For research use only. Not for therapeutic Use.
C16-PAF (PAF (C16)), a phospholipid mediator, is a platelet-activating factor and ligand for PAF G-protein-coupled receptor (PAFR). C16-PAF exhibits anti-apoptotic effect and inhibits caspase-dependent death by activating the PAFR. C16-PAF is a potent MAPK and MEK/ERK activator. C16-PAF induces increased vascular permeability[1][2][3][4][5].
C16-PAF (PAF (C16); 0.5-1.5 μM; for 24 hours) elicits significant concentration-dependent neuronal loss in PAFR?/? but not PAFR+/+ cultures. C16-PAF (1 μM) elicits neuronal death in PAFR?/? cells infected with EGFP alone[1]. ?
C16-PAF (1 μM; for 24 hours) activates caspase 7 but not caspase 3 in PAFR?/? neurons[1]. ?
C16-PAF is 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]. ?
C16-PAF (1-25 μg/ml; 6, 12, 24 h) inhibits M. smegmatis and M. bovis BCG growth in a time-dependent manner[3].
| Catalog Number | I010654 |
| CAS Number | 74389-68-7 |
| Synonyms | [(2R)-2-acetyloxy-3-hexadecoxypropyl] 2-(trimethylazaniumyl)ethyl phosphate |
| Molecular Formula | C26H54NO7P |
| Purity | ≥95% |
| InChI | InChI=1S/C26H54NO7P/c1-6-7-8-9-10-11-12-13-14-15-16-17-18-19-21-31-23-26(34-25(2)28)24-33-35(29,30)32-22-20-27(3,4)5/h26H,6-24H2,1-5H3/t26-/m1/s1 |
| InChIKey | HVAUUPRFYPCOCA-AREMUKBSSA-N |
| SMILES | CCCCCCCCCCCCCCCCOCC(COP(=O)([O-])OCC[N+](C)(C)C)OC(=O)C |
| Reference | [1]. Scott D Ryan, et al. Heterogeneity in the sn-1 carbon chain of platelet-activating factor glycerophospholipids determines pro- or anti-apoptotic signaling in primary neurons. J Lipid Res. 2008 Oct;49(10):2250-8. [2]. Z Honda, et al. Transfected platelet-activating factor receptor activates mitogen-activated protein (MAP) kinase and MAP kinase kinase in Chinese hamster ovary cells. J Biol Chem. 1994 Jan 21;269(3):2307-15. [3]. Muhammad S Riaz, et al. Direct Growth Inhibitory Effect of Platelet Activating Factor C-16 and Its Structural Analogs on Mycobacteria. Front Microbiol. 2018 Sep 11;9:1903. [4]. Jing Chu, et al. IGHG1 Regulates Prostate Cancer Growth via the MEK/ERK/c-Myc Pathway. Biomed Res Int. 2019 Jul 4;2019:7201562. [5]. Nina Bögershausen, et al. RAP1-mediated MEK/ERK pathway defects in Kabuki syndrome. J Clin Invest. 2015 Sep;125(9):3585-99. |
