For research use only. Not for therapeutic Use.
NPS2390 is a group I mGlu antagonist. It displays noncompetitive antagonist activity at both mGlu1 and mGlu5 receptors. NPS2390 is thought to act on a site separate from the glutamate binding pocket.
| Catalog Number | I008336 |
| CAS Number | 226878-01-9 |
| Synonyms | NPS2390; NPS 2390; NPS-2390.;N-(1-adamantyl)quinoxaline-2-carboxamide |
| Molecular Formula | C19H21N3O |
| Purity | ≥95% |
| Target | Neuronal Signaling |
| Solubility | Soluble in DMSO |
| Storage | Store at RT |
| IUPAC Name | N-(1-adamantyl)quinoxaline-2-carboxamide |
| InChI | InChI=1S/C19H21N3O/c23-18(17-11-20-15-3-1-2-4-16(15)21-17)22-19-8-12-5-13(9-19)7-14(6-12)10-19/h1-4,11-14H,5-10H2,(H,22,23) |
| InChIKey | ZKFVOZCCAXQXBU-UHFFFAOYSA-N |
| SMILES | C1C2CC3CC1CC(C2)(C3)NC(=O)C4=NC5=CC=CC=C5N=C4 |
| Reference | 1:Biochem Biophys Res Commun. 2017 Apr 29;486(2):589-594. doi: 10.1016/j.bbrc.2017.03.097. Epub 2017 Mar 20. Calcium-sensing receptor antagonist NPS2390 attenuates neuronal apoptosis though intrinsic pathway following traumatic brain injury in rats.Xue Z,Song Z,Wan Y,Wang K,Mo L,Wang Y, PMID: 28336431 DOI: 10.1016/j.bbrc.2017.03.097 </br><span>Abstract:</span> Traumatic brain injury (TBI) initiates a complex cascade of neurochemical and signaling changes that leads to neuronal apoptosis, which contributes to poor outcomes for patients with TBI. Previous study indicates that calcium-sensing receptor (CaSR) activation contributes to neuron death in focal cerebral ischemia-reperfusion mice, however, its role in neuronal apoptosis after TBI is not well-established. Using a controlled cortical impact model in rats, the present study was designed to determine the effect of CaSR inhibitor NPS2390 upon neuronal apoptosis after TBI. Rats were randomly distributed into three groups undergoing the sham surgery or TBI procedure, and NPS2390 (1.5 mg/kg) was infused subcutaneously at 30 min and 120 min after TBI. All rats were sacrificed at 24 h after TBI. Our data indicated that NPS2390 significantly reduced the brain edema and improved the neurological function after TBI. In addition, NPS2390 decreased caspase-3 levels and the number of apoptotic neurons. Furthermore, NPS2390 up-regulated anti-apoptotic protein Bcl-2 expression and down-regulated pro-apoptotic protein Bax, and reduced subsequent release of cytochrome c into the cytosol. In summary, this study indicated that inhibition of CaSR by NPS2390 attenuates neuronal apoptosis after TBI, in part, through modulating intrinsic apoptotic pathway.Copyright © 2017 Elsevier Inc. All rights reserved. |
