ACA是一种广谱磷脂酶 A2 (PLA2) 的抑制剂，TRP channel的阻滞剂。ACA 也是一种有效的钙离子激活氯通道 (calcium-activated chloride channels) 的可逆抑制剂，有潜力用于心律失常的相关研究。 ACA通过抑制人血小板中的磷脂酶A2（PLA2）来抑制肾上腺素刺激的血栓烷生成。还阻断胰岛中葡萄糖诱导的胰岛素分泌。具有中等程度的白三烯拮抗剂活性。 ACA可阻断肾上腺素刺激的血小板中血栓烷的产生。抑制肺泡II型细胞中ATP刺激的磷脂酰胆碱（PC）分泌。还可以阻断佛波酯和A23187诱导的II型细胞中PC的分泌。据报道可阻断胰腺β细胞中葡萄糖诱导的胰岛素分泌。表现出中等程度的白三烯拮抗剂活性。 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.