Anti-Inflammatory Molecule Halts Progression of Multiple Sclerosis

Multiple sclerosis (MS) inflammation can be stopped with a newly developed molecule that functions like a drug, according to findings published in Nature Communications.

Researchers from the Walter and Eliza Hall Institute in Australia developed a drug-like molecule which they called WEHI 345 designed to bind to and inhibit an immune system-signaling protein called RIPK2, which prevents the release of inflammatory cytokines in MS. The researchers aimed to examine the potential of WEHI 345 to treat immune diseases in experimental animal models of MS. They found that cytokine production was halted in both in vitro and in vivo models of MS.

“We treated preclinical models with WEHI 345 after symptoms of MS first appeared, and found it could prevent further progression of the disease in 50 percent of cases,” explained researcher Ueli Nachbur in a press release. “These results are extremely important, as there are currently no good preventive treatments for MS.”

The researchers were driven to create the molecule because of MS currently has no real cure — but there is “a desperate need for new and better treatments,” the press release emphasized. The inflammatory disease damages the central nervous system, including the brain, spinal cord, and optic nerves.

“This molecule will be a great starting point for a drug discovery program that may one day lead to new treatments for MS and other inflammatory diseases,” concluded researcher Guillame Lessene in the statement. “This signaling pathway must be finely balanced, because WEHI 345 only delayed signaling rather than blocked it. Nevertheless, this delay is enough to completely shut off cytokine production.”

In the future, the researchers want to use WEHI 345 to further investigate the signaling pathway that produces inflammatory cytokines in order to develop a better and stronger inhibitor of RIPK2 for treating various inflammatory diseases.

“Our study highlights the importance of the kinase activity of RIPK2 for proper immune responses and demonstrates the therapeutic potential of inhibiting RIPK2 in inflammatory diseases,” the authors concluded in the paper.