Exhibit 99.1

Biomea fusion tm Corporate Presentation November 2021

Disclaimer and Forward-Looking Statement Certain statements in this presentation and the accompanying oral commentary are forward-looking statements. These statements relate to future events or the future financial performance of Biomea Fusion, Inc. (the “Company”) and involve known and unknown risks, uncertainties and other factors that may cause the actual results, levels of activity, performance or achievements of the Company or its industry to be materially different from those expressed or implied by any forward-looking statements. In some cases, forward-looking statements can be identified by terminology such as “may,” “will,” “could,” “would,” “should,” “expect,” “plan,” “anticipate,” “intend,” “believe,” “estimate,” “predict,” “potential” or other comparable terminology. All statements other than statements of historical fact could be deemed forward-looking, including any projections of financial information or profitability, the initiation, timing and results of pending or future clinical trials, the actions or potential action of the FDA, the status and timing of ongoing research, corporate partnering activities, any statements about historical results that may suggest trends for the Company’s business; any statements of the plans, strategies, and objectives of management for future operations; any statements of expectation or belief regarding future events, potential markets or market size, or technology developments, and other factors affecting the Company’s financial condition or operations. The Company has based these forward-looking statements on its current expectations, assumptions, estimates and projections. While the Company believes these expectations, assumptions, estimates and projections are reasonable, such forward-looking statements are only predictions and involve known and unknown risks and uncertainties, many of which are beyond the Company’s control. These and other important factors may cause actual results, performance or achievements to differ materially from those expressed or implied by these forward-looking statements. The forward-looking statements in this presentation are made only as of the date hereof. Except as required by law, the Company assumes no obligation and does not intend to update these forward-looking statements or to conform these statements to actual results or to changes in the Company’s expectations. This presentation also contains estimates and other statistical data made by independent parties and by us relating to market size and growth and other data about our industry. This data involves a number of assumptions and limitations, and you are cautioned not to give undue weight to such estimates. In addition, projections, assumptions, and estimates of our future performance and the future performance of the markets in which we operate are necessarily subject to a high degree of uncertainty and risk.

Experienced and Successful Management Team Novel FUSION™ Platform BMF-219—Clinical Stage Oncology Asset Multiple Oncology Programs built from FUSIONTM Platform revolutionize current medicine by creating and developing novel single agent and combination therapies that maximizes patient benefit Biomea Fusion is a clinical-stage biopharmaceutical company focused on the discovery and development of irreversible small-molecule drugs to treat patients with genetically defined cancers. Our discovery team is engaged in all phases of development, including target selection, small molecule design, and preclinical and clinical studies to develop innovative medicines

Our Team Experienced and successful team designed, discovered, and developed breakthrough therapies Thomas Butler Ramses Erdtmann Franco Valle Naomi Cretcher Heow Tan Steve Morris MD Thorsten Kirschberg Jim Palmer Chairman & CEO President & COO Chief Financial Chief of People Chief Technical & Chief Medical Officer EVP of Chemistry VP of Drug Officer Quality Officer Consultant Discovery 15 years in Life Science 15 years in Life Science 15 years in Life Science 15 years in Life Science 22 years in Life Science 25+ years in Life Science 25 years in Life Science 30 years in Life Science Pharmacyclics Pharmacyclics Eidos Therapeutics Pharmacyclics Pharmacyclics HealthChart LLC Terns Pharmaceuticals Biota Ltd Gilead Sciences Oxygen Investments Iovance Biotherapeutics Genentech Collegium Pharmaceutical Insight Genetics Gilead Sciences Cytopia Ltd. UCLA – MBA Finance Commerzbank Pharmacyclics UC Irvine, BA Comm Praecis Pharmaceuticals St. Jude Children’s Cell Gate Rigel, Inc. UCSB, MS – Chemistry University of Münster, CallidusCloud SF State University, Comm Ohio State University Research Hospital Golden Gate University, Celera Genomics Master’s in Banking & PricewaterhouseCoopers Santa Clara University Board certified internist MBA Prototek Inc. Corp Finance San Jose State University, BS Leavey School of Business, (Univ. of Texas SW HSC) University of Münster, Purdue University Corporate Finance MBA – Finance & Mgmt and medical oncologist Ph.D., Chemistry Ph.D. Organic Chemistry (Yale University School of Medicine)

