Exhibit 99.1

Biomea Fusion Presents at the 2022 ASH Annual Meeting Preclinical Data on BMF-500 Supporting its Potential as the Most Potent and Selective FLT3 Inhibitor to Date

REDWOOD CITY, Calif., December 12, 2022 (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 preclinical data today for BMF-500, an investigational covalent FLT3 inhibitor, at the 64^{th American Society of Hematology (ASH) Annual Meeting. The preclinical poster can be viewed at Biomea’s website at https://biomeafusion.com/publications.}

BMF-500, a novel, orally bioavailable, highly potent and selective covalent small molecule inhibitor of FLT3, was discovered and developed in-house at Biomea using the company’s proprietary FUSION^™ System and designed to have a therapeutic profile to allow for combinations with standard of care and/or novel targeted agents like BMF-219, Biomea’s investigational covalent menin inhibitor. The company is on track to submit an investigational new drug (IND) application for BMF-500 in the first half of 2023 and, subject to successful IND clearance, plans to initiate clinical trials evaluating BMF-500 as a single agent and in novel combinations shortly thereafter.

“The majority of late-stage and approved FLT3 inhibitors fall short of providing sufficient and sustained inhibition of FLT3 signaling required for maximal benefit. We believe the exquisite potency, selectivity and durability of BMF-500, all of which are possible through the design of this novel covalent molecule with our proprietary FUSION system, have the potential to translate to deep and durable remissions in patients with FLT3-mutant AML, representing nearly a third of all AML patients,” said Steve Morris, M.D., Biomea’s Chief Medical Officer. “We look forward to advancing BMF-500 toward the clinic in 2023, which will mark our second clinical-stage novel covalent small molecule program for cancer and further solidify our position as a leader in next-generation covalent medicines.”

“The impressive profile of BMF-500 speaks to the bench strength of our Discovery Team and to our ability to design and deliver novel therapeutics. We believe that targeting FLT3 with a covalent inhibitor, as we did with menin, represents another significant opportunity to improve the outcomes that reversible inhibition provide. BMF-500 has the potential to be an effective option as a monotherapy as well as in combination,” said Thomas Butler, Biomea’s Chief Executive Officer and Chairman of the Board.

The data presented at the ASH conference today showed that in FLT3-driven AML cell lines, three-hour exposure to BMF-500 produced complete phospho-FLT3 inhibition, which was maintained following washout of the compound. The commercially available reversible (i.e., non-covalent) FLT3 inhibitor gilteritinib required 16 times higher concentration than BMF-500 and continuous exposure for 96 hours to produce the same effect. The covalent small molecule inhibitor BMF-500 exhibited potent inhibition of FLT3 receptor kinase and marked cell killing in FLT3-ITD AML cell lines, as demonstrated by IC_90s at physiologically relevant doses. In addition, the kinase profile of BMF-500 revealed high target selectivity and selective cytotoxicity profile against a panel of non-target cancer cell lines suggesting the potential for minimal off-target liabilities. As part of the poster presentation, Biomea also presented the results of two preclinical animal xenograft models in which BMF-500 demonstrated antitumor activity with sustained tumor regression and improved survival while being well tolerated, with body weight maintenance across treatment groups.

About BMF-500

BMF-500 is a novel orally bioavailable, highly potent and selective covalent small molecule inhibitor of FLT3 in preclinical development, which has been shown to exhibit favorable durability, selectivity and tolerability in preclinical studies in comparison to commercially available FLT3 inhibitor gilteritinib. BMF-500 was discovered and developed in-house by Biomea using its proprietary FUSION^™ System and designed to have a therapeutic profile to allow for combinations with standard of care and novel targeted agents like BMF-219, Biomea’s investigational covalent menin inhibitor. The kinase profile of BMF-500 showed high target selectivity, suggesting the potential for minimal off-target liabilities.

About FLT3 (fms-like tyrosine kinase 3)

FLT3 is a receptor tyrosine kinase (RTK) that plays a central role in the survival, proliferation, and differentiation of immature blood cells. Notably, FLT3 gene mutations are common in patients with AML and are associated with a poor prognosis. Nearly 30% of AML patients have a FLT3 mutation, representing more than 6,000 incident patients in the United States each year. While FLT3-specific and pan-tyrosine kinase inhibitors are approved by the FDA across various lines of therapy in AML, these agents have produced relatively low rates of durable responses and overall survival remains an unmet need.

