# EDGAR Filing Document

**Accession Number:** 0001840439
**File Stem:** 0001193125-23-007186
**Filing Date:** 2023-1
**Character Count:** 67737
**Document Hash:** 9a2c24f8c79221d6cb5ab584c7da1563
**Contains OCR:** False
**Source Format:** 

## Filing Content

## Filing Summary
**0001193125-23-007186.hdr.sgml**: 20230112

**ACCESSION NUMBER**: 0001193125-23-007186

**CONFORMED SUBMISSION TYPE**: 8-K

**PUBLIC DOCUMENT COUNT**: 67

**CONFORMED PERIOD OF REPORT**: 20230109

**ITEM INFORMATION**: Other Events

**ITEM INFORMATION**: Financial Statements and Exhibits

**FILED AS OF DATE**: 20230112

**DATE AS OF CHANGE**: 20230112

**FILER**: 

**COMPANY DATA:**
- **COMPANY CONFORMED NAME:** Biomea Fusion, Inc.
- **CENTRAL INDEX KEY:** 0001840439
- **STANDARD INDUSTRIAL CLASSIFICATION:** PHARMACEUTICAL PREPARATIONS [2834]
- **IRS NUMBER:** 000000000
- **STATE OF INCORPORATION:** DE
- **FISCAL YEAR END:** 1231

**FILING VALUES:**
- **FORM TYPE:** 8-K
- **SEC ACT:** 1934 Act
- **SEC FILE NUMBER:** 001-40335
- **FILM NUMBER:** 23526002

**BUSINESS ADDRESS:**
- **STREET 1:** 900 MIDDLEFIELD ROAD
- **STREET 2:** 4TH FLOOR
- **CITY:** REDWOOD CITY
- **STATE:** CA
- **ZIP:** 94063
- **BUSINESS PHONE:** (650) 980-9099

**MAIL ADDRESS:**
- **STREET 1:** 900 MIDDLEFIELD ROAD
- **STREET 2:** 4TH FLOOR
- **CITY:** REDWOOD CITY
- **STATE:** CA
- **ZIP:** 94063

?xml version="1.0" encoding="utf-8" ? 8-K

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### UNITED STATES

### SECURITIES AND EXCHANGE COMMISSION

#### WASHINGTON, D.C. 20549

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### FORM 8-K

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#### CURRENT REPORT

#### Pursuant to Section 13 or 15(d)

#### of the Securities Exchange Act of 1934

#### Date of Report (Date of earliest event reported): January 9, 2023

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## Biomea Fusion, Inc.

#### (Exact name of Registrant as Specified in Its Charter)

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| | | |
|:---|:---|:---|
| **Delaware** | **001-40335** | **82-2520134** |
| **(State or Other Jurisdiction**<br> **of Incorporation)** | **(Commission**<br> **File Number)** | **(IRS Employer**<br> **Identification No.)** |

---

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| | |
|:---|:---|
| **900 Middlefield Road, 4<sup>th</sup> Floor**<br> **Redwood City, CA** | **94063** |
| **(Address of Principal Executive Offices)** | **(Zip Code)** |

---

#### Registrant's Telephone Number, Including Area Code: (650) 980-9099

#### Not Applicable

#### (Former Name or Former Address, if Changed Since Last Report)

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Check the appropriate box below if the Form 8-K filing is intended to simultaneously satisfy the filing obligation of the registrant under any of the following provisions:

☐ Written communications pursuant to Rule 425 under the Securities Act (17 CFR 230.425)

☐ Soliciting material pursuant to Rule 14a-12 under the Exchange Act (17 CFR 240.14a-12)

☐ Pre-commencement communications pursuant to Rule 14d-2(b) under the Exchange Act (17 CFR 240.14d-2(b))

☐ Pre-commencement communications pursuant to Rule 13e-4(c) under the Exchange Act (17 CFR 240.13e-4(c))

Securities registered pursuant to Section 12(b) of the Act:

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| | |
|:---|:---|
| **Title of each class** | **Name of each exchange**<br> **on which registered** |
| Common Stock, $0.0001 par value BMEA | The Nasdaq Global Select Market |

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Indicate by check mark whether the registrant is an emerging growth company as defined in Rule 405 of the Securities Act of 1933 (§ 230.405 of this chapter) or Rule 12b-2 of the Securities Exchange Act of 1934 (§ 240.12b-2 of this chapter).

Emerging growth company ☒

If an emerging growth company, indicate by check mark if the registrant has elected not to use the extended transition period for complying with any new or revised financial accounting standards provided pursuant to Section 13(a) of the Exchange Act. ☐

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| | |
|:---|:---|
| **Item 8.01.** | **Other Events.**  |

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On January 9, 2023, Biomea Fusion, Inc. (the "Company") issued a press release titled, "Biomea Fusion to Present at 41<sup>st</sup> Annual J.P. Morgan Healthcare Conference and Highlight 2023 Corporate Milestones." The information described in the press release was presented by the Company in an updated corporate presentation at the 41<sup>st</sup> Annual J.P. Morgan Healthcare Conference, which took place from January 9-12, 2023 in San Francisco, California.

Copies of the press release and the Company's presentation are attached to this Current Report on Form 8-K as Exhibits 99.1 and 99.2 and are incorporated herein by reference.

#### Forward-Looking Statements
Statements made or incorporated by reference in this Current Report on Form 8-K 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 the clinical and therapeutic potential of the Company's product candidates and development programs, including BMF-219 and BMF-500, the potential of BMF-500 as an FLT3 inhibitor, the potential of BMF-219 as a treatment for various types of cancer and diabetes, the Company's research, development and regulatory plans, the progress of the Company's ongoing clinical trials, including COVALENT-101, COVALENT-102 and the Company's Phase I/II clinical COVALENT-111 study of BMF-219 in Type 2 diabetes, the Company's plans to present clinical data from the Company's COVALENT-101 study and the first two cohorts of the Phase II portion of the Company's COVALENT-111 study, the Company's plans to dose the first patient in the Company's COVALENT-102 study, the Company's plans to submit an IND application for BMF-500 in patients with FLT3 mutations, the Company's plans to provide clinical updates on the healthy volunteer section of the Company's Phase I/II Type 2 diabetes study of BMF-219, the Company's plans to announce a third development candidate from the FUSION platform, and the timing of such events, may be deemed to be forward-looking statements. The Company intends 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 is making this statement for purposes of complying with those safe harbor provisions.

Any forward-looking statements made or incorporated by reference in this Current Report on Form 8-K are based on the Company's current expectations, estimates and projections only as of the date of this Current Report on Form 8-K 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 the Company may encounter delays in preclinical or clinical development, the preparation, filing and clearance of INDs, patient enrollment and in the initiation, conduct and completion the Company's ongoing and planned clinical trials and other research and development activities. These risks concerning the Company'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. The Company explicitly disclaims any obligation to update any forward-looking statements except to the extent required by law.

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| | |
|:---|:---|
| **Item 9.01.** | **Financial Statements and Exhibits.**  |

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(d) Exhibits

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| | |
|:---|:---|
| **Exhibit**<br> **Number** | **Description** |
| 99.1 | [Press release titled, "Biomea Fusion to Present at 41<sup>st</sup> Annual J.P. Morgan Healthcare Conference and Highlight 2023 Corporate Milestones."](d417295dex991.htm) |
| 99.2 | [Corporate Slide Presentation of Biomea Fusion, Inc., titled "JP Morgan 2023 Corporate Presentation"](d417295dex992.htm) |
| 104 | Cover Page Interactive Data File (embedded within the Inline XBRL document) |

---

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#### SIGNATURES
Pursuant to the requirements of the Securities Exchange Act of 1934, the registrant has duly caused this report to be signed on its behalf by the undersigned thereunto duly authorized.

