Felzartamab

The 2025 ASN Kidney Week in Houston, TX marked a pivotal moment in nephrology, signaling a shift from broad-stroke treatments toward precision-driven approaches tailored to individual patient needs. From groundbreaking therapies for rare glomerular diseases to the first major advances in Type 1 Diabetes-related CKD in decades, the meeting highlighted how innovation is reshaping care. Generative AI emerged as a powerful tool for uncovering disease subtypes and guiding drug development, while advances in xenotransplantation, APOL1-targeted therapies, and novel biological pathways pointed to a future where treatment is increasingly personalized, predictive, and proactive. In this blog, Dr. Ajay Srivastava, Vice President, Medical Department, reflects on these key takeaways from 2025 ASN Kidney Week and what they mean for the future of renal drug development. Marked a transition for nephrology, moving from “broad-stroke” treatments like SGLT2 inhibitors toward Precision Nephrology. Meeting was dominated by breakthroughs in rare glomerular diseases, the first major therapeutic advance for Type 1 Diabetes (T1D) with CKD in decades, and the rising role of generative AI in drug discovery. The 2025 meeting featured several “practice-changing” trials, particularly in the fields of T1D, IgA Nephropathy (more detailed review later in this summary) and Alport Syndrome. Several notable biological pathways emerged as the primary focus for future drug development: BAFF/APRIL Dual Inhibition: This was the highlight for IgA Nephropathy. Drugs like Atacicept and Telitacicept target these two cytokines to deplete the pathogenic B-cell populations responsible for Gd-IgA1 production. Aldosterone Synthase Inhibition (ASI): Unlike traditional MRAs, ASIs like Lorundrostat block the production of aldosterone itself. This addresses “aldosterone escape,” a common issue where aldosterone levels rise despite ACE/ARB therapy. See also below additional meeting highlights. APOL1-Mediated Kidney Disease (AMKD): A major focus on precision medicine for Black patients. Discussion centered on small molecule inhibitors (like Inaxaplin) that specifically target the toxic function of APOL1 risk variants (G1/G2) in podocytes. See also below additional meeting highlights. NOX1/4 & Oxidative Stress: The Setanaxib data highlighted a shift toward targeting Reactive Oxygen Species (ROS) to combat interstitial fibrosis, particularly in genetic conditions like Alport Syndrome. Anti-CD38 Platform: Felzartamab was highlighted for its ability to target long-lived plasma cells, which are often resistant to standard anti-CD20 (Rituximab) therapy in refractory glomerular diseases. The 2025 meeting confirmed that IgAN treatment has moved well past simple BP control and steroid use. Phase 3 data for BAFF/APRIL inhibitors showed remarkable efficacy with surprisingly manageable safety profiles. The “Advances in Research” conference showcased how AI is moving beyond “chatbots” into structured science. Spatial Proteomics/Lipidomics: Sessions (e.g., Pinaki Sarder, PhD) discussed how AI can now map specific proteins and lipids directly onto a biopsy slide with sub-cellular resolution. This allows us to see exactly where a drug like an SGLT2i is active versus where fibrosis is still pervasive. “Digital Twins” [virtual models] in Trials: Dr. Navdeep Tangri’s group presented on using AI to create prognostic enrichment models. Using AI to select only the “fast progressors” for trials, which significantly increases the power of a study with a smaller sample size. Pathology 2.0: Generative AI is being used to “reconstruct” 3D models of the glomerulus from 2D slides, identifying podocyte foot process effacement that was previously only visible via expensive Electron Microscopy. APOL1-mediated kidney disease (AMKD) was a major focus, specifically for its role in health disparities. Inaxaplin: New data showed that small molecule inhibition of the APOL1 pore is not just stopping progression but potentially reversing some podocyte damage in FSGS patients with high-risk genotypes. Mechanism: Focus is on the G1/G2 variants which cause a “gain of toxicity” through pore formation in the podocyte membrane, leading to cell death. Inaxaplin: New data showed that small molecule inhibition of the APOL1 pore is not just stopping progression but potentially reversing some podocyte damage in FSGS patients with high-risk genotypes. Mechanism: Focus is on the G1/G2 variants which cause a “gain of toxicity” through pore formation in the podocyte membrane, leading to cell death. This was the first major trial in 30 years to show a significant reduction in albuminuria (25%) specifically in Type 1 Diabetes patients. Until now, they were largely excluded from the big MRA/SGLT2 trials. With decades of experience conducting phase I-IV nephrology clinical trials, Medpace is a globally recognized leader in nephrology clinical research. Our seasoned medical in-house nephrologists, operational, and regulatory teams are fully embedded throughout your project – providing unmatched support for your program. Combined with our strong site network and KOL relationships to accelerate development and enhance patient recruitment, we’ve successfully led Phase III studies (several to regulatory approval) in key indications such as acute kidney injury, chronic kidney disease, glomerulonephritis, genetic and rare kidney diseases, and renal transplantation.