170568-47-5
基本信息
Imidazo[1,5-a]quinoline-3-carboxylic acid, 7-chloro-5-[[(3R,5S)-3,5-dimethyl-1-piperazinyl]carbonyl]-, 1,1-dimethylethyl ester, rel-
物理化学性质
| 密度 | 1.33±0.1 g/cm3(Predicted) |
| 储存条件 | -20°C储存 |
| 溶解度 | 溶于二甲基亚砜 |
| 酸度系数(pKa) | 8.16±0.60(Predicted) |
常见问题列表
PNU-101017 potentiates GABA-stimulated Cl - currents at low concentrations (<1 μM). U-101017 concentration-dependently inhibits the binding of [ 3 H]FNZ to the membrane preparation of rat cerebral cortex in vitro with K i of 3.37±0.22 nM.
Pre-ischemic treatment with either PNU-101017 significantly protects the CA1 neuronal population, and PNU-101017 reduces the loss to 50%. Delaying PNU-101017 administration until immediately after reperfusion does not reduce the neuroprotective activity. U-101017 (30 μmol/kg, p.o.) time-dependently blocks [ 3 H]FNZ binding to the mouse cerebral cortex. U-101017 dose-dependently decreases the levels of cGMP with ED 50 s of 260.0 (163-425) and 0.37 (0.12-1.04) in nonstressed and foot shock-stressed mice, respectively. Flumazenil, an antagonist of GABAA receptors, has no significant effect on cGMP in nonstressed mice, but pretreatment with flumazenil significantly blocks U-101017 (10 μmol/kg, p.o.)-induced reductions in cGMP. In stressed mice, flumazenil is ineffective in altering cerebellar cGMP, but pretreatment with these doses of flumazenil significantly (p < 0.01) blocks U-101017-induced attenuation of stress-induced elevations in cGMP.