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 Date03 Feb 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 Date17 Jan 2025

Sponsor / Collaborator

National Cancer Institute

NCT06240754 / RecruitingPhase 2IIT

A Pilot Study of Enasidenib for Patients With Clonal Cytopenia of Undetermined Significance and Mutations in IDH2: A Decentralized Trial

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 Date10 Oct 2024

Sponsor / Collaborator

Washington University School of Medicine

[+2]

100 Clinical Results associated with Enasidenib Mesylate

100 Translational Medicine associated with Enasidenib Mesylate

100 Patents (Medical) associated with Enasidenib Mesylate

271

Literatures (Medical) associated with Enasidenib Mesylate

01 Oct 2024·JTO clinical and research reports

Differentiation Syndrome in a Patient With NSCLC Harboring IDH2 Mutation Treated With Enasidenib: Case Report

Article

Author: Sukhadia, Bhoomika ; Shah, Zunairah ; Tan, Dean ; Chae, Young Kwang ; Oh, Youjin

IDH2 gain-of-function mutations cause DNA hypermethylation interfering with cellular differentiation and are linked to poor disease outcomes in NSCLC. IDH2-inhibitor enasidenib is approved for refractory acute myeloid leukemia but has been associated with delayed onset of differentiation syndrome-a potentially fatal inflammatory reaction caused by differentiating agents, namely all-trans retinoic acid and arsenic trioxide. We report the first case of differentiation syndrome in a patient with NSCLC treated with enasidenib, who after 7 weeks experienced bilateral peripheral edema and shortness of breath, with scans exhibiting pericardial effusion and ground-glass opacities suggestive of pneumonitis. Differentiation syndrome should be considered as a differential diagnosis in patients with solid tumors undergoing IDH2-inhibitor targeted therapy.

01 Oct 2024·JAMA Oncology

Contemporary Management of Acute Myeloid Leukemia

Review

Author: Sekeres, Mikkael A. ; Venugopal, Sangeetha

Importance:

Acute myeloid leukemia (AML) is a clonal hematopoietic cancer that disrupts normal hematopoiesis, ultimately leading to bone marrow failure and death. The annual incidence rate of AML is 4.1 per 100 000 people in the US and is higher in patients older than 65 years. Acute myeloid leukemia includes numerous subgroups with heterogeneous molecular profiles, treatment response, and prognosis. This review discusses the evidence supporting frontline therapies in AML, the major principles that guide therapy, and progress with molecularly targeted therapy.

Observations:

Acute myeloid leukemia is a genetically complex, dynamic disease. The most commonly altered genes include FLT3, NPM1, DNMT3A, IDH1, IDH2, TET2, RUNX1, NRAS, and TP53. The incidence of these alterations varies by patient age, history of antecedent hematologic cancer, and previous exposure to chemotherapy and/or radiotherapy for any cancer. Since 2010, molecular data have been incorporated into AML prognostication, gradually leading to incorporation of targeted therapies into the initial treatment approach of induction chemotherapy and subsequent management. The first molecularly targeted inhibitor, midostaurin, was approved to treat patients with AML with FLT3 variants in 2017. Since then, the understanding of the molecular pathogenesis of AML has expanded, allowing the identification of additional potential targets for drug therapy, treatment incorporation of molecularly targeted therapies (midostaurin, gilteritinib, and quizartinib targeting FLT3 variants; ivosidenib and olutasidenib targeting IDH1 variants, and enasidenib targeting IDH2), and identification of rational combination regimens. The approval of hypomethylating agents combined with venetoclax has revolutionized the therapy of AML in older adults, extending survival over monotherapy. Additionally, patients are now referred for hematopoietic cell transplant on a more rational basis.

Conclusions and Relevance:

In the era of genomic medicine, AML treatment is customized to the patient’s comorbidities and AML genomic profile.

19 Sep 2024·Blood Cancer Journal

Current status and research directions in acute myeloid leukemia.