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 and BMF-500, the potential of BMF-500 as a treatment for various types of cancer, our research, development and regulatory plans, including our plans to submit an IND for BMF-500 and to initiate clinical trials of BMF-500 as a single agent and in novel combinations, 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 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:

Sasha Blaug

SVP Corporate Development

sb@biomeafusion.com

(650) 460-7759

Exhibit 99.2

Abstract 2756 ASH Dec. 10 – 13, 2022 BMF-500: An Orally Bioavailable Covalent Inhibitor of FLT3 with High Selectivity and Potent Antileukemic Activity in FLT3-Mutated AML Brian Law, BS1, Tripta Rughwani, MS1, Tenley Archer PhD1, Lekha Kumar, MS1, Daniel Lu, MS1, Priyanka Somanath, PhD1, Yan Ma, PhD1, Xiaodong Wang, MS*1, David Sperandio, PhD1, Steve Morris, MD1, Thorsten Kirschberg, PhD1, Mini Balakrishnan, PhD1 and Thomas Butler, MSc MBA1 1Biomea, Fusion, Inc. Redwood City, CA Introduction Potent and Durable Target Inhibition Leading to Effective Cell Killing Fms-like tyrosine kinase 3 (FLT3), a member of the receptor tyrosine kinase Figure 2. family, is overexpressed on AML blasts and widely expressed in hematopoietic A. Protein Modification of FLT3 B. Target Inhibition C. Compound Pulse-Chase Study progenitor cells (Carow et al., 1996). Read cell viability on Day Activating mutations of FLT3 are the most frequent genetic alterations in AML MV-4-11 cells Wash 4 by CTG leading to FLT3 ligand-independent signaling and cellular proliferation, which exposed to out compound kDa DMSO 3nM 50nM 3nM DMSO 3nM 50nM 3nM compound or after 3 hours account for approximately 30% of newly diagnosed adult AML patients and are vehicle control Measure target 160 - inhibition by p-FLT3 associated with poor prognosis (Papaemmanuil et al., 2016). Western blot 130 - 160 - t-FLT3 Although, several FLT3 inhibitors have entered clinical trials and reached 4 Day Cell Viability Assay 130 - commercialization; however, phospho-FLT3 target duration coverage, adverse 120 44 - p-ERK events and dose-limiting toxicities often restrict the therapeutic window and 100 No washout 98 98 96 42 -limit their long-term use and efficacy (Kennedy VE & Smith CC, 2020). Washout at 3 hrs 67 44 - Figure 2. A) Protein Modification of FLT3. LC/MS protein modification assay using recombinant 80 t-ERK 55 42 - FLT3 protein in the presence of BMF-500. B) Target Inhibition. MV-4-11 cells treated for 1 hr with Killing 32 BMF-500 is a novel orally bioavailable, highly potent and selective covalent serial dilutions of BMF-500 (right), Gilteritinib (left) or vehicle control were lysed and the impact on 60 90 - p-STAT5 FLT3 phosphorylation analyzed by WES. C) Compound Pulse Chase. MV-4-11 cells were Cell 80 - small molecule inhibitor of FLT3 with best-in-class potential, given its efficacy, 40 treated with BMF-500 (3nM), Gilteritinib (3 nM and 50nM) or vehicle control for 3hrs after which the % 90 - t-STAT5 durability, and selectivity in comparison to an existing FLT3 inhibitor. compound was either washed out (pink) or the incubation continued in the presence of drug (black). 20 80 -Viable cell count was measured at the end of Day 4 by CTG readout and % cell killing calculated 0 relative to vehicle-treated control. In addition, effects on phosphorylated and total protein levels for Gilteritinib-3nM Gilteritinib-50nM BMF-500-3nM 116 - vinculin Potent Target Inhibition FLT3, ERK and STAT5 were measured by immunoblot at the end of 3 hrs pulse and at 24 hrs. A Figure .. 