The hypothesis of inhibitory signaling of sesamol in platelet activation. Collagen binds to its receptors, and then activates both the PLCγ2-DAG-PKC and NF-κB pathways. Activated phospholipase Cγ2 (PLCγ2) catalyses phosphatidylinositol 4,5-bisphosphate (PI4,5-P2) into 1,2-diacylglycerol (DAG) and inositol 1,4,5-trisphosphate (IP3). DAG activates protein kinase C (PKC), followed by phosphorylation of a 47-kDa protein (p47). IP3 induces the release of Ca2+ from the dense tubular system (DTS). On the other hand, IKKβ activates NF-κB signaling including IκBα degradation and p65 phosphorylation, which further activates the PLCγ2-PKC pathway. Sesamol can activate cyclic AMP-protein kinase A (PKA), followed by inhibition of both the PLCγ2 and NF-κB cascade (i.e., IKKβ), and finally inhibits platelet activation.