| Stereochemistry | ACHIRAL |
| Molecular Formula | C23H26N2O |
| Molecular Weight | 346.4653 |
| Optical Activity | NONE |
| Defined Stereocenters | 0 / 0 |
| E/Z Centers | 0 |
| Charge | 0 |
SHOW SMILES / InChI
SMILES
OC1=CC2=C(NC=C2CCCCN3CCC(=CC3)C4=CC=CC=C4)C=C1
InChI
InChIKey=HGEYJZMMUGWEOT-UHFFFAOYSA-N
InChI=1S/C23H26N2O/c26-21-9-10-23-22(16-21)20(17-24-23)8-4-5-13-25-14-11-19(12-15-25)18-6-2-1-3-7-18/h1-3,6-7,9-11,16-17,24,26H,4-5,8,12-15H2
| Molecular Formula | C23H26N2O |
| Molecular Weight | 346.4653 |
| 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 |
Roxindole (EMD-49,980) is a dopaminergic and serotonergic drug which was originally developed for the treatment of schizophrenia. Roxindole has also been investigated as a therapy for the major depressive disorder, Parkinson's disease, and prolactinoma. Roxindole is dopamine autoreceptor-selective agonistic drug with high affinity to D2-like receptors and with much lower affinities to D1-like, % and ol2, muscarinic and 5HT 2 receptors. Additionally, Roxindole exerts 5HT uptake inhibition and 5HT1A agonistic effects. The bioavailability of Roxindole has been estimated at 5% due to a high first-pass metabolization. On the other hand, in 14C distribution studies, Roxindole has crossed the blood-brain barrier readily and the brain concentrations at all intervals have been much higher than corresponding plasma levels. In clinical trials, Roxindole ‘s antipsychotic efficacy was only modest but it was unexpectedly found to produce potent and rapid antidepressant and anxiolytic effects. However, the clinical development of Roxindole was discontinued.
CNS Activity
Originator
Approval Year
Doses
Overview
| CYP3A4 | CYP2C9 | CYP2D6 | hERG |
|---|---|---|---|
OverviewOther
| Other Inhibitor | Other Substrate | Other Inducer |
|---|---|---|
Drug as perpetrator
Drug as victim
Tox targets
PubMed
Patents
Sample Use Guides
Roxindole was administered at increasing daily doses from 0.3 to 30 mg for 28 days.
Route of Administration:
Oral
Roxindole activity was evaluated in [35S]GTPγS binding assay. Membranes of CHO cells stably expressing recombinant human 5-HT1A receptor were treated with [35S]GTPγS (0.1 nM) in assay buffer (HEPES (20 mM), pH 7.4, NaCl (100 mM), GDP (3 µM), MgCl2 (3 mM)) for 20 min at 22 °C. Efficacy is expressed as the increase in [35S]GTPγS binding observed with the agonist relative to that induced by a maximally effective concentration (10 µM) 5HT.
