https://www.selleckchem.com/pr....oducts/abtl-0812.htm
fected cells while sparing and mobilizing healthy immune cells and thereby enable control of EBV-associated lymphoproliferation. Increased β-adrenergic receptor (β-AR) signaling has been shown to promote the creation of an immunosuppressive tumor microenvironment (TME). Preclinical studies have shown that abrogation of this signaling pathway, particularly β2-AR, provides a more favorable TME that enhances the activity of anti-PD-1 checkpoint inhibitors. We hypothesize that blocking stress-related immunosuppressive pathways would impro
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