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BMF-219 demonstrated early signs of clinical activity and ability to achieve durable and sustained complete responses (CRs) with minimal residual disease negativity (MRD-neg) in acute myeloid leukemia (AML) patientsPharmacodynamic data further supports the mechanism of action of BMF-219 as a menin inhibitor; in-line with preclinical models, BMF-219 downregulated key leukemogenic genes (e.g. HOXA9, MEIS1) as well as MEN1BMF-219, the first and only investigational covalent oral menin inhibitor in clinical development for AML, was generally well tolerated with no dose-limiting toxicities observed and without adverse event (AE) related treatment discontinuationsClinical data to date support protocol enhancements to COVALENT-101 to include focusing exclusively on patients with menin sensitive mutations such as MLL-r and NPM1 mutant acute leukemias and higher dose levels for CYP3A4 inhibitor Arm (Arm B) REDWOOD CITY, Calif., Dec. 11, 2023 (GLOBE NEWSWIRE) -- Biomea Fusion, Inc. (Nasdaq: BMEA), a clinical-stage biopharmaceutical company dedicated to discovering and developing novel covalent small molecules to treat and improve the lives of patients with genetically defined cancers and metabolic diseases, presented positive clinical data for BMF-219, an investigational covalent menin inhibitor, in relapsed / refractory AML patients with menin-dependent mutations at the 65th American Society of Hematology (ASH) Annual Meeting. The poster can be viewed at Biomea’s website at https://biomeafusion.com/publications. “We are very excited to present the clinical update at ASH on our targeted, covalently binding menin inhibitor, BMF-219, achieving durable and sustained CRs in patients with menin inhibitor-sensitive acute leukemia, even at suboptimal dosing levels. The gene expression data we presented here validates the proposed mechanism of action of BMF-219 and is in-line with our preclinical models,” said Steve Morris, M.D., Chief Development Officer at Biomea. As of the October 31, 2023, out of 29 patients dosed in the Phase I of COVALENT-101, nearly half (45%) of the participants received prior Hematopoietic Stem Cell Transplant (HSCT) and the median prior lines of therapy was 3. A total of 7 patients were selected as evaluable for efficacy. The efficacy evaluable population includes AML patients who meet the following criteria: dosed at or near predicted efficacious dose (500 mg or above [Arm A – non-CYP inhibitor Arm]; 125 mg or above [Arm B]), had known menin-dependent mutations, and completed at least two cycles of therapy. Within this patient population 2 Complete Responses (CRs) (CR rate 2/7 = 29%) were observed with a mean time to response of 1.8 months (1 CR patient had a NUP-98 mutation and 1 CRi patient had a NPM1 mutation). In the CYP inhibitor arm, BMF-219 showed increasing plasma pharmacokinetic (PK) exposure with escalating dose levels, and the ability to achieve systemic exposures predicted to be efficacious based on preclinical acute leukemia models. Further dose escalation is still needed to achieve target AUC. Pharmacodynamic data from a case study of an AML patient containing NUP98-NSD1 mutation showed suppression of key leukemogenic genes (e.g. HOXA9, MEIS1) as well as downregulation of MEN1, without noticeable increases in differentiation markers (e.g. CD14, ANPEP, ITGAM) in contrast to non-covalent menin inhibitors. Across all patients enrolled in the trial as of the data cutoff date (n=29), BMF-219 was generally well-tolerated with no dose-limiting toxicities observed and without treatment discontinuations due to toxicity. Four participants experienced Differentiation Syndrome (DS) ≤ Grade 3, with onset 1-3 weeks after initiation of therapy and an average duration of 10 days, managed by cytoreductive therapy (hydroxyurea and steroids). Two participants recovered without dose modification or interruption, and none of the participants discontinued due to DS. Initially, patients were enrolled agnostic to mutational status; subsequently, the study protocol was amended to enrich for patients with AML harboring menin-dependent mutations. Dose Level 4 is the first dose level which focused primarily on enrolling