Icovamenib Treatment in Patients with Severe Insulin-Deficient Diabetes Led to a Significant Improvement in Pancreatic Beta-cell Function with a 53% Mean Increase in C-peptide Levels 3 Months After Last Dose
Biomea Fusion (NASDAQ: BMEA) has presented groundbreaking clinical data for icovamenib, their investigational covalent menin inhibitor, at the ATTD 2025 Conference. The drug demonstrated significant improvement in pancreatic beta-cell function in patients with severe insulin-deficient diabetes.
Key findings include:
- 53% mean increase in C-peptide levels 3 months after the last dose
- Strong correlation between C-peptide increase and HbA1c reduction (r=-0.73, p<0.0001)
- Statistically significant placebo-adjusted mean reduction in HbA1c of 1.47% at Week 26 (p=0.022)
- Enhanced responsiveness to GLP-1-based medicines in preclinical studies
The results suggest icovamenib's potential as a first-in-class, disease-modifying therapy by targeting beta-cell restoration and enhancing insulin secretion, with benefits persisting beyond the treatment period. The treatment shows particular promise for severe insulin-deficient diabetes, affecting over 100 million people worldwide.
Biomea Fusion (NASDAQ: BMEA) ha presentato dati clinici innovativi per icovamenib, il loro inibitore covalente della menina in fase di sperimentazione, durante la Conferenza ATTD 2025. Il farmaco ha dimostrato un miglioramento significativo nella funzione delle cellule beta pancreatiche nei pazienti con diabete severo da carenza di insulina.
I principali risultati includono:
- Aumento medio del 53% dei livelli di C-peptide 3 mesi dopo l'ultima dose
- Fortissima correlazione tra l'aumento del C-peptide e la riduzione dell'HbA1c (r=-0.73, p<0.0001)
- Riduzione media statisticamente significativa dell'HbA1c aggiustata per placebo dell'1.47% alla Settimana 26 (p=0.022)
- Maggiore reattività ai farmaci basati su GLP-1 negli studi preclinici
I risultati suggeriscono il potenziale di icovamenib come terapia di prima classe modificante la malattia, mirata al ripristino delle cellule beta e al potenziamento della secrezione di insulina, con benefici che persistono oltre il periodo di trattamento. Il trattamento mostra particolare promessa per il diabete severo da carenza di insulina, che colpisce oltre 100 milioni di persone in tutto il mondo.
Biomea Fusion (NASDAQ: BMEA) ha presentado datos clínicos innovadores para icovamenib, su inhibidor covalente de menina en investigación, en la Conferencia ATTD 2025. El fármaco demostró una mejora significativa en la función de las células beta pancreáticas en pacientes con diabetes severa por deficiencia de insulina.
Los hallazgos clave incluyen:
- Aumento medio del 53% en los niveles de C-péptido 3 meses después de la última dosis
- Fuerte correlación entre el aumento de C-péptido y la reducción de HbA1c (r=-0.73, p<0.0001)
- Reducción media estadísticamente significativa de HbA1c ajustada por placebo del 1.47% en la Semana 26 (p=0.022)
- Mayor respuesta a los medicamentos basados en GLP-1 en estudios preclínicos
Los resultados sugieren el potencial de icovamenib como una terapia de primera clase modificadora de la enfermedad, al dirigirse a la restauración de células beta y mejorar la secreción de insulina, con beneficios que persisten más allá del período de tratamiento. El tratamiento muestra una promesa particular para la diabetes severa por deficiencia de insulina, que afecta a más de 100 millones de personas en todo el mundo.
Biomea Fusion (NASDAQ: BMEA)는 ATTD 2025 컨퍼런스에서 그들의 연구용 공유 결합 메닌 억제제인 이코바메닙에 대한 획기적인 임상 데이터를 발표했습니다. 이 약물은 중증 인슐린 결핍 당뇨병 환자에서 췌장 베타 세포 기능의 상당한 개선을 나타냈습니다.
