Bruton's Tyrosine Kinase Inhibitors for Multiple Sclerosis Treatment: A New Frontier

BTK presents a novel and exciting therapeutic target in MS. Based on its role in the activation of autoreactive B cells, inhibition of BTK may result in fewer relapses and potentially less progression independent of relapse activity. Additionally, inhibition of BTK results in blunting of the proinflammatory phenotype of microglia. This alteration of microglia may therapeutically benefit patients by preventing neurodegeneration. Although multiple agents are undergoing study in phase 3 trials, practitioners should be wary of lumping these medications into a "class" with shared efficacy and/or safety experiences. The profoundly unique pharmacologic characteristics of the medications, including binding site specificity, CNS penetration, half-life, and enzyme inhibition properties will mandate that each agent be judged on its own data. If one agent achieves therapeutic success for progressive disease, it does not mean that all will. Similarly, if one agent is associated with certain adverse events or side effects, it does not mean that all will. Regardless of these caveats, the potential addition of new medications with novel mechanisms of action to the therapeutic arsenal in MS is an exciting and welcome milestone.