patients with known menin-dependent mutations. Biomea is planning to amend the dosing protocol to explore higher dosing levels in Arm B. Dose escalation is to be followed by a dose optimization/expansion to determine the recommended phase 2 dose. About BMF-219 BMF-219 is a covalently binding inhibitor of menin, a protein known to play an essential role in oncogenic signaling in genetically defined leukemias as well as in diabetes. Preclinically, BMF-219 has demonstrated in well-established acute leukemia cell lines robust downregulation of key leukemogenic genes in addition to menin itself. Additionally, BMF-219 has shown anticancer activity in multiple in vitro, in vivo, and ex vivo models of acute leukemia, multiple myeloma, diffuse large B-cell lymphoma and chronic lymphocytic leukemia. BMF-219 is currently being evaluated in first-in-human clinical trials enrolling patients with specific menin-dependent mutations in liquid and solid tumors as well as patients with diabetes. About COVALENT-101 COVALENT-101 is a Phase I, open-label, multi-center, dose-escalation and dose-expansion study designed to assess the safety, tolerability, and pharmacokinetics/pharmacodynamics of oral dosing of BMF-219 in patients with relapsed/refractory (R/R) acute leukemias — including subpopulations where menin inhibition is expected to provide therapeutic benefit (e.g., patients with MLL1/KMT2A gene rearrangements or NPM1 mutations). The study is designed to enroll subsets of acute leukemia patients who are receiving a CYP3A4 inhibitor and also those not receiving a CYP3A4 inhibitor. COVALENT-101 is also investigating the dosing of BMF-219 in other patient populations where preclinical studies have shown high menin dependence, such as multiple myeloma, diffuse large B-cell lymphoma, and chronic lymphocytic leukemia. Additional information about this Phase I clinical trial of BMF-219 can be found at ClinicalTrials.gov using the identifier NCT05153330. About Acute Myeloid Leukemia (AML) AML is the most common form of acute leukemia in adults and represents the largest number of annual leukemia deaths in the U.S. and Europe. AML originates within the white blood cells in the bone marrow and can rapidly move to the blood and other parts of the body, including the spleen, central nervous system, and other organs. Approximately 30,000 people in the U.S. and Europe are diagnosed with AML each year, and the five-year overall survival rate in adults is roughly 29%. Among patients with relapsed/refractory disease, the need is greatest, as the overall survival is only approximately 3 to 9 months. It is estimated that upwards of 45% of AML patients have menin-dependent genetic drivers (MLL1-r, NPM1 mutant, and certain additional less common but recurrent gene mutations). About Biomea Fusion Biomea Fusion is a clinical stage biopharmaceutical company focused on the discovery and development of covalent small molecules to treat patients with genetically defined cancers and metabolic diseases. A covalent small molecule is a synthetic compound that forms a permanent bond to its target protein and offers a number of potential advantages over conventional non-covalent drugs, including greater target selectivity, lower drug exposure, and the ability to drive a deeper, more durable response. The company is utilizing its proprietary FUSION™ System to advance a pipeline of covalent-binding therapeutic agents against key oncogenic drivers of cancer and metabolic diseases. Biomea Fusion is a leader in advancing next-generation covalent small molecule medicines designed to maximize clinical benefit to treat various cancers and metabolic diseases. Forward-Looking Statements Statements we make in this press release may include statements which are not historical facts and are considered forward-looking statements within the meaning of Section 27A of the Securities Act of 1933, as amended (the “Securities Act”), and Section 21E of the Securities Exchange Act of 1934, as amended (the “Exchange Act”). These statements may be identified by words such as “aims,” “anticipates,” “believes,” “could,” “estimates,” “expects,” “forecasts,” “goal,” “intends,” “may,” “plans,” “possible,” “potential,” “seeks,” “will,” and