| 包装 | 价格(元) |
| 5mg | 电议 |
| 10mg | 电议 |
| 25mg | 电议 |
| 50mg | 电议 |
Cell lines | HIP-009 cells |
Preparation Method | Assessed the effects of NBQX disodium salt and CNQX—antagonists of AMPARs and KARs—on the AMPA- or KA-evoked calcium rise to confirm the functions of these receptors in differentiated HIP-009 cells. |
Reaction Conditions | 30 µM NBQX disodium salt |
Applications | NBQX disodium salt inhibited both AMPA or kainic acid (KA) induced signals in a concentration-dependent manner, with IC50 values being 0.7 ± 0.1 and 0.7 ± 0.03 µM, respectively. The AMPA-evoked calcium rise was completely inhibited by NBQX disodium salt, whereas 68.6% ± 1.3% inhibition of the KA-induced signal was observed with 30 µM of NBQX disodium salt treatment. |
Animal models | Male Wistar rats |
Preparation Method | To observe anti-epileptic effects of NBQX disodium salt in PTZ induced epilepsy,rats into four groups: rats in saline + saline group were treated with saline only; rats in PTZ + saline group were treated with 50 mg/kg of PTZ and saline for 28 days; rats in saline + NBQX disodium salt group were treated with saline for 28 days, and 20 mg/kg of NBQX disodium salt for next 3 days; rats in PTZ + NBQX disodium salt group were treated with 50 mg/kg of PTZ for 28 days and were treated with 20 mg/kg of NBQX disodium salt for next 3 days. Behavioral tests and neurochemical analysis were performed on the following 2 days. |
Dosage form | 20 mg/kg NBQX disodium salt Once daily by intraperitoneal injection for 3 days |
Applications | NBQX disodium salt was sufficient to decrease pentylenetetrazole-induced seizures through increasing the latency to seizures, decrease the duration of seizure onset, and reduce the scores for the severity of seizures. |
| 产品描述 | NBQX disodium salt is a potent, highly selective and competitive antagonist of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) receptors (AMPARs). Inhibition of AMPARs with NBQX disodium salt shows neuroprotective and anticonvulsant activity. In HIP-009 cells, NBQX disodium salt inhibited both AMPA or kainic acid (KA) induced signals in a concentration-dependent manner, with IC50 values being 0.7 ± 0.1 and 0.7 ± 0.03 μM, respectively. The AMPA-evoked calcium rise was completely inhibited by NBQX disodium salt, whereas 68.6% ± 1.3% inhibition of the KA-induced signal was observed with 30 μM of NBQX disodium salt treatment[1]. NBQX disodium salt had an effect on acute seizure development, resulting in a significantly higher number of mice experiencing seizures, an increase in the number of seizures per mouse, a greater cumulative seizure score per mouse and a significantly higher mortality rate among the mice[6]. NBQX disodium salt was sufficient to decrease pentylenetetrazole-induced seizures through increasing the latency to seizures, decrease the duration of seizure onset, and reduce the scores for the severity of seizures[2]. SRS develop after status epilepticus (SE) induced by intrahippocampal injection of kainate. they were markedly suppressed by NBQX disodium salt and perampanel. However, perampanel was less tolerable than NBQX disodium salt in epileptic mice[3]. In Male Wistar rats,Although NBQX disodium salt did not affect nicotine maintenance, it significantly suppressed the drug-paired responding in the relapse session[4]. Adult male Wistar rats were trained in drinking in dark paradigm (3 weeks), and following stable alcohol intake, ketamine, NBQX disodium salt as well as their combination were injected prior to a 90 min drinking session Both doses of ketamine (5 and 10 mg/kg) and NBQX disodium salt (5 and 10 mg/kg) significantly attenuated percent alcohol intake[5]. In mice lacking NCAM and PSA, NBQX disodium salt-induced ataxia proved to be more intense as compared with wild-type mice. On both mutant backgrounds, NBQX disodium salt significantly elevated seizure thresholds during i.v. infusion of the chemoconvulsant pentylenetetrazole[7]. References: |
m.cnreagent.com