Our Scientific Advisory Board Bruce Lipshutz PhD Urte Gayko, PhD Dave Ball PhD Rohit N. Kulkarni, M.D., Ph.D. Xianxin Hua, M.D., Ph.D. David Smith, Ph.D. Jeffery Rubnitz, M.D., Ph.D. Professor of Chemistry SVP, Drug Dev. & Reg. Professor of Chemistry Professor of Medicine Professor of Cancer Biostatistician; Former Director, Leukemia / Lymphoma UCSB Affairs Nektar CSUC Harvard Medical School Biology BOD Pharmacyclics Division Therapeutics Joslin Diabetes Center & University of Pennsylvania St. Jude Children’s Research Hospital Broad Institute 40+ year academic career 20+ years industry 40+ year academic career 20+ year academic and clinical 20+ years in academics, 20+ years academic and clinical Ph.D.: Yale University experience Ph.D.: UCSB career NIH/FDA, Industry career at Amgen, Nodality, • Research has focused on M.D. and Ph.D.: St. John’s Medical College and the Royal Postgraduate •Dr. Hua has over 100 publications with • David Smith, Ph.D. was a • Developing new technologies Pharmacyclics, AbbVie, novel synthesis of organic board member of more than 50 in the field to assist with the transition of Nektar compounds including Medical School in London Dr.Kulkarni’s of menin biology. Pharmacyclics. Prior to organic chemistry to a Ph.D.: Harvard University activators of PKC, and • academic work explores growth factor signaling •Dr. Hua’s lab has investigated the critical Pharmacyclics, he was a sustainable discipline, focusing analogs of indolactam V. senior biostatistician at City role and mechanism for the Menin on both chemo- and bio- • Currently SVP at Nektar. mechanisms in the regulation of human islet biology, and pathway in a wide variety of biological of Hope and served as a catalysis, all done in water. Prior roles at Biostatistical Reviewer for and physiological functions, including AbbVie (Global Head of pathways that allow regeneration of beta cells in type 1 diabetes. epigenetic regulation of gene the Division of Oncology Regulatory Affairs), Drug Products, U.S. Food transcription, beta cell signaling Pharmacyclics (SVP, • Translational work includes creating genetic and and proliferation, neuro- and Drug Administration Regulatory Affairs), (“FDA”) for 3 years. During endocrine tumors , colorectal Nodality, (VP of Regulatory knockout models to examine the roles of various drivers of cancer (CRC), and AML. his tenure at FDA, he and Clinical Affairs), Amgen reviewed more than 40 •He has also investigated how inhibition of (Director Global Regulatory diabetes and insulin homeostasis. menin by small molecules inhibitors chemotherapy INDs and Leader and Program NDAs. influences beta cell proliferation and Manager). dysregulation of metabolism in colorectal cancer (CRC) cells. 20+ years as academic and clinician M.D. and Ph.D.: UCSD School of Medicine • Dr. Rubnitz’s academic work at St Jude explores the potential for developing new strategies for the treatment of acute myeloid leukemia (AML). Prior to St. Jude, Dr. Rubnitz completed his pediatrics residency and heme/onc fellowship at Stanford Children’s Hospital.

Our Vision – We Aim to Cure Biomea leverages the FUSIONTM Platform to create a suite of novel agents to maximize the depth and durability of response Validated Targets For Covalent Inhibition Biology Breakthrough Covalent Chemistry Chemistry Proprietary Combinations Medicine Drugs pursuing validated targets have a ~2x higher likelihood of approval than molecules pursuing a new mechanism of action Source: Nelson et al. (2015) Nat Genet.; Thomas et al. (2016) BIO; In a Landscape of ‘Me Too’ Drug Development, What Spurs Radical Innovation? HBS Weekly Review (Jun 2018); Irreversible inhibitors provide deep target inactivation and a large therapeutic window, allowing for longer duration on therapy Source: Singh et al. (2011) Nature Reviews Drug Discovery; Cheng et al. (2020) Journal of Hematology & Oncology; Combination therapy with non-overlapping resistance mechanisms results in more durable responses and better outcomes Source: Strelow (2017) SLAS Discovery; Kalgutkar & Dalvie (2012) Expert Opin. Drug Discov.; Palmer et al. (2019) eLife; Mokhtari et al. (2017) Oncotarget

