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The following table summarizes our product candidate pipeline. We own full worldwide development and commercialization rights to all of our programs.

All our assets are in house designed, developed, and wholly owned by Biomea Fusion Inc.

Biomea Diabetes Pipeline

About Diabetes

Diabetes is a chronic health condition that affects how the body metabolizes nutrients. It results in too much glucose (sugar) in the bloodstream. Over time, this can cause serious health problems by damaging vital tissues and organs. Most people with diabetes have a shorter life expectancy than people without this disease. The Centers for Disease Control (CDC) estimates about 2 in 5 adults in the USA will develop diabetes during their lifetime. More than 37 million people of all ages (about 11% of the US population) have diabetes today. 96 million adults (more than 1 in 3) have prediabetes, glucose levels that are higher than normal but not high enough to be classified as diabetes. Diabetes is also one of the largest economic burdens on the health care system, with $1 out of every $4 in US health care costs being spent on caring for people with diabetes.

Beta cells are found in the pancreas and are responsible for the synthesis and secretion of insulin. Insulin is a hormone that helps the body use glucose for energy and helps control blood glucose levels. In patients with diabetes, beta-cell mass and function are diminished, leading to insufficient insulin secretion and elevated glucose levels (hyperglycemia).

There are two major types of diabetes: type 1 diabetes (T1D) and type 2 diabetes (T2D). T1D is caused by an autoimmune reaction (the body “attacks itself” by mistake). This reaction destroys insulin-producing beta cells in the pancreas, stopping the body’s ability to produce and secrete insulin. Approximately 5-10% of the people who have diabetes have T1D. With T2D, the body doesn’t use insulin well and can’t keep blood sugar at normal levels. About 90-95% of people with diabetes have T2D. Loss of functional beta-cell mass is a core component of the natural history in both T1D and T2D.

Despite significant advances in pharmacotherapy and diabetes-related devices over the past 2 decades, it is estimated that approximately 50% of persons with diabetes in the US do not have adequate glucose control, as defined by a glycated hemoglobin (HbA1C) of 7% or less. One important reason is that current agents for the management of T2D and T1D do not address the root cause of diabetes – a progressive decline in beta-cell mass and function.

Different abnormalities that contribute to the hyperglycemia that occurs in patients with T2D
(adapted from DeFronzo et al. Diabetes 2009)

Progressive decline in beta-cell function (Lebovitz et al. Diabetes Review 1999) 

Menin in Diabetes


Menin is a transcriptional scaffold protein that controls the expression and activity of proteins that regulate beta-cell proliferation. Menin is thought to control beta-cell proliferation and mass by acting as a brake on beta-cell turnover / beta-cell growth, supporting the notion that inhibition of menin could lead to the regeneration of normal, healthy beta cells, which could be a disease-modifying approach to treat diabetes.

Normal Role of Menin in beta cell regulation

BMF-219 – Mechanism of Action

BMF-219, is an orally bioavailable, potent and selective covalent inhibitor of menin, built using Biomea Fusion’s FUSION™ System. BMF-219 is an investigational agent currently being studied in clinical trials of T1D and T2D and is not yet approved for the treatment of any human disease.

Loss of functional beta cell mass is a core component of the natural history in both types of diabetes — type 1 diabetes (mediated by autoimmune beta cell death) and type 2 diabetes (mediated by metabolic dysfunction leading to beta cell death). Beta cells are found in the pancreas and are responsible for the synthesis and secretion of insulin. Insulin is a hormone that helps the body use glucose for energy and helps control blood glucose levels. In patients with diabetes, beta cell mass and function are diminished, leading to insufficient insulin secretion and hyperglycemia. Menin is thought to act as a brake on beta-cell turnover and growth, supporting the notion that inhibition of menin could lead to the regeneration of normal, healthy beta cells.

BMF-219’s proposed mechanism of action in diabetes is to enable the proliferation, preservation, and reactivation of a patient’s own healthy, functional, insulin-producing beta cells. As the potentially first disease-modifying therapy for type 1 and type 2 diabetes, BMF-219 could be an important addition and complement to the diabetes treatment landscape, if approved.


Preclinical Development

Biomea conducted two diabetes animal experiments to measure the potential impact of BMF-219 for the treatment of type 2 diabetes: the Zucker Diabetic Fatty (ZDF) rat, a widely studied model of obesity and insulin resistance in rats, and the Streptozotocin (STZ)-induced diabetic rat, another frequently used model in which diabetes is induced using a chemical (STZ) that selectively destroys beta cells. In both models, BMF-219 was able to normalize glucose levels in the majority of animals after just 2 weeks of treatment. Notably, the majority of the effect was maintained efven after the two week BMF-219 treatment period. (Butler et al, EASD 2022; Somanath et al. EASD 2022). 

