| Stereochemistry | ABSOLUTE |
| Molecular Formula | C17H18ClNO.C4H4O4 |
| Molecular Weight | 403.856 |
| Optical Activity | UNSPECIFIED |
| Defined Stereocenters | 1 / 1 |
| E/Z Centers | 1 |
| Charge | 0 |
SHOW SMILES / InChI
SMILES
OC(=O)\C=C/C(O)=O.CN1CCC2=CC(Cl)=C(O)C=C2[C@H](C1)C3=CC=CC=C3
InChI
InChIKey=FGHVSEXHEAUJBT-HFNHQGOYSA-N
InChI=1S/C17H18ClNO.C4H4O4/c1-19-8-7-13-9-16(18)17(20)10-14(13)15(11-19)12-5-3-2-4-6-12;5-3(6)1-2-4(7)8/h2-6,9-10,15,20H,7-8,11H2,1H3;1-2H,(H,5,6)(H,7,8)/b;2-1-/t15-;/m1./s1
| Molecular Formula | C17H18ClNO |
| Molecular Weight | 287.784 |
| Charge | 0 |
| Count |
MOL RATIO
1 MOL RATIO (average) |
| Stereochemistry | ABSOLUTE |
| Additional Stereochemistry | No |
| Defined Stereocenters | 1 / 1 |
| E/Z Centers | 0 |
| Optical Activity | UNSPECIFIED |
| Molecular Formula | C4H4O4 |
| Molecular Weight | 116.0722 |
| Charge | 0 |
| Count |
MOL RATIO
1 MOL RATIO (average) |
| Stereochemistry | ACHIRAL |
| Additional Stereochemistry | No |
| Defined Stereocenters | 0 / 0 |
| E/Z Centers | 1 |
| Optical Activity | NONE |
SCH-23390 is a potent and selective antagonist of the dopamine-1 and dopamine-5 receptors (Ki = 0.2 and 0.3 nM respectively). It was found to prevent death from d-amphetamine overdose in rats and has also been investigated as a potential treatment for Parkinson's Disease and Bipolar Disorder. A single clinical trial was conducted in healthy humans where SCH-23390 induced akathisia (motor restlessness). Preclinical and clinical trials as therapeutic have been discontinued due to side-effects and lack of efficacy. However, it should be noted that a C11 radiolabeled version of the compound has been synthesized and used as a PET imaging probe for the study of Parkinson's Disease and Huntington's Disease.
CNS Activity
Originator
Approval Year
PubMed
Sample Use Guides
SCH-23390 was tested in four healthy subjects at doses of 310–810 micrograms delivered intravenously. SCH-23390 induced akathisia at the three highest doses.
Route of Administration:
Intravenous
Rat brain striatal slices were preincubated with [3H]GABA