Kura Oncology has launched Caspian Therapeutics, a separately financed company developing small-molecule menin inhibitors for diabetes and cardiometabolic diseases, after closing a $50 million financing that included Eli Lilly and Company.
BVF Partners led the financing, with participation from the T1D Fund, Invus, Montanova, Lilly, Kura, members of Kura’s leadership team and several biotechnology entrepreneurs.
Caspian was formed around KO-7246, a selective menin inhibitor designed for chronic metabolic diseases, along with related intellectual property and know-how contributed by Kura. The financing is intended to fund investigational new drug-enabling work and initial clinical proof-of-concept studies of KO-7246 in diabetes. It will also support a second menin inhibitor candidate for diabetes and cardiometabolic diseases.
Kura will retain an ownership stake of about 50% in Caspian on a fully diluted basis and hold board representation. Caspian will have dedicated leadership and outside funding while accessing Kura research, development and corporate functions through an intercompany services arrangement.
Kura said the structure allows it to continue focusing on its oncology strategy while retaining an interest in the new company.
Diabetes is associated with the loss or dysfunction of pancreatic beta cells, which produce insulin. Caspian’s approach is intended to increase the number and function of beta cells rather than solely manage blood glucose or replace insulin.
Menin is a scaffold protein involved in gene expression and acts as a regulator of beta-cell proliferation. Kura said its preclinical research found that menin inhibition selectively stimulated beta-cell proliferation, increased functional beta-cell mass and raised endogenous insulin production across Type 1 and Type 2 diabetes animal models.
The company said improvements in insulin production and glycemic control continued after treatment was stopped in those models. It also reported selective beta-cell proliferation and improved beta-cell function in human pancreatic islet microtissues and organoid systems, without observed proliferation of non-beta cells.
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