The FDA has approved the drug FTY720 for the treatment of multiple sclerosis.

Specifically, Hla and colleagues outlined a mechanism by which FTY270 causes S1P receptor degradation on the cells lining the blood vessels of the lungs and found that this reduction in S1P receptor levels causes leakage of the blood vessel contents into the lungs, impairing lung function. In contrast, S1P receptor degradation appears not to be required for the effects of FTY720 on immune cells, which are the effects that mediate its therapeutic efficacy. Hla and colleagues therefore suggest that developing a drug that does not act on S1P receptor on the cells lining the blood vessels of the lungs but does target S1P receptor on immune cells may provide a therapeutic with decreased side effects.
Source-Eurekalert