Review

Author: Yilmaz, Musa ; Daver, Naval ; Kadia, Tapan ; Kantarjian, Hagop ; Short, Nicholas J ; Ravandi, Farhad ; Sasaki, Koji ; Borthakur, Gautam ; Issa, Ghayas ; DiNardo, Courtney D ; Jabbour, Elias

The understanding of the molecular pathobiology of acute myeloid leukemia (AML) has spurred the identification of therapeutic targets and the development of corresponding novel targeted therapies. Since 2017, twelve agents have been approved for the treatment of AML subsets: the BCL2 inhibitor venetoclax; the CD33 antibody drug conjugate gemtuzumab ozogamicin; three FLT3 inhibitors (midostaurin, gilteritinib, quizartinib); three IDH inhibitors (ivosidenib and olutasidenib targeting IDH1 mutations; enasidenib targeting IDH2 mutations); two oral hypomethylating agents (oral poorly absorbable azacitidine; fully absorbable decitabine-cedazuridine [latter approved as an alternative to parenteral hypomethylating agents in myelodysplastic syndrome and chronic myelomonocytic leukemia but commonly used in AML]); and CPX-351 (encapsulated liposomal 5:1 molar ratio of cytarabine and daunorubicin), and glasdegib (hedgehog inhibitor). Other targeted therapies (menin inhibitors, CD123 antibody-drug conjugates) are showing promising results. To achieve optimal results in such a rare and heterogeneous entity as AML requires expertise, familiarity with this rare cancer, and the access to, and delivery of disparate therapies under rigorous supportive care conditions. In this review, we update the standard-of-care and investigational therapies and outline promising current and future research directions.

News (Medical) associated with Enasidenib Mesylate

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

12 Jul 2024

·www.biopharmadive.com

Bristol Myers’ leukemia blockbuster set to face generic rivals

Pharmaceutical companies face a looming patent cliff over the next several years, as generic rivals could erode sales of some of the industrys best-selling medicines. For some drugmakers, copycat competitors are already on the doorstep.Bristol Myers Squibb, for one, could soon hit headwinds for its blockbuster Sprycel as the first generic of the leukemia drug is expected to hit the market in September.Sprycel, or dasitinib, is a kinase inhibitor that was approved in 2006 to treat chronic myeloid leukemia, a type of blood cancer thats diagnosed in about 10,000 people in the U.S. each year. The tablet has been a reliable blockbuster for Bristol Myers over the years, reaching $1.9 billion in global sales in 2023. Sales topped $2.1 billion in both 2022 and 2021.Bristol Myers has faced several challenges to Sprycels patents, and filed a patent infringement lawsuit again Swedish biopharma company XSpray Pharma in 2022, as well as a handful of other companies that were challenging two patents listed in the Food and Drug Administrations Orange Book that expire in 2025 and 2026.Bristol Myers settled with XSpray last year, clearing the way for the challenger to launch a generic dasatinib as soon as Sept. 1, 2024. XSpray has an FDA decision date of July 31 for its optimized version of dasatinib, Dasynoc.If Dasynoc is approved, it will join dozens of new generics cleared by the FDA this year, including several copies of cancer drugs. Their entry could lead to price declines in oncology, according to IDP Analytics. Sprycel has a list price of more than $18,000 per month. CML mostly affects adults 65 and older, and Sprycel treatment is therefore often covered under Medicare.Biocon, Teva Pharmaceutical and several other companies also have developed dasitinib generics and secured tentative FDA approval.Sprycels patent expiration isnt the only generic threat Bristol Myers faces. Copycat competitors to Revlimid are available in limited fashion already, while protection for top-sellers Eliquis and Opdivo run out in 2026 and 2028 in the U.S., respectively.In oncology, Bristol Myers is focused on expanding the market for Breyanzi, a CAR-T cell therapy for different types of lymphoma and leukemia, as well as for Abecma, for multiple myeloma. Opdualag, a combination immunotherapy for melanoma, also figures heavily in the companys plans.Elsewhere in Bristol Myers pipeline are two candidates for acute myeloid leukemia, or AML, that are in early clinical stages. The company co-markets with Servier Idhifa for AML, which is considered a hard-to-treat disease, '

ImmunotherapyDrug ApprovalPatent InfringementBiosimilar

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
CCUS Clonal Cytopenia of Undetermined Significance	Phase 2	US	Bristol Myers Squibb Co.	10 Oct 2024
Anemia	Phase 2	US	Celgene Corp.	12 Jan 2022
Monocytic leukemia	Phase 2	US	Celgene Corp.	12 Jan 2022
IDH2 mutation Acute Myeloblastic Leukemia	Phase 2	DE	Celgene Corp.	27 Aug 2020
Myelodysplastic Syndromes	Phase 2	DE	Celgene Corp.	27 Aug 2020
Refractory acute myeloid leukemia	Phase 2	US	Celgene Corp.	02 Dec 2019
Relapsing acute myeloid leukemia	Phase 2	US	Celgene Corp.	02 Dec 2019
Chronic Myelomonocytic Leukemia	Phase 2	US	Celgene Corp.	17 Jan 2018
High Risk Myelodysplastic Syndrome	Phase 2	US	Celgene Corp.	17 Jan 2018
Advanced Malignant Solid Neoplasm	Phase 2	US	Celgene Corp.	08 Dec 2014