Our Technology Platform Traditional Small Molecule Design (Library Screening and Synthesis) FUSION™ Platform (AI/VR Matching + Custom Synthesis) Year 1 Year 2 Year 3 Year 4 Year 5 Year Target To Hit Hit To Lead Lead Optimization Preclinical Library Screening Small Molecule Target Exploration 2 3 4 Lead Optimization Synthesis Detailed crystal structures Library approach provides Emphasis on optimizing Traditional medicinal required to understand starting points for drug potency and specificity can chemistry methods may potential binding sites used design, uncovering insights force trade offs not completely improve to generate “hits” on optimal engagement key drug properties Insilico Medicine & Paul, S. M.et al. (2010). How to improve R&D productivity: the pharmaceutical industry’s grand challenge. Nature Reviews Drug Discovery, 9(3), 203–214. Year 1 Year 2 Year 3 Year 4 Target Custom Lead Custom design at lead stage Preclinical To Hit Lead Optimization accelerates timeline Biomea Library of Custom Scaffold Target Validation 2 3 4 Refinement Covalent Engagers Creation Crystal structures leveraged AI/VR driven matching Small molecules created Custom scaffolds put for deep structural process that is validated from scratch through through refinement process knowledge and biologic through insights from custom synthesis based on for optimal drug like relevance physical synthesis insights from AI/VR properties

Biomea Pipeline A suite of novel agents in multiple cancer indications and metabolic disease IND Target Population Program Discovery Phase 1 Phase 2 Phase 3 Next Milestone Enabling (US) MLL-R & NPM1 Liquid Tumors 2.5K 7.5K Patient enrollment (AML/ALL) MLL-r NPM1 BMF-219 Additional Liquid Tumors ~6K ~10K Additional preclinical (Oncology) (MM, DLBCL) DLBCL MM data Q1 2022 KRAS Solid Tumors 34K 26K 17K Additional preclinical (Lung, Pancreatic, CRC) Lung Panc. CRC data Q1 2022 Menin Pathway validation Diabetes Mellitus 1.5M 28.5M Inhibition studies to be released (Type 2, Type 1) Type 1 Type 2 (Metabolic) in Q1 2022 Lead Candidate and Target #2 Oncology N/A Target to be announced Undisclosed in H1 2022 Target #3 Oncology N/A To be announced Undisclosed Menin Programs Additional Oncology Programs

Biomea’s Value Proposition Team Vision Platform Pipeline Execution Strategy Process Value Creation Experience designing and Combining validated Leveraging our platform Developing best-in-class developing leading small biology and proven with non-traditional drug covalent inhibitors for molecule drugs chemistry to optimize design for continuous underserved indications therapeutic value discovery of novel agents

Irreversible Inhibitors Have a History of Medical Success Notable Irreversible Inhibitors Aspirin Penicillin Osimertinib (TAGRISSO) Tenofovir (VIREAD) Sofosbuvir (SOVALDI) Ibrutinib (IMBRUVICA) • Aspirin was the first commercialized irreversible drug—Discovered in 1899, Aspirin is the most utilized drug in the world • Notable precision oncology and infectious disease programs leverage irreversible mechanisms—Precision Oncology: Osimertinib and Ibrutinib both target kinases and are used in subpopulations with specific genetic biomarkers—Antivirals: Sofosbuvir and Tenofovir both target reverse transcriptases and are leveraged to treat HCV and HIV

