The US FDA has approved Kerendia (finerenone) for a third indication: reducing urinary albumin-to-creatinine ratio (UACR), which is expected to slow progression to sustained estimated glomerular filtration rate (eGFR) decline and end-stage kidney disease in adults with chronic kidney disease (CKD) associated with type 1 diabetes (T1D). Bayer said the agency granted Priority Review to the supplemental New Drug Application (sNDA), and the company described the approval as the first new therapeutic advance for this patient population in more than 30 years.
The new indication covers once-daily oral finerenone at 10 mg or 20 mg added to standard of care. Approval rested on UACR reduction as a surrogate endpoint, with the label stating this reduction is "expected to" translate into reduced kidney disease progression — a bridging approach supported by UACR-outcome associations established in finerenone's earlier CKD trials in type 2 diabetes (T2D). Finerenone is a non-steroidal mineralocorticoid receptor antagonist (MRA) that selectively blocks mineralocorticoid receptor overactivation in the kidneys and heart, suppressing pro-inflammatory and pro-fibrotic signaling driven by aldosterone excess.
The pivotal FINE-ONE trial (NCT05901831) was a randomized, double-blind, placebo-controlled Phase III study enrolling 242 adults with CKD associated with T1D. The primary endpoint was UACR reduction averaged over months 3 and 6. Finerenone reduced UACR by 22% versus placebo at month 3 and by 28% at month 6 (p=0.0001), with effects sustained throughout the observation period. Hyperkalemia occurred in 10.1% of finerenone-treated patients versus 3.3% on placebo, leading to treatment discontinuation in 1.7% and 0%, respectively. Results were published in the New England Journal of Medicine and presented at the American Society of Nephrology (ASN) Kidney Week 2025, as previously reported.
Unlike steroidal MRAs such as spironolactone and eplerenone, finerenone's non-steroidal structure confers higher MR selectivity and a more balanced kidney-to-cardiac tissue distribution, reducing off-target hormonal effects.