The United States Food and Drug Administration (FDA) has granted approval to KERENDIA® (finerenone) for the treatment of chronic kidney disease (CKD) associated with type 1 diabetes (T1D). This landmark decision, announced by Bayer on September 17, marks the first time in over three decades that a new pharmacological intervention has been approved to specifically address the progression of kidney disease in the type 1 diabetes patient population. The approval focuses on the reduction of the urinary albumin-to-creatinine ratio (UACR), a clinical marker that serves as a proxy for the risk of sustained decline in the estimated glomerular filtration rate (eGFR) and the eventual onset of end-stage kidney disease (ESKD).
The FDA’s decision followed a Priority Review of Bayer’s supplemental New Drug Application (sNDA), a designation reserved for treatments that offer significant improvements over existing options or provide a treatment where none exists. For patients with type 1 diabetes, the management of kidney complications has long relied on blood pressure control and glucose management, primarily utilizing ACE inhibitors or ARBs. However, these therapies often fall short of halting the progression toward dialysis or transplantation. The introduction of finerenone, a non-steroidal mineralocorticoid receptor antagonist (MRA), represents a paradigm shift in the standard of care.
A New Era for Chronic Kidney Disease Management in Type 1 Diabetes
Chronic kidney disease is a common and devastating complication of diabetes, characterized by the progressive loss of renal function. While much of the recent pharmaceutical innovation has targeted type 2 diabetes, the type 1 population has remained largely underserved. Type 1 diabetes involves an autoimmune destruction of insulin-producing beta cells, leading to absolute insulin deficiency. Over time, high blood sugar levels cause inflammation and fibrosis in the kidneys.
Finerenone operates differently from previous generations of MRAs. Traditional steroidal MRAs, such as spironolactone or eplerenone, are often limited by side effects like hyperkalemia (excessive potassium levels) and hormonal imbalances. As a non-steroidal MRA, KERENDIA binds to mineralocorticoid receptors with high potency and selectivity. By blocking these receptors, which are overactivated in patients with CKD and diabetes, the drug reduces the inflammatory and fibrotic processes that drive kidney damage.
Dr. Janet McGill, Professor of Medicine at Washington University School of Medicine and Co-Chair of the FINE-ONE study’s Executive Committee, emphasized the clinical void this approval fills. She noted that for more than 30 years, physicians have had "limited options" to address the risk of kidney disease progression in this specific cohort. The approval provides an oral, once-daily treatment option that directly targets the physiological drivers of renal decline.
The FINE-ONE Clinical Trial: Data and Outcomes
The FDA’s approval was primarily supported by data from the FINE-ONE trial (NCT05901831), a pivotal Phase III, global, randomized, double-blind study. The trial was designed to evaluate whether KERENDIA, when added to the current standard of care, could outperform a placebo in reducing albuminuria—a key indicator of kidney stress and damage.
The study enrolled 242 adult participants with CKD and type 1 diabetes. Patients were randomized to receive either 10 mg or 20 mg of KERENDIA once daily or a placebo. The primary objective was to measure the change in UACR over a six-month period. The results, which were presented at the American Society of Nephrology (ASN) Kidney Week 2025 and subsequently published in the New England Journal of Medicine, demonstrated a statistically significant reduction in UACR among those treated with finerenone compared to the placebo group.
The reduction in UACR is critical because it is a modifiable risk factor. Clinical evidence from previous trials in type 2 diabetes—specifically the FIDELIO-DKD and FIGARO-DKD studies—has already established that lowering UACR leads to a direct reduction in the risk of end-stage kidney disease and cardiovascular death. By bridging this evidence to the type 1 population through the FINE-ONE results, the FDA recognized the potential for finerenone to alter the long-term trajectory of renal health for T1D patients.
Expanding Indications and the Clinical Timeline
The September 2026 approval for type 1 diabetes is the latest in a series of regulatory milestones for KERENDIA. Since its initial entry into the market, the drug has rapidly expanded its therapeutic reach:
- July 2021: Initial FDA approval for KERENDIA to reduce the risk of sustained eGFR decline, end-stage kidney disease, cardiovascular death, non-fatal myocardial infarction, and hospitalization for heart failure in adults with CKD associated with type 2 diabetes.
- July 2025: The FDA approved the drug for a second indication: reducing the risk of cardiovascular death and heart failure-related hospitalizations or urgent visits in adults with heart failure and a left ventricular ejection fraction (LVEF) of 40% or greater.