주요 발견 사항은 다음과 같습니다:
- 마지막 투여 후 3개월 동안 C-펩타이드 수치의 평균 53% 증가
- C-펩타이드 증가와 HbA1c 감소 간의 강한 상관관계 (r=-0.73, p<0.0001)
- 26주차에 플라세보 조정된 HbA1c의 평균 통계적으로 유의미한 1.47% 감소 (p=0.022)
- 전임상 연구에서 GLP-1 기반 약물에 대한 반응성 향상
결과는 이코바메닙이 베타 세포 복원과 인슐린 분비 개선을 목표로 하는 최초의 질병 수정 치료제로서의 잠재력을 제시하며, 치료 기간 이후에도 혜택이 지속됨을 나타냅니다. 이 치료법은 전 세계적으로 1억 명 이상의 사람들에게 영향을 미치는 중증 인슐린 결핍 당뇨병에 특히 유망합니다.
Biomea Fusion (NASDAQ: BMEA) a présenté des données cliniques révolutionnaires pour l'icovamenib, leur inhibiteur covalent de la ménine en cours d'investigation, lors de la Conférence ATTD 2025. Le médicament a montré une amélioration significative de la fonction des cellules bêta pancréatiques chez les patients atteints de diabète sévère par carence en insuline.
Les résultats clés incluent:
- Augmentation moyenne de 53% des niveaux de C-peptide 3 mois après la dernière dose
- Corrélation forte entre l'augmentation du C-peptide et la réduction de l'HbA1c (r=-0.73, p<0.0001)
- Réduction moyenne statistiquement significative de l'HbA1c ajustée pour placebo de 1.47% à la Semaine 26 (p=0.022)
- Réactivité améliorée aux médicaments basés sur le GLP-1 dans les études précliniques
Les résultats suggèrent le potentiel de l'icovamenib en tant que thérapie de première classe modifiant la maladie, en ciblant la restauration des cellules bêta et en améliorant la sécrétion d'insuline, avec des bénéfices qui persistent au-delà de la période de traitement. Ce traitement montre une promesse particulière pour le diabète sévère par carence en insuline, qui touche plus de 100 millions de personnes dans le monde.
Biomea Fusion (NASDAQ: BMEA) hat auf der ATTD 2025-Konferenz bahnbrechende klinische Daten zu icovamenib, ihrem experimentellen kovalenten Menin-Inhibitor, präsentiert. Das Medikament zeigte eine signifikante Verbesserung der Funktion der pankreatischen Beta-Zellen bei Patienten mit schwerem insulinabhängigem Diabetes.
Wichtige Ergebnisse umfassen:
- 53% durchschnittliche Erhöhung der C-Peptid-Spiegel 3 Monate nach der letzten Dosis
- Starke Korrelation zwischen dem Anstieg des C-Peptids und der Reduktion des HbA1c (r=-0.73, p<0.0001)
- Statistisch signifikante placebo-adjustierte durchschnittliche Reduktion des HbA1c um 1.47% in Woche 26 (p=0.022)
- Erhöhte Reaktivität auf GLP-1-basierte Medikamente in vorklinischen Studien
Die Ergebnisse deuten auf das Potenzial von icovamenib als erstklassige, krankheitsmodifizierende Therapie hin, die auf die Wiederherstellung der Beta-Zellen und die Verbesserung der Insulinsekretion abzielt, mit Vorteilen, die über den Behandlungszeitraum hinaus anhalten. Die Behandlung zeigt besondere Versprechen für schweren insulinabhängigen Diabetes, der über 100 Millionen Menschen weltweit betrifft.
- Significant 53% mean increase in C-peptide levels, indicating improved insulin production
- Strong efficacy with 1.47% HbA1c reduction at Week 26
- Therapeutic effects sustained 3 months after treatment cessation
- Potential synergy with GLP-1 medications, expanding treatment options
- Large addressable market of over 100 million patients worldwide
- Still in clinical-stage development, pending regulatory approval
- Long-term safety and efficacy data beyond 3 months post-treatment not yet available
Insights
Biomea Fusion's icovamenib data represents a potentially significant breakthrough in diabetes treatment. The
The placebo-adjusted
The strong correlation (r=-0.73) between C-peptide increases and HbA1c reduction provides compelling evidence for icovamenib's proposed mechanism of action. Most current therapies manage glucose through various mechanisms but don't address declining insulin production capacity.