Greater Deep Target High Selectivity Therapeutic Inactivation Window • Irreversible drugs have non- • Irreversible permanent inactivation inhibitors can of cause • Irreversible to maintain drugs their effect are designed in the covalent and covalent interactions, which increase bound protein drug absence exposure, of sustained unlike systemic target selectivity • Irreversible binding may result which conventional typically reversible need to be drugs, • Unlike reversible inhibitors, in the target elimination through irreversible drugs can achieve normal cellular degradation present to provide benefit without high selectivity jeopardizing and potency processes • Uncoupling of drug effects from pharmaceutical properties drug exposure can potentially • Target inactivation can trigger rapid apoptosis or enable lower drug dosing and • High selectivity reduces non- less frequent dosing regimens specific, off-target interactions differentiation into a normal, mature cell versus reversible approaches that tolerability often lead challenges to safety and Important Benefits of Irreversible Small Molecule Inhibition Biomea only develops optimized irreversible small molecule inhibitors due to their favorable properties

Irreversible Inhibition Enables Large Therapeutic Window Irreversible small molecule inhibitors have uncoupled drug effect from drug exposure, resulting in more optimal PD/PK profile that maximizes target engagement Drug Exposure over 24 hrs Irreversible drugs: • Can quickly achieve nearly complete and sustained occupancy (long kinetic half-life) • Drive high specificity via engaging a single amino acid within the target • Designed with a short biologic half-life to minimize systemic off target toxicity Thus, IC90 may be reached and maintained with relatively low exposure Sources: Cheng, S.-S. et al, (2020). The design and development of covalent protein-protein interaction inhibitors for cancer treatment. Journal of Hematology & Oncology, 13(1).; Strelow, J. M. (2016). A Perspective on the Kinetics of Covalent and Irreversible Inhibition. SLAS DISCOVERY: Advancing Life Sciences R&D, 22(1), 3–20. Type of Inhibition Reversible Non-Covalent Irreversible Covalent

Menin-MLL: A Complex Interaction Role of Menin-MLL Complex Modified after Uckelmann (Scott Armstrong Lab) , ASH 2018, Abstract # 546 BMF-219 an irreversible covalent inhibitor at the Menin-MLL interface Menin-MLL Fusions Different fusions result in different binding affinities between MLL fusion proteins and Menin MLL Fusions (AML/ALL) Prevalence (%) AF4 36% AF9 19% ENL 13% AF10 8% ELL 4% PTD 4% …80+ additional fusions 16% Source: Meyer, C. et al. (2017). The MLL recombinome of acute leukemias in 2017. Leukemia, 32(2), 273–284.

BMF-219 Impacts More than MLL Driven Tumors Mechanism of Action NPM1 BMF-219 covalent binding to menin disrupts menin-MLL protein-protein interaction, resulting in global change of function Menin MLL Other Resulting change of function of menin impacts important binding partners involved in oncogenesis Target Patient Population MLL • MLL-r Acute Leukemia NPM1 • NPM1 mutant Acute Leukemia • DHT / DEL DLBCL MYC • Multiple Myeloma • KRAS mutant (CRC, Lung, Pancreatic) Other • Liquid and Solid Tumors BMF-219 has the potential to address additional patient populations that are dependent on menin or some of its binding partners

BMF-219 Shows Strong Cell-Growth Inhibition Across Menin Dependent Cell Lines MLLr BAL Cell Line MLLr AML Cell Line FLT3-ITD/NPM1 AML Cell Line (MV4;11) (MOLM-13) (OCI-AML3) 1200 5000 4000 (K) 1000 3500 4000 Units 3000 800 2500 600 3000 2000 Fluorescent 2000 1500 400 1000 200 1000 Relative 500 0 0 0 T4 T7 T11 T14 T4 T7 T11 T14 T4 T7 T11 T14 DMSO BMF-219 MI-503 • BMF-219 demonstrated rapid shut down of metabolic activity, sustained over the 14-day study duration • BMF-219 responses were superior to a tested reversible menin inhibitor (MI-503) with respect to both onset and durability of metabolic suppression

