Biomea Fusion announces presentation of icovamenib preclinical, clinical data

Biomea Fusion (BMEA) announced the presentation of preclinical and clinical data from studies assessing icovamenib at the Advanced Technologies & Treatments for Diabetes 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. 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. 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 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 experienced a mean increase in C-peptide index levels. In particular the severe insulin-deficient diabetes patients who received icovamenib experienced the largest mean increase in C-peptide index levels by Week 26. Long-Term Beta-Cell Restoration Potential: Insulin deficient patients who received icovamenib 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 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. 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.