Stereochemistry | ACHIRAL |
Molecular Formula | C28H38N2O2 |
Molecular Weight | 434.6135 |
Optical Activity | NONE |
Defined Stereocenters | 0 / 0 |
E/Z Centers | 0 |
Charge | 0 |
SHOW SMILES / InChI
SMILES
CCCCN(CCCC)CCCOC1=CC=C(C=C1)C(=O)C2=C(CC)C=C3C=CC=CN23
InChI
InChIKey=NRTGWAAGLRTUJZ-UHFFFAOYSA-N
InChI=1S/C28H38N2O2/c1-4-7-17-29(18-8-5-2)19-11-21-32-26-15-13-24(14-16-26)28(31)27-23(6-3)22-25-12-9-10-20-30(25)27/h9-10,12-16,20,22H,4-8,11,17-19,21H2,1-3H3
Molecular Formula | C28H38N2O2 |
Molecular Weight | 434.6135 |
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 |
Butoprozine increased the action potential duration like amiodarone, depressed the plateau phase like verapamil and decreased the amplitude and the maximum rate of depolarization. Butoprozine injected intravenously depressed sino-atrial node function, lengthened A-V nodal conduction time and the A-V nodal refractory period, and prolonged the atrial refractory period. Thus butoprozine acted preferentially on parts of the myocardial tissue where the slow inward current seems to be particularly involved. In this respect, butoprozine was more active than amiodarone, but in contrast to this drug, butoprozine did neither prolong the ventricular monophasic action potential duration nor the ventricular refractory period.