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 ...

Published in the peer reviewed journal BMJ Open (March 2024, Vol 14, Issue 3), this paper by key members of the Arch Biopartners scientific team, led by Dr. Daniel Muruve at the University of Calgary, and their collaborators, describes the clinical highlights, outcomes and biomarker results of the study.

The results of the Phase II trial provided first-ever evidence validating Dipeptidase-1 (DPEP1) as a mediator of organ inflammation and therapeutic target in humans. In addition, LSALT peptide was well tolerated with no safety issues related to the drug.

The Phase II trial was an international, multicenter, randomized, double-blind, placebo-controlled, proof of concept study of LSALT peptide for the prevention of organ inflammation such as acute respiratory distress syndrome (ARDS) and acute kidney injury (AKI) in hospitalised patients infected with SARS-CoV-2. The exploratory, adaptive trial was initiated in the early stages of the global pandemic to ...

Published in the AAAS journal Science Advances this paper by key members of the Arch Biopartners scientific team led by Dr. Daniel Muruve at the University of Calgary, and their collaborators, demonstrated the mechanism by which DPEP-1 regulates the recruitment of leukocytes (i.e. inflammation) to the kidney following ischemia reperfusion injury, which is injury that occurs after a reduction in blood flow to the kidney. Ischemia reperfusion injury is a common cause of AKI in humans undergoing cardiac surgery or kidney transplantation.

Importantly, the study also confirmed the mechanism of action of two DPEP-1 inhibitors, the LSALT peptide (Metablok) and cilastatin that effectively protected the kidney during ischemia reperfusion injury. Both the LSALT peptide and cilastatin are protected by composition and method of use patents for AKI respectively and held by Arch Biopartners.

Publication Details

Science Advances, ...