Vitae Earns $8M Milestone from Boehringer Ingelheim
Firm identified a lead 11beta-HSD-1 inhibitor candidate for the treatment of diabetes.!--h2>
Vitae Pharmaceuticals achieved a milestone in its collaboration with Boehringer Ingelheim, triggering an $8 million payment. The partnership is centered around 11beta-hydroxysteroid dehydrogenase (HSD)-1 inhibitors for diabetes and other metabolic diseases.
“The quality of the lead candidate and the speed at which the program progresses is a testament to the efficiency of our work together with Boehringer Ingelheim,” says Richard Gregg, M.D., Vitae’s CSO. “Our lead may have potential as a once-a-day drug for treating diabetes and other metabolic syndrome related indications.”
Vitae and Boehringer Ingelheim initiated their agreement in October 2007. The companies combined their research programs, working together to identify and advance novel 11beta-HSD-1 inhibitors for clinical development.
Vitae received $36.5 million in up-front and committed payments and is eligible to receive up to $300 million in milestones based on the achievement of development, regulatory, and commercial program goals. Further milestone payments may be achieved with additional compounds and/or additional approved indications.
Vitae will receive royalties on sales of products commercialized under the collaboration. The initial research term was for two years, however, the companies recently agreed to extend the term into 2010.
11beta-HSD-1 is an enzyme that converts the biologically inactive steroid cortisone into the active hormone cortisol. Cortisol is known to cause resistance to the action of insulin in multiple target tissues including liver, muscle, and adipose tissue. Overexpression of 11beta-HSD-1 in mouse adipose tissue leads to a metabolic syndrome-like phenotype including increased central obesity, hypertension, impaired glucose tolerance, and hypertriglyceridemia.
In contrast 11beta-HSD-1 knockout mice resist visceral obesity and diabetes through improved function of insulin in liver and adipose tissues, consistent with the beneficial effects of enzyme inhibition. Early evidence has shown that inhibiting 11beta-HSD-1 can reduce glucose and lipids in diabetic patients.