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Biomea Fusion Corporate Presentation 1st QUARTER 2026 1
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Legal disclaimer & forward-looking statements Certain statements in this presentation and the accompanying oral commentary are forward-looking statements. These statements relate to future events or the future business and 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, including our expected cash runway, the initiation, timing and results of pending or future preclinical studies and clinical trials, the actual or potential actions of the U.S. Food and Drug Administration (FDA), the status and timing of ongoing research, development and 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 and any statements of expectation or belief regarding future events, potential markets or market size, or technology developments. 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. For a discussion of these and other risks and uncertainties, and other important factors, any of which could cause our actual results to differ from those contained in the forward-looking statements, see the section entitled "Risk Factors" in our most recent annual report on Form 10-K filed with the Securities and Exchange Commission (the SEC), as well as discussions of potential risks, uncertainties, and other important factors in our other subsequent filings with the SEC. 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. 2
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Transforming diabetes and obesity with novel oral medicines 3 ICOVAMENIB Potential first-in-class oral menin inhibitor - the control switch to beta cell restoration Restores functional beta-cell mass to address disease biology in type 2 diabetes • Increased insulin production and synergy with GLP-1 shown in preclinical models • Durable HbA1c reduction and C-peptide increase through 52 weeks after a 12-week course in the first Phase II trial in T2D patients failing standard of care • Two Phase II studies underway with 26 weeks primary endpoint data anticipated in 4Q 2026 with the potential to address over 10M U.S. T2D diabetes patients Critical unmet need: 1/3 of all diabetes patients fail standard of care and progress to insulin dependence driving complications such as kidney disease, nerve damage, vision loss, and cardiovascular issues.1-3 BMF-650 Next-generation oral GLP-1 receptor agonist Designed for consistent exposure, higher bioavailability and improved tolerability with scalable weight reduction • Improved bioavailability, better plasma protein binding, greater oral exposure with lower variability • Demonstrated weight reduction and generally well tolerated in preclinical models • Phase I clinical study in obese healthy volunteers ongoing with 28-day weight reduction data anticipated in 2Q 26, aiming to address over 100M U.S. obese patients Critical unmet need: Real world evidence indicates that up to 70% of patients on currently available GLP-1 based therapies drop out within the first year due to gastrointestinal adverse events and other tolerability considerations.4 Biomea Fusion founded in 2017 (public in 2021; NASDAQ: BMEA ) Clinical-stage company advancing two differentiated metabolic investigative programs 1.Scherer et al., Scientific Reports, 2020; 2. Nichols et al., Diabetes Care, 2015; 3.UKPDS Group. Lancet, 1998; 4. Prime Therapeutics & Magellan Rx Management, 2023 real-world claims analysis. Biomea funded through key clinical readouts for icovamenib and BMF-650 into Q1 of 2027.