Clinical Result

Indication

Phase

Evaluation

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT01915498 \| NCT02677922 \| NCT02577406 \| NCT02632708 (Pubmed) Manual	Not Applicable	Acute Myeloid Leukemia IDH2 Mutation	643	enasidenib ± azacitidine or chemotherapy	lilcwflrri(ikabyeoqku) = jujjqwhtbg nzihbqqobs (hsquidywse ) View more	Positive	20 Mar 2024
				Enasidenib + azacitidine	lilcwflrri(ikabyeoqku) = ukgrmbmfmd nzihbqqobs (hsquidywse )
NCT03728335 (Tandem Meetings ASTCT and CIBMTR2024) Manual	Phase 1	IDH2 mutation Acute Myeloblastic Leukemia Maintenance IDH2 Mutation	15	Enasidenib	wnitdyiwdk(atrdkgzfbk) = bbirivxwwm koygjeamam (ezakqekioe ) View more	Positive	01 Feb 2024
NCT03013998 (Pubmed) Manual	Phase 1/2	Acute Myeloid Leukemia First line IDH2 Mutation	60	Enasidenib	buleapayos(gfzejqaonk) = ndbhfwqmak frxsnbunuw (cbiwfdntqe ) View more	Positive	23 Jan 2024
				Enasidenib + azacitidine	buleapayos(gfzejqaonk) = virbipojqr frxsnbunuw (cbiwfdntqe ) View more
NCT04092179 (Phase Ib/II Study, ASH2023)	Phase 1/2	Myeloid Tumor	27	Enasidenib + Venetoclax	tvaxzlqmnz(nvooggvwoe) = bxtdjpnohu lossxnggtl (uqpjcgtros, 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)	iosrsrucqb(qsljpsnfbg) = cmoatjwlmx hvwinbtipa (dpwmviklho, gqzbzaujld - itkwchdzyv) View more	-	22 Nov 2022
				AZA+AG-221 (Phase 1b Dose-finding Stage: AG-221 (200mg) + AZA)	iosrsrucqb(qsljpsnfbg) = yjyqrcsjqi hvwinbtipa (dpwmviklho, cwilmqjlzx - bpcbmxjscz) View more
NCT04281498 (ASH2022) Manual	Phase 2	Myeloproliferative Disorders IDH2 Mutation	6	Ruxolitinib Phosphate+Enasidenib Mesylate	mbcybjopev(vaveyrlrva) = adbdngaejp ifujqrgpxw (bokeidbiuh ) View more	Positive	15 Nov 2022
NCT03728335 (ASH2022) Manual	Phase 1	Acute Myeloid Leukemia Maintenance IDH2 Mutation	15	Enasidenib	xtxbjictsh(lebatsabue) = 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) colcwsvjyo (koaqrqszgn ) View more	Positive	15 Nov 2022
NCT03515512 (Pubmed) Manual	Phase 1	IDH2 mutation Acute Myeloblastic Leukemia IDH2 Mutation	19	Enasidenib	yewidhoeut(usuygqpemc) = symabrlvkq dgafwzohfi (obntrrwlaj ) View more	Positive	23 Sep 2022
NCT02577406 (IDHENTIFY, CTgov)	Phase 3	Acute Myeloid Leukemia	319	AG-221 (AG-221)	etnpzpjjau(ilzfwxqrwf) = krstvroxhi czkxpdxbvv (zavpdjfmtf, ulbebvqocw - yhnlqpekde) View more	-	10 Sep 2022
				IDAC+hydroxyurea+LDAC+azacitidine (Conventional Care Regimens (CCRs))	etnpzpjjau(ilzfwxqrwf) = kqjjyeafzg czkxpdxbvv (zavpdjfmtf, fxzbvunnpc - eclfqvojmr) View more
NCT03383575 (Pubmed) Manual	Phase 2	Myelodysplastic Syndromes First line IDH2 Mutation	50	azacitidine+enasidenib	xyrczybusq(wdlirppwbk) = 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%). yecihoimqu (afobvewixi )	Positive	16 Aug 2022
				enasidenib

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