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| | | |
|:---|:---|:---|
|  | **BIOMEA FUSION, INC.** | **BIOMEA FUSION, INC.** |
| Date: January 12, 2023 | By: | /s/ Thomas Butler |
|  |  | **Thomas Butler** |
|  |  | **Principal Executive Officer** |

---

## Exhibit 99.1

**Exhibit 99.1** 

**Biomea Fusion to Present at 41<sup>st</sup> Annual J.P. Morgan Healthcare Conference and Highlight 2023 Corporate Milestones** 

REDWOOD CITY, Calif., Jan. 9, 2023 (GLOBE NEWSWIRE) — Biomea Fusion, Inc. (Nasdaq: BMEA), a clinical-stage biopharmaceutical company dedicated to discovering and developing novel covalent small molecules to treat and improve the lives of patients with genetically defined cancers and metabolic diseases, today announced that Thomas Butler, Biomea Fusion's Chief Executive Officer and Chairman of the Board, will present recent progress and 2023 corporate milestones at the 41st Annual J.P. Morgan Healthcare Conference on Wednesday, January 11, 2023 from 11:15 – 11:55 am ET, and that Biomea management will hold 1x1 meetings during the conference January 9 – 11.

A live webcast of the presentation will be available on the Investors & Media page of Biomea's website at:

<u>https://investors.biomeafusion.com/news-events/events.</u>

"2022 was a year of strong execution and fundamental infrastructure build as we transitioned to a clinical-stage company and expanded our pipeline. We enter 2023 with three clinical trials studying BMF-219 across 8 cancer indications covering both blood cancers and solid tumors as well as in Type 2 diabetes, the 7<sup>th</sup> leading cause of death in the United States," stated Thomas Butler, Biomea Fusion's Chief Executive Officer and Chairman of the Board. "We anticipate advancing BMF-500 into the clinic during the first half of 2023, subsequent to FDA clearance of an IND, which will increase our clinical pipeline to 4 clinical trials covering 10 indications. COVALENT-111, our Phase I/II study in Type 2 diabetes is now due to report initial safety and efficacy from the first two cohorts of the Phase II portion by the end of Q1."

Mr. Butler further commented, "we continue to activate sites and enroll patients in our Phase I/Ib (COVALENT-101) study of BMF-219 in patients with several liquid tumor types, and plan to report initial clinical data from this study in the first half of 2023. In addition, we anticipate initiating dosing imminently in our Phase I/Ib (COVALENT-102) study of BMF-219 in patients with KRAS-mutated solid tumors. In 2023, we will continue the patient-centric urgency and disciplined execution that are now well-established hallmarks of Team Biomea."

**RECENT & ANTICIPATED MILESTONES** 

**ONCOLOGY** 

&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;• COVALENT-101 (BMF-219)

&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;• Presented robust anti-tumor activity of covalent menin small molecule inhibitor, BMF-219, as a single agent and mechanistic evidence for novel inhibition of the menin protein in preclinical models of diffuse large B-cell lymphoma (DLBCL), multiple
myeloma (MM), and chronic lymphocytic leukemia (CLL). BMF-219 displayed single agent potency, surpassing greater than 90% cell killing at clinically relevant exposures in DLBCL, MM and CLL cell lines and
patient-derived samples.

&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;• BMF-219 is the first investigational menin inhibitor in clinical
development to show potential as a therapeutic agent in hematologic malignancies outside of MLLr and NPM1 mutated acute myeloid leukemia/acute lymphoblastic leukemia (AML/ALL) patients, specifically in subsets of DLBCL, MM and CLL patients.

&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;• Biomea continued site activation and patient enrollment for the dosing of BMF-219 across four liquid tumor cohorts in the COVALENT-101 study, including patients with AML/ALL, DLBCL, MM and CLL.

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&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;• **Next Anticipated Milestone:** 

On track to present initial clinical data of AML/ALL patients (including those with MLL rearrangement and NPM1 mutation) dosed in the COVALENT-101 study in the first half of 2023.

&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;• COVALENT-102 (BMF-219)

&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;• Presented strong and highly specific pan-KRAS anti-cancer activity of BMF-219 as a single agent across KRAS G12C, G12D, G12V and G13D mutant cell lines including in non-small cell lung cancer (NSCLC), colorectal cancer (CRC) and the most
prevalent type of pancreatic cancer, PDAC.

&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;• BMF-219 is the first investigational menin inhibitor in development to
enter clinical trials for the treatment of solid tumors. A targeted pan-KRAS inhibitor could have the potential to treat 25-35% of NSCLC, 35-45% of CRC, and approximately 90% of PDAC patients.

&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;• Biomea received FDA clearance of its IND in the fourth quarter of 2022 and has since initiated a Phase I/Ib
clinical trial of BMF-219 as a monotherapy in patients who have unresectable, locally advanced, or metastatic NSCLC, CRC or PDAC with an activating KRAS mutation.

&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;• **Next Anticipated Milestone:** 

On track to dose first patient in COVALENT-102 study in January 2023.

&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;• COVALENT-103 (BMF-500)

&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;• Presented data showing multi-fold higher potency and increased cytotoxicity of Biomea's covalent FLT3
small-molecule inhibitor BMF-500 compared to the commercially available reversible, non-covalent FLT3 inhibitor gilteritinib, and complete, sustained tumor regression in
mouse models of FLT3-ITD AML with maintenance of effect after cessation of therapy.

&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;• **Next Anticipated Milestone:** 

On track to file IND for BMF-500 in the first half of 2023 to initiate COVALENT-103 study of the covalent FLT3 inhibitor in patients with acute leukemia.

**DIABETES** 

&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;• COVALENT-111 (BMF-219)

&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;• Presented preclinical data highlighting the ability of BMF-219 in a Type
2 diabetes rat model to restore normal HOMA-B, a measure of pancreatic beta cell function, following only 4-weeks of treatment and to significantly lower HbA1c compared
to active control, liraglutide, -3.5% vs -1.7%, respectively.

&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;• BMF-219 is the first investigational menin inhibitor in development to
enter clinical trials for the improvement of glycemic control and insulin sensitivity in Type 2 diabetes patients.

&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;• Biomea completed the healthy volunteer portion of the Phase I/II COVALENT-111 study of BMF-219 in Canada. BMF-219 was well tolerated with an encouraging pharmacokinetic and pharmacodynamic
profile in healthy volunteers and with no safety signals detected.

&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;• Biomea received FDA clearance in December 2022 to expand the Phase II portion of COVALENT-111 to sites in the U.S. and in January 2023 announced dosing of the first U.S. patient with Type 2 diabetes. The company continues to enroll Type 2 diabetes patients in the Phase II portion of the
study in Canada as well.

&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;• **Next Anticipated Milestones:** 

On track to present initial clinical data from the first two cohorts of the Phase II portion of the study by the end of Q1 2023, and to present details of the healthy volunteer (Phase I) portion of the study at a scientific medical meeting in 2023.

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**FUSION<sup>TM</sup> SYSTEM DISCOVERY PLATFORM** 

&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;• Developed two covalently binding small molecules (BMF-219 and BMF-500), each within 18 months from target identification to IND candidate, leveraging the proprietary FUSION<sup>TM</sup> System Discovery Platform and showing excellent
preclinical profiles.

&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;• **Next Anticipated Milestone:** 

On track to announce a third development candidate from the FUSION platform in the first half of 2023.

**About Biomea Fusion** 

Biomea Fusion is a 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<sup>™</sup> System to advance a pipeline of covalent-binding therapeutic agents against key oncogenic drivers of cancer and metabolic diseases. Biomea Fusion's goal is to utilize its capabilities and platform to become a leader in developing covalent small molecules in order to maximize the clinical benefit when treating 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 the clinical and therapeutic potential of our product candidates and development programs, including BMF-219 and BMF-500, the potential of BMF-500 as an FLT3 inhibitor, the potential of BMF-219 as a treatment for various types of cancer and diabetes, our research, development and regulatory plans, the progress of our ongoing clinical trials, including COVALENT-101, COVALENT-102 and our Phase I/II clinical COVALENT-111 study of BMF-219 in Type 2 diabetes, our plans to present clinical data from our COVALENT-101 study and the first two cohorts of the Phase II portion of our COVALENT-111 study, our plans to dose the first patient in our COVALENT-102 study, our plans to submit an IND application for BMF-500 in patients with FLT3 mutations, our plans to provide clinical updates on the healthy volunteer section of our Phase I/II Type 2 diabetes study of BMF-219, our plans to announce a third development candidate from the FUSION platform, 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 preclinical or clinical development, the preparation, filing and clearance of INDs, patient enrollment and in the initiation, conduct and completion of our ongoing and planned clinical trials and other research and development activities. These risks concerning Biomea Fusion's business and operations are described in additional detail in its periodic filings with the U.S. Securities and Exchange Commission (the "SEC"), including its most recent periodic report filed with the SEC and subsequent filings thereafter. Biomea Fusion explicitly disclaims any obligation to update any forward-looking statements except to the extent required by law.

