In the presence of R59949, vasopressin- as well as collagen-induced release reaction and aggregation was strongly increased, independently of the formation of arachidonate metabolites[1]. In THP‐1 monocytes, R59949 attenuates CCL2‐evoked Ca2+ signalling with a half‐maximal concentration of 8.6 μM[2]. R59949 inhibits inducible nitric oxide production through decreasing transplasmalemmal L-arginine uptake in vascular smooth muscle cells[4].
Kinase Assay
Cell Assay
Animal Administration
References
[1]. de Chaffoy de Courcelles D, 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. J Biol Chem. 1989;264(6):3274-3285.
[2]. Day P, et al. Inhibitors of DAG metabolism suppress CCR2 signalling in human monocytes. Br J Pharmacol. 2019;176(15):2736-2749.
[3]. Meinhardt G, et al. Effect of novel modulators of protein kinase C activity upon chemotherapy-induced differentiation and apoptosis in myeloid leukemic cells. Anticancer Drugs. 2002;13(7):725-733.
[4]. Shimomura T, et al. R59949, a diacylglycerol kinase inhibitor, inhibits inducible nitric oxide production through decreasing transplasmalemmal L-arginine uptake in vascular smooth muscle cells. Naunyn Schmiedebergs Arch Pharmacol. 2017;390(2):207-214.
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