1. In Vivo Efficacy in Mouse Xenograft Models Potent Cell-Based Activity in AML Cell Lines with FLT3 Mutations Figure 3. C. Overall Survival MOLM-13 D. Individual Tumor Volume MV-4-11 A. Subcutaneous MOLM-13 Xenograft Model B. Subcutaneous MV-4-11 Xenograft Model Xenograft Model Xenograft Model 100 4000 2500 2400 3 ) 3500 2000 Survival Vehicle PO,QD x 28 (mm 2000 Gilteritinib 6 mg/kg,PO,QD x 28 Gilteritinib 10mg/kg,PO,QD x 28 BMF-500 5 mg/kg,PO,BID x 28 ) 1600 of 1500 BMF-500 15 mg/kg,PO,BID x 28 ) BMF-500 30 mg/kg,PO,BID x 28 3 3000 3 50 BMF-500 50 mg/kg,PO,BID x 8, 1200 BMF-500 60mg/kg,PO,QD x 28 volume 1000 QD from D9 to D28 (mm 2500 (mm 800 No treatment Probability Tumor 500 2000 400 0 0 1500 300 0 7 14 21 282758275827582758 y y y y y y y y Volume volume a a a a a a a a D D D D D D D D Days 1000 200 Figure 3. Efficacy of BMF-500 in subcutaneous AML xenograft models. Female nude mice bearing MOLM-13 (A), or MV-4-11 (B), xenograft tumors were dosed with BMF-500, gilteritinib or vehicle control for 28 days, and Compound MV-4-11 MOLM-13 Tumor 500 Tumor 100 tumor volume was measured through the dosing phase and beyond. Vertical dotted line indicates termination of ID IC (nM) IC (nM) dosing (day 28). Data points represent group mean tumor volume. Error bars represent standard error of the mean 50 50 0 0 (SEM). C.) Overall Survival MOLM-13 Xenograft Model. Kaplan-Meier probability of survival of female nude mice BMF-500 0.03 0.30 Treatment Period (28-days) Treatment Period (28-days) bearing MOLM-13 xenograft. D.) Individual Tumor Volume MV-4-11 Xenograft Model. Individual tumor volume trace of female nude mice bearing MV-4-11 xenograft model. Gilteritinib 1.7 6.5 0 7 14 21 28 0 7 14 21 28 35 42 49 56 63 Days post treatment initiation (day) Days post treatment initiation (day) Conclusion Potent Coverage of FLT3 Inhibitor Resistance Mutations Ve PO, x 2 BMF-500 30 mg/kg,PO,BID x 28 Vehicle PO,BID x 28 BMF-500 15 mg/kg,PO,BID x 28 Vehicle PO,QD x 28 The covalent small molecule inhibitor BMF-500 exhibits potent inhibition of FLT3 Gilteritinib 6 mg/kg,PO,QD x 28 BMF-500 50 mg/kg,PO,BID x 8, QD from D9 to D28 B. NanoBRET Target Engagement Assay, IC (nM) Gilteritinib 10mg/kg,PO,QD x 28 BMF-500 60mg/kg,PO,QD x 28 receptor kinase and excellent cell killing in FLT3-ITD AML cell lines. 50 BMF-500 5 mg/kg,PO,BID x 28 Transformed cells expressing key FLT3 inhibitor resistance variants, including D835Y/V/H FLT3 FLT3 FLT3 FLT3 activation loop and F691L gatekeeper point mutations show high sensitivity to BMF-500, Cmpd ID High Selectivity WT (D835H) (D835V) (D835Y) Figure 4. highlighting a clear differentiation to gilteritinib. BMF-500 0.31 0.18 0.22 0.25 B. 5-Day Cytotoxicity Profile A. Kinase Profile Covalent modification of FLT3 by BMF-500 leads to constitutive on-target inhibition of Cell Line Tumor Type BMF-500 Gilteritinib Cell Line Tumor Type BMF-500 Gilteritinib phospho-FLT3 and its down-stream signaling in a dose dependent manner in the target Gilteritinib 23.4 1.45 1.1 1.4 BMF-500 @ 50 nM Gilteritinib @ 50 nM 4 Interactions Mapped 11 Interactions Mapped cell. SW684 Fibrosarcoma >1 >1 MCF7 Adenocarcinoma >1 >1 C. FLT3 Inhibitor Resistance Mutations Coverage, IC50 (nM) A549 