variations of these words or similar expressions that are intended to identify forward-looking statements. Any such statements in this press release that are not statements of historical fact, including statements regarding our cash runway, the clinical and therapeutic potential of our product candidates and development programs, including BMF-219, the potential of BMF-219 as a treatment for various types of cancer, our research, development and regulatory plans, including the progress of our ongoing COVALENT-101 clinical trial of BMF-219, the availability of data from the trial, and the timing of such events, may be deemed to be forward-looking statements. We intend these forward-looking statements to be covered by the safe harbor provisions for forward-looking statements contained in Section 27A of the Securities Act and Section 21E of the Exchange Act and are making this statement for purposes of complying with those safe harbor provisions. Any forward-looking statements in this press release are based on our current expectations, estimates and projections only as of the date of this release and are subject to a number of risks and uncertainties that could cause actual results to differ materially and adversely from those set forth in or implied by such forward-looking statements, including the risk that we may encounter delays in the initiation, conduct and completion of preclinical studies, including IND-enabling studies, the submission and clearance of IND applications, and our ongoing and planned clinical trials and other research and development activities. These risks concerning Biomea Fusion’s business and operations are described in additional detail in its periodic filings with the U.S. Securities and Exchange Commission (the “SEC”), including its most recent periodic report filed with the SEC and subsequent filings thereafter. Biomea Fusion explicitly disclaims any obligation to update any forward-looking statements except to the extent required by law.

BMF-219 demonstrated early signs of clinical activity and ability to achieve durable and sustained complete responses (CRs) with minimal residual disease negativity (MRD-neg) in acute myeloid leukemia (AML) patients Pharmacodynamic data further supports the mechanism of action of BMF-219 as a menin inhibitor; in-line with preclinical models, BMF-219 downregulated key leukemogenic genes (e.g. HOXA9, MEIS1) as well as MEN1 BMF-219, the first and only investigational covalent oral menin inhibitor in clinical development for AML, was generally well tolerated with no dose-limiting toxicities observed and without adverse event (AE) related treatment discontinuations Clinical data to date support protocol enhancements to COVALENT-101 to include focusing exclusively on patients with menin sensitive mutations such as MLL-r and NPM1 mutant acute leukemias and higher dose levels for CYP3A4 inhibitor Arm (Arm B) REDWOOD CITY, Calif., Dec. 11, 2023 (GLOBE NEWSWIRE) -- Biomea Fusion, Inc. (Nasdaq: BMEA), a clinical-stage biopharmaceutical company dedicated to discovering and developing novel covalent small molecules to treat and improve the lives of patients with genetically defined cancers and metabolic diseases, presented positive clinical data for BMF-219, an investigational covalent menin inhibitor, in relapsed / refractory AML patients with menin-dependent mutations at the 65th American Society of Hematology (ASH) Annual Meeting. The poster can be viewed at Biomea’s website at . “We are very excited to present the clinical update at ASH on our targeted, covalently binding menin inhibitor, BMF-219, achieving durable and sustained CRs in patients with menin inhibitor-sensitive acute leukemia, even at suboptimal dosing levels. The gene expression data we presented here validates the proposed mechanism of action of BMF-219 and is in-line with our preclinical models,” said Steve Morris, M.D., Chief Development Officer at Biomea. As of the October 31, 2023, out of 29 patients dosed in the Phase I of COVALENT-101, nearly half (45%) of the participants received prior Hematopoietic Stem Cell Transplant (HSCT) and the median prior lines of therapy was 3. A total of 7 patients were selected as evaluable for efficacy. The