Currently Enrolling Trials
Kerendia (finerenone) is a non-steroidal mineralocorticoid receptor antagonist.
Kerendia is specifically indicated to reduce the risk of sustained eGFR decline, end-stage kidney disease, cardiovascular death, nonfatal myocardial infarction, and hospitalization for heart failure in adult patients with chronic kidney disease (CKD) associated with type 2 diabetes.
Kerendia is supplied as tablets for oral administration. Measure serum potassium levels and estimated glomerular filtration rate (eGFR) before initiation of treatment. Do not initiate treatment if serum potassium is > 5.0 mEq/L.
For patients who are unable to swallow whole tablets, Kerendia may be crushed and mixed with water or soft foods such as applesauce immediately prior to use and administered orally.
The recommended starting dose of Kerendia is based on eGFR. The target daily dose of Kerendia is 20 mg.
|eGFR (mL/min/1.73m2||Starting Dose|
|≥ 60||20 mg once daily|
|≥ 25 to < 60||10 mg once daily|
|< 25||Not Recommended|
Mechanism of Action
Kerendia (finerenone) is a nonsteroidal, selective antagonist of the mineralocorticoid receptor (MR), which is activated by aldosterone and cortisol and regulates gene transcription. Finerenone blocks MR mediated sodium reabsorption and MR overactivation in both epithelial (e.g., kidney) and nonepithelial (e.g., heart, and blood vessels) tissues. MR overactivation is thought to contribute to fibrosis and inflammation. Finerenone has a high potency and selectivity for the MR and has no relevant affinity for androgen, progesterone, estrogen, and glucocorticoid receptors.
Adverse effects associated with the use of Kerendia may include, but are not limited to, the following:
Clinical Trial Results
The FDA approval of Kerendia was based on results of the pivotal Phase III FIDELIO-DKD trial. The randomized, double-blind, placebo-controlled, multicenter study in adult patients with CKD associated with T2D, defined as either having an UACR of 30 to 300 mg/g, eGFR 25 to 60 mL/min/1.73 m2 and diabetic retinopathy, or as having an UACR of ≥300 mg/g and an eGFR of 25 to 75 mL/min/1.73 m2. The trial excluded patients with known significant non-diabetic kidney disease and a clinical diagnosis of chronic heart failure with reduced ejection fraction and persistent symptoms (NYHA class II to IV). All patients were to have a serum potassium ≤4.8 mEq/L at screening and be receiving standard of care background therapy, including a maximum tolerated labeled dose of an angiotensin-converting enzyme inhibitor (ACEi) or angiotensin receptor blocker (ARB). A total of 5,674 patients were randomized to receive Kerendia (N=2833) or placebo (N=2841) and were followed for a median of 2.6 years.
Over a median of 10.8 months, a primary-outcome event occurred in 897 of 2526 patients (35.5%) in the vericiguat group and in 972 of 2524 patients (38.5%) in the placebo group. A total of 691 patients (27.4%) in the vericiguat group and 747 patients (29.6%) in the placebo group were hospitalized for heart failure. Death from cardiovascular causes occurred in 414 patients (16.4%) in the vericiguat group and in 441 patients (17.5%) in the placebo group. The composite of death from any cause or hospitalization for heart failure occurred in 957 patients (37.9%) in the vericiguat group and in 1032 patients (40.9%) in the placebo group. Symptomatic hypotension occurred in 9.1% of the patients in the vericiguat group and in 7.9% of the patients in the placebo group, and syncope occurred in 4.0% of the patients in the vericiguat group and in 3.5% of the patients in the placebo group.