Published in the peer-reviewed Journal of the American Society of Nephrology (JASN), this abstract reports on new research led by Dr. Justin Chun and collaborators that identifies interleukin-32 (IL-32) as a key mediator of diabetic chronic kidney disease (CKD).

The findings provide the scientific foundation for Arch Biopartners’ new CKD platform, expanding the Company’s kidney therapeutics pipeline beyond acute injury to chronic disease.

Overview

The research published in JASN shows that the inflammatory protein IL-32 localizes to lipid droplets in kidney tubular cells, where it drives mitochondrial dysfunction contributing to injury in DKD. This is the first evidence that lipid droplets function as inflammatory platforms linking metabolic stress to progressive kidney damage.

In preclinical models, blocking IL-32 reduced tubular injury, while treatment with the SGLT2 inhibitor canagliflozin lowered IL-32 expression, underscoring the immediate clinical relevance of this pathway. As a human-specific cytokine, IL-32 offers a differentiated and targetable mechanism for next-generation therapies and biomarker development in DKD, the leading cause of kidney failure worldwide.

Publication Details

Journal of the American Society of Nephrology, October 2024 - Volume 35 - S, Kidney Week, ...