For research use only. Not for therapeutic Use.
NPS2390（Cat No.:I008336）is a selective inhibitor of the ion channel TRPC6 (transient receptor potential cation channel subfamily C member 6), which is involved in regulating calcium influx in various cells. TRPC6 plays a key role in processes such as vascular smooth muscle contraction, neuronal signaling, and cardiac function. Overactivation of TRPC6 has been implicated in diseases like heart failure, hypertension, and certain neurological disorders. NPS2390 is being investigated for its potential therapeutic applications in these conditions. Preclinical studies suggest that targeting TRPC6 with NPS2390 may help modulate calcium-related dysfunctions and improve outcomes in cardiovascular and neurodegenerative diseases.
| 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. |
