Researchers have identified the arthritis drug auranofin as a potential treatment for coronary artery disease using a computational drug-repurposing method, according to a study published in Nature Communications on September 2, 2026.
The scientists developed a gene-regulatory network strategy to dissect the molecular architecture of arterial disease. Their framework integrated transcriptional signatures generated by silencing key driver genes of GRN 42, a regulator of human arterial wall foam cells, with drug-induced gene expression profiles sourced from the National Institutes of Health Library of Integrated Network-Based Cellular Signatures program.
Laboratory screening of candidate compounds confirmed the computational predictions in cellular models. Testing demonstrated that auranofin, an FDA-approved gold salt prescribed for rheumatoid arthritis, effectively reduced foam cell formation in vitro. In subsequent animal testing, the drug attenuated both atherosclerosis and inflammation in male mice and rabbits. Furthermore, a retrospective cohort study of patients with rheumatoid arthritis linked auranofin treatment to reduced cardiovascular risk.
Study authors Johan L. M. Bjorkegren and Chiara Giannarelli contributed equally to leading the research, which included teams from the NYU Grossman School of Medicine, the Icahn School of Medicine at Mount Sinai, and the VA Boston Healthcare System. The paper noted that Bjorkegren founded and chairs Clinical Gene Networks, a company developing commercial clinical gene networks for cardiovascular conditions, while Giannarelli disclosed consulting fees from Novartis.