- September 2026: The current approval for CKD associated with type 1 diabetes, solidifying the drug’s role as a versatile tool in cardio-renal metabolic medicine.
Carolina Aldworth, M.D., MSc, Executive Medical Director at Bayer, highlighted that this third indication validates the "breadth of its clinical trial program" and addresses a population that has historically been clinically underserved.
Arrowhead Pharmaceuticals Reports Breakthrough Data in Hypertriglyceridemia
In a separate but equally significant development for metabolic medicine, Arrowhead Pharmaceuticals presented Phase 3 data for its investigational drug, plozasiran. During the European Society of Cardiology (ESC) Congress 2026 in Munich, Germany, the company revealed results from the SHASTA-3 and SHASTA-4 studies. These trials focused on patients with severe hypertriglyceridemia (sHTG), a condition characterized by dangerously high levels of triglycerides in the blood, which significantly increases the risk of acute pancreatitis (AP).
Severe hypertriglyceridemia is often defined as triglyceride levels exceeding 500 mg/dL. For many patients, diet and existing medications are insufficient to bring these levels into a safe range. Plozasiran is an RNA interference (RNAi) therapeutic designed to reduce the production of Apolipoprotein C-III (APOC3), a key regulator of triglyceride metabolism.
Deep Reductions in Triglycerides and Pancreatitis Risk
The SHASTA-3 and SHASTA-4 trials met all primary and secondary endpoints. Across a pool of 757 patients, those treated with plozasiran (25 mg administered subcutaneously every three months) experienced median triglyceride reductions of 79% and 81% at Month 12. Perhaps more importantly, more than 90% of treated patients saw their triglyceride levels drop below the critical 500 mg/dL threshold, and over half achieved levels below 150 mg/dL, which is considered normal.
The most striking clinical outcome, however, was the reduction in acute pancreatitis events. Acute pancreatitis is a painful and potentially life-threatening inflammation of the pancreas. In a pooled analysis, plozasiran reduced the rate of all AP events by 78% compared to a placebo. In high-risk patients—those with a prior history of pancreatitis and TG levels above 500 mg/dL—the drug reduced the event rate by a staggering 91%. This translates to a "Number Needed to Treat" (NNT) of only 3 to prevent one episode of pancreatitis over one year in high-risk individuals.
James Hamilton, MD, MBA, Chief Medical Officer at Arrowhead, noted that the reduction in AP events became "increasingly more meaningful in patients at higher risk," suggesting that plozasiran could become a cornerstone of preventative care for this population.
Safety Profile and Regulatory Future
Plozasiran demonstrated a favorable safety profile. While some patients (14.3%) reported worsening glycemic control compared to the placebo group (8.7%), the mean HbA1c levels showed minimal change, suggesting that the drug did not significantly disrupt long-term glucose management. Other common side effects included minor injection-site reactions and diarrhea. Crucially, there were no signals of liver toxicity or significant platelet count changes, which are often concerns with RNA-based therapies.
Arrowhead Pharmaceuticals has announced plans to seek global marketing authorization, starting with an sNDA filing with the FDA before the end of 2026. To expedite this process, the company purchased an FDA Priority Review Voucher, which could shorten the review period by several months, potentially bringing the drug to market by mid-2027.
Broader Implications for Metabolic and Renal Health
The dual announcements from Bayer and Arrowhead underscore a significant trend in modern medicine: the move toward highly targeted, molecular-level therapies for chronic metabolic conditions.
For the millions of adults living with type 1 diabetes, the approval of KERENDIA offers a shield against the most feared complication of the disease—kidney failure. By reducing UACR, clinicians can now intervene earlier and more effectively, potentially delaying the need for dialysis by years or even decades. This has profound implications not only for patient quality of life but also for healthcare economics, as the cost of managing end-stage renal disease is a massive burden on global health systems.
Similarly, the success of plozasiran represents a major advancement in lipidology. By utilizing RNAi technology to silence the APOC3 gene, Arrowhead has demonstrated that it is possible to achieve near-normal lipid levels in patients who were previously considered "untreatable." The dramatic reduction in pancreatitis events suggests that this therapy will move beyond mere "number management" to provide tangible protection against acute medical emergencies.
As these two therapies move into clinical practice, they represent a new standard of "precision endocrinology," where treatments are tailored to the specific biological pathways of the disease, offering hope to populations that have waited decades for innovation.
