Diseases

Heart failure is one of the largest unmet needs in medicine — and half of its patients have almost no effective options.

60M+

people worldwide are living with heart failure

>50%

of heart failure patients have preserved ejection fraction (HFpEF)

1 class

of drugs — SGLT2 inhibitors — has shown clear efficacy in HFpEF

Heart failure with preserved ejection fraction

In HFpEF, the heart contracts normally but cannot relax and fill properly. It represents more than half of all heart failure worldwide, is growing with the aging population, and has historically resisted nearly every therapy that works in reduced ejection fraction. SGLT2 inhibitors are the only drug class with demonstrated efficacy in this population — which makes the mechanism behind that efficacy, PANK1 activation, an extraordinary starting point for new medicine.

The energy hypothesis

A failing heart is an energy-starved heart. Coenzyme A sits at the center of every major fuel pathway the heart uses — sugars, fats, amino acids, and ketones — and CoA levels are depleted in failing human hearts. PANK1 controls the first and rate-limiting step of CoA synthesis. By activating PANK1 selectively, CoArdia aims to restore the heart's capacity to produce energy and improve its ability to contract and relax.

Beyond the limits of SGLT2 inhibition

The side effects of SGLT2 inhibitors — including urinary tract infections and euglycemic diabetic ketoacidosis — arise from their action on SGLT2 in the kidney, not from PANK1. A selective PANK1 activator is designed to capture the cardiac benefit while leaving those liabilities behind and may allow dosing beyond the ceiling that SGLT2-related effects impose.