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Program Indications Pre-clinical Phase I Phase II Phase III Key Catalysts Obesity Phase I weight reduction data expected Q2 2026 Phase II 26-week data (primary endpoint) anticipated 4Q 2026 COVALENT-211 (study initiated) GLP-131 (study enrolling) Biomea Fusion pipeline – targeting diabetes & obesity Biomea Fusion retains full worldwide rights across all programs COVALENT-212 (study initiated) 52-week follow-up data presented 4Q 2025 52-week follow-up data expected in Q2 2026 COVALENT-111 (study completed)Type 2 diabetes Patients – all comers Type 1 diabetes Patients – all comers Patients not controlled on GLP-1-based therapies Type 2 diabetes Type 2 diabetes Patients with Insulin- deficiency COVALENT-112 (study completed) BMF-650 ICOVAMENIB ICOVAMENIB ICOVAMENIB 4 Phase II 26-week data (primary endpoint) anticipated 4Q 2026
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ICOVAMENIB Potential first-in-class menin inhibitor aimed to restore functional beta-cells Aims to serve a significant unmet need for millions of diabetes patients failing on standard of care Employ and enhance body’s natural response to hyperglycemia as evidenced in pregnancy Conditionally drive beta-cell proliferation and activity only in presence of high glucose levels Enhance GLP-1 efficacy by upregulating GLP-1 receptors on the beta-cell surface Severe insulin-deficient diabetes patients after 12-weeks of dosing GLP-1 RA uncontrolled diabetes patients after 12 weeks of dosing Early signs of clinical activity with 12 weeks of dosing in diabetes patients failing standard of care therapies 5 Target beta-cell restoration and potentially delay or prevent onset of end-stage disease + + + + Post-hoc analysis of patients on GLP-1 based therapy not achieving stable HbA1c <7% at enrollment (9 months after last dose) Icovamenib is developed to:
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Phase IIa completed and proposed mechanism supported • Persistent 52-week HbA1c reduction after 12 weeks of treatment • Increased C-peptide OFF DRUG in both responding patient populations validating mechanism of action of restored beta-cell mass • Go-forward regimen generally well- tolerated Two transformative phase II trials ongoing Near term readouts expected in 4Q 2026 COVALENT-211 Insulin-deficient T2D failing standard of care • Enrollment ongoing • 26-week topline data expected 4Q 2026 COVALENT-212 T2D inadequately controlled on GLP-1 therapy • Enrollment ongoing • 26-week topline data expected 4Q 2026 Two Phase II trials underway ICOVAMENIB 6
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Diabetes patients are poorly controlled with over 7M US patients currently needing insulin as a last resort of people with diabetes will die from the disease1 The end-stage in the evolution of diabetes is insulin-dependence, which drives complications such as kidney disease, nerve damage, vision loss, and cardiovascular issues. 80% of life lost from diabetes2 Diabetes today remains poorly controlled in 50% of patients treated with standard of care agents3 The burden to the healthcare system is immense. There is no current therapy except for insulin replacement 12-14 years 60+ Approved therapies are not adequately resolving the growing problem of type 2 diabetes. No current therapy restores beta-cell function 1.T abish Int J Health Sci. 2007 Jul;1(2):V–VIII. 2.National library of Medicine 1(2); 2007 Jul PMC3068646 3.Zohu Lancet 2024; 404: 2077–93 38M PEOPLE IN THE US WITH DIABETES 4 PEOPLE IN US WITH T2D5 35M 7M PEOPLE IN US WITH T2D USING INSULIN6 7 Icovamenib targets beta-cell restoration and may delay or prevent onset of end-stage disease 4. CDC, Natl. Diabetes Stat. Rep., 2022 5. ADA, Standards of Care in Diabetes, Diabetes Care, 2024 6. Ahlqvist, Lancet Diabetes Endocrinol., 2018
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BMF-650 Oral GLP-1 RA developed for improved patient friendly tolerability Greater oral exposure and bioavailability with lower variability observed in preclinical models Higher plasma protein binding supporting better tolerability Potential for simplified dose escalation schedule with generally well-tolerated safety profile ~15% Body Weight Reduction in 28-day Obese Monkey Study 8 Built on the orforglipron scaffold with key structural improvements Aims to serve a significant unmet need with millions of obese Americans dropping off the available GLP -1 RAs agents within the first year 1 + + + + 1. Prime Therapeutics & Magellan Rx Management, 2023 real-world claims analysis. BMF-650 is developed to:
