DCP-LA

DCP-LA (FR236924), a linoleic acid derivative, selectively and directly activates PKCε. DCP-LA activates Ca(²⁺)/calmodulin-dependent protein kinase II (CaMKII) and inhibits protein phosphatase-1 (PP-1) to stimulate AMPA receptor exocytosis. DCP-LA inhibits activation of caspase-3/-9 and protects neurons at least in part from oxidative stress-induced apoptosis^[1][2][3]. IC50 & Target:PKCε^[1]; CaMKII, PP-1, caspase-3/-9^[3] In Vitro:DCP-LA (100 nM; 15 min) activates cytosolic PKCε by binding to the phosphatidylserine binding/associating sites Arg50 and Ile89, without translocation towards the cell surface in PL-12 cells^[1].
DCP-LA (10, 100, 100 nM; 10 min; 35 ℃) activates CaMKII and inhibits PP-1 in rat hippocampal neurons^[2].
DCP-LA (100 nM; 20 min) increases expression of the receptors on the plasma membrane, responsible for potentiate AMPA receptor responses in rat hippocampal slices^[2].
DCP-LA (100 nM; 10 min) results facilitation of hippocampal synaptic transmission^[2].
DCP-LA (100 nM; 24 h) prevents the Sodium nitroprusside (SNP, HY-10219) effect and rescues neurons from SNP-induced degradation^[3].
DCP-LA (100 nM; 12 h) abolishes the caspase-3/9 activation induced by Sodium nitroprusside (SNP, HY-10219) (1 mM)^[3].
In Vivo:DCP-LA (1 mg/kg; p.o.; once daily; 7 d) exhibits a protective effect against ischemic brain damage, decreasing cerebral cortical defect due to middle cerebral artery (MCA) occlusion in mouse model^[3].