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**Contact:** 

Sasha Blaug

Senior Vice President, Corporate Development

SB@biomeafusion.com

(650) 460-7759

## Exhibit 99.2

![](g417295ex99_2p1g1.jpg)

Exhibit 99.2 JP Morgan 2023 Corporate Presentation 1

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![](g417295ex99_2p2g1.jpg)

Disclaimer 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, the initiation, timing and results of pending or future preclinical studies and clinical trials, the actual or potential actions of the 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; 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. Page 2

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![](g417295ex99_2p3g1.jpg)

Excellent Science - Combining Validated Targets with Breakthrough Chemistry We aim to cure TM Experienced Management Team Biomea Fusion is a clinical-stage biopharmaceutical company focused on the discovery and development of oral covalent small-molecule drugs to treat Novel FUSION™ System patients with genetically defined cancers and metabolic diseases. We believe that our approach may lead to significant improvement and extension of life for patients. Our team is engaged in all phases of drug discovery and development, including target selection, BMF-219 - Clinical Stage Lead Asset small molecule design, and preclinical and clinical studies to develop innovative medicines. BMF-500 and additional Programs Page 3

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![](g417295ex99_2p4g1.jpg)

Developing some of the most impactful medicines of our time A long history of developing successful drugs together Heow Tan Steve Morris MD Ramses Erdtmann Naomi Cretcher Franco Valle Thomas Butler Thorsten Kirschberg Jim Palmer Chief Technical & Chief Medical President & COO Chief of People Chief Financial Chairman & CEO EVP of Chemistry VP of Drug Quality Officer Officer Officer Discovery 22+ years in Life Science 25+ years in Life Science 15+ years in Life Science 15+ years in Life Science 15+ years in Life Science 15+ years in Life Science 30+ years in Life Science 25+ years in Life Science Pharmacyclics Pharmacyclics HealthChart LLC Eidos Therapeutics Pharmacyclics Pharmacyclics Biota Ltd Terns Pharmaceuticals Gilead Sciences Oxygen Investments Genentech Collegium Pharmaceutical Insight Genetics Iovance Biotherapeutics Cytopia Ltd. Gilead Sciences UC Irvine, BA Comm Praecis Pharmaceuticals St. Jude Children's Research UCLA – MBA Finance Commerzbank Pharmacyclics Rigel, Inc. Cell Gate UCSB, MS – Chemistry SF State University, Comm Ohio State University Hospital CallidusCloud Celera Genomics University of Münster, Golden Gate University, Santa Clara University Board certified internist Master's in Banking & Corp PricewaterhouseCoopers Prototek Inc. MBA University of Leavey School of Business, (Univ. of Texas SW HSC) San Jose State University, Finance Purdue University Münster, Ph.D., Chemistry MBA – Finance & Mgmt and medical oncologist BS Corporate Finance Ph.D. Organic Chemistry (Yale University School of Medicine) Co-lead of Ledipasvir at Gilead Co-inventor of Remdesivir at Gilead Co-inventor of ibrutinib at Celera Page 4

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![](g417295ex99_2p5g1.jpg)

TM Biomea leverages the FUSION System to Create a Suite of Novel Covalent Agents to Improve and Extend the Lives of Patients Biomea's Development Principles Drugs pursuing Validated Disease Targets have a ~2x higher likelihood of approval than molecules pursuing Validated Validated Targets Breakthrough a new mechanism of action Targets Sources: Nelson et al. (2015) Nat Genet.; Thomas et al. (2016) BIO; In a Landscape of 'Me Too' Drug For Covalent Validated Targets Breakthrough Covalent Chemistry Development, What Spurs Radical Innovation? HBS Weekly Review (Jun 2018) Inhibition For Covalent Covalent Inhibition Chemistry Biology Covalent Small Molecule Inhibitors provide deep Chemistry target inactivation and a wider therapeutic window, allowing for longer duration on therapy Covalent Sources: Singh et al. (2011) Nature Reviews Drug Discovery; Cheng et al. (2020) Journal of Hematology & Inhibitors Oncology; Strelow (2017) SLAS Discovery; Kalgutkar & Dalvie (2012) Expert Opin. Drug Discov.; Proprietary Combinations Combination Therapy with non-overlapping resistance mechanisms results in more durable Medicine Proprietary Chemistry responses and better outcomes Sources: Palmer et al. (2019) eLife; Mokhtari et al. (2017) Oncotarget Combinations Page 5

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![](g417295ex99_2p6g1.jpg)

TM Our Technology Platform – The FUSION SYSTEM TM Biomea created the Fusion System specifically to address unique targets and rapidly create highly potent and safe covalent inhibitors for them. Protein-protein interactions Shallow, limited, or dynamic binding sites Difficult to target kinases, including avoiding high homology family High affinity competitive ligands members Transcriptional factors Systemic tolerability issues at efficacious dose Low expressing targets Targeting optimal confirmation Scaffold proteins Identify small molecules for new targets Small GTPases Most proteins are considered undruggable because it's impossible to get high enough drug exposure to effectively silence the target without significant side effects… Our Optimized Covalent Inhibitors Uniquely Solve That Problem. 6

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![](g417295ex99_2p7g1.jpg)

TM Our Technology Platform – The FUSION SYSTEM – provided 3 Program leads over the past 4 years! Target identification to IND candidate in 18 months IND Target to Hit Custom Lead Lead Optimization Custom scaffold creation Target validation Library of custom engagers Refinement Proprietary AI platform with VR Custom built Synthesis to Building in drug-like Visual integration of validation matches novel DRUG create candidates with properties, optimizing PK/PD crystal structures of target and reactive LIKE PROBES to cysteines; we do desired profile, and maintaining cysteine not screen via library probes. specificity Utility: Utility: Utility: Utility: Differentiated insights from Library of covalent scaffolds AI/VR program platform yields Scaffolds are further refined X-ray crystal structures, provide for ~1,000 de novo over 300 scaffolds, which are with Mass spec, animal, and identifying target cysteines scaffolds for AI/VR scoring synthesized for in vitro testing cell-based assays to two IND candidates Page 7

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![](g417295ex99_2p8g1.jpg)

Covalent Chemistry creates very powerful results Covalent Inhibitors - a History of Medical & Commercial Success Notable Covalent Inhibitors • Aspirin was the first commercialized covalent drug Aspirin Penicillin Osimertinib (TAGRISSO) • Notable precision oncology and infectious disease programs leverage covalent mechanisms - Precision Oncology: Osimertinib and Ibrutinib both target kinases and are used in subpopulations with specific genetic biomarkers - Antivirals: Remdesivir and Tenofovir both target reverse transcriptases and are Remdesivir (VEKLURY) Ibrutinib (IMBRUVICA) Sofosbuvir (SOVALDI) leveraged to treat HCV and other viruses including HIV and COVID-19 Compounds in blue were invented or developed by Biomea Fusion senior leadership Page 8

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![](g417295ex99_2p9g1.jpg)

