R 59-022 (DKGI-I) hydrochloride is a DGK inhibitor ( IC 50 : 2.8 µM). R 59-022 hydrochloride inhibits the phosphorylation of OAG to OAPA. R 59-022 hydrochloride is a 5-HT Receptor antagonist, and activates protein kinase C (PKC). R 59-022 hydrochloride potentiates thrombin-induced diacylglycerol production in platelets and inhibits phosphatidic acid production in neutrophils. In Vitro R 59-022 (10 μM, 1 min) hydrochloride potentiates aggregation, but not shape change induced by sub-maximal concentrations of thrombin. R 59-022 (30 μM, 0-60 min) hydrochloride increases release of Noradrenaline in chromaffin cells. R 59-022 (40 μM, 30 min) hydrochloride activates PKC in HeLa and U87 cells . R 59-022 (0-10 μM, 4 h) hydrochloride blocks EBOV GP-mediated entry into Vero cells . MCE has not independently confirmed the accuracy of these methods. They are for reference only. Western Blot Analysis Cell Line: HeLa cells Concentration: 40 uM Incubation Time: 30 min Result: Increased the phosphorylation of PKC downstream targets by about 2.5-fold. In Vivo R 59-022 (2 mg/kg, i.p., 12 days) hydrochloride significantly increases median survival in SCID mice implanted with U87 GBM cells . MCE has not independently confirmed the accuracy of these methods. They are for reference only. Animal Model: SCID mice implanted with U87 GBM cells Dosage: 10 mg/kg Administration: Intraperitoneal injection (i.p.) Result: Increased median survival and decreased tumor volume. Form:Solid