R-59-949

R-59-949 is an inhibitor of diacylglycerol kinase α (DGK-α) with an IC₅₀ value of 300 nM in isolated platelet plasma membranes using exogenous diacylglycerol as a substrate.¹ DGK-α inhibition with R-59-949 increases diacylglycerol-dependent PKC activity, serotonin secretion, and aggregation of thrombin-stimulated platelets. R-59-949 inhibits DGK-α activity induced by platelet-derived growth factor (PDGF) in intact vascular smooth muscle cells (VSMCs).² It inhibits high K⁺- and glucose-induced insulin secretion in MIN6 pancreatic β-cells in a dose-dependent manner.³ In vivo, administration of R-59-949 prevents retinal neovascularization in a mouse model of oxygen-induced retinopathy.⁴

WARNING This product is not for human or veterinary use.

1. de Chaffoy de Courcelles, D., Roevens, P., Van Belle, H., et al. The role of endogenously formed diacylglycerol in the propagation and termination of platelet activation. A biochemical and functional analysis using the novel diacylglycerol kinase inhibitor, R 59 949. The Journal of Biological Chemisty 264(6), 3274-3285 (1989).

2. Du, X., Jiang, Y., Qian, W., et al. Fatty acids inhibit growth-factor-induced diacylglycerol kinase alpha activation in vascular smooth-muscle cells. Biochem J. 357(Pt. 1), 275-282 (2001).

3. Kurohane Kaneko, Y., Kobayashi, Y., Motoki, K., et al. Depression of type I diacylglycerol kinases in pancreatic β-cells from male mice results in impaired insulin secretion. Endocrinology 154(11), 4089-4098 (2013).

4. Yang, L., Xu, Y., Li, W., et al. Diacylglycerol kinase (DGK) inhibitor II (R59949) could suppress retinal neovascularization and protect retinal astrocytes in an oxygen-induced retinopathy model. J. Mol. Neurosci. 56(1), 78-88 (2015).