Case Study PCI-32765 IMBRUVICA - Prolonged Target Occupancy Effect Without prolonged Systemic Exposure Imbruvica – a Covalent Inhibitor with Long Kinetic but very Short Biological Half Life High Selectivity Long Kinetic Half Life Two-step inhibition: 1) Initial reversible binding followed by % Active-Site Occupancy (left axis) indicates 2) covalent interaction, increasing target selectivity irreversible BTK Inhibition at cancer sites Deep Target Inactivation Short Biologic Half Life Plasma concentration (right axis) reflects Permanent inactivation of bound protein drives target systemic exposure to body elimination through normal cellular degradation processes Greater Therapeutic Window Designed to maintain an effect without sustained systemic exposure, unlike conventional non-covalent inhibitors Page 9 9 (ng/ml)

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![](g417295ex99_2p10g1.jpg)

JPM 2022 Announcement BMF-219 Goals for the year 2022 Initiation of "Clinical Trials in 7 tumor types and in Diabetes" – and WE DID IT! Completion of Healthy Volunteer Completed Portion of Study Enrollment of First Diabetes Patient Completed Plus CLL Additional Programs nd 2 Pipeline Candidate H1 2022 Announced rd To be 3 Pipeline Candidate announced Announced Page 10

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In 2022 Biomea Expanded into Eight Different Solid and Liquid Tumors as well as Type 2 Diabetes Biomea's Pipeline as of January 2023 Addressable Population IND Discovery Phase 1 Phase 2 Phase 3 Enabling (US Incidence) AML/ALL (Leukemia) ~2.5K MLL-r ~6K NPM1 DLBCL (Lymphoma) ~6.5K DLBCL (r/r MYC) COVALENT-101 (Liquid Tumors) MM (Myeloma) ~9.5K MM (r/r MYC) CLL (Leukemia) ~8K CLL (r/r) BMF-219 Menin NSCLC (Lung) ~58K NSCLC (KRAS) COVALENT-102 Program (KRAS PDAC (Pancreas) ~53K PDAC (KRAS) Solid Tumors) ~60K CRC (KRAS) CRC (Colon) COVALENT-111 Type 2 Diabetes ~37M Prevalent T2 Diabetics (Diabetes) BMF-500 COVALENT-103 AML/ALL (Leukemia) FLT3 ~6K FLT3+ AML (Liquid Tumors) Program Additional Oncology Target # 3 Undisclosed Oncology Program Page 11

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BMF-219 and BMF-500 Patient Populations in the US Cancer Indications: >200K and Diabetes: >125M Addressable Annual US Patient Population for BMF-219 Diabetes Patient Population Oncology Patient Population 70,000 100 M ~90M 60K 90 M ~58K 60,000 ~53K 80 M MLL-R and 50,000 70 M NPM1 AML Initial Target 60 M 40,000 Patient 50 M Population 30,000 ~37M for menin 40 M inhibitors 30 M 20,000 20 M 9.5K 8K 10,000 6K 6K ~6.5K 10 M 2.5K 1.6M 0 M FLT3 MLL-R NPM1 DLBCL r/r with MM r/r with CLL r/r KRAS Mut. KRAS Mut. KRAS Mut. Diabetes Pre Diabetc Diabetes (BMF-500) MYC MYC Pancreatic NSCLC Colon Cancer (Type I) (Type 2) (Type II) Implication Implication Cancer Acute Leukemias Lymphoma & Myelomas Solid Tumors Metabolic Sources: Jovanović, K. K., Roche-Lestienne, C., Ghobrial, I. M., Facon, T., Quesnel, B., & Manier, S. (2018). Targeting MYC in multiple myeloma. Leukemia, 32(6), 1295–1306. https://doi.org/10.1038/s41375-018-0036-x ; Riedell, P. A., & Smith, S. M. (2018). Double hit and double expressors in lymphoma: Definition and treatment. Cancer, 124(24), 4622–4632. https://doi.org/10.1002/cncr.31646; Kempf, E., Rousseau, B., Besse, B., & Paz-Ares, L. (2016). KRAS oncogene in lung cancer: focus on molecularly driven clinical trials. European respiratory review : an official journal of the European Respiratory Society, 25(139), 71–76. https://doi.org/10.1183/16000617.0071-2015; Lanfredini, S., Thapa, A., & O'Neill, E. (2019). RAS in pancreatic cancer. Biochemical Society transactions, 47(4), 961–972. https://doi.org/10.1042/BST20170521; Serna-Blasco, R., Sanz-Álvarez, M., Aguilera, Ó., & García-Foncillas, J. (2019). Targeting the RAS-dependent chemoresistance: The Warburg connection. Seminars in cancer biology, 54, 80–90. https://doi.org/10.1016/j.semcancer.2018.01.016; Park, W., Chawla, A., & O'Reilly, E. M. (2021). Pancreatic Cancer: A Review. JAMA, 326(9), 851–862. https://doi.org/10.1001/jama.2021.13027; NCI SEER Estimated 2021 Incidence Page 12 US Incident Patient Population

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BMF-219 a covalent inhibitor of menin with unique properties Restoring Balance in Menin Dependents Diseases is Context Specific Pathological State Effector Genes CDK inhibition results in beta-cell quiescence Treating Cancer Treating Diabetes • Menin dependent effector genes • Menin dependent effector genes in beta-cells express proteins that in certain cancers express or repress beta-cell growth regulate proteins that drive oncogenesis BMF-219 selectively enables BMF-219 selectively enables cell cell homeostasis of menin homeostasis of menin dependent dependent cancer cells beta cells Menin suppressing Menin disrupting cell homeostasis cell homeostasis Page 13

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First Development Success with BMF-219 in MLL Fusion and NPM1 Driven Tumors BMF-219 has the Potential to Impact Important Binding Partners in Multiple Tumors Mechanism of Action Target Patient Population • Acute Leukemia: MLL-r MLL HOXA9/ BMF-219 covalent binding to MEIS1 • Acute Leukemia: NPM1 mutant NPM1 menin disrupts menin-MLL NPM1 • Acute Leukemia: Ras mutant protein-protein interaction, MYC resulting in global change of • DLBCL: DHT / DEL function • Multiple Myeloma: MYC addicted Menin MYC • KRAS mutant Solid Tumors: Colorectal Lung MLL Other Pancreatic • CLL: r/r population Other • Liquid and Solid Tumors BMF-219 has the potential to address additional patient populations Resulting change of function of menin impacts important binding with tumors that are dependent on menin or some of its binding partners involved in oncogenesis partners Page 14

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Novel Covalent Inhibitor of Menin BMF-219 Pipeline-in-a-Pill – Single Agent for Multiple Indications MLL Fusion & NPM1 Driven Tumors Initial clinical validation in r/r acute leukemias with MLL fusions in addition to NPM1 mutations MYC Addicted and MYC Driven Tumors Expansion into r/r diffuse large b cell lymphoma, r/r multiple myeloma and r/r chronic lymphocytic leukemia RAS/RAF Driven Solid Tumors Further expansion into KRAS and RAS mutant colorectal, lung, and pancreatic cancer Diabetes Pathway and clinical validation of covalent menin inhibition Page 15

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First Development Success with BMF-219 in MLL Fusion and NPM1 Driven Tumors In Acute Leukemia Development Stage: Phase I Clinical Trial (COVALENT-101) enrolling patients with relapsed/refractory acute leukemia Key Facts MOA Relevant Pathway BMF-219 covalently blocks menin / MLL Menin / MLL interaction can modify chromatin, Estimated Addressable Population interaction activating key leukemic genes Estimated US Patient Acute Leukemia Population (Annual MLL1 (Mutation) H3K4me3 Incidence) HOXA9 MLL2 Menin MEIS1 MLL-r ~2,500 MYC NPM1 mutant ~6,000 Ras Driven ~6,000 Menin / MLL complex forms and modifies chromatin • BMF-219 directly inhibits MLL-menin interaction and at histone H3, activating HOXA9 and MEIS1 was optimized to cause cell killing, rather than cell differentiation. • In preclinical studies, BMF-219 shows robust cell killing and reduction of expression of key genes (including MYC, MEIS1, HOXA9, and BCL2) Page 16

