A research team led by scientists from Brigham and Women's Hospital found that Fingolimod interferes with signals sent by lipid receptors, and may reduce the disease-producing activities by cells in the nervous system. The findings suggest the treatment may hold promise for difficult-to-treat secondary progressive MS.
 
According to Francisco Quintana, a researcher in the Ann Romney Center for Neurologic Diseases, "One of the most important unmet clinical needs in MS is to design therapeutic approaches for the progressive phase of the disease, and a key unanswered question related to that is, what are the biological processes that drive disease pathogenesis at this stage?"
 
The study, published in PNAS and led by Quintana sheds new light on the role of sphingosine-1-phosphate, a type of lipid, and its receptors in SPMS. The researchers found that blockage of these signals with Fingolimod had important effects on astrocytes in both mice and humans, decreasing their proinflammatory and neurotoxic properties while also increasing the cells' anti-inflammatory capabilities.
 
The neuroprotective effects the team observed are not as strong as those they have recorded in previous studies of other drugs. The results suggest Fingolimod may help mitigate some aspects of SPMS in humans. A clinical trial of a highly related drug, led by Novartis, is now underway and encouraging preliminary results have been recently released.