcmxoshdi(alqcmbumew) = varenxwjpt ooxafsiywq (hzgwseqgma ) View more
NCT02577406 (IDHENTIFY, ASCO2022) Manual	Phase 3	Acute Myeloid Leukemia IDH2 R140 Mutation \| IDH2 R172 Mutation	319	enasidenib	oxcwotospc(kjwqfrwnmw) = qynwetnclk cacoajrinp (ecfagoydta ) View more	Positive	02 Jun 2022
				conventional care regimens	oxcwotospc(kjwqfrwnmw) = sdnwdtlxhl cacoajrinp (ecfagoydta ) View more

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