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GLP and non-GLP IND-Enabling Toxicology Studies BMF-219 Was Highly Selective in Key Screening and Safety Panels No Histopathology Findings Were Observed with BMF-219 in GLP and non-GLP IND-Enabling Toxicology Studies Kinase Screening P BMF-219 Vehicle Metabolic Activity (%) 169 kinases screened; only two showed >50% inhibition with BMF- 100 219 80 60 Oncopanel Screen P 40 20 Minimal impact of BMF-219 on cell metabolism in leukemia and lymphoma cell lines that have wild type MLL1 0 BC-1 BCP-1 BV-173 K562 U937 Safety Screen P SafetyScreen44 panel (CEREP/Eurofins Discovery)\* showed no meaningful impact (>50% activation or inhibition) Mean half-life Drug \*SafetyScreen44 in-vitro panel of 44 common selected targets to identify significant off-target (min) interactions Omeprazole 123.3 Neratinib 197.7 Glutathione Reactivity P Ibrutinib >360 BMF-219 had less reactivity than the approved covalent drugs omeprazole BMF-213 322.3 and neratinib BMF-214 >360 BMF-219 >360 Page 17

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First Development Success with BMF-219 in MLL Fusion and NPM1 Driven Tumors BMF-219 Demonstrated Rapid and Near Complete Reduction of Expression of Oncogenes Gene Expression Changes in AML cells following treatment • Covalent inhibitor, BMF-219, w/ BMF-219 (0.500µM dose) downregulates expression of Menin (via the target MEN1 gene) and critical leukemogenic genes (e.g., MEIS1 and HOXA9) @6 hours - 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 @24 hours • BMF-219 demonstrated up to 80% reduction in readout genes by 6 hours and approximately 90%+ reduction at 24 hours (Transcripts per Million is a measure of gene expression) Page 18

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First Development Success with BMF-219 in MLL Fusion and NPM1 Driven Tumors BMF-219 Superior Cell killing of the Target AML Cell Lines at Half the Dose vs Reversible Competitive Menin Inhibitors Source Data from ASH 2021 Publications BMF-219 Non-covalent Inhibitors KO-539 is 15% effective @ 1000nM in MOLM-13 cells and 46% effective @ 1 100nM in OCI-AML3 cells 100% 15% effective 90% @ 1000nM 80% 70% 60% 50% 46% effective 40% @ 100nM 30% 20% SNDX-50469 is 12% effective @ 1000nM in MOLM-13 cells 10% And 68% effective @ 1000nM in OCI-AML3 cells 0% MOLM-13 OCI-AML3\* MV4;11 MOLM13 OCI-AML3 12% effective Average of Clinical Non- BMF-219 @ 560nM @ 1000nM covalent Inhibitors @ 1000nM Approximately half the dose of non-covalent inhibitors \*Only SNDX-50469 was tested at 1000 nM in this cell line • BMF-219 killed >90% of AML cells in MLL-rearranged and NPM1 mutant cell lines at 4 days 68% effective post-treatment @ 1000nM • Non-covalent menin inhibitors generally report significantly less cell killing of AML cell lines as a single agent Blood (2021) 138 (Supplement 1): 3340., ASH 2021. Page 19 % of Cells with Calcein Staining

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Novel Covalent Inhibitor of Menin BMF-219 Pipeline-in-a-Pill – Single Agent for Multiple Indications MLL Fusion & NPM1 Driven Tumors Initial clinical validation in r/r acute leukemias with MLL fusions in addition to NPM1 mutations MYC Addicted and MYC Driven Tumors Expansion into r/r diffuse large b cell lymphoma, r/r multiple myeloma and r/r chronic lymphocytic leukemia RAS/RAF Driven Solid Tumors Proprietary Further expansion into KRAS and RAS mutant colorectal, lung, and pancreatic cancer Combinations Chemistry Diabetes Pathway and clinical validation of covalent menin inhibition Pathway and clinical Page 20

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Menin Dependencies Observed in Multiple Tumors Acute Leukemia, DLBCL, MM & Other Tumor Types Have High Menin Dependency Based on Broad Institute DEPMAP Dataset BROAD Institute Cancer Dependency Map (DEPMAP) for Menin (MEN1) • 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 clinically exploring the potential for covalent inhibition of menin in a variety of liquid and solid tumor types 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 Page 21

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BMF-219 Covalent Binding of Menin has Broad Impact BMF-219 Shown to Disrupt MYC Genomic Function via Broad Impact on the Complexes Surrounding Menin Covalent Menin Inhibitor – BMF-219 Non-Covalent Menin Inhibitor – SNDX-50469 TF activity inference scores greater than 10 are highly significant TF activity inference using ChIP-seq of differentially expressed genes in MOLM-13 cells incubated with 500 nM BMF-219 at 24 Blood (2021) 138 (Supplement 1): 3340. hours. Each bar represents a study in the GEO repository using the specified TF antibody. • In MOLM-13 cells treated with BMF-219, the top transcription factors • Significantly less impact on MYC expression (2x fold) and genomic function by clinical non-covalent menin inhibitor regulating gene expression are MYC and MAX • IRF4, MYC, and MAX are known drivers for some forms of DLBCL, • In contrast, BMF-219 treatment led to a ~100-200x reduction in MYC (addicted) multiple myeloma, and multiple additional tumors expression at 24 hours Page 22

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First Development Success with BMF-219 in MYC Addicted and MYC Driven Tumors BMF-219 Led to near Complete Inhibition of Growth at 1μM in DLBCL in ex-vivo Samples Triple Hit Lymphoma MYC Amplified DLBCL • At ~1µM exposure, BMF-219 produces robust growth BM-101 125 BM-100 inhibition in both THL (triple hit 125 100 lymphoma) and MYC amplified 100 DLBCL ex-vivo cell lines 75 75 50 50 • BMF-219 responses were 25 25 superior to clinical reversible 0 0 (non-covalent) inhibitors with -25 -25 respect to cell growth -50 -50 inhibition at the concentrations 0.01 0.1 1 10 100 0.01 0.1 1 10 100 -75 -75 tested Compound concentration (μM) Compound concentration (μM) Clinical Reversible 1 Clinical Reversible 2 B BM MF F -2 -219 19 Clinical Reversible 1 Clinical Reversible 2 Somanath et al., AACR 2022 Abstract 2654 Growth Inhibition IC (mM) 50 Treatment BM100 BM101 BMF-219 0.250 0.151 Clinical Reversible-1 0.969 5.63 Clinical Reversible-2 6.31 Max killing <30% Page 23 % Growth Inhibition % Growth Inhibition

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First Development Success with BMF-219 in MYC Addicted and MYC Driven Tumors BMF-219 Achieves >98% Cell Lethality Against Diverse CLL ex vivo models Growth inhibition of BMF-219 in CLL ex vivo models grouped by genetic background and Rai stage Growth Inhibition of Ex Vivo CLL Models Response based on Cytogenetics Response based on Rai Stage by Genetic Background 100 100 80 75 BMF-219 (1.1µM) 60 Clinical Reversible 50 40 Menin Inhibitor (1.1µM) Venetoclax (0.8µM) 25 20 0 0 -20 -2 5 Stage 1 Stage 2 Stage 2 Relapsed Stage 3 Rai Binet Stage Cytogenetic Background Somanath et al., ASCO 2022 Abstract 7541 Page 24 Normal Normal Normal Trisomy 11 13q Del Trisomy 12, KRAS NOTCH1, ATM NOTCH1 WT1 ATM TP53 TP53 % Growth Inhibition % Growth Inhibition