Particularly noteworthy is icovamenib's synergistic potential with GLP-1 medications, demonstrated through increased GLP-1 receptor expression in preclinical models. This could enhance efficacy while potentially allowing lower GLP-1 doses, improving tolerability.
The target population—severe insulin-deficient diabetes affecting over 100 million patients globally—represents a substantial unmet need. Current therapies for this subgroup often fail to provide adequate glycemic control.
If these results translate through late-stage trials, icovamenib could represent the first therapy addressing a root cause of type 2 diabetes progression rather than merely managing symptoms—a paradigm shift in treatment approach.
Biomea's icovamenib data exhibits several characteristics that differentiate it from typical incremental diabetes advances. The disease-modifying potential demonstrated by sustained glycemic control after treatment cessation represents a fundamentally different value proposition from maintenance therapies requiring lifelong administration.
The targeted approach to severe insulin-deficient diabetes—a difficult-to-treat subpopulation estimated at over 100 million patients—positions Biomea in a less crowded market segment with significant unmet need. The
Mechanistically, icovamenib's ability to increase beta-cell function addresses the progressive nature of type 2 diabetes that eventually leads to insulin dependence. This contrasts with competitors focused primarily on insulin sensitivity or glucose excretion.
The preclinical evidence showing enhanced responsiveness to GLP-1 receptor agonists suggests potential for combination therapy with blockbuster medications like semaglutide and tirzepatide. This complementary mechanism could carve out a valuable position in treatment algorithms.
The endorsements from key opinion leaders in diabetes (Edelman, Cheng, Pettus, Kulkarni) significantly enhance icovamenib's credibility. Their emphasis on the uniqueness of icovamenib's mechanism and potential disease modification validates Biomea's approach.
While Biomea remains a clinical-stage company with execution risks ahead, these results represent a significant derisking event that validates their menin inhibition platform in diabetes and potentially expands its market opportunity beyond initial expectations.
- Therapeutic effects were sustained off treatment, with persistent reduction in HbA1c and improvement in beta-cell function 3 months after last dose, suggesting disease-modifying potential of icovamenib
- Strong correlation between C-peptide increase and HbA1c reduction (r = -0.73, p<0.0001) across all dosing groups (n=23) support the proposed mechanism of beta cell restoration
- Best response observed in prespecified, beta-cell deficient patients on one or more antihyperglycemic agents at baseline, achieving a statistically significant placebo-adjusted mean reduction in HbA1c of
1.47% at Week 26 (p=0.022), after only 12 weeks of 100 mg once daily icovamenib - Preclinical in vivo experiments indicated that icovamenib enhanced the responsiveness of human islets to GLP-1-based medicines, consistent with the increase in expression levels (transcript and protein) of both the GLP-1 receptor and intracellular insulin
- Severe Insulin Deficient Diabetes represents an underserved patient population within type 2 diabetes and is estimated to be over 100 million people worldwide.
REDWOOD CITY, Calif., March 24, 2025 (GLOBE NEWSWIRE) -- Biomea Fusion, Inc. (“Biomea”) (Nasdaq: BMEA), a clinical-stage diabetes and obesity medicines company, today announced the presentation of preclinical and clinical data from studies assessing icovamenib at the Advanced Technologies & Treatments for Diabetes (ATTD) 2025 Conference in Amsterdam, The Netherlands. The new findings support icovamenib’s potential as a first-in-class, disease-modifying therapy by targeting beta-cell restoration, enhancing insulin secretion, and sustaining glycemic improvements beyond icovamenib’s treatment period.
“At ATTD, we presented data on icovamenib’s ability to drive a significant increase in C-peptide production in patients who need it most, demonstrating a durable effect that lasted well beyond the treatment period. This is an exciting moment for icovamenib, but most importantly an exciting moment for patients who are in need of an alternative mechanism of action for their diabetes. This data validates the topline analysis reported last December, highlighting the impactful responses seen in those with poor beta cell function at baseline. With icovamenib, we look to increase the fundamental capability of our patients, enabling them to produce more insulin on their own and take back control of their diabetes. We look forward to providing further updates with this study as we continue to uncover the broad potential of icovamenib in type 2 diabetes,” said Thomas Butler, Chief Executive Officer and Chairman of Biomea Fusion.
