paf c 18

PAF C-18 is a naturally occurring phospholipid produced upon stimulation through two distinct pathways known as the remodeling and 'de novo' pathways. It is less potent than PAF C-16 in the induction of platelet aggregation

PAF C-18:1 is a naturally occurring phospholipid produced by cells upon stimulation and plays a role in the establishment and maintenance of the inflammatory response. It is less potent than PAF C-16 and PAF C-18 in the induction of neutrophil chemotaxis, but is equipotent to PAF C-16 and PAF C-18 in promoting eosinophil migration. PAF C-18:1 activates the PAF receptor and has been used in antibody binding experiments to determine the importance of an acyl linkage at the sn-2 position for recognition at this receptor.

Lyso-PAF C-16 is a biologically inactive precursor of platelet activating factor.

2-O-methyl PAF C-16 is a synthetic analog of platelet-activating factor (PAF) featuring a methyl group attached via an ether linkage at the sn-2 position. While the specific biological activities of 2-O-methyl PAF C-16 remain undercharacterized, studies with its C-18 counterpart have demonstrated its ability to modulate various biological processes. These processes include reducing plasma membrane fluidity and hindering the invasiveness of tumor cells in embryonic chick hearts. Furthermore, in rat astrocytes, the C-18 analog prompts the release of significant amounts of nitric oxide (NO) through a mechanism that involves the activation of nitric oxide synthase (NOS).

C-Met-IN-18, an ATP-competitive type-III inhibitor, targets both wild-type (WT) and D1228V mutant c-MET with IC50 values of 0.013 µM and 0.20 µM, respectively. It is utilized in research pertaining to c-MET-driven cancers [1].

2-O-Ethyl PAF C-16, a homolog of Platelet-activating Factor (PAF) and competitive ligand for the Platelet-activating Factor Receptor (PAFR), inhibits the binding of PAF antagonist WEB 2086 to PAFR with an IC50 of 21 nM [1].

PAF C-16 is a naturally occurring phospholipid produced upon stimulation through two distinct pathways known as the remodeling and 'de novo' pathways. It is a potent mediator of neutrophil migration and the production of reactive oxygen species and IL-6. Pathological processes involving PAF include necrotizing enterocolitis

L-threo-Sphingosine C-18 is a protein kinase C inhibitor.

Methylcarbamyl PAF C-16 is a stable analog of PAF C-16 with a half-life greater than 100 minutes in platelet poor plasma due to its resistance to degradation by PAF-AH. It is nearly equipotent with PAF C-16 in its ability to induce platelet aggregation both in isolated platelets and in platelet-rich plasma. In NRK-49 cells overexpressing the PAF receptor, both PAF C-16 and methylcarbamyl PAF C-16 cause the induction of c-myc and c-fos and the activation of mitogen-activated protein kinase. Methylcarbamyl PAF C-16 induces G1 phase cell cycle arrest, suggesting a potential role for PAF in the inhibition of oncogenic transformation.