Targeted cardiometabolic therapeutics
We are developing a novel, targeted therapy for patients with type 2 diabetes.
Leveraging scientific insights into the intracellular regulation of cortisol, Sparrow is pioneering a precision approach to type 2 diabetes (T2D).
Our lead candidate, clofutriben, is a HSD-1 inhibitor designed to reduce elevated intracellular cortisol – a key driver of impaired glucose control and treatment resistance in millions of patients with T2D.
This novel, differentiated, and complimentary mechanism addresses an underlying cause of metabolic dysfunction across multiple pathways in varied organ systems and may enable improved glycemic control and metabolic health for patients underserved by existing options.
A new way to treat metabolic dysfunction
Nearly half of patients with difficult-to-control diabetes display increased cardiometabolic risk associated with elevated cortisol, yet there are no therapies approved for the vast majority of patients with type 2 diabetes that address this underlying cause of disease.
Cortisol acts across multiple organ system pathways to decrease insulin production, increase insulin resistance, and increase gluconeogenesis.
By utilizing a therapy that inhibits HSD-1, we can lower intracellular levels of cortisol in key metabolic tissues to reduce many of the adverse effects of cortisol excess.
Introducing clofutriben: a highly potent and selective HSD-1 inhibitor
In development for type 2 diabetes with elevated cortisol:
Millions of patients with type 2 diabetes struggle to adequately control their blood sugar levels, leaving them exposed to dangerous health risks. New research suggests that many of these patients have undiagnosed elevated cortisol that is causing or exacerbating their disease.
The targeted agent clofutriben may be perfectly suited to improve glycemic control in this population.
Clofutriben is a once-daily, oral HSD-1 inhibitor designed to reduce intracellular cortisol levels and mitigate the numerous adverse metabolic effects caused or exacerbated by excess cortisol.
