The US Food and Drug Administration has extended the label of finerenone, sold by Bayer as Kerendia, to adults with chronic kidney disease associated with type 1 diabetes. The clearance rests on a single pivotal study of 242 adults, an endpoint that is a urinary biomarker rather than a kidney outcome, and an inferential bridge from two earlier type 2 diabetes outcome trials. Bayer describes it as the first new treatment in more than 30 years for this population. For UK readers the relevant point is jurisdictional: there is no stated MHRA or EMA decision for the type 1 diabetes indication, and nothing in the public record on a NICE appraisal. What follows separates what the trial measured from what the announcements say it means.
What the FDA has approved and on what evidence
The FDA has approved finerenone to reduce urinary albumin-to-creatinine ratio, or UACR, in adults with chronic kidney disease associated with type 1 diabetes. Bayer says the agency granted the expansion after Priority Review of a supplemental New Drug Application, making this the product's third US indication after type 2 diabetes kidney disease in 2021 and heart failure in July 2025.
The wording of the indication is the whole story. Bayer's company announcement states that finerenone is approved to reduce UACR, which is "expected to reduce the risk of sustained estimated glomerular filtration rate (eGFR) decline and end-stage kidney disease" in this population. Expected is doing considerable work in that sentence. The approval does not assert a demonstrated reduction in kidney failure in type 1 diabetes; it accepts a biomarker movement as a surrogate for one.
Bayer says the application was supported by FINE-ONE together with phase 3 data from FIDELIO-DKD and FIGARO-DKD, both conducted in type 2 diabetes, on the basis that UACR reductions in those trials were associated with improved kidney outcomes. That is a class of regulatory reasoning, extrapolation across a related population via a shared biomarker, that UK and EU sponsors and their regulatory consultancy partners will be reading closely, because it sets a template for small-population filings where an outcome trial is not feasible.
The 25% headline against the trial's own figures
Coverage of the approval has settled on a single number. Zacks Investment Research reported a "statistically significant 25% reduction from baseline in the urine albumin-to-creatinine ratio (UACR) over six months compared with placebo", and pharmaphorum reported a 25% reduction from baseline over six months. Bayer's own announcement of the FINE-ONE results does not use 25% at all.
What the company announcement reports is a primary objective of superiority to placebo in reducing UACR over six months, averaged over months 3 and 6, in line with the registered protocol for NCT05901831. Against placebo, the announcement gives a 22% reduction at month 3, with a least squares geometric mean ratio of 0.78 and a 95% confidence interval of 0.68 to 0.90, and a 28% reduction at month 6, ratio 0.72, confidence interval 0.60 to 0.86, with p=0.0001 for the comparison over six months.
So the widely quoted 25% is a mid-point between two timepoints, and it is a ratio, not an absolute difference. No absolute UACR values at baseline or follow-up appear in the material Bayer has released publicly for this approval, and without them the clinical size of the effect cannot be judged. A 28% ratio reduction from a UACR of 800 mg/g and the same reduction from 60 mg/g are not the same event. Detailed results were presented at American Society of Nephrology Kidney Week 2025 and published in the New England Journal of Medicine in March, and absolute values are the figures a UK formulary committee would need.
Context: FINE-ONE enrolled 242 adults and ran its primary assessment over six months, according to Bayer's company announcement. FIDELIO-DKD and FIGARO-DKD, the trials supplying the outcome evidence being bridged from, were conducted in type 2 diabetes.
The adverse event numbers reported in FINE-ONE
Hyperkalaemia was recorded in 10.1% of participants taking finerenone and 3.3% of those on placebo, an absolute difference of 6.8 percentage points, with treatment discontinuation due to hyperkalaemia in 1.7% and 0% respectively. Treatment-emergent adverse events occurred in 47.1% of the finerenone group and 49.2% of placebo. Serious treatment-emergent events were 11.8% and 11.5%. All of these figures come from Bayer's announcement of the trial.
Bayer states that tolerability was consistent with existing evidence in type 2 diabetes kidney disease. Two qualifications belong alongside that. First, 242 participants over six months cannot characterise the frequency of uncommon harms, and the confidence intervals around a 6.8 percentage point potassium signal in a cohort this size would be wide. Second, the population that would receive the drug in NHS renal practice is already on renin-angiotensin blockade, which carries its own potassium burden.