BMF-219 Produces Near Complete Inhibition of Growth in AML ex-vivo Samples Growth Inhibition of Ex-Vivo AML Cells from Patients (1μM 100% Patient 320: NPM1 AML, Treatment Patient 340: NPM1 AML, Treatment 90% Patient 400: MLL-r AML, Treatment 80% 70% tion 60% Inhibi 50% Growth 40% 30% 20% 10% 0% BMF-219 MI-503 • 1µM exposure of BMF-219 produces robust growth inhibition in both NPM1 and MLL-R ex-vivo cell lines • BMF-219 responses were superior to a tested reversible menin inhibitor, MI-503, with respect to cell growth inhibition

BMF-219 Shuts Down Target Gene – MEN1 MEN1 Gene Expression Decreases w/ BMF-219 Treatment @6 hours @6 hours No significant change in MEN1 expression was observed after Wu Y et al. Disruption of the menin-MLL treatment of a reversible menin interaction triggers menin protein degradation inhibitor, MI-503 via ubiquitin-proteasome pathway. Am J Cancer Res. 2019 Aug 1;9(8):1682-1694. Menin Half Life Varies By Compartment Half Life in Cytoplasm: <1hr Half Life in Nucleus: 6-8 hrs Menin’s half-life in nucleus is most relevant for pharmacological intervention BMF-219 produces robust decrease in expression of target protein (Menin) Effect continues beyond established nuclear half-life of menin, indicating robust effect that is not impacted by protein turnover

BMF-219 Shuts Down Gene Expression of Oncogenes w/ BMF-219 @6 hours @24 hours (Transcripts per Million is a measure of gene expression) • Irreversible inhibitor, BMF-219, downregulates expression of Menin (via the target MEN1 gene) and critical leukemogenic genes (e.g. MEIS1 and HOXA9)—MEIS1 is a gene that can be an accelerator of leukemic transformation (along with HOXA9)—HOXA9 is a gene involved in myeloid differentiation and can be leukemogenic—DNMT3A is a gene that codes for a methyltransferase, which can be leukemogenic when mutated • BMF-219 demonstrated up to 80% reduction in readout genes by 6 hours and approximately 90%+ reduction at 24 hours

BMF-219 Showed Significant Survival Benefit in a Disseminated Leukemia Xenograft Model vs. Standard of Care • Mice were inoculated with xenograft cancer cells at high levels (1x107 MV4;11-luc) with greater than 90% viability • BMF-219 treatment showed notable reduction in tumor burden and survival benefit over vehicle control (72% at 20mg/kg and 94% at 40mg/kg) • Daily dosing for 14 days was well-tolerated and caused minimal body weight changes

Menin Can Play a Key Role in the Regulation of Oncogenesis Transcription Histone Histone Regulators Factors Regulators • MLL1/MLL2 Menin • HDAC/SIRT • PRMT5 • SUV39H1 • DOT1L Menin Target Transcription Factors Genes • MYC / NPM1 • Beta Catenin Menin Target Genes • PTEFb • LEDGF • HOXA9 • TERT • AP-1/JunD • MEIS1 • P53 • FOXA2 • NPM1 • AXIN • FLT3 • IL-1B13 • IL-17 Modified after Issa, G. C., et al. (2021). Therapeutic implications of menin inhibition in acute leukemias. Leukemia, 35(9), 2482–2495. AML/ ALL Implications • MLLr • NPM1 • FLT3 • MYC DLBCL MM Implications • MYC • BCL2 • CREB • PI3K/MTOR Solid Tumors Implications • MAPK/KRAS • MYC • CDK

DLBCL, MM, & Other Tumors Have High Menin Dependency Double knock-out of MEN1 via Broad Institute’s DEPMAP dataset shows that menin is essential for a wide variety of tumor types, including DLBCL, MM, leukemias and lymphomas BROAD Institute Cancer Dependency Map (DEPMAP) for Menin (MEN1) Note: CERES MENIN Dependency scores less than -1 in various tumor types imply that menin is considered essential for cell survival in those tumor types • Cell viability scores have shown that menin plays a key role in survival of multiple tumors • High menin dependency in liquid and solid tumors, beyond acute leukemias, provides rationale for further analysis in dependent tumor types • Biomea is exploring the potential for irreversible inhibition of menin in a variety of liquid and solid tumor types