In additional preclinical studies, ex vivo human pancreatic islet cultures were performed to assess the effect of BMF-219. Dependent on the concentration and duration of exposure, BMF-219 was shown to increase the beta-cell mass and function, promoting glucose-dependent proliferation and enhancement of insulin production. Beta cell proliferation was observed only under elevated glucose conditions, which mimic diabetic levels, and with continuous drug exposure. BMF-219 was demonstrated to upregulate the expression of key proteins involved in cell-cycle regulation such as PbK and CCNA2 (Cyclin A2) in a glucose-dependent fashion. (Kulkarni et al. WCIRDC 2023) 

Clinical Development

COVALENT-111 (Type 2 Diabetes)

Biomea reported
initial clinical data from the first two cohorts of the Phase 2 portion of the T2D trial COVALENT-111 (NCT05731544) in March 2023. As reported, 89% of patients enrolled in Cohort 3 (n=10 patients at 100 mg dosed daily without food for 4 weeks) achieved a reduction in HbA1c, with 78% achieving ≥ 0.5% reduction and 56% achieving ≥ 1% reduction (median and mean reduction over the entire cohort: -1.0% and -0.81%, respectively). BMF-219 was well tolerated and demonstrated a favorable safety profile with no dose discontinuations.
Additional clinical data were presented in June 2023 at the annual meeting of the American Diabetes Association from the first two cohorts of patients with T2D enrolled in the Phase 2 portion of COVALENT-111. This new data highlighted specific patients treated with BMF-219 for 4 weeks who maintained or experienced a further decrease in HbA1c levels 8 weeks after treatment was completed, highlighting up to a 2.4% reduction from baseline.
 (Rodriguez et al. ADA 2023)

Clinical data presented at 2023 ADA. The top 50% of responders with T2D after 4 weeks of treatment in Cohorts 2 and 3  (100 mg BMF-219 once daily administered either fed or fasted, respectively) demonstrated durable and ongoing reduction in HbA1c while off treatment up to Week 12; a continued reduction in HbA1c was observed in both Cohort 2 (additional 114%) and Cohort 3 (additional 62%) (Rodriguez et al. ADA 2023). Left panel, All patients; Right panel, Top 50% of responders.

In December 2023 at the World Congress Insulin Resistance Diabetes & Cardiovascular Disease (WCIRDC), Biomea presented long-term follow-up data showing improved glycemic control after 22 weeks off treatment in the ongoing COVALENT-111 study of BMF-219 in T2D. At Week 26 – 22 weeks following the last dose of BMF-219 – participants in the 100 mg QD (dosed without food) cohort saw a placebo-adjusted mean reduction in HbA1c of 0.8% (compared to a 0.7% placebo-adjusted mean reduction in HbA1c at Week 4, immediately after the completion of BMF-219 dosing). The observed HbA1C reduction was supported by an increase from baseline in placebo-adjusted mean HOMA-B (+270%) and in mean stimulated C-peptide AUC (+22%) at Week 26 in responders (defined as those T2D subjects achieving HbA1c reduction ≥0.5% at Week 26) and with baseline HOMA-B below the upper limit of normal of <200). BMF-219 was generally well tolerated; there were no dose reductions, dose discontinuations, or severe or serious adverse events, and no symptomatic or asymptomatic hypoglycemia was observed. In addition, Biomea reported that the 200 mg BMF-219 dosing cohorts nearly doubled the percentage of patients (~36%) achieving durable HbA1c reduction of 1% or more compared to the 100 mg cohorts, reported earlier at 20%. (Frias et al. WCIRDC 2023)

