| Stereochemistry | ACHIRAL |
| Molecular Formula | C31H44N2O10.2ClH |
| Molecular Weight | 677.61 |
| Optical Activity | NONE |
| Defined Stereocenters | 0 / 0 |
| E/Z Centers | 0 |
| Charge | 0 |
SHOW SMILES / InChI
SMILES
Cl.Cl.COC1=CC(=CC(OC)=C1OC)C(=O)OCCCN2CCCN(CCCOC(=O)C3=CC(OC)=C(OC)C(OC)=C3)CC2
InChI
InChIKey=VILIWRRWAWKXRW-UHFFFAOYSA-N
InChI=1S/C31H44N2O10.2ClH/c1-36-24-18-22(19-25(37-2)28(24)40-5)30(34)42-16-8-12-32-10-7-11-33(15-14-32)13-9-17-43-31(35)23-20-26(38-3)29(41-6)27(21-23)39-4;;/h18-21H,7-17H2,1-6H3;2*1H
| Molecular Formula | C31H44N2O10 |
| Molecular Weight | 604.6885 |
| 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 |
| Molecular Formula | ClH |
| Molecular Weight | 36.461 |
| Charge | 0 |
| Count |
MOL RATIO
2 MOL RATIO (average) |
| Stereochemistry | ACHIRAL |
| Additional Stereochemistry | No |
| Defined Stereocenters | 0 / 0 |
| E/Z Centers | 0 |
| Optical Activity | NONE |
Dilazep is a coronary and cerebral vasodilator as an adenosine reuptake inhibitor. Dilazep is an inhibitor of platelet aggregation and of membrane transport of nucleosides. Dilazep is also known to have a vasodilating effect on renal vessels and is often used in patients with ischaemic heart disease, cerebral ischemia or renal dysfunction to improve tissue circulation.
Originator
Approval Year
Doses
AEs
Overview
| CYP3A4 | CYP2C9 | CYP2D6 | hERG |
|---|---|---|---|
OverviewOther
| Other Inhibitor | Other Substrate | Other Inducer |
|---|---|---|
Drug as perpetrator
Drug as victim
Tox targets
PubMed
Sample Use Guides
Dilazep dihydrochloride was administered orally at 300 mg/day for 24 months in 15 of these patients
Route of Administration:
Oral
The effect of dilazep or adenosine on the mechanical function was examined in both palmitoyl-L-camitine (PALCAR) treated heart (PALCAR-treated heart experiments) and normal (PALCAR-untreated) heart (normal heart experiments). Dilazep, adenosine or vehicle was infused into the aortic cannula for 45 mm at a constant flow rate of 0.1 ml/min. In the PALCAR-treated heart experiments, PALCAR was infused into the aortic cannula at the constant flow rate of 0.1 ml /min for 10 min from 10 min after the start of infusion of dilazep, adenosine or vehicle. The experimental condition and protocol of the normal heart experiments were essentially the same as in the PALCAR-treated heart experiments, except for an infusion of KHB buffer instead of PALCAR solution. In each group, LVSP, LVEDP and LVDP were recorded continuously before and during the infusion of dilazep, adenosine or vehicle.