Finerenone is a selective non-steroidal mineralocorticoid receptor antagonist, a class distinct from the steroidal MRAs spironolactone and eplerenone, and its contraindications as listed by Bayer include concomitant use with strong CYP3A4 inhibitors and adrenal insufficiency. Potassium and eGFR monitoring requirements sit in the US prescribing information and are a matter for the prescribing clinician.
Finerenone measured against SGLT2 inhibitors in UK renal pathways
UK renal protection in diabetic kidney disease currently runs on ACE inhibitors or angiotensin receptor blockers plus SGLT2 inhibitors, with GLP-1 receptor agonists increasingly part of the metabolic picture. That infrastructure is licensed, cheap in generic form at the ACE inhibitor layer, and supported by hard outcome data. Finerenone in type 1 diabetes arrives as an addition to standard care, not a replacement for any part of it, which is how FINE-ONE was designed.
The comparator question resolves awkwardly, because the two bodies of evidence are not aligned. SGLT2 inhibitor and GLP-1 evidence in kidney disease is overwhelmingly in type 2 diabetes. A cohort study of more than 75,000 patients with type 2 diabetes, published in the British Medical Journal and reported by Nursing Times in September 2026, found that over an average 32 months of follow-up the renal benefit of these agents appeared only in the 18% of participants with albuminuria, who were 40% less likely than patients on DPP-4 inhibitors to lose significant kidney function over five years. The authors, at Brigham and Women's Hospital in Boston, reported no such effect in patients without albuminuria, and the absolute event rates behind that 40% were not given in the report. The relationship between these agents and cardiovascular risk reduction is a separate evidence stream again.
Read together, the two datasets point the same way on patient selection. Albuminuria is where the measurable benefit of renal-protective pharmacology concentrates, and FINE-ONE selected for it by making UACR the endpoint. That strengthens the positioning argument for finerenone in albuminuric type 1 diabetes and weakens any wider one.
Where UK and EU approval stands
No MHRA or EMA decision on finerenone in type 1 diabetes has been reported. Finerenone is approved for chronic kidney disease associated with type 2 diabetes in Europe, Japan and China, and for heart failure with left ventricular ejection fraction of at least 40% in Europe, Japan, China and several other markets, according to Zacks Investment Research. Approval in the United States confers no availability elsewhere.
The commercial pressure behind a European filing is visible in the numbers. Bayer's first-half finerenone sales rose 75% to more than 600 million euros, pharmaphorum reported, and Zacks put second-quarter growth at 82.9% on US and Chinese volumes, against a company peak sales estimate above 3 billion euros across all indications. Bayer is also pursuing a non-diabetic CKD indication on FIND-CKD, which the company says met its primary endpoint by slowing the annual rate of eGFR decline against placebo, with marketing applications filed in China and Japan. Regulatory decisions of this kind are tracked by trade titles such as BioPharma Dive.
The case against a surrogate-led approval
The strongest objection is straightforward. UACR is a surrogate endpoint, and the evidence that lowering it reduces kidney failure in type 1 diabetes specifically has not been generated; it has been inherited from type 2 diabetes trials in a different population with different disease mechanics. Bayer's own framing concedes the structure of the argument by saying the FIDELIO-DKD and FIGARO-DKD associations were used "to bridge" the evidence across.
Weighing it fairly, the counter-argument has force. Roughly 20% to 30% of people with type 1 diabetes in the US also have CKD on Bayer's figures, and an event-driven outcome trial in that group would take years and a cohort far larger than 242. Regulators accept surrogates precisely when that arithmetic does not work. Dr Janet McGill of Washington University School of Medicine in St Louis, co-chair of the study's executive committee and therefore not an independent voice, said in Bayer's announcement that the population "has continued to face substantial unmet need".
The question for a NICE appraisal, if one follows a UK licence, is different from the question the FDA answered. Cost-effectiveness modelling needs a quantified link between UACR change and avoided dialysis, in type 1 diabetes, at a British price. That link is currently an association carried over from another population.
What would resolve it
Three things remain unknown. The absolute UACR values and dropout rate in FINE-ONE, which the company announcement does not give. Whether Bayer has filed, or will file, for the type 1 diabetes indication with the EMA and the MHRA, neither of which has published a decision. And whether any type 1 diabetes outcome data will follow, from the FINEOVATE programme Bayer says comprises 12 phase 3 studies, or from registry follow-up. Until a UK licence exists there is no appraisal to model and no pathway position to argue over. Clinicians deciding treatment for individual patients should work from the licensed indication in their own territory and from the published trial.