Menin is Critical for MYC-dependent Aggressive DLBCL MYC is a transcription factor implicated in oncogenesis. MYC regulates genes associated with cellular proliferation, differentiation, and apoptosis MYC Overexpression Is a Critical Factor For Menin is Critical for Expression of MYC Target Genes Highly Aggressive DLBCL Subtypes Menin-MYC complex shown to be essential for transcription of MYC target genes, which includes NPM1 Source: Cabanillas, F., & Shah, B. (2017). Advances in Diagnosis and Management of Diffuse Large B-cell Lymphoma. Clinical Lymphoma Myeloma and Leukemia, 17(12), 783–796. Source: Wu, G. et al. Menin enhances c-Myc-mediated transcription to promote cancer progression. Nat. Commun. 8, 15278 (2017).

BMF-219 Elicits Broad Impact on the Complexes Surrounding Menin. Resulting in Strong Modulation of MYC Driven Expression Figure: Transcription factor (TF) activity inference using ChIP-seq of differentially expressed genes in MOLM-13 cells incubated with 500 nM BMF-219 at 24 hours. Each bar represents a study in the GEO repository using the specified TF antibody. TFs with more than one bar represent multiple study sets in GEO that overlap with BMF-219 mediated differentially expressed genes. MYC and MAX are top TFs regulating this subset of differentially expressed genes (p=10-49.5). Established menin co-factors (KMT2A, JUND) also emerged as top candidates in this dataset. • MYC and co-factor MAX emerged as top candidates based on the analysis • KMT2A and JUND, which are known menin co-factors, also emerged as top candidates in the analysis • These results strongly point toward altered MYC-activity mediated by BMF-219 in leukemia cells and provided rationale for pursuing MYC-dependent lymphoid malignancies

BMF-219 Inhibits Growth in Double Hit DLBCL Cell Lines. Providing Initial Validation of Anti-Cancer Activity Beyond AML DB TOLEDO 120 IC50 IC50 Top %Max 120 IC50 %Max BMF-219 0.316 98.64 IC50 Top 100 60 BMF-219 0.2877 99.47 Clinical Reversible ) 100 BMF-219 0.2877 99.47 (%) Clinical Reversible Inhibitor-1 3.07 100 (% 80 n Inhibitor-1 1.49 99.84 io 80 ibition i t h ib In 60 60 Inh n ati o ion 40 rat 40 Cell Lines Cell Type Translocations er if e olif DB and Toledo cells l DB GCB-DLBCL MYC/BCL2 Pr 20 20 Pro ell were incubated with TOLEDO GCB-DLBCL MYC/BCL2 C 0 Cell compounds for 4 days 0 -20 -20 0.001 0.01 0.1 1 10 0.001 0.01 0.1 1 10 Compound Concentration (uM) Compound Concentration (uM) • Irreversible menin inhibition by BMF-219 leads to marked growth inhibition in multiple DLBCL cell lines • We believe this is due to disruption of Menin-MYC • One of the clinical stage reversible menin inhibitors tested displays activity, but at 5-10x higher concentration

BMF-219 Impairs Growth in Multiple Myeloma and KRAS Solid Tumor Cell Lines Multiple Myeloma Cell Viability (KMS-20 cells, 0.560µM dose) 80000 70000 60000 (relativeunits) 50000 Cellst 40000 30000 Survivingfluorescen 20000 10000 0 Day 4 Day 7 Day 11 Day 14 DMSO BMF-219 Impairment of survival in multiple myeloma model (KMS-20 cell line, 0.56µM doses) by irreversible menin inhibitor BMF-219 KRAS Pancreatic Cancer Viability (MIA-PaCa--2 cells, 0.560µM) 3500000 3000000 2500000 2000000 1500000 1000000 500000 0 Day 4 Day 7 Day 11 DMSO BMF-219 MI-503 Impairment of survival in G12C KRAS mutation driven pancreatic cancer model (MIA-PaCa-2, 0.56µM doses) by irreversible menin inhibitor BMF-219 versus a reversible menin inhibitor (MI-503)