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COVALENT-101 (ENROLLING 4 COHORTS) Phase I first-in-human dose-escalation and dose-expansion study of BMF-219 enrolling adult patients with r/r acute leukemia, r/r diffuse large B cell lymphoma, r/r multiple myeloma, and r/r chronic lymphocytic leukemia (CLL) (NCT05153330) Dose Escalation Dose Expansion Study Treatment: BMF-219 R/R ALL, AMPL, AML R/R ALL, AMPL, AML A covalent small molecule menin inhibitor, administered orally N = var Total N = 30 daily in 28-day cycles R/R ALL, AMPL, AML R/R ALL, AMPL, AML Objectives N = var Total N = 30 Primary: Determine OBD & RP2D of BMF-219 monotherapy independently for each Cohort and Arm R/R DLBCL R/R DLBCL Secondary: Evaluate safety and tolerability of BMF-219 N = var Total N < 20 Determine PK/ PD parameters of BMF-219 Explore additional evidence of efficacy and antitumor activity R/R MM R/R MM N = var Total N < 20 BMF-219 is being studied in seven different blood cancers. The design of COVALENT-101 is the following: Dose escalation of each cohort is done in parallel followed by independent dose selection and dose expansion phase. R/R CLL/SLL R/R CLL/SLL N = var Total N < 20 Accelerated titration design followed by classical 3+3 Cohort 1 for R/R AML/AMPL/AML patients Cohort 2 for R/R DLBCL with ≥ 2L of prior therapy Abbreviations: ALL Acute Lymphoblastic Leukemia AML Acute Myeloid Leukemia AMPL Acute Mixed-Phenotype Cohort 3 for R/R MM with ≥ 3L of prior therapy Leukemia CYP3A4 Cytochrome 450 OBD Optimal biologic dose DLBCL diffuse large B-cell lymphoma MM multiple Cohort 4 for R/R CLL/SLL with ≥ 2L of prior therapy myeloma R/R Relapsed/Refractory Page 25 Cohort 4 Cohort 3 Cohort 1 Cohort 2 Arm A Arm A Arm A Arm A Arm B No No No No CYP3A4 CYP3A4 CYP3A4 CYP3A4 CYP3A4

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Novel Covalent Inhibitor of Menin BMF-219 Pipeline-in-a-Pill – Single Agent for Multiple Indications MLL Fusion & NPM1 Driven Tumors Initial clinical validation in r/r acute leukemias with MLL fusions in addition to NPM1 mutations MYC Addicted and MYC Driven Tumors Expansion into r/r diffuse large b cell lymphoma, r/r multiple myeloma and r/r chronic lymphocytic leukemia RAS/RAF Driven Solid Tumors Further expansion into KRAS and RAS mutant colorectal, lung, and pancreatic cancer Chemistry Diabetes Pathway and clinical validation of covalent menin inhibition Pathway and clinical Page 26

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First Development Success with BMF-219 in RAS/RAF Driven Solid Tumors BMF-219 Produced Near Complete Inhibition of Growth at 1.1μM Across KRAS G12C, G12D, G13D, and G12V Mutant Cell Lines but not WT KRAS Growth inhibition of In Vitro KRAS Mutant Cell Lines Growth Inhibition of In Vitro KRAS Mutant Cell Lines 100 90 BMF-219 (1.1 μM) 80 Clinical Menin Reversible 1 (1.1 μM) Clinical Menin Reversible 2 (1.1 μM) 60 Clinical Kras G12C Irreversible 1 (1.1 μM) 50 Sotorasib KRAS G12C (1.1 μM) 40 20 0 -20 Lung Pancreas Colon Lung Pancreas Colon Stomach ALL Colon Colon Colon G12C G12D G13D G12V WT • Covalent menin inhibition by BMF-219 led to robust growth inhibition, comparable to clinical G12C inhibitors in G12C cell lines • In non-G12C cell lines, BMF-219 achieved robust growth inhibition, higher than clinical KRAS G12C inhibitors • Clinical reversible (non-covalent) inhibitors did not achieve greater than 30% growth inhibition in any cell lines at the concentrations tested Law et al., AACR 2022 Abstract 2665 Page 27 % Growth Inhibition

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First Development Success with BMF-219 in RAS/RAF Driven Solid Tumors BMF-219 Produced Near Complete Inhibition of Growth at 1.1μM in KRAS G12C and G12D ex-vivo Patient Samples Growth Inhibition of ex-vivo KRAS mutant Cells from Patients (1μM Exposure) % Growth Inhibition of Ex Vivo PDX Tumors BM-208 (NSCLC) • 1.1µM exposure of BMF-219 produces robust growth inhibition in both G12C and BM-207 (Panc.) G12D ex-vivo cell lines BM-206 (Panc.) • BMF-219 responses were superior to BM-205 (CRC) clinical reversible (non-covalent) inhibitors with respect to cell growth inhibition at the BM-204 (CRC) concentrations tested BM-203 (CRC) BM-202 (NSCLC) BM-201 (NSCLC) 0 20 40 60 80 100 BMF-219 (1.1 μM) Clinical Menin Reversible 1 (1.1 μM) Law et al., AACR 2022 Abstract 2665 Clinical Menin Reversible 2 (1.1 μM) Page 28 KRAS G12C KRAS G12D

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COVALENT-102 (ENROLLING 3 COHORTS) Phase I/Ib Study of BMF-219, an oral covalent menin inhibitor, in patients with KRAS Mutant, Unresectable, Locally Advanced, or Metastatic Non-Small Cell Lung Cancer (NSCLC), Pancreatic Cancer (PDAC), and Colorectal Carcinoma (CRC) (NCT05631574) Study Treatment: BMF-219 A covalent small molecule menin inhibitor, administered orally daily in 28 day cycles Objectives Primary: Determine OBD & RP2D of BMF-219 monotherapy independently for each Cohort / Indication Secondary: Classical 3+3 dose escalation design Evaluate safety and tolerability of BMF-219 Determine PK/ PD parameters of BMF-219 Explore additional evidence of efficacy and antitumor activity Abbreviations: NSCLC Non-Small Cell Lung Cancer PDAC Pancreatic Cancer CRC Colorectal Carcinoma OBD optimal biologic dose RP2D recommended phase 2 dose PK/PD pharmacokinetic/pharmacodynamic ECOG Eastern Cooperative Oncology Group var variable L prior line of systemic therapy Page 29

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Novel Covalent Inhibitor of Menin BMF-219 Pipeline-in-a-Pill – Single Agent for Multiple Indications MLL Fusion & NPM1 Driven Tumors Initial clinical validation in r/r acute leukemias with MLL fusions in addition to NPM1 mutations MYC Addicted and MYC Driven Tumors Expansion into r/r diffuse large b cell lymphoma, r/r multiple myeloma and r/r chronic lymphocytic leukemia RAS/RAF Driven Solid Tumors Further expansion into KRAS and RAS mutant colorectal, lung, and pancreatic cancer Diabetes Pathway and clinical validation of covalent menin inhibition Page 30

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st Diabetes – the biggest Epidemic of the 21 century 1 in 3 Americans will develop Diabetes in their life 34.2 million US Adults have • One of the largest economic burdens on the US diabetes today a total of $380 health care system and the 7th leading cause of Billion was spent in 2021 death in the US Source: Diabetes.org • 80% of people with diabetes will die from this disease. Premature mortality caused by diabetes results in an estimated 12-14 years of life lost. Source: National library of Medicine 1(2); 2007 Jul PMC3068646 • In the United States $1 out of every $4 in US health care costs is being spent on caring for people with diabetes. In 2021 the US spent $380 Billion to treat diabetes. • According to the CDC, worldwide 463 million adults have diabetes. In the United States alone, 34.2 million adults have diabetes, 10.5% of the population. 96 million adults (more than 1 in 3) in the US have pre-diabetes. = Diabetes is an uncontrolled disease despite the availability of current medication. There is a significant need for the treatment and care of diabetes patients. Page 31

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st Diabetes – the biggest Epidemic of the 21 century Types 2 Diabetes Progression: Beta Cell Loss Type 2 Diabetic Healthy Individual Pancreatic Islet • Type 1 and Type 2 Diabetes = Islet alpha-cell results in Beta Cell Loss and a Reduction in Beta = Islet beta-cell Cell Mass = Islet beta-cell containing IAPP oligomers • Standard of Care Agents = Islet delta-cell are not addressing the Loss = Enlarged islet of Beta Cells alpha-cell = Extracellular • Type 1 and Type 2 Diabetes amyloid plaque Patients remain un- controlled and continue to = Islet alpha-cell = Islet delta-cell progress = Islet beta-cell = Enlarged islet alpha-cell = Islet beta-cell = Extracellular amyloid containing IAPP plaque oligomers \*Int. J. Mol. Sci. 2016, 17, 744; doi:10.3390/ijms17050744` Page 32

