NNC 711 is an anticonvulsant agent and a selective GABA uptake inhibitor (1,2).
NO-711 hydrochloride is suitable for use as γ-aminobutyric acid (GABA) transporter-1 (GAT-1) antagonists or GABA uptake inhibitor.
Potent and selective inhibitor of GABA uptake by GAT-1 (IC 50 values are 0.04, 171, 1700 and 622 μ M for hGAT-1, rGAT-2, hGAT-3 and hBGT-1 respectively). Anticonvulsant following systemic administration in vivo .
NO-711 is a potent and selective GABA uptake inhibitor that crosses the blood-brain barrier.
NNC-711 (0.25-3 mg/kg; i.p.; 30 min prior to training) prevents amnesia for a passive avoidance task induced by the acetylcholine receptor antagonist Scopolamine (HY-N0296) in male Wistar rat[2].
NNC-711 (0.5-3 mg/kg; i.p.; immediately prior to occlusion) protects against ischemia-induced death of CA1 pyramidal neurons in a model of bilateral common carotid artery occlusion in the gerbil[2].
NNC-711 (0.5-1.5 mg/kg; i.p.; immediately prior to training) exhibits significant cognition-enhancing actions in postnatal day 80 male and 28-month old female Wistar rats[2].
NNC-711 (NO-711) (50-200 μg/10 μL; i.t.; once) effectively develops analgesic effect in sciatic nerve CCI rats modelc[3].
NNC-711 (0.3-30 mg/kg, i.p.; 30 min before testing) exhibits anticonvulsant effects in Multiple mices and rats epilepsy model[4].
| Animal Model: | DMCM (HY-100369A)-induced seizures in female NMRI mice (20 g), pentylenetetrazole-induced seizures in male NMRI mice and male albino Wistar SPF rats (150-200 g), Audiogenic seizures in male DBA/2 mice (8 g) [4] |
| Dosage: | 0.3-30 mg/kg |
| Administration: | Intraperitoneal injection (i.p.); 30 min prior to the seizure test |
| Result: | Inhibited DMCM-induced clonic seizures in NMRI mice with an ED50 = 1.2 mg/kg. |
| Animal Model: | Postnatal day 80 male Wistar rats (300-350 g)[2] |
| Dosage: | 0.25, 0.5, 1, 3 mg/kg |
| Administration: | Intraperitoneal injection (i.p.); 30 min prior to training |
| Result: | Significantly reversed the amnesia induced by scopolamine administration 6-h post-training when retrieval was tested at 24-h post-training.
Had no effect on learning in the 0.25-0.5 mg/kg dose range, and induced amnesia at 3.0 mg/kg.
Not to directly interact with the cholinergic system, but rather to have a more general neuroprotective action on the consolidation process.
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| Animal Model: | Postnatal day 80 male Mongolian gerbils (50-65 g)[2] |
| Dosage: | 0.5, 3 mg/kg |
| Administration: | Intraperitoneal injection (i.p.); immediately prior to occlusion |
| Result: | Administrated immediately prior to occlusion significantly reduced CA1 cell death. |
| Animal Model: | Postnatal day 80 male Wistar rats (300-350 g) and 28-month old female Wistar rats[2] |
| Dosage: | 0.5, 1.5 mg/kg |
| Administration: | Intraperitoneal injection (i.p.); immediately prior to training |
| Result: | Significantly reduced escape latencies in both mature postnatal day 80 and aged 28 months rats.
Improved rats ability to locate the hidden platform at 0.5 mg/kg, but the effect was reduced at 1.5 mg/kg.
Had no effect on memory retention.
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| Animal Model: | Sciatic nerve chronic constriction injury (CCI) rats[3] |
| Dosage: | 50, 100, 200 μg/10 μL |
| Administration: | Intrathecal (i.t.); once |
| Result: | Increased withdrawal thresholds (WT) and withdrawal latency (WL) values after 1 day compared with CCI + saline group.
The maximum value of WT was achieved 3 days after administration and maximum value of WL was achieved 1 day after administration.
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![1,2,5,6-Tetrahydro-1-[2-[[(diphenylmethylene)amino]oxy]ethyl]-3-pyridinecarboxylic acid hydrochloride Structure](/CAS/GIF/145645-62-1.gif)
