| Stereochemistry | ACHIRAL |
| Molecular Formula | C15H10BrF3N6O |
| Molecular Weight | 427.179 |
| Optical Activity | NONE |
| Defined Stereocenters | 0 / 0 |
| E/Z Centers | 0 |
| Charge | 0 |
SHOW SMILES / InChI
SMILES
FC(F)(F)C1=CC(NC(=O)NC2=CC=C(Br)C=C2C3=NN=NN3)=CC=C1
InChI
InChIKey=JXPULDIATMTIIN-UHFFFAOYSA-N
InChI=1S/C15H10BrF3N6O/c16-9-4-5-12(11(7-9)13-22-24-25-23-13)21-14(26)20-10-3-1-2-8(6-10)15(17,18)19/h1-7H,(H2,20,21,26)(H,22,23,24,25)
| Molecular Formula | C15H10BrF3N6O |
| Molecular Weight | 427.179 |
| Charge | 0 |
| Count |
MOL RATIO
1 MOL RATIO (average) |
| Stereochemistry | ACHIRAL |
| Additional Stereochemistry | No |
| Defined Stereocenters | 0 / 0 |
| E/Z Centers | 0 |
| Optical Activity | NONE |
NS3623 is a human ether-a-go-go (hERG) KV11.1 potassium channel activator. It was shown that treatment of transgenic mouse model of sickle cell disease (SAD mice) with NS3623 improves erythrocyte hydration and diminishes sickling, probably by lowering of the Cl-conductance, which limits salt and concomitant water loss mediated by the Gardós channel, that makes NS3623 antisickling agent in vivo
Approval Year
PubMed
Patents
Sample Use Guides
SAD mice (transgenic mouse model of sickle cell disease): were treated for 3 weeks with 2 daily administrations of 10, 35, and 100 mg/kg NS3623
Route of Administration:
Oral
Application of the hERG agonist NS3623 (10 uM) prolonged the QRS rate dependently. A significant prolongation (16 +/- 6%) was observed at short basic cycle length (BCL 90 ms) but not at longer cycle lengths (BCL 250 ms). The effect could be reversed by the I(Kr) blocker E4031 (1 uM). While partial I(Na) inhibition with flecainide (1 uM) alone prolonged the QRS (34 +/- 3%, BCL 250 ms), the QRS was further prolonged by 19 +/- 2% when NS3623 was added in the presence of flecainide. These data suggest that the effect of NS3623 was dependent on sodium channel availability.