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Biology, mechanism of action & preclinical findings ICOVAMENIB
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IMPROVED BETA CELL MASS & FUNCTION Icovamenib promotes selective and partial reduction in menin levels Induction of beta cell proliferation Increased expression of • GLP-1 • GLP-1 receptor IMPROVED INCRETIN EFFECTS Icovamenib’s mechanism of action ICOVAMENIB | PRECLINICAL 10 Lowering menin levels releases the break on beta cell proliferation and GLP-1 and GLP-1 receptor expression Decrease in blood glucose Increase in insulin Synergistic with GLP-1 based therapies Potential for lean mass/muscle preservation Potential for weight loss Improved beta cell function Decrease in blood glucose Pancreatic islet
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Icovamenib increased beta cell quantity, function & GLP-1 receptor expression following a short treatment period BUILDING OF THE BET A CELL POOL MA TURA TION OF BETA CELL POOL DECREASE IN BET A CELL MASS INSULIN DEPENDENCE Use of icovamenib for patients failing standard of care ICOVAMENIB Diagnosis of Type 2 Diabetes Use of standard of care agents Dosing 12 weeks 1/3 of Type 2 Diabetes patients end up on insulin Follow-up period additional 14 weeks Long-term follow-up period additional 26 weeks ICOVAMENIB | PRECLINICAL 11 FURTHER DECREASE IN BETA CELL MASS INSULIN DEPENDENCE Improved beta cell mass and function
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ICOVAMENIB | PRECLINICAL 12 ICOVAMENIB | PRECLINICAL Icovamenib downregulated menin protein levels & promoted beta cell proliferation in ex vivo human islet cultures MENIN LEVELS DOWNREGULA TED Standard Glucose (5.5 mM) High Glucose (8 mM) ICOVAMENIB CONDITIONALL Y PROMOTED BETA CELL PROLIFERA TION ONL Y UNDER HYPERGL YCEMIC CONDITIONS
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13 ICOVAMENIB | PRECLINIAL Icovamenib enhanced GLP-1 receptor & insulin expression and demonstrated potential synergy in combination with semaglutide ex vivo ICOVAMENIB | PRECLINICAL Cadaver derived human islets • Gene expression & Protein analysis • Glucose Stimulated Insulin Secretion -/+ Semaglutide (200nM) Culture 7 days under glucotox conditions (8mM glucose) 13 ICOVAMENIB INCREASED GLP-1 RECEPTOR AND INSULIN EXPRESSION GLP-1 Receptor Insulin ICOVAMENIB IN COMBINA TION WITH SEMAGLUTIDE INCREASED GLUCOSE-STIMULA TED INSULIN SECRETION
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14 APPETITE SUPPRESSION BODY WEIGHT REDUCTION ❑ SUPERIOR APPETITE SUPPRESSION WITH ABOUT 10% GREA TER BODY WEIGHT REDUCTION THAN LOW-DOSE SEMAGLUTIDE ALONE ❑ THE OBSERVED BODY WEIGHT REDUCTION WAS PRIMARIL Y DUE TO FA T MASS LOSS WITH PRESERVA TION OF LEAN MASS Combination treatment of icovamenib & low-dose semaglutide reduced food intake & body weight ICOVAMENIB WITH GLP-1RA
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Potential first-in-class oral menin inhibitor clinical study results ICOVAMENIB
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*Per the COVALENT-111 Protocol the population analyzed includes only subjects who received ≥80% of their planned dosing. A clinical hold interrupted the dosing. Patients were also excluded if they had significant protocol deviation. Baseline demographics & characteristics Per Protocol Population* on 1 or More Antihyperglycemic Agents at Baseline (N=163) ICOVAMENIB | COVALENT-111 Parameter Mean (SD) or % Arm A icovamenib (8 wks 100mg QD) (N=45) Arm B icovamenib (12 wks 100 mg QD) (N=36) Arm C icovamenib (8 wks 100 mg QD then 4 wks of 100 mg BID) (N=33) Combined Arms icovamenib (N=114) Combined Arms placebo (N=49) Age (yr) 55 (7) 56 (6) 51 (10) 54 (8) 55 (7) Duration of T2D Diagnosis (yr) 4.3 (1.8) 4.7 (1.8) 4.2 (2.2) 4.4 (1.9) 4.3 (2.0) Sex (% Female) (31) (56) (36) (40) (43) HbA1c % (SD) 8.3 (1.1) 8.3 (1.0) 8.0 (0.8) 8.2 (1.0) 8.3 (1.0) Fasting C-peptide (ng/mL) 3.4 (1.2) 3.8 (1.5) 3.7 (1.8) 3.6 (1.5) 3.5 (1.4) BMI (kg/m2) 30.9 (4.7) 32.7 (4.5) 32.4 (4.9) 31.9 (4.7) 32.6 (4.2) BMI <30 kg/m2 (%) (49) (22) (30) (35) (27) BMI ≥30 kg/m2 (%) (51) (75) (70) (64) (73) Number of T2D Medications, n (%) 1 39 (87) 23 (64) 23 (70) 85 (75) 41 (84) 2 4 (9) 11 (31) 7 (21) 22 (19) 6 (12) 3 2 (4) 2 (6) 3 (9) 7 (6) 2 (4) 16