Icovamenib, an investigational, covalent menin inhibitor, is being evaluated for its ability to restore pancreatic beta-cell mass and function, which are key drivers of disease progression in insulin-deficient diabetes. The presentations provided comprehensive insights into icovamenib’s mechanism of action, long-term clinical activity, biomarker responses, safety profile, and potential as a combination therapy with GLP-1-based medicines.
“These findings reinforce the potential role of icovamenib in improving beta-cell function even after treatment cessation. The significant increase in C-peptide levels observed in icovamenib-treated patients more than 3 months after stopping therapy supports the proposed mechanism of action, the restoration of beta cell mass and function,” said Juan Pablo Frías, MD, Chief Medical Officer of Biomea Fusion. “Additionally, we have observed benefits consistent with a potential synergy between icovamenib and GLP-1-based medicines, highlighting icovamenib’s potential to complement existing and broadly used therapies. We are eager to continue advancing this novel approach and are working towards bringing a first-in-class, potentially disease-modifying therapy to patients. The ability to restore beta-cell function, thereby improving insulin production and secretion, could be a game-changer for patients with severe insulin deficiency, a population that has long been underserved by current treatment options.”
ATTD 2025 Conference Highlights:
- First Large-Scale Analysis of C-Peptide Response: The data represents the first large-scale assessment of C-peptide levels in icovamenib-treated patients, providing robust evidence supporting its proposed mechanism of action. C-peptide, a key biomarker of endogenous insulin production, demonstrated significant increases, indicating improved pancreatic beta-cell function over 3 months after the final dose of icovamenib.
- OGTT-Based Beta-Cell Function Assessment: An oral glucose tolerance test (OGTT) was conducted at baseline and six timepoints over 26 weeks, providing a detailed evaluation of beta-cell insulin secretory capacity. This test is considered a robust and well-validated method of assessing beta cell insulin secretory capacity via assessment of the C-peptide index, the ratio of plasma C-peptide per unit of glucose. This offers critical insights into icovamenib’s impact on pancreatic beta-cell function.
- C-Peptide Increases in Insulin-Deficient Subgroups: Patients with insulin deficient diabetes (n=45) experienced a mean increase in C-peptide index levels. In particular the severe insulin-deficient diabetes patients who received icovamenib (n=23) experienced the largest mean increase in C-peptide index levels by Week 26 (
53% mean increase from baseline). - Long-Term Beta-Cell Restoration Potential: Insulin deficient patients who received icovamenib (n=45) demonstrated a persistent increase in C-peptide levels beyond the active treatment period, over 3 months after the final dose of icovamenib, suggesting a durable effect on insulin secretion and reinforcing our belief in icovamenib’s potential to drive long-term improvements in beta-cell function.
- Strong Correlation between C-peptide and HbA1c: An analysis of the severe insulin-deficient diabetes subgroup of participants (n=23) who were uncontrolled on at least one prior antihyperglycemic therapy revealed a strong correlation between changes in C-peptide index and HbA1c at Week 26 (r=-0.73). The strong correlation between the improvement in HbA1c and the increase in C-peptide index, 14 weeks after cessation of icovamenib therapy, supports the proposed mechanism of action of icovamenib, a durable improvement in beta-cell function. These data suggests that icovamenib fundamentally impacted the disease, potentially restoring the patient’s ability to produce more insulin, after a short treatment period.
- Precision Medicine Potential: Analysis across different diabetes subtypes demonstrated that icovamenib preferentially increased insulin secretion in insulin-deficient patients, highlighting its potential as a targeted therapy for individuals with severe insulin deficiency, a population with limited treatment options and the highest risk profile.
- Enhanced Impact of GLP-1 based Therapeutic Agents with Icovamenib Combination: Icovamenib enhanced responsiveness of human islets to the GLP-1-based medicines, semaglutide and tirzepatide. Enhancement in beta-cell function was correlated with an increase in the expression levels of the GLP-1 receptor as well as intracellular insulin – both transcript and protein levels were increased. These effects induced by icovamenib may allow lower doses of GLP-1-based medicines to achieve glycemic targets, potentially improving tolerability of these agents.
ATTD 2025 Presentations:
All abstracts will be published in the peer-reviewed Journal of Diabetes Technology & Therapeutics. All presentations and the symposium slides are also available on Biomea Fusion’s Investor Relations Page under the Events section https://investors.biomeafusion.com/news-events.
Global Experts across the Diabetes Field have also Recognized the Significance of these Findings:
“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 proposed 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.
“We do not have an agent today that addresses one of the root causes of diabetes – beta cell dysfunction – icovamenib, if approved, would be the first. Patients in the COVALENT-111 trial have achieved lasting benefits without continuous chronic dosing, suggesting that icovamenib may be disease-modifying. I am very impressed.”
Alice Cheng, M.D., Endocrinologist, Associate Professor of Medicine, University of Toronto.
“The C-peptide data which was presented during ATTD is a meaningful update, as we now have insight into why insulin-deficient patients may respond better to icovamenib treatment. The potential to restore endogenous insulin production capacity is an exciting development in the treatment of type 2 diabetes.”
Jeremy Pettus, M.D., Endocrinologist, Professor of Medicine UCSD.
“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 icovamenib driven inhibition of menin will provide to patients.”
Rohit N. Kulkarni, M.D., Ph.D., Professor of Medicine at Harvard Medical School.
About Menin’s Role in Diabetes
Loss of functional beta-cell mass and function is a core component of the natural history in both types of diabetes – type 1 diabetes (“T1D”) (mediated by autoimmune dysfunction) and type 2 diabetes (“T2D”) (mediated by metabolic dysfunction). 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 have been observed to be diminished, leading to insufficient insulin secretion and hyperglycemia. Menin is thought to act as a brake on beta-ell turnover and growth, supporting the notion that inhibition of menin could lead to the regeneration of normal, healthy beta cells. Based on these and other scientific findings, Biomea is exploring the potential for icovamenib-mediated menin inhibition as a viable therapeutic approach to potentially halt or reverse progression of T2D.
About Type 2 Diabetes
Diabetes is considered a chronic health condition that affects how the body turns food into energy and results in excessive glucose in the bloodstream. Over time, this can cause serious health problems and damage vital organs. Most people with diabetes have a shorter life expectancy than people without this disease. The Centers for Disease Control and Prevention estimates about two in five adults in the United States are now expected to develop diabetes during their lifetime. More than 37 million people of all ages (about
About Icovamenib
Icovamenib is an investigational, orally bioavailable, potent, and selective covalent inhibitor of menin. The molecule was built using Biomea’s FUSION™ System and is designed to regenerate insulin-producing beta cells with the aim to cure diabetes. Icovamenib’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 T1D and T2D, icovamenib could become an important addition and complement to the diabetes treatment landscape once it has successfully completed its ongoing clinical studies and received regulatory approval.
About Biomea Fusion
Biomea is a clinical-stage diabetes and obesity medicines company focused on the discovery and development of oral covalent small molecules to improve the lives of patients with diabetes, obesity, and metabolic disease. 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.
We are utilizing our proprietary FUSION™ System to discover, design and develop a pipeline of next-generation covalent-binding small-molecule medicines designed to maximize clinical benefit for patients. We aim to have an outsized impact on the treatment of disease for the patients we serve. We aim to cure.
Visit us at biomeafusion.com and follow us on LinkedIn, X and Facebook.
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, the potential of BMF-219 as a treatment for T1D and T2D, our research, development and regulatory plans, the progress of our ongoing and planned clinical trials, including COVALENT-111, the availability of data from our clinical trials 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.
Contact:
Meichiel Jennifer Weiss
Sr. Director, Investor Relations and Corporate Development
IR@biomeafusion.com
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