Including data published for the first time in a peer-reviewed journal, this paper in Inflammation Research (Springer Nature, Volume 75, Article 33, 2026), by a scientific team led by Dr. Justin Chun at the University of Calgary, identifies interleukin-32 (IL-32) as a lipid droplet–associated cytokine that may contribute to tubular injury and inflammation in diabetic kidney disease (DKD). The findings, based on human kidney tissue, show that kidney cells accumulate lipid droplets coated with IL-32, potentially linking metabolic dysregulation to inflammation and disease progression.

The publication builds on earlier findings and strengthens the scientific rationale for Arch Biopartners’ CKD platform, which aims to develop novel therapeutics targeting IL-32 in chronic kidney disease.

Background

Diabetic kidney disease (DKD) is a severe complication of diabetes mellitus and the leading cause of chronic kidney disease worldwide. Among the many drivers of tubular injury, lipid accumulation and inflammation are emerging as major contributors to kidney disease progression, but the molecular link between lipid metabolism and inflammatory signaling remains to be determined.

Publication Details

Inflammation Research (Springer Nature, Volume 75, Article 33, 2026)

Citation

Meadows, ...

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, ...