BMF-219 is Highly Selective In Key Screening and Safety Panels Kinase screening • 169 kinases screened; only two wild type kinases showed greater than 50% inhibition upon treatment with BMF-219 • In-house analysis of menin revealed no relevant structural similarity between targeted binding pocket and tyrosine kinases with known involvement in hematological cancers Oncopanel screening • Minimal impact of BMF-219 treatment on cell metabolism in leukemia and lymphoma cell lines that have wild type MLL, but no menin-linked mechanism for disease • Findings are consistent with external studies, showing that menin-MLL interaction is not generally cell-essential and only critical to survival in those cells that contain aberrant biology Glutathione reactivity Mean half-Drug life (min) Omeprazole 123.3 Neratinib 197.7 Ibrutinib >360 BMF-213 322.3 BMF-214 >360 BMF-219 >360 Safety screen Metabolic Activity (%) BMF-219 Vehicle 100 80 60 40 20 0 BC-1 BCP-1 BV-173 K562 U937 Drugs with limited non-specific interactions have long half-lives BMF-219 less reactivity than the approved irreversible drugs omeprazole and neratinib BMF-219 was also profiled on the SafetyScreen44 panel (CEREP/Eurofins Discovery), an in-vitro panel of 44 common selected targets to identify significant off-target interactions Findings showed no meaningful impact (greater than 50% activation or inhibition) of BMF-219 across these key safety assays

Biomea Pipeline A suite of novel agents in multiple cancer indications and metabolic disease IND Target Population Program Discovery Phase 1 Phase 2 Phase 3 Next Milestone Enabling (US) MLL-R & NPM1 Liquid Tumors 2.5K 7.5K Patient enrollment (AML/ALL) MLL-r NPM1 Menin Programs BMF-219 Additional Liquid Tumors ~6K ~10K Additional preclinical (Oncology) (MM, DLBCL) DLBCL MM data Q1 2022 KRAS Solid Tumors 34K 26K 17K Additional preclinical (Lung, Pancreatic, CRC) Lung Panc. CRC data Q1 2022 Menin Pathway validation Diabetes Mellitus 1.5M 28.5M Inhibition studies to be released (Type 2, Type 1) Type 1 Type 2 (Metabolic) in Q1 2022 Additional Lead Candidate and Oncology Target #2 Oncology N/A Target to be announced Programs Undisclosed in H1 2022 Target #3 Oncology N/A To be announced Undisclosed

BMF-219: Biomea’s Covalent Menin Inhibitor BMF-219: A Molecule That Really Grabs You and Won’t Let Go BMF-219 Properties Molecular Weight Approximately 500 kD Nanomolar Potency in Key Targeted Cell Lines: MLL-r NPM1 FLT3-ITD DLBCL MYC Driven Tumors MM KRAS Mutants (pan mutation) hERG inhibition ~5% at 10 ìM Significant Downregulation of HOXA9, MEN1, and MYC No Histopath Findings in IND Enabling Tox Studies Predicted Efficacious Human AUC for BMF-219 ~500,000 ’219 Expected hERG AUC MTD Not Determined in IND (ng/hr/ml) Enabling Tox 2,000 ‘219 Targeted Efficacious AUC

BMF-219 Phase I Study in r/r Acute Leukemia Patients Phase I first-in-human dose-escalation and dose-expansion study of BMF-219 will enroll adult patients with acute leukemia, including those with an MLL/KMT2A gene rearrangement or NPM1 mutation Phase I Study Design Dose Escalation Dose Expansion R/R ALL, AMPL, AML R/R ALL, AMPL, AML A CYP3A4ACYP3A4 Arm Arm N = 12 No N = TBD No R/R ALL, AMPL, AML R/R ALL, AMPL, AML B B ArmCYP3A4 ArmCYP3A4 N = 12 N = TBD Additional Study Details Eligibility: • All patients: – R/R ALL, AMPL, AML agnostic of mutation – > 18 years Endpoints: • Phase I: Safety, PK, determine the Optimal Biological Dose and the Recommended Phase II Dose Treatment: • BMF-219 will be administered PO daily Accelerated titration design followed by 3+3 Abbreviations: ALL Acute Lymphoblastic Leukemia AML Acute Myeloid Leukemia AMPL Acute Mixed-Phenotype Leukemia CEBP/A CCAAT Enhancer Binding Protein Alpha CRR Complete Response Rate CYP3A4 Cytochrome 450 3A4 FIH first-in-human FLT3 FMS-like Tyrosine Kinase KMT2A Lysine Methyltransferase 2A MLL Mixed Lineage Leukemia MLLr Mixed Lineage Leukemia-rearranged MN1 Meningioma 1 gene NPM1 Nucleophosmin 1 OBD Optimal biologic dose PICALM-AF10 Phosphatidylinositol Binding Clathrin Assembly Protein AF10 PK Pharmacokinetic R/R Relapsed/Refractory RP2D Recommended Phase 2 Dose TEAE Treatment Emergent Adverse Event