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All presented data utilized a while-on-treatment estimand with mixed model repeated measures (MMRM) analysis and was censored for use of rescue medication, defined as any modification in anti-diabetic therapy. Change in HbA1c from baseline through week 52 – all subtypes ICOVAMENIB | COVALENT-111 Across treatment durations (Arm A = 8 weeks 100 mg, Arm B = 12 weeks 100 mg, Arm C = 8 weeks 100 mg 4 weeks at 200 mg) per protocol participants taking one or more antihyperglycemic medications at baseline 17 -0.6 -0.5 -0.4 -0.3 -0.2 -0.1 0.0 0.1 0.2 0 8 12 26 36 42 52 Mean Change HbA1c (%) Weeks Pooled Placebo (N=49) Arm A (N=45) Arm B (N=36) Arm C (N=33) -0.5% threshold for clinical significance CMS Clinical Endpoints Review (2024) TREATMENT OFF-TREATMENT
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• Dosing timing relative to food will impact icovamenib’s pharmacokinetics (PK) • In a ‘Food Effect Study’ icovamenib achieved optimal PK exposure when administered within 30 minutes after a meal • These findings now inform the dosing strategy for the ongoing Phase II studies Higher HbA1c reduction was associated with higher icovamenib exposure Week 52, All Dosing Arms (N=114), HbA1c Reduction vs. Icovamenib Exposure (Mean AUC) ICOVAMENIB | COVALENT-111 18 273 218 207 184 0 50 100 150 200 250 300 ≥2.0 ≥1.5% ≥1.0% ≥0.5% PK (Mean AUC) Reduction HbA1c % at Week 52
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-2.0 -1.5 -1.0 -0.5 0.0 0.5 1.0 0 8 12 26 36 42 52 Mean Change HbA1c (%) Week Pooled Placebo (N=12) icovamenib (N=10) -0.5% threshold for clinical significance CMS Clinical Endpoints Review (2024) TREATMENT OFF-TREATMENT -0.5 -0.8 -1.2 P=0.01 -0.3 0.1 0.3 12 weeks of dosing (arms B&C) delivered lasting benefit through 52 weeks for severe insulin-deficient diabetes patients Arm A was excluded from this analysis because it included only 8 weeks of dosing which the company is not planning to pursue. ICOVAMENIB 19 INITIAL T ARGET POPULATION FOR ICOVAMENIB
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Icovamenib increased insulin secretion as measured by C -peptide index in severe insulin-deficient patients (arms B&C) ICOVAMENIB 0.7 0.8 0.9 1.0 1.1 1.2 1.3 1.4 1.5 1.6 0 12 52 Fold Change in C-peptide Index Weeks Icovamenib (N=10) Placebo (N=12) TREATMENT OFF-TREATMENT 2% 24% 20 Data censored at onset of rescue medication, defined as any modification in antihyperglycemic therapy
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Patients on a GLP-1 based therapy at enrollment showed durable & clinically meaningful response in reduction of blood sugar (HbA1c) ICOVAMENIB 21 -2.0 -1.5 -1.0 -0.5 0.0 0.5 1.0 1.5 0 8 12 52 Mean Change HbA1c (%) Weeks Pooled Placebo (N=4) icovamenib (N=12) -1.2 P=0.05 -0.5% threshold for clinical significance CMS Clinical Endpoints Review (2024) TREATMENT OFF-TREATMENT 0.6 -0.7 -0.3 0.1 1.1
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Icovamenib increased insulin secretion as measured by C -peptide index in GLP-1 RA treated patients – 9 months post last dose ICOVAMENIB 0.4 0.6 0.8 1.0 1.2 1.4 1.6 0 12 52 Mean Change HbA1c (%) Weeks Icovamenib (N=11) Placebo (N=4) 22 35% -4% Data censored at onset of rescue medication, defined as any modification in antihyperglycemic therapy TREATMENT OFF-TREATMENT