Clinical data presented at 2023 WCIRDC. Pharmacokinetics and HbA1c Response

Case study. 29-year-old man with 4-year history of T2D

Biomea presented additional clinical data sets from the dose escalation phase of COVALENT-111 in March 2024, highlighting BMF-219’s novel mechanism of action in patients with T2D. Patients in COVALENT-111 displayed improving glycemic control while off therapy, supporting enhanced pancreatic islet function following BMF-219 treatment. Consistent with the mechanism of action, patients who demonstrated the greatest HbA1c reduction at Week 26 (22 weeks off treatment) had the greatest improvement in beta cell function as measured by HOMA-B and C-peptide. In patients failing current standard of care medications, at Week 26, following only a 28-day dosing cycle of BMF-219, a general dose-response association was observed with placebo-adjusted mean percent changes of HbA1c of -0.04% (50mg QD*), -0.2% (100mg QD with food), -0.8% (100mg without food), -0.4% (200mg QD), -0.4% (100mg BID), and -1.4% (200mg with food) (*50mg data out to Week 20, at the time of data cut). Across 100mg QD, 200mg QD, and 100mg BID cohorts (N=40), 38% of patients had ≥0.5% HbA1c reduction (with a mean reduction of 1.2%), and 23% of patients had ≥1.0% HbA1c reduction (with a mean reduction of 1.5%) at Week 26. Patients with >7 years duration of diabetes and failing dual- or triple-agent therapy (including GLP1 RA and/or SGLT2i) (n=2) also demonstrated improved glycemic control (HbA1c -0.4%, -1.1%, and -1.1% at Weeks 4, 12, and 26, respectively) following BMF-219 dosing at 200mg with food. Increases in HOMA-B and C-peptide generally correlated with glycemic control, consistent with BMF-219’s core mechanism of action: increased beta-cell proliferation and improved beta-cell function. BMF-219 was generally well tolerated with no serious adverse events and no adverse event-related study discontinuations, and no symptomatic or clinically significant hypoglycemia. 100mg and 200mg BMF-219 dose levels have been selected for the first 3 Arms of the Expansion Phase of COVALENT-111, which will dose patients for up to 12 weeks (compared to 4 weeks in the Escalation Phase) and with extended off-treatment follow-up to Week 52. (Rodriguez et al. ATTD 2024, Abitbol et al. ATTD 2024, Denham et al. ATTD 2024

COVALENT-112 (Type 1 Diabetes)


COVALENT-112 is a randomized, placebo-controlled, double-blind Phase II study (n=150) designed to examine the safety, efficacy, and durability of BMF-219 in adults diagnosed with type 1 diabetes at two oral dose levels, 100 mg and 200 mg, for 12 weeks of treatment followed by a 40 week off-treatment period. The trial includes an open label portion for adults with type 1 diabetes up to 15 years since diagnosis. The open label portion (n=40) also examines the safety, efficacy, and durability of BMF-219 at two oral dose levels, 100 mg and 200 mg, for 12 weeks of treatment followed by a 40 week off-treatment period.

The first patient in the COVALENT-112 study was dosed at the end of December 2023. In April 2024, Biomea presented data from the first two type 1 diabetes patients enrolled in COVALENT-112, both of whom demonstrated early signs of clinical activity including improved measures of beta-cell function as indicated by c-peptide responses following initial treatment with BMF-219.


Biomea Publications


Oral menin inhibitor, BMF-219, displays a significant and durable reduction in HbA1c in a type 2 diabetes rat model

Priyanka Somanath, Sanchita Mourya, Weiqun Li, Tenley C. Archer, Brian Law, Daniel Lu, Tripta Rughwani, Lekha Kumar, Taisei Kinoshita, Mini Balakrishnan, Thomas Butler;
EASD 2022 Short Oral Discussion (#590).

Oral long-acting menin inhibitor normalises type 2 diabetes in two rat models

Thomas Butler, Sanchita Mourya, Weiqun Li, Brian Law, Tenley Archer, Taisei Kinoshita, Priyanka Somanath
EASD 2022 Oral Presentation (#197).

Oral Menin Inhibitor, BMF-219, Displays a Significant and Durable Reduction in HbA1c in a Type 2 Diabetes Mellitus Rat Model

Priyanka Somanath, Sanchita Mourya, Weiqun Li, Tenley C. Archer, Brian Law, Daniel Lu, Tripta Rughwani, Lekha Kumar, Taisei Kinoshita, Mini Balakrishnan, Thomas Butler
ADA Scientific Sessions 2022 (113-LB)

Oral Long-Acting Menin Inhibitor Normalizes Type 2 Diabetes Mellitus (T2DM) in Two Rat Models

Thomas Butler, Weiqun Li, Brian Law, Tenley Archer, Taisei Kinoshita, Priyanka Somanath
ADA Scientific Sessions 2022 (P-851)

Literature References


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John M. Strelow
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Expert Opinion on Drug Discovery – 2012 May 19



Diabetes and Beta Cell Function


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Beta Cell Proliferation


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Beta cell adaptation to pregnancy requires prolactin action on both beta and non-beta cells

