DCP-LA

DCP-LA is a derivative of linoleic acid (Item No. 90150) and a potent activator of PKCε.¹ It activates PKCε with a greater than 7-fold stronger potency over PKCα, βI, βII, γ, δ, μ, η, and ζ in a cell-free assay. DCP-LA activates PKC in PC12 cells in a concentration-dependent manner, an effect that is blocked by the PCK inhibitor bisindolylmaleimide I (Item Nos. 13298 | 21180) and a PCKε-selective peptide inhibitor. It decreases intracellular levels of amyloid-β (Aβ) in Neuro2 neuroblastoma cells transfected with human APPSwe/PS1Δ9.² DCP-LA also stimulates hippocampal glutamate release, striatal dopamine release, and hypothalamic serotonin release in rat brain slices in a PKC- and α7-containing nicotinic acetylcholine receptor-dependent manner.³ In vivo, DCP-LA (3 mg/kg, i.p.) prevents synaptic loss and amyloid plaque formation and decreases escape latency in the Morris water maze in the 5XFAD transgenic mouse model of Alzheimer's disease.⁴

WARNING This product is not for human or veterinary use.

1. Kanno, T., Yamamoto, H., Yaguchi, T., et al. The linoleic acid derivative DCP-LA selectively activates PKC-ε, possibly binding to the phosphatidylserine binding site. J. Lipid. Res. 47(6), 1146-1156 (2006).

2. Nelson, T.J., Cui, C., Luo, Y., et al. Reduction of β-amyloid levels by novel protein kinase Cϵ activators. The Journal of Biological Chemisty 284(50), 34514-34521 (2009).

3. Shimizu, T., Kanno, T., Tanaka, A., et al. α, β-DCP-LA selectively activates PKC-ε and stimulates neurotransmitter release with the highest potency among 4 diastereomers. Cell Physiol. Biochem. 27(2), 149-158 (2011).

4. Hongpaisan, J., Sun, M.-K., and Alkon, D.L. PKC ε activation prevents synaptic loss, Aβ elevation, and cognitive deficits in Alzheimer’s disease transgenic mice. J. Neurosci. 31(2), 630-643 (2011).