969P Effect of angiotensin II inhibition on non-small cell lung cancer response to immune checkpoint blockers

The renin-angiotensin system (RAS) is an important signaling system within the tumor microenvironment, promoting both malignant and stromal cell proliferation. Angiotensin II (AngII) is the main effector hormone, acting predominantly by the signaling of angiotensin II type 1 receptor (AT1R). Preclinical data show that AngII increases TGF-β production through AT1R signaling and decreases TGF-β through AT2R signaling. Thus, the overlap of these pathways may have a critical role in carcinogenesis, as well as immune evasion and inhibiting AT1R may enhance clinical responses in combination with immune checkpoint inhibitors (ICI).