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23 Favorable 52-week safety profile Data are n (%) TEAE = T reatment Emergent Adverse event. SAE = Serious Adverse Event. Data are n (%) of TEAE with ≥5% frequency in any arm. ALT (alanine aminotransferase) or AST (aspartate aminotransferase) increase irrespective of incidence %. *Arm A had an SAE of atrial fibrillation, unrelated to study treatment and occurred during the treatment period. *Arm C had an SAE of COVID -19. Unrelated to study treatment and occurred during the treatment period. *Placebo Arm had an SAE of nephrolithiasis. Unrelated to study treatment and occurred during the treatment period. ALT increase: In the icovamenib arms, 4 of the 5 events were Grade 1 and 1 event was Grade 2. AST increase: In the icovamenib arms, all 4 events were Grade 1. All incidences of ALT and AST elevations resolved without interruption. Parameter Arm A icovamenib (N=67) Arm B icovamenib (N=67) Arm C icovamenib (N=67) Combined Arms icovamenib (N=201) Combined Arms placebo (N=66) Patients with ≥1 TEAE, N (%) 19 (28) 22 (33) 14 (21) 55 (27) 18 (27) Treatment-Related SAEs, N (%) 0 (0) 0 (0) 0 (0) 0 (0) 0 (0) SAEs*, N (%) 1 (1) 0 (0) 1 (1) 2 (1) 1 (1) Treatment Discontinuation due to TEAE, N (%) 0 (0) 0 (0) 0 (0) 0 (0) 0 (0) Study Discontinuation due to TEAE, N (%) 0 (0) 0 (0) 0 (0) 0 (0) 0 (0) ALT increase, N (%) 3 (4) 0 2 (3) 5 (3) 0 AST increase, N (%) 3 (4) 0 1 (1) 4 (2) 0 Resolution of AL T/AST w/o treatment interruption (%) 100 100 100 100 N/A Deaths, N (%) 0 (0) 0 (0) 0 (0) 0 (0) 0 (0) ICOVAMENIB | COVALENT-111
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Menin Inhibition Potentially Leads to Increased Clinical Benefit Key findings through week 52 after a short treatment course • COVALENT-211 PHASE IIB IN SEVERE INSULIN DEFICIENT T2D, FIRST P ATIENT ENROLLMENT IN 1Q 2026. • COVALENT-212 PHASE II T2D P A TIENTS NOT CONTROLLED ON GLP-1 BASED THERAPIES. FIRST P A TIENT ENROLLED IN 1Q 2026. Durable Clinical Activity in Insulin Deficient T2D Durable Clinical Activity in T2D Not Controlled on GLP-1-based Therapies Favorable Safety Profile Higher exposure aligned with deeper HbA1c reductions. Data also supports potential for exposure improvements 1.2% mean HbA1c reduction (p=0.01) maintained through Week 52 after 12 weeks of dosing 1.3% mean HbA1c reduction (p=0.05) maintained through Week 52 after 12 weeks of dosing Generally well tolerated, no treatment-related serious adverse events NEXT STEPS: ICOVAMENIB 24
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Potential first-in-class oral menin inhibitor Ongoing Phase II Studies ICOVAMENIB
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Phase IIa key derisking-insights • Optimal dose selected • Food Effect Study confirmed optimal PK exposure of icovamenib within 30 minutes after a meal • 12-week treatment observed to drive durable and lasting effects, no chronic treatment required • Strong clinical activity in insulin-deficient and GLP-1 inadequate responder populations • Treatment-emergent AEs comparable to placebo Optimal dose, dose-duration, target population identified for phase IIb program ICOVAMENIB 26 COVALENT-211 Phase IIb trial in type 2 insulin deficient diabetes patients failing standard of care • Adult participants with Type 2 Diabetes who were treated with 1-3 antidiabetic medications • HbA1c 7.5%-10.5% • BMI ≤ 32 kg/m2 • Background therapy maintained unless rescue required COVALENT-212 Phase II trial in Type 2 Diabetes Patients failing standard of care while on a GLP-1 RA • Adult participants with T2D who are not achieving glycemic targets despite GLP-1-based therapy • HbA1c ≥7.5% and ≤9.5% • BMI 25 to 40 kg/m2 • Background therapy maintained unless rescue required Direct application in Phase II/IIb’s
