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Liao X, Zeng Q, Xie L, et al

Insufficient or disorganized TJ complex formation, an expression of claudin-1 with decreased levels of claudin-5 trans interaction, and claudin-5/ZO-1 interaction in leaky vessels (219) are among the proposed mechanisms behind an incomplete recovery of BBB permeability

The c-MET receptor tyrosine kinase is overexpressed in H69 cells and is inducible by exogenous HGF, resulting in induction of tyrosine phosphorylation at the major autophosphorylation sites pY1230/1234/1235 in the catalytic kinase domain, and also the pY1003 site in the juxtamembrane domain of c-MET (Figure 1)

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No oncological concerns specific to the TREK-1 blockade mechanism have been identified

Drug interactions have not been extensively studied, warranting caution when combined with immunomodulatory or anticoagulant medications