efficacy evaluable population includes AML patients who meet the following criteria: dosed at or near predicted efficacious dose (500 mg or above [Arm A – non-CYP inhibitor Arm]; 125 mg or above [Arm B]), had known menin-dependent mutations, and completed at least two cycles of therapy. Within this patient population 2 Complete Responses (CRs) (CR rate 2/7 = 29%) were observed with a mean time to response of 1.8 months (1 CR patient had a NUP-98 mutation and 1 CRi patient had a NPM1 mutation). In the CYP inhibitor arm, BMF-219 showed increasing plasma pharmacokinetic (PK) exposure with escalating dose levels, and the ability to achieve systemic exposures predicted to be efficacious based on preclinical acute leukemia models. Further dose escalation is still needed to achieve target AUC. Pharmacodynamic data from a case study of an AML patient containing NUP98-NSD1 mutation showed suppression of key leukemogenic genes (e.g. HOXA9, MEIS1) as well as downregulation of MEN1, without noticeable increases in differentiation markers (e.g. CD14, ANPEP, ITGAM) in contrast to non-covalent menin inhibitors. Across all patients enrolled in the trial as of the data cutoff date (n=29), BMF-219 was generally well-tolerated with no dose-limiting toxicities observed and without treatment discontinuations due to toxicity. Four participants experienced Differentiation Syndrome (DS) ≤ Grade 3, with onset 1-3 weeks after initiation of therapy and an average duration of 10 days, managed by cytoreductive therapy (hydroxyurea and steroids). Two participants recovered without dose modification or interruption, and none of the participants discontinued due to DS. Initially, patients were enrolled agnostic to mutational status; subsequently, the study protocol was amended to enrich for patients with AML harboring menin-dependent mutations. Dose Level 4 is the first dose level which focused primarily on enrolling patients with known menin-dependent mutations. Biomea is planning to amend the dosing protocol to explore higher dosing levels in Arm B. Dose escalation is to be followed by a dose optimization/expansion to determine the recommended phase 2 dose. About BMF-219 BMF-219 is a covalently binding inhibitor of menin, a protein known to play an essential role in oncogenic signaling in genetically defined leukemias as well as in diabetes. Preclinically, BMF-219 has demonstrated in well-established acute leukemia cell lines robust downregulation of key leukemogenic genes in addition to menin itself. Additionally, BMF-219 has shown anticancer activity in multiple in vitro, in vivo, and ex vivo models of acute leukemia, multiple myeloma, diffuse large B-cell lymphoma and chronic lymphocytic leukemia. BMF-219 is currently being evaluated in first-in-human clinical trials enrolling patients with specific menin-dependent mutations in liquid and solid tumors as well as patients with diabetes. About COVALENT-101 COVALENT-101 is a Phase I, open-label, multi-center, dose-escalation and dose-expansion study designed to assess the safety, tolerability, and pharmacokinetics/pharmacodynamics of oral dosing of BMF-219 in patients with relapsed/refractory (R/R) acute leukemias — including subpopulations where menin inhibition is expected to provide therapeutic benefit (e.g., patients with MLL1/KMT2A gene rearrangements or NPM1 mutations). The study is designed to enroll subsets of acute leukemia patients who are receiving a CYP3A4 inhibitor and also those not receiving a CYP3A4 inhibitor. COVALENT-101 is also investigating the dosing of BMF-219 in other patient populations where preclinical studies have shown high menin dependence, such as multiple myeloma, diffuse large B-cell lymphoma, and chronic lymphocytic leukemia. Additional information about this Phase I clinical trial of BMF-219 can be found at ClinicalTrials.gov using the identifier NCT05153330. About Acute Myeloid Leukemia (AML) AML is the most common form of acute leukemia in adults and represents the largest number of annual leukemia deaths in the U.S. and Europe. AML originates within the white blood cells in the bone marrow and can rapidly move to the blood and other parts of the body, including the spleen, central nervous system, and other