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ICOVAMENIB | COVALENT-211 A Phase II trial of icovamenib in T2D insulin deficient participants who are not achieving glycemic targets Objectives Endpoints Placebo 100 mg QD Icovamenib 100 mg QDARM A (n=40) ARM B (n=20) Stable Background Therapy SCREENING: 28 DA YS TREA TMENT : 12 WEEKS FOLLOW-UP: 52 WEEKS Week 26: Primary endpoint Week 52: Secondary endpoint Inclusion Criteria 27 FOLLOW-UP: 26 WEEKS • Adult participants with Type 2 Diabetes who were treated with 1-3 antidiabetic medications • HbA1c 7.5%-10.5% • BMI ≤ 32 kg/m2 • Background therapy maintained unless rescue required To demonstrate that icovamenib 100 mg once daily for 12 weeks is superior to placebo for glycemic control at Week 26 and Week 52 • Mean change in HbA1c from baseline at Week 26 and 52 • Mean change in fasting plasma glucose (FPG) from baseline at Week 26 • Safety Objectives Endpoints Inclusion Criteria
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ICOVAMENIB | COVALENT-212 Phase II trial of icovamenib in participants with T2D who are not achieving glycemic targets while using GLP-1-based therapy Objectives Endpoints Placebo 100 mg QD Icovamenib 100 mg QDARM A (n=40) ARM B (n=20) Background Therapy: Stable GLP -1-based-therapy Inclusion Criteria SCREENING: 28 DA YS TREA TMENT : 12 WEEKS FOLLOW-UP: 52 WEEKS Week 26: Primary endpoint Week 52: Secondary endpoint FOLLOW-UP: 26 WEEKS 28 • Adult participants with T2D who are not achieving glycemic targets despite GLP-1-based therapy • HbA1c ≥7.5% and ≤9.5% • BMI 25 to 40 kg/m2 • Background therapy maintained unless rescue required To demonstrate that icovamenib 100 mg once daily for 12 weeks is superior to placebo for glycemic control at Week 26 and Week 52 • Mean change in HbA1c from baseline at Week 26 and 52 • Mean change in fasting plasma glucose (FPG) from baseline at Week 26 • Safety Objectives Endpoints Inclusion Criteria
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An investigational next-generation oral GLP-1 receptor agonist for obesity BMF-650 Preclinical results and clinical overview
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Improved PK Profile Greater oral exposure with lower variability observed in preclinical studies Generally Favorable Safety Profile Better tolerability associated with higher plasma protein binding in preclinical models Patient Friendly Design Oral delivery with the potential for simplified dose escalation • Only 3 of 10 patients remain on GLP -1 therapy at one year due to tolerability, GI effects and complexity of use. • An oral agent with improved tolerability could potentially expand the long -term use. Greater therapeutic window matters Developed to deliver strong efficacy with improved oral tolerability An Investigational Next-Generation Oral GLP-1 Receptor Agonist BMF-650 1. Khan, et al. JAMA 2024 doi:10.1001/jama.2024.22284. 1 30 Intellectual Property • U.S. patent allowance received December 2025 covering BMF-650 composition. • U.S. and PCT applications published and proceeding through examination. Proposed differentiated properties of BMF-650
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Disclaimer: No head-to-head studies of BMF-650 and CT-996 have been conducted. Comparing results from different preclinical studies may be unreliable due to differences in study designs, study endpoints, and other parameters. BMF-650 up to ~15% body weight reduction after 28-days BMF-650 demonstrated robust, dose dependent weight loss in obese monkeys Weight loss in cross-study comparison with CT-996 (Roche/Carmot), while not head-to-head appeared favorable CT-996 body weight change Literature data; Carmot Therapeutics (now part of the Roche group), ADA 2024. BMF-650 | PRECLINICALBMF-650 | PRECLINICAL 31
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10 mg (fasted) 25 mg (fed)25 mg (fasted) 50 mg (fasted) 100 mg (fed)100 mg (fasted) 200 mg (fasted) Design BMF-650 | GLP-131 A Randomized, Double-blind, Placebo-controlled, FIH Study of an Oral Non-peptide GLP-1 Receptor Agonist Part 1 is a single ascending dose (SAD) study and Part 2 is a multiple ascending dose (MAD) study. Single Ascending Dose (SAD) Multiple Ascending Dose (MAD) Objectives Safety and tolerability, PK, and food effect Safety and tolerability, and efficacy (weight -loss) Eligibility Healthy overweight or obese patients (BMI 25.0–40.0 kg/m²) Healthy overweight or obese patients (BMI 30.0–45.0 kg/m²) 10 mg → 25 mg → 50 mg → 100 mg COHORT 1 2 3 4 BMF-650 active drug placebo 50 mg → 100 mg → 200 mg → 200 mg 75 mg → 150 mg → 300 mg → 300 mg 75 mg → 200 mg → 400 mg → 400 mg 7 DAYS → 7 DAYS → 7 DAYS → 21 DAYS 5 cohorts N=40 N=40 x 4 cohorts x Body weight at Baseline versus Day 28 and Day 42 on treatment 32
