N-(p-Amylcinnamoyl) anthranilic Acid (ACA), a cell permeable inhibitor of PLA2, has been reported to inhibit α-ketoisocaproic acid and glyceraldehyde-induced insulin secretion, as well as glucose-induced insulin secretion. Additionally, by inhibiting PLA2, ACA consequentially suppresses glucose-induced arachidonic acid formation in cells. Furthermore, research has shown ACA to modulate the activity of different transient receptor potential channels. In particular, ACA's blocking ability of diacylglycerol-activated TRP channels is of special interest since it offers the opportunity to interfere with receptor-induced Ca2+-dependent signaling processes in vascular smooth muscle cells and platelets.