organs. Approximately 30,000 people in the U.S. and Europe are diagnosed with AML each year, and the five-year overall survival rate in adults is roughly 29%. Among patients with relapsed/refractory disease, the need is greatest, as the overall survival is only approximately 3 to 9 months. It is estimated that upwards of 45% of AML patients have menin-dependent genetic drivers (MLL1-r, NPM1 mutant, and certain additional less common but recurrent gene mutations). About Biomea Fusion Biomea Fusion is a clinical stage biopharmaceutical company focused on the discovery and development of covalent small molecules to treat patients with genetically defined cancers and metabolic diseases. A covalent small molecule is a synthetic compound that forms a permanent bond to its target protein and offers a number of potential advantages over conventional non-covalent drugs, including greater target selectivity, lower drug exposure, and the ability to drive a deeper, more durable response. The company is utilizing its proprietary FUSION™ System to advance a pipeline of covalent-binding therapeutic agents against key oncogenic drivers of cancer and metabolic diseases. Biomea Fusion is a leader in advancing next-generation covalent small molecule medicines designed to maximize clinical benefit to treat various cancers and metabolic diseases. Forward-Looking Statements Statements we make in this press release may include statements which are not historical facts and are considered forward-looking statements within the meaning of Section 27A of the Securities Act of 1933, as amended (the “Securities Act”), and Section 21E of the Securities Exchange Act of 1934, as amended (the “Exchange Act”). These statements may be identified by words such as “aims,” “anticipates,” “believes,” “could,” “estimates,” “expects,” “forecasts,” “goal,” “intends,” “may,” “plans,” “possible,” “potential,” “seeks,” “will,” and variations of these words or similar expressions that are intended to identify forward-looking statements. Any such statements in this press release that are not statements of historical fact, including statements regarding our cash runway, the clinical and therapeutic potential of our product candidates and development programs, including BMF-219, the potential of BMF-219 as a treatment for various types of cancer, our research, development and regulatory plans, including the progress of our ongoing COVALENT-101 clinical trial of BMF-219, the availability of data from the trial, and the timing of such events, may be deemed to be forward-looking statements. We intend these forward-looking statements to be covered by the safe harbor provisions for forward-looking statements contained in Section 27A of the Securities Act and Section 21E of the Exchange Act and are making this statement for purposes of complying with those safe harbor provisions. Any forward-looking statements in this press release are based on our current expectations, estimates and projections only as of the date of this release and are subject to a number of risks and uncertainties that could cause actual results to differ materially and adversely from those set forth in or implied by such forward-looking statements, including the risk that we may encounter delays in the initiation, conduct and completion of preclinical studies, including IND-enabling studies, the submission and clearance of IND applications, and our ongoing and planned clinical trials and other research and development activities. These risks concerning Biomea Fusion’s business and operations are described in additional detail in its periodic filings with the U.S. Securities and Exchange Commission (the “SEC”), including its most recent periodic report filed with the SEC and subsequent filings thereafter. Biomea Fusion explicitly disclaims any obligation to update any forward-looking statements except to the extent required by law. Contact: Investor Relations Chunyi Zhao, PhD Sr. Manager of Investor Relations & Corporate Development czhao@biomeafusion.com Media Relations Neera Chaudhary, PhD Chief Commercial Officer – Diabetes nchaudhary@biomeafusion.com

