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

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 M nster, 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 M nster, 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 (1 M 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 1 M 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

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.