NSCLC >1 0.278 MV-4-11 Leukemia (acute myelomonocytic <0.001 0.003 In MV-4-11 cells, 3-hour exposure followed by washout of BMF-500 was sufficient to produce longer duration of response and greater cell killing that outperformed BV-173 Leukemia (CML) >1 0.740 RS4;11 Leukemia (acute lymphoblastic) >1 0.233 FLT3-ITD- FLT3-ITD- continuous exposure of gilteritinib at 3 nM. Cmpd ID FLT3-ITD CGTH-W-1 Carcinoma, metastatic >1 0.455 SaOS2 Osteosarcoma >1 0.236 D835Y F691L BMF-500 demonstrates antitumor activity with sustained tumor regression, improved Daudi Burkitt’s lymphoma >1 >1 SK-N-AS Neuroblastoma >1 >1 BMF-500 2 nM 5 nM 7 nM survival and is well tolerated with body weight maintenance across treatment groups in HCT-116 Carcinoma >1 >1 SKOV3 Adenocarcinoma >1 0.804 two preclinical mouse xenograft models. Gilteritinib 7 nM 19 nM 98 nM Jurkat Acute T-cell leukemia >1 0.947 Thp1 Leukemia (acute monocytic) >1 >1 The kinase profile of BMF-500 revealed high target selectivity and selective cytotoxicity Leukemia, acute profile against a panel of non-target cancer cell lines suggesting minimal off target Figure 1. A.) Potent Cell-Based Activity in AML Cell Lines with FLT3 Mutations. Potency of HL-60 >1 0.445 WiDr Colorectal adenocarcinoma >1 0.268 promyelocytic BMF-500 and gilteritinib against FLT3 (WT) and FLT3-ITD enzyme-based biochemical assay (left) liabilities. and cell-based 4-day CTG readout using MV-4-11 and MOLM-13 (right) cell lines. Representative LS411N Carcinoma, Duke’s type B >1 >1 CCRFCEM Leukemia (acute lymphoblastic) >1 >1 Figure 4A. Kinase Profile. Map of the human kinome is dose response curves are shown for MV4-11 and MOLM-13 cell killing. B.) NanoBRET Target shown for 169 kinases for BMF-500 (left) and gilteritinib RL95-2 Carcinoma >1 0.868 References Engagement Assay, IC (nM). C.) FLT3 Inhibitor Resistance Mutations Coverage, IC (nM). MOLT-4 Leukemia (ALL) >1 >1 50 50 (right) as profiled against a panel of 169 kinases at 50 nM Transformed cells expressing wild-type (WT), FLT3 D835H/V/Y variants, FLT-ITD, FLT-ITD-D835Y, top concentration (>100x target IC of BMF-500). The red Figure 4B. 5-Day Cytotoxicity Profile. BMF-500 and gilteritinib were profiled against a panel of 20 cancer cell lines in a 5-day cell viability assay, using CTG ? Carow, CE., Levenstein, M., Kaufmann, SH. et al. Expression of the hematopoietic growth factor receptor FLT3 (STK-1/Flk2) in human leukemias. Blood (1996) 87(3):1089–96. and FLT3-ITD-F691L mutations were profiled via NanoBRET target engagement and Ba/F3 cell- 50? Papaemmanuil, E., Gerstung, M., Bullinger, L. et al. Genomic Classification and Prognosis in Acute Myeloid Leukemia. N Engl J Med (2016) 374(23):2209–21. circles denote inhibition of activity greater with size scale readout. Top concentration tested was 1 M. IC values are listed. Cell lines represent different tumor tissue types as indicated. MV-4-11 was the only cell line ? Gilliland DG, Griffin JD. The roles of FLT3 in hematopoiesis and leukemia. Blood (2002) 100(5):1532–42. based assays, respectively. 50? Dohner H, Weisdorf DJ, Bloomfield CD. Acute Myeloid Leukemia. N Engl J Med (2015) 373(12):1136–52. as shown in legend. in the panel known to h arbor a FLT3 activating mutation (FLT3-ITD). ? Kennedy, VE., Smith, CC. FLT3 Mutations in Acute Myeloid Leukemia: Key Concepts and Emerging Controversies. Front Oncol. 2020 Dec 23;10:612880.