– DSP-5336, an Investigational Menin and Mixed-lineage Leukemia Inhibitor, is Being Evaluated in Patients with Relapsed or Refractory Acute Leukemia, with Positive Preliminary Data Presented at ASH – CAMBRIDGE, Mass., Dec. 11, 2023 /PRNewswire/ -- Sumitomo Pharma America, Inc. (SMPA) today announced new data from the ongoing Phase 1/2 first-in-human study of DSP-5336, in patients with relapsed or refractory acute leukemia, presented at the 65th American Society of Hematology (ASH) Annual Meeting & Exposition. DSP-5336 is an investigational small molecule inhibitor of the menin and mixed-lineage leukemia (MLL) protein interaction, which plays key roles in biological pathways, including cell growth regulation, cell cycle control, genomic stability, bone development, and hematopoiesis.1,2,3 Data from the open-label, ongoing dose determination portion of the Phase 1/2 study enrolling patients with relapsed or refractory acute leukemia with relevant genomic alterations receiving oral DSP-5336 up to 200 mg twice-daily were presented at the meeting. In the ongoing study, patients are continuing to dose escalate and are now at therapeutic levels. Preliminary results presented at ASH 2023 included four evaluable patients treated with DSP-5336 200 mg twice-daily, three of whom showed objective responses. Clinical remission with partial hematologic recovery and clinical remission with incomplete count recovery (CRh/CRi) was achieved by one patient, CRi was achieved by one patient, and morphologic leukemia-free state (MLFS) was achieved by one patient. All patients cleared peripheral blasts. To date, DSP-5336 has been well-tolerated, notably, with no treatment-related cardiac effects, including QT prolongation. Additionally, differentiation syndrome has not been observed at the 200 mg twice-daily dose. "While these data are early-stage, it is encouraging to see promising clinical activity from DSP-5336, particularly with limited safety signals and a clean tolerability pro date," said Navel Daver, M.D., Director, Department of Leukemia, Division of Leukemia Research Alliance Program, The University of Texas MD Anderson Cancer Center and lead author on the DSP-5336 poster at ASH. "DSP-5336 is an investigational targeted therapy that inhibits menin-MLL protein interaction. Inhibition of the menin-MLL protein interaction may be able to reverse the leukemogenic activity of MLL fusion proteins and may be a future therapeutic option for acute leukemia." Leukemia is a type of cancer that forms in blood-forming tissue, characterized by the uncontrolled growth of blood cells, usually white blood cells in the bone marrow.4 Acute leukemia, a form of leukemia, requires immediate treatment as blood cells multiply rapidly leading to a sudden onset of symptoms.4 "There is a high unmet need for new and innovative approaches in the treatment of relapsed or refractory acute leukemia, as many patients have limited options to treat the disease or do not respond to currently available cancer therapies," said Jatin Shah, M.D., Chief Oncology Development Officer, SMPA. "We believe we are close to determining the appropriate therapeutic dose of DSP-5336 in our ongoing study and were encouraged by our discussions on these results with the leading hematological oncology community at ASH. We look forward to continuing the study of DSP-5336 as a monotherapy and to exploring additional combination studies." Additional SMPA data presented at ASH included an oral presentation of encouraging preliminary results from the ongoing Phase 1/2 study of TP-3654 monotherapy in patients with relapsed or refractory myelofibrosis who were previously treated with or ineligible for a JAK inhibitor. About DSP-5336 DSP-5336 is an investigational small molecule inhibitor of the menin and mixed-lineage leukemia (MLL) protein interaction. Menin is a scaffold nuclear protein that plays various key roles in biological pathways, including cell growth regulation, cell cycle control, genomic stability, bone development, and hematopoiesis.1,2 In preclinical studies, DSP-5336 has shown selective growth inhibition in human acute leukemia cell lines with KMT2A (MLL) rearrangements or NPM1 mutations.1,3 DSP-5336 showed induced reduction of gene expression of HOXA9 and MEIS1, which are highly expressing leukemia associate genes, and increased