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PROGRAM INDICATION PHASE I PHASE II PHASE III Biomea pipeline Biomea Fusion retains full worldwide rights across all programs and is currently funded through major catalysts into 1Q 2027 UPCOMING MILESTONES ICOVAMENIB Potential first-in- class oral menin inhibitor BMF-650 Potential best-in- class oral GLP-1 RA (study enrolling) GLP-131 (study completed) COVALENT-112 (study initiated) COVALENT-211 (study initiated) COVALENT-212 Phase II 26-week data (primary endpoint) anticipated 4Q 2026 Phase II 26-week data (primary endpoint) anticipated 4Q 2026 52-week follow-up data of those patients who completed dosing expected 2Q 2026 Phase I 28-day weight reduction data expected 2Q 2026 Type 1 diabetes Patients - All comers (>2M US Patients) 1 Type 2 diabetes Patients with insulin deficiency (~7M US Patients) 2 Patients not controlled on GLP-1 based therapies Type 2 diabetes (>3M US Patients) 3,4 Obesity (>100M US Patients) 5 1.National Diabetes Statistics Report, Accessed January 28, 2026 2. International Diabetes Federation. IDF Diabetes Atlas www.diabetesatlas.org (Based on company calculations) 3.NCHS Data Brief dated August 2025. Accessed January 28, 2026 (Based on company calculations) 4.Chitnis AS. Clinical effectiveness of liraglutide across body mass index in patients with type 2 diabetes in the United States: a retrospective cohort study. Adv Ther. 2014 Sep;31(9):986-99 (Based on company calculations) 5.National Center for Health Statistics August 2023. Accessed January 28, 2026 33
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THANK YOU (NASDAQ: BMEA) For questions or inquiries, please reach out to Meichiel Weiss at ir@biomeafusion.com www.biomeafusion.com
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Slowing the clock on diabetes Turning a healthcare crisis into a huge opportunity 36 The problem: Diabetes is a global healthcare crisis, with over 800 million people affected worldwide. The disease is expanding at an estim ated ~4% annually. In the United States, one in every four healthcare dollars is spent on people living with diabetes, totaling ov er $400 billion per year. More than 100 million Americans have prediabetes; approximately 40% will progress to diabetes, and ~60% are diagnosed only after reaching late -stage disease. The economic impact: Late-stage diabetes drives over 50% of healthcare related costs due to complications such as kidney failure, cardiovascular dise ase, amputations and visual loss. With late -stage diabetes the healthcare system is burden by additional $15,000 - $20,000 per patient. Assuming 10m US diabetes patients are in late stage, delaying the progression could save the system $150 -200billion. Our breakthrough: We are developing a novel mechanism of action developed to restore beta -cell function and slow the progression of hyperglycemia. By rebuilding a functional beta -cell pool, the body may regain the ability to regulate its own insulin production . The true burden of diabetes is not early disease, but late -stage progression with irreversible organ damage. Slowing that clock by e ven a few years could generate societal returns exceeding the annual economic output of the entire pharmaceutical sector. Icovame nib would delay the need for unwieldy and often unreliable insulin therapy for years! Our vision: Keeping diabetes patients durably controlled, preventing progression to late -stage disease and avoiding the devastating complications that drive cost, morbidity, and mortality.