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Prolactin-regulated Pbk is involved in pregnancy-induced β-cell proliferation in mice

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Pancreatic islet cell type-specific transcriptomic changes during pregnancy and postpartum

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Menin and Beta Cell Proliferation

Menin regulates pancreatic islet growth by promoting histone methylation and expression of genes encoding p27Kip1 and p18INK4c

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Menin controls growth of pancreatic beta-cells in pregnant mice and promotes gestational diabetes mellitus

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The potential of β‐cell growth promotion, continued

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Menin Science

Menin dynamics and functional insight: take your partners
Katalin BaloghAttila PatócsLászló HunyadyKároly Rácz

Molecular and Cellular Biology – 2010 Sep 15;326(1-2):80-4.doi: 10.1016/j.mce.2010.04.011. Epub 2010 Apr 24.

The role of menin in hematopoiesis

Ivan Maillard and Jay L. Hess
Advances in Experimental Medicine and Biology – 2009:668:51-7.doi: 10.1007/978-1-4419-1664-8_5.

Regulation cyclin B2 expression and cell cycle G2-M transition by menin

Ting Wu, Xiuli Zhang, Xiaohua Huang, Yuqing Yang,and Xianxin Hua
Journal of Biological Chemistry – 2010 Jun 11; 285(24): 18291–18300.
Published online 2010 Apr 19. doi: 10.1074/jbc.M110.106575

Leah Wuescher, Kristine Angevine, Terry Hinds, Sadeesh Ramakrishnan, Sonia M. Najjar, and Edith J. Mensah-Osman
Endocrinology and Metabolism – 
A Review of the Scaffold Protein Menin and its Role in Hepatobiliary Pathology
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Menin in Hematological Malignancies

Therapeutic implications of menin inhibition in acute leukemias

Issa, G. C., Ravandi, F., DiNardo, C. D., Jabbour, E., Kantarjian, H. M., & Andreeff, M.
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Challenges and opportunities in targeting the menin–MLL interaction

Cierpicki, T., & Grembecka, J.
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The Spectrum of MYC Alterations in Diffuse Large B-Cell Lymphoma

Xia, Y., & Zhang, X.
Acta haematologica – 2020, 143(6), 520–528.

Targeting MYC in multiple myeloma

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Targeting Chromatin Regulators Inhibits Leukemogenic Gene Expression in NPM1 Mutant Leukemia

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Menin in Solid Tumors

The same pocket in menin binds both MLL and JUND but has opposite effects on transcription

Jing Huang, Buddha Gurung, Bingbing Wan, Ke Wan, Xianxin Hua, and Ming Lei
Nature. 2012 Feb 12; 482(7386): 542–546. Published online 2012 Feb 12. doi: 10.1038/nature10806

JunD, not c-Jun, is the AP-1 transcription factor required for Ras-induced lung cancer
E Josue Ruiz et. al.
JCI Insight – 
2021 Jul 8;6(13):e124985. doi: 10.1172/jci.insight.124985.


Loss of MLL Induces Epigenetic Dysregulation of Rasgrf1 to Attenuate Kras-Driven Lung Tumorigenesis
Ling-Yu ZhuJun-Bo YuanLi ZhangChun-Xiao HeXiao LinBin XuGuang-Hui Jin
Cancer Research – 
2022 Nov 15;82(22):4153-4163. doi: 10.1158/0008-5472.CAN-22-1475.
Menin enhances c-Myc-mediated transcription to promote cancer progression. Nature communications
Gongwei Wu, Mengqiu Yuan, Shengqi Shen, Xiaoyu Ma, Jingwen Fang, Lianbang Zhu, Linchong Sun, Zhaoji Liu, Xiaoping He, De Huang, Tingting Li, Chenchen Li, Jun Wu, Xin Hu, Zhaoyong Li, Libing Song, Kun Qu, Huafeng Zhang, and Ping Gao
Nature Communications Vol 8, Article number: 15278 (2017)
The scaffold protein menin is essential for activating the MYC locus and MYC-mediated androgen receptor transcription in androgen receptor-dependent prostate cancer cells
Yakun LuoVirginie Vlaeminck-GuillemRomain TeinturierRazan Abou ZikiPhilippe BertolinoMuriel Le RomancerChang Xian Zhang
Cancer Communications (London, England) 
2021 Dec;41(12):1427-1430. doi: 10.1002/cac2.12217. Epub 2021 Dec 1.
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