expression of differentiation marker gene CD11b in the human acute leukemia cell lines with MLL rearrangements.5,6 DSP-5336 also showed growth inhibition and changes of gene expression levels of HOXA9, MEIS1 and CD11b on human acute leukemia patient samples with MLL rearrangements or NPM1 mutations.5,6 The safety and efficacy of DSP-5336 is currently being clinically evaluated in a Phase 1/2 dose escalation/dose expansion study in patients with relapsed or refractory acute leukemia (NCT04988555). The FDA granted Orphan Drug Designation for DSP-5336 for the indication of acute myeloid leukemia in June 2022. About TP-3654 TP-3654 is an oral investigational inhibitor of PIM1 kinase, which has shown potential antitumor and antifibrotic activity through multiple pathways, including induction of apoptosis in preclinical models.7,8 TP-3654 was observed to inhibit proliferation and induce apoptosis in murine and human hematopoietic cells expressing the clinically relevant JAK2V617F mutation.7 TP-3654 alone and in combination with ruxolitinib showed white blood cell and neutrophil count normalization, and also reduced spleen size and bone marrow fibrosis in JAK2V617F and MPLW515L murine models of myelofibrosis.8 The safety and efficacy of TP-3654 is currently being clinically evaluated in a Phase 1/2 study in patients with intermediate and high-risk myelofibrosis (NCT04176198). The U.S. Food and Drug Administration (FDA) granted Orphan Drug Designation for TP-3654 for the indication of myelofibrosis in May 2022. About Sumitomo Pharma Sumitomo Pharma Co., Ltd. is a global pharmaceutical company based in Japan with key operations in the U.S. (Sumitomo Pharma America, Inc.), Canada (Sumitomo Pharma Canada, Inc.) and Europe (Sumitomo Pharma Switzerland GmbH) focused on addressing patient needs in psychiatry & neurology, oncology, urology, women's health, rare disease, and cell & gene therapies. With several marketed products in the U.S., Canada, and Europe, a diverse pipeline of early- to late-stage assets, and in-house advanced technology capabilities, we aim to accelerate discovery, research, and development to bring novel therapies to patients sooner. For more information, please visit and LinkedIn to follow us. The Sumitomo Pharma icon is a trademark of Sumitomo Pharma Co., Ltd., used under license. SUMITOMO PHARMA is a trademark of Sumitomo Pharma Co., Ltd., used under license. SUMITOMO is a registered trademark of Sumitomo Chemical Co., Ltd., used under license. Sumitomo Pharma America, Inc. is a U.S. subsidiary of Sumitomo Pharma Co., Ltd. © 2023 Sumitomo Pharma America, Inc. All rights reserved. For a copy of this release, visit Sumitomo Pharma America's website at . References Cierpicki T, Grembecka J. Challenges and opportunities in targeting the menin-MLL Interaction. Future Med Chem. 2014; 6(4):447-462. doi:10.4155/fmc.13.214. Matkar S, Thiel A, Hua X. Menin: a scaffold protein that controls gene expression and cell signaling. Trends Biochem Sci. 2013; 38(8):394-402. doi:10.1016/j.tibs.2013.05.005. Kuhn MWM, Song E, Feng Z, et al. Targeting chromatin regulators inhibits leukemogenic gene expression in NPM1 mutant leukemia. Cancer Discov. 2016; 6(10):1166-1181. doi:10.1158/2159-8290.CD-16-0237. Chennamadhavuni A, Lyengar V, Mukkamalla SKR, et al. Leukemia. [Updated 2023 Jan 17]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: . Eguchi K, Shimizu T, Kato D, et al. Preclinical Evaluation of a Novel Orally Bioavailable Menin-MLL Interaction Inhibitor, DSP-5336, for the Treatment of Acute Leukemia Patients with MLL-Rearrangement or NPM1 Mutation. Blood (2021) 138 (Supplement 1): 3339. . Daver N, Zeidner JF, Yuda J, et al. 2911 Phase 1/2 First-in-Human Study of the Menin-MLL Inhibitor DSP-5336 in Patients with Relapsed or Refractory Acute Leukemia. American Society of Hematology 2023. Available at: Foulks JM, Carpenter KJ, Luo B, et al. A small-molecule inhibitor of PIM kinases as a potential treatment for urothelial carcinomas. Neoplasia. 2014;16(5):403-412. Dutta A., Nath D, Yang Y, et al. Genetic ablation of Pim1 or pharmacologic inhibition with TP-3654 ameliorates myelofibrosis in murine models. Leukemia. 2022; 36 (3): 746-759. doi: 10.1038/s41375-021-01464-2.