| Stereochemistry | ACHIRAL |
| Molecular Formula | C18H19ClN4O |
| Molecular Weight | 342.823 |
| Optical Activity | NONE |
| Defined Stereocenters | 0 / 1 |
| E/Z Centers | 0 |
| Charge | 0 |
SHOW SMILES / InChI
SMILES
C[N+]1([O-])CCN(CC1)C2=NC3=CC(Cl)=CC=C3NC4=CC=CC=C24
InChI
InChIKey=OGUCZBIQSYYWEF-UHFFFAOYSA-N
InChI=1S/C18H19ClN4O/c1-23(24)10-8-22(9-11-23)18-14-4-2-3-5-15(14)20-16-7-6-13(19)12-17(16)21-18/h2-7,12,20H,8-11H2,1H3
| Molecular Formula | C18H19ClN4O |
| Molecular Weight | 342.823 |
| Charge | 0 |
| Count |
MOL RATIO
1 MOL RATIO (average) |
| Stereochemistry | RACEMIC |
| Additional Stereochemistry | No |
| Defined Stereocenters | 0 / 1 |
| E/Z Centers | 0 |
| Optical Activity | NONE |
Clozapine N-oxide is a phase 1 metabolite of antipsychotic drug clozapine, produced by oxidation of clozapine by CYP3A4. Clozapine N-oxide is inert with respect to a wide range of GPCRs. It was used a tool compound in the DREADD (designer receptors exclusively activated by designer drugs) system in which a mutated muscarinic G protein-coupled receptor is activated by an otherwise inert compound, however interpretation of experiments is confounded by the ability of clozapine-N-oxide to convert to clozapine upon administration. Clozapine N-oxide exhibits neuroprotective action by inhibiting of microglial NADPH oxidase.
CNS Activity
Approval Year
Targets
| Primary Target | Pharmacology | Condition | Potency |
|---|---|---|---|
Conditions
| Condition | Modality | Targets | Highest Phase | Product |
|---|---|---|---|---|
PubMed
Patents
Sample Use Guides
In a study of reversibility of clozapine metabolism, 100 mg of clozapine N-oxide was orally administered to schizophrenic patients.
Route of Administration:
Oral
To investigate neuroprotective effects of clozapine N-oxide (CNO), the in vitro model of inflammation elicited neurotoxicity was used. Neuron-glia cultures with Escherichia coliendotoxin LPS, and dopamine uptake capacity and cell counts of THir neurons were performed to determine the function and survival of DA neurons 7 days after LPS treatment. Pretreatment with CNO protected DA neurons against an LPS-induced reduction of uptake capacity in a bell-shaped curve with a maximal effect achieved at 0.1 uM.
