PAF (C16) is a potent MAPK and MEK/ERK activator that induces increased vascular permeability. PAF (C16) (PAF (C16)) is a platelet-activating factor, a phospholipid-derived mediator and a ligand for PAF G protein-coupled receptor (PAFR). PAF (C16) has shown anti-apoptotic and anti-inflammatory activity in vitro, inhibiting Caspase-dependent apoptosis by interacting with its receptor (PAF-R) to perform cell signaling.

In PAFR+/+ cultures, C16-PAF (PAF (C16); 0.5-1.5 μM; for 24 hours) does not elicit significant concentration-dependent neuronal loss, whereas it does induce significant concentration-dependent neuronal loss in PAFR?/? cultures. Specifically, C16-PAF (1 μM) induces neuronal death in PAFR?/? cells infected with EGFP alone[1].In PAFR neurons, C16-PAF (1 μM; for 24 hours) activates caspase 7 but not caspase 3[1].
Synthesized by two distinct pathways, the remodeling pathway and the de novo synthesis pathway, C16-PAF acts by binding to a unique G-protein-coupled seven-transmembrane receptor[2][3].
Furthermore, C16-PAF (1-25 μg/ml; 6, 12, 24 h) exhibits time-dependent inhibition of M. smegmatis and M. bovis BCG growth[3].