Abstract: SA-PO1264
Protecting the Kidney Without Compromising Cancer Therapy: Integrin α3β1 Antibody Treatment for Chemotherapy-Induced Injury
Session Information
- Onconephrology: Epidemiological Trends, Risk Stratification, and Clinical Outcomes
October 24, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Onconephrology
- 1600 Onconephrology
Authors
- Balza Pineda, Santiago, Allosite Therapeutics, MIAMI, Florida, United States
- Lopez-Rodriguez, Darlah M., Allosite Therapeutics, MIAMI, Florida, United States
- Gonzalez-Lerma, Paola, Allosite Therapeutics, MIAMI, Florida, United States
- Barbosa, Antonio, Allosite Therapeutics, MIAMI, Florida, United States
- Gupta, Vineet, The University of Texas Medical Branch at Galveston, Galveston, Texas, United States
Background
Chemotherapy-induced kidney injury remains a major-dose limiting toxicity that compromises cancer treatment, worsens patient outcomes, and limits therapeutics options for patients with pre-existing renal vulnerability. Podocyte injury and disruption of the glomerular filtration barrier are key contributors to chemotherapy-associated proteinuria and progressive renal dysfunction. Integrin α3β1 is highly expressed in podocytes and plays a central role in maintaining podocyte adhesion, cytoskeletal organization, and glomerular basement membrane attachment. We hypothesize that activation of integrin α3β1 using a protective agonist antibody can preserve podocyte structure and function during chemotherapy exposure, thereby reducing kidney injury without interfering with anti-tumor efficacy.
Methods
Here we evaluate a candidate anti-integrin a3 antibody as a renal-protective biologic in models of chemotherapy-induced nephrotoxicity. In vitro studies revealed antibody-mediated enhancement of podocyte adhesion, cytoskeletal stability, and survival under chemotherapy-associated injury conditions. Lead candidates will be tested for their ability to prevent albuminuria, histopathologic glomerular damage, and podocyte loss following chemotherapy challenge. Finally, to evaluate renal protection in the setting of active malignancy and concurrent chemotherapy, we incorporated a tumor-bearing mouse model.
Results
We anticipate that treatment with the anti-integrin α3 antibody will enhance podocyte adhesion and cytoskeletal stability under chemotherapy-induced stress conditions. In vivo, antibody treatment is expected to prevent albuminuria and preserve renal function limiting glomerular injury. This approach will allow simultaneous assessment of kidney protection, antibody safety, tumor compatibility and preservation of chemotherapeutic anti-tumor activity.
Conclusion
Successful completion of this work will provide proof-of-concept for first-in-class integrin α3β1-targeted strategy to protect the kidney during cancer therapy. By evaluating renal protection in both nephrotoxicity and tumor-bearing models, this approach is designed to support development of a tumor-compatible biologic therapy that reduces chemotherapy-associated kidney injury while preserving anti-cancer activity.