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Ralph DeFronzo, M.D . ENDOCRINOLOGIST , PROFESSOR OF MEDICINE UTHSCSA Melanie Davies, M.D. DIABETOLOGIST , PROFESSOR OF DIABETES MEDICINE AT THE UNIVERSITY OF LEICESTER “Icovamenib's recent data has shown an impressive restoration of beta cell function as demonstrated by significant elevations in C-peptide even after the treatment period ended. This data validates the mechanism of action of this menin inhibitor as a disease modifying agent and helps address the poor adherence and persistence commonly seen in type 2 diabetes. ” Steve Edelman, M.D . ENDOCRINOLOGIST , PROFESSOR OF MEDICINE UCSD / VA SAN DIEGO “The icovamenib data looks exciting. The data presented today help to confirm icovamenib’s mechanism of action. We have not previously seen data like this with any antihyperglycemic agent. As more trials are conducted, I believe that inhibition of menin may lead to benefits across all subtypes of diabetes. I applaud Biomea for developing a potential new treatment option that may be disease modifying for patients with diabetes. ” “Great foray into precision medicine. We need to be addressing patients in a much more individualized manner . By addressing insulin-deficient diabetes patients with icovamenib, we have seen post treatment that the beta cell pool is being restored and producing a higher level of insulin, as measured by C- peptide. This indicates a fundamental and potentially lasting impact on the disease and validates the mechanism of action of menin inhibition. ” Key opinion leaders highlight icovamenib’s potential to redefine diabetes care 37
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Alice Cheng, M.D. ENDOCRINOLOGIST , ASSOCIATE PROFESSOR OF MEDICINE UNIVERSITY OF TORONTO “Icovamenib is a very interesting molecule that acts quite differently than anything I have seen before. We are observing glucose controlled and beta cell-specific proliferation and an increase in stimulated C-peptide secretion leading to patient benefits that continued after the icovamenib dosage ended. I am very excited to further explore the many opportunities that the covalent inhibition of menin will provide to patients. ” Rohit Kulkarni, M.D ., Ph.D . PROFESSOR OF MEDICINE AT HARVARD MEDICAL SCHOOL Julio Rosenstock, M.D. DIRECTOR VELOCITY CLINICAL RESEARCH A T MEDICAL CITY DALLAS AND CLINICAL PROFESSOR OF MEDICINE, UNIV . OF TEXAS SOUTHWESTERN MEDICAL CENTER “The icovamenib data are quite interesting because of the continued effects despite having stopped it. Usually, one would expect to see the HbA1c levels climb towards baseline when the medication is stopped, but with icovamenib, the HbA1c levels decreased, which is quite intriguing and unprecedented. ” “We do not have an agent today that addresses one of the root cause of diabetes - beta cell dysfunction - icovamenib would be the first. Patients are achieving lasting benefits without continuous chronic dosing, suggesting that icovamenib may be disease modifying. I am very impressed. ” Key opinion leaders highlight icovamenib’s potential to redefine diabetes care 38