Drug-like molecule halts inflammation, could prevent progression of MS
Scientists at the Walter and Eliza Hall Institute of Medical Research in Melbourne, Australia, have developed a new drug-like molecule with the ability to inhibit a key signal that triggers inflammation in the body. The scientists say the molecule has already shown promise for putting the brakes on the progression of multiple sclerosis (MS).
Although still not completely understood, MS is widely believed to be triggered by an over-active immune system damaging cells that produce myelin, an electrically insulating material that is essential for the proper functioning of the nervous system.
"Inflammation results when our immune cells release hormones called cytokines, which is a normal response to disease," says Dr Ueli Nachbur. "However when too many cytokines are produced, inflammation can get out-of-control and damage our own body, all of which are hallmarks of immune or inflammatory diseases."
The small drug-like molecule developed by Dr Nachbur and his colleagues is called WEHI-345 and prevents the release of inflammatory cytokines by binding to and inhibiting a key immune signaling protein called RIPK2.
"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 per cent of cases," says Professor Andrew Lew. "These results are extremely important, as there are currently no good preventive treatments for MS."
Because WEHI-345 only delayed signaling rather than blocking it, Dr Nachbur says the molecule will be used to further investigate the pathway responsible for producing inflammatory cytokines, with the goal of developing a stronger inhibitor of RIPK2.
The team hopes WEHI-345 will ultimately lead to the development of new treatments for not only MS, but other inflammatory diseases.
"Not only is this a potential new treatment," says Dr Nachbur. "It is a great tool we can use to unravel this signaling pathway and identify other important proteins that control inflammation that could be a drug target."
The team's research was published in the journal Nature Communications.
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