Role of Menin in Diabetes: Beta Cell Regeneration Menin is implicated in the proliferation of beta islet cells, providing rationale for a menin inhibitor as an agent for beta cell regeneration and turnover Pancreatic beta cells proliferation regulated via the menin/JunD/Pbk axis • Pbk is crucial for regulating compensatory pancreatic beta cell proliferation of high fat diet (HFD) fed mice • Menin and HDAC3 complex are recruited by JunD to epigenetically repress Pbk expression • Menin-JunD interaction was interrupted by small molecule menin inhibitors (MIs), leading to upregulating of Pbk gene expression, beta cell proliferation, and improved glucose tolerance in diet-induced obese and diabetic mice • Pbk is required for MI-induced beta cell proliferation and improved glucose tolerance in HFD-induced diabetic mice Sources: Ma et al. (2021) Menin-regulated Pbk controls high fat diet-induced compensatory beta cell proliferation May 7;13(5):e13524.

Role of Menin in Diabetes: Glucose Tolerance Potential for menin inhibition demonstrated by beta cell ablation diabetes model in MEN1 excised mice MEN1 Excision Prevents Development of STZ-induced Hyperglycemia Multiple low-dose streptozotocin (MLD-STZ) administered to the control and Men1-excised mice to induce beta cell damage and a diabetes-like environment Men1-excised mice did not develop hyperglycemia in STZ model, which was observed in the control group Sources: Yang et al. (2010) Deletion of theMen1Gene Prevents Streptozotocin-Induced Hyperglycemia in Mice. Experimental Diabetes Research, 2010, 1–11. doi:10.1155/2010/876701

Near Term Milestones BMF-219 – Liquid Tumors Completed IND Clearance DLBCL Preclinical Completed ASH 2021 Abstract BMF-219 Ph. I In Progress AML Trial Initiation Additional Preclinical Q1 2022 Data in DLBCL/MM BMF-219 – Solid Tumors Additional Preclinical Q1 2022 Data in KRAS Tumors BMF-219 – Diabetes T2D Menin Pathway Q1 2022 Validation Additional Programs 2nd Pipeline Candidate H1 2022 Announced 3rd Pipeline Candidate To be announced Announced

Company Financials Detailed Financials (unaudited) Three Months Ended Nine Months Ended September 30, September 30, 2021 2020 2021 2020 Operating expenses: R&D $ 7,886 $ 789 $ 16,908 $ 1,339 G&A $ 4,752 $ 346 $ 10,022 $ 489 Total Operating Expenses $ 12,638 $ 1,135 $ 26,930 $ 1,828 Loss from operations $ (12,638) $ (1,135) $ (26,930) $ (1,828) Interest and other income, net $ 32 — $ 73 $ 2 Net loss $ (12,606) $ (1,135) $ (26,857) $ (1,826) Other comprehensive loss: Changes in unrealized gain on short term investments, net — — $ 2 —Comprehensive loss $ (12,606) $ (1,135) $ (26,855) $ (1,826) Net loss per common share, basic and diluted $ (0.43) $ (0.10) $ (1.21) $ (0.18) Weighted-averaged number of common shares used to compute 29,001,213 11,724,100 22,105,321 10,082,667 basic and diluted net loss per common share $192M Cash, cash equivalents, and investments as of the end of Q3 2021

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