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st Diabetes – the biggest Epidemic of the 21 century Diabetes Progression of Type 1 and Type 2 Driven by Beta Cell Loss Prior Paradigm Current Paradigm Causes Type 1 and Type 2 Diabetes results in Beta Cell Loss and Insulin Resistance leads to an increase in Beta Cell Workload which ultimately leads to Reduction in Beta Cell Mass Beta Cell Failure and Death and the Progression of Type 2 Diabetes. \*Int. J. Mol. Sci. 2016, 17, 744; doi:10.3390/ijms17050744 Page 33

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st Diabetes – the biggest Epidemic of the 21 century Diabetes Patient Segments Patient Population Proposed BMF-219 MOA Initial Decline in Glycemic Control Pre-Diabetes Increasing HbA1c, Increasing Insulin Resistance 90M Beta Cell Preservation Decreasing beta cell numbers and function Beta Cell Growth 6.3M Beta Cell Reactivation Beta Cell Growth 5.3M Beta Cell Reactivation Beta Cell Preservation 7.7M Beta Cell Reactivation Beta Cell Growth 13.65M Beta Cell Reactivation Beta Cell Preservation Initial Diagnosis/Disease – Stage 2/Stage 3 T1D 1.5M Beta Cell Growth Increasing HbA1c, Initial Reduction in Insulin Beta Cell Preservation Significant Decrease in beta cell numbers Page 34

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st Diabetes – the biggest Epidemic of the 21 century BMF-219 Value Proposition in Diabetes First in class molecule with paradigm shifting potential for the treatment of diabetes Oral Treatment for the Regeneration, Preservation, and Reactivation of Beta Cells • Disease modification as the first treatment to potentially provide a functional cure of diabetes via restoration of beta cell homeostasis • Synergistic with GLP-1 based treatments while potentially insulin sparing. Potential utility in: • Prevention of T2D (90M prediabetic patients in the US) • 90% of T2D patients with beta cell impact • 50% of T2D patients on SOC but not at target A1C • T1D • Diabetic patients at risk for hypoglycemia • Potential reduction in insulin dependance • MOA could positively impact • NASH, CKD, CV benefit • Weight loss as monotherapy or in combination • Patients at risk for hypoglycemia under current SOC Page 35

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First Development Success with BMF-219 in Type II Diabetes Potential for Menin Inhibition Demonstrated by Beta Cell Ablation Diabetes Model in MEN1 Excised Mice MEN1 Excision Prevents Development of STZ-induced Hyperglycemia Control Control Men1-excised Men1-excised Multiple low-dose streptozotocin (MLD-STZ) administered to the control Men1-excised mice did not develop hyperglycemia in STZ and Men1-excised mice to induce beta cell damage and a diabetes-like model, which was observed in the control group environment 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 Page 36

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First Development Success with BMF-219 in Type II Diabetes STZ Rat Model Study Design The Streptozotocin (STZ)-Induced Rat Model Study Design Only direct insulin injection shows an effect in this model with high fat diet STZ treatment typically results in ~50% Beta Cell Loss Page 37

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First Development Success with BMF-219 in Type II Diabetes BMF-219 Demonstrates Strong Efficacy in Beta Cell Loss Animal Model (STZ Rat) BMF-219 Achieves Glycemic Control in STZ (Beta Cell Loss) Rat Model STZ + HFD model Oral Glucose Tolerance Test (Day 17) Non-Fasting Glucose Vehicle Non-fasting Glucose Pioglitazone (30 mg/kg) 800 800 BMF-219 (175mg/kg) 600 600 400 400 200 \* \* 200 \* \* \* \* p<0.05 vs Vehicle 0 0 -7 -6 -5 -4 -3 -2 -1 1 8 14 0 15 30 60 90 120 Days Minutes TA dosing Vehicle Pioglitazone (30 mg/kg) BMF-219 (175mg/kg) start BMF-219 achieves lower glucose level than pioglitazone at all BMF-219 achieves lower non-fasting glucose than pioglitazone at day timepoints in OGTT (day 17) in STZ rat model 8 and day 14 in STZ rat model Butler et al., ADA 2022 (P-851) Page 38 Blood Glucose (mg/dL) Mean± SEM Mean±SE (mg/dL)

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First Development Success with BMF-219 in Type II Diabetes BMF-219 Demonstrates Recovery of Beta Cell Activity • HOMA-Beta, a measurement of Beta Cell Function, was analyzed using 4-hr fasting glucose and insulin levels in animal plasma. • BMF-219 displayed a significant level of Beta Cell function compared to vehicle at Day 17 in a Beta +96% Cell Type 2 Diabetes Model. • This data supports the observed results from the Beta Cell Mass Quantitative Analysis using IHC. Importantly, Beta Cell Function is observed despite cessation of dosing. ~96% increase represents near doubling of beta cell function (Type 2 STZ Model represents ~ 50% Beta Cell Destruction) Page 39

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First Development Success with BMF-219 in Type II Diabetes Zucker Diabetic Fatty Rat - a Model of Insulin Resistance The ZDF Rat Study Design Day • The ZDF rat is a model of pancreatic exhaustion, thus Treatment groups (n = 10/group): mimicking some aspects of human diabetes. 1. Vehicle 2. BMF-219 175 mg/kg • Pioglitazone and metformin provide therapeutic efficacy in this 3. Pioglitazone 30 m g/kg model. • The ZDF rat is a translatable model for studying the development of T2D. Page 40

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First Development Success with BMF-219 in Type II Diabetes BMF-219 Displays Durable Glycemic Control during Drug Washout and Two Weeks after the Last Dose After 2-week Drug Washout Oral Glucose Tolerance Test (OGTT) Day 29 800 OGTT AUC on day 29 100000 600 80000 \*p<0.05 vs Vehicle 400 60000 \* 75% glycemic control \* \* maintained on day 29 40000 \* \* post-dosing compared to 200 \* 20000 day 15 \* \* p<0.05 vs Vehicle 0 0 0 15 30 60 90 120 Minutes Vehicle Pioglitazone (30 mg/kg) BMF-219 (175mg/kg) ZDF rats treated with BMF-219, pioglitazone or vehicle control for 16 days were monitored for blood glucose levels by OGTT on day 29, ~2 weeks after administration of the last dose, displaying an AUC reduction of 40%, (p<0.05). Page 41 Blood Glucose (mg/dL) Mean± SEM

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Fir Firs st t De Dev ve elo lop pm me en nt t S Su uc cc ce es ss s w wit ith h B BM MF F- -2 21 19 9 in in T Ty yp pe e I II I Diab Diabe et te es s BMF-219 Increases Β-islets in Pancreas Sections of ZDF Diabetic Model +2.0% • Quantitative Analysis of pancreatic islet tissue cross sections shows BMF-219 treated animals show novel effects in Beta Cell Area growth and maintenance. -28% -33% • BMF-219 was able to maintain Beta Cell function and prevent Beta Cell Area Loss in an Insulin Resistance Type 2 Diabetes Model. • Importantly, Beta Cell Area is maintained, despite cessation of dosing. Page 42

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First Development Success with BMF-219 in Type II Diabetes BMF-219 Demonstrates Strong Β-cell Activity - Supporting Quantitative Analysis +351% Normal (Adequate) State • HOMA-Beta, a measurement of Beta Cell Function, was analyzed using 4-hr fasting glucose and insulin levels in animal plasma. • BMF-219 displayed a significant level of Beta Cell function compared to vehicle at Day 31 in an Insulin Resistance Type 2 Diabetes Model. • This data supports the observed results from the Beta Cell Area Quantitative Analysis using IHC. Importantly, Beta Cell Function is observed despite cessation of dosing. O.J. Fasipe et al. / Can J Diabetes 44 (2020) 663e669 Page 43

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First Development Success with BMF-219 in Type II Diabetes BMF-219 Demonstrates Strong Efficacy in Insulin Resistant Animal Model (ZDF Rat) BMF-219 Reduces HbA1c After 28 days of Treatment and Maintains Effect After 14-day Washout \* p<0.05 \*\* p<0.01 BMF-219 demonstrated significant decrease HbA1c (%) \*\*\*\*p<0.0001 in HbA1c (-3.5% at day 29) vs. control ✱ ✱✱ starting on day 21 of treatment ✱ ✱ ✱ ✱ ✱ ✱ ✱ ✱ ✱ ✱ ✱ ✱ ✱ ✱ 15 Vehicle 0mg/kg BMF-219 treated group demonstrated ✱ ✱ ✱ ✱ ✱ ✱ ✱ ✱ BMF-219 40mg/kg (days 1-16), significant weight reduction starting at 200mg/kg (days 17-28) PO day 25 BMF-219 85mg/kg PO 10 BMF-219 170mg/kg PO Liraglutide 0.2 mg/kg BID 5 HbA1c reduction in BMF-219 highest dose groups maintained through washout period 0 Day 29 Day 43 Somanath et al., ADA 2022 (113-LB) Page 44 44 HbA1c (%), Mean± SEM

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First Development Success with BMF-219 in Type II Diabetes BMF-219 Treated Groups Display Body Weight and Cholesterol Reduction BMF-219 200 mg/kg group reduces body weight during BMF-219 reduces blood lipemic levels treatment in ZDF rats measured on Day 29 Triglycerides Total Cholesterol Body weight ✱ ✱ ✱ ✱ 425 ✱ ✱ ✱ 250 400 1000 \*\*\* p<0.0005 \*\*\*\*p<0.0001 200 800 375 150 600 350 100 400 325 50 200 13% body weight reduction on Day 29 0 0 300 1 3 5 8 10 12 15 17 19 21 22 25 28 29 31 Days Vehicle 0mg/kg BMF-219 170mg/kg PO Liraglutide 0.2mg/kg BID BMF-219 40mg/kg (days 1-16), 200mg/kg (days 17-28) PO Page 45 Vehicle 0mg/kg BMF-219 200mg/kg PO BMF-219 170mg/kg PO Liraglutide 0.2 mg/kg BID Vehicle 0mg/kg BMF-219 200mg/kg PO BMF-219 170mg/kg PO Liraglutide 0.2 mg/kg BID Body weight (g) Mean± SEM TC (mg/dL) Mean± SEM TG (mg/dL) Mean± SEM

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First Development Success with BMF-219 in Type II Diabetes COVALENT – 111 (Enrolling) A Phase 1/2 Randomized, Double-Blind, Placebo-Controlled Single and Multiple Ascending Dose Study to Evaluate the Safety, Tolerability, Pharmacokinetics, and Pharmacodynamics of BMF-219, an Oral Covalent Menin Inhibitor, in Healthy Adult Subjects and in Adult Subjects with Type 2 Diabetes Mellitus Study Treatment: BMF-219 SAD C1 to SAD C4 (HVs) Total N=40 A covalent small molecule menin inhibitor, administered orally daily in 28 day cycles Dose [100, 200, 400, and 600 mg] Primary Objective: MAD C1 (HVs) Evaluate safety and tolerability of BMF-219 Total N = 16 Secondary Objectives: Evaluate PK of BMF-219 MAD C2 to MAD C8 (T2D) Evaluate the effect on BMF-219 on glycemic parameters (HbA1C, PG) Total N=108 and few additional parameters using OGTT, 7-day CGM Dose [100, 200, 300, 400, 600 mg] Evaluate the changes in beta cell function Evaluate impact on lipid parameters, body weight etc. Exploratory Objectives: In the Phase 2, COVALENT-111 will enroll subjects with a HbA1C of 7-10% despite being on standard of care, up to To assess the durability of response to glycemic parameters three agents of therapy. Page 46 Phase 2 Phase 1 (MAD) (SAD)

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Second Development Success with BMF-500 BMF-500 A Third Generation FLT3 Inhibitor Generation Second Generation First Generation Third Generation of FLT3 FLT3 / multi-kinase Inhibitors FLT3 Inhibitors FLT3 Inhibitors Inhibitor Quizartinib Midostaurin Lestaurtinib Sorafenib Gilteritinib Crenolanib BMF-500 (FDA Rejected (FDA Approved as (FDA Approved as (FDA Approved as (Failed in clinical due to (Phase 3 in US) (Covalent Inhibitor, Preclinical) RYDAPT) NEXAVAR) XOSPATA) trials) Products Cardiotox) • More selective • Improved PK • Improved • Drives cell death • In vitro potency against FLT3 for FLT3 properties potency D835 • Improved FLT3 potency and • Oral route of administration • Reduced KIT selectivity inhibition • Improved activity in known resistance mechanisms • Limited impact on cKIT at projected physiological dose Benefits • Adverse • Drives • TID Dosing • Limited history of covalent FLT3 • Poor kinase selectivity Events Differentiation • F619 experience in the clinic • Challenging pharmacokinetic (PK) profile • QTc impact • Myelo- Resistance • Novel scaffold with emerging • Low steady state free drug concentration • Cytopenia suppression • Drives profile • Low potency resulting from challenging PK at tolerable doses • Frequent Dose Differentiation Adj Challenges • QTc impact BMF-500 Kinome Selectivity Gilteritinib Crenolanib Sources: Levis M. (2017). Midostaurin approved for FLT3-mutated AML. Blood, 129(26), 3403–3406. https://doi.org/10.1182/blood-2017-05-782292; Drugs@FDA.gov Page 47

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Second Development Success with BMF-500 BMF-500 Highly Effective FLT3 Inhibitor Against Resistance Mutations Page 48

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Second Development Success with BMF-500 BMF-500 Highly Potent and Durable FLT3 Inhibitor Page 49

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Second Development Success with BMF-500 BMF-500: Highly Potent and Durable FLT3 Inhibitor Individual Tumor Volume MV-4-11 Subcutaneous MV-4-11 Xenograft Model Xenograft Model

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Biome Fusion WE AIM TO CURE 2023 : Exploring 8 Different Tumor Types and Type II Diabetes in the Clinic Present initial Phase II clinical data in Type 2 Diabetes: 1Q 2023 Present initial Phase I clinical data in AML: 1H 2023 Continue enrolling patients in trials exploring BMF-219 utility in KRAS driven Solid Tumors (PDAC, NSCLC, CRC) and Liquid Tumors (AML/ALL, MM, CLL, DLBCL) File IND for BMF-500: 1H 2023 Initiate Phase I trial for BMF-500: 1H 2023 Announce third pipeline asset from FUSION™ platform technology : 1H 2023 Cash as of 30 Sept 2022 $133.8M - Capitalized into 2024 Page 51

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As of September 30, 2022 Company Financials (NASDAQ: BMEA) Three Months Ended Sept 30 2022 2021 Operating expenses: R&D $18,242 $7,886 G&A $5,242 $4,752 Total Operating Expenses $23,484 $12,638 $(23,484) $(12,638) Loss from operations $594 $32 Interest and other income, net $(22,890) $(12,606) Net loss Other comprehensive loss: Changes in unrealized gain on short term investments, net $4 - $(22,886) $(12,606) Comprehensive loss Net loss per common share, basic and diluted $(0.78) $(0.43) Weighted-average number of common shares used to compute basic and diluted net loss per 29,319,042 29,001,213 common share Cash as of 31 June 2022 $150.2M Net Cash Burn Q3 $16.4M Cash as of 30 Sept 2022 $133.8M Page 52

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THANK YOU Biomea Fusion 900 Middlefield Road, 4th floor Redwood City, CA, 94063 biomeafusion.com 53