SAN DIEGO — September 29, 2026
Caspian Therapeutics and Kura Oncology announced new preclinical data for KO-7246, an investigational, orally bioavailable menin inhibitor being developed for diabetes and other cardiometabolic diseases. Presented at the 62nd European Association for the Study of Diabetes (EASD) Annual Meeting in Milan, the data showed that KO-7246 increased functional pancreatic β-cell mass, endogenous insulin production and glycemic control in preclinical models of Type 1 and Type 2 diabetes. In human pancreatic islet models, the compound selectively increased β-cell proliferation and improved glucose-responsive insulin secretion. Caspian said the findings support its development strategy of using menin inhibition to restore endogenous insulin-producing capacity. The company is advancing KO-7246 through IND-enabling development and plans to evaluate the candidate in an initial Phase 1 clinical program.
KO-7246 Demonstrates Durable β-Cell Regeneration
In a rat model of Type 1 diabetes, KO-7246 normalized fasting blood glucose in a majority of animals and increased stimulated C-peptide, a marker of endogenous insulin production. Among responding animals, pancreatic islets regenerated to approximately 40% to 90% of levels observed in healthy controls by Day 56. The company reported that normalized glucose levels and increased C-peptide were maintained for at least one month after treatment was discontinued, while residual β-cell proliferation was negligible. The findings are consistent with the proposed mechanism in which menin inhibition removes a molecular constraint on pancreatic β-cell proliferation and may restore functional β-cell capacity. However, these results are derived from animal models and do not establish clinical efficacy or durability in people with diabetes. Caspian said the response also appeared dependent on the amount of residual β-cell capacity present at baseline.
Preclinical Type 2 Diabetes Data Support Combination Strategy
KO-7246 also reduced fasting blood glucose and increased insulin and C-peptide levels in a mouse model of Type 2 diabetes, while producing a reported 3.4-fold increase in β-cell mass. The compound demonstrated additional activity when combined with semaglutide, suggesting a potential complementary approach alongside established GLP-1-based glucose-lowering therapy. According to Caspian, the increase in insulin was not associated with hypoglycemia in the model. Studies using human pancreatic islets provided further translational evidence, with KO-7246 increasing β-cell proliferation without stimulating proliferation of other islet-cell populations and improving glucose-responsive insulin release. Together, the findings support continued investigation of the candidate as a potential regenerative approach for diabetes, although the therapeutic relevance of the preclinical combination and human-islet findings remains to be established through clinical studies.
Advertisement
Caspian Advances Menin Program Toward Clinical Testing
Caspian is positioning KO-7246 as a highly selective menin inhibitor for diabetes, with the company highlighting pharmacology data from biochemical, cellular and in vivo models. Comparative experiments reported by Caspian indicated that KO-7246 demonstrated menin inhibition in biochemical and cellular assays and produced activity in a menin-dependent leukemia model, while the company reported different pharmacologic findings for BMF-219. In Type 1 diabetes models, Caspian said KO-7246 restored glycemic control and increased β-cell mass, whereas BMF-219 did not produce those effects under the tested conditions. These comparisons are company-generated preclinical findings and do not establish comparative clinical efficacy or safety. Caspian plans to advance KO-7246 through IND-enabling studies toward Phase 1 evaluation, with the longer-term objective of developing menin-directed therapies for diabetes and other cardiometabolic diseases. Management is scheduled to host a virtual investor event on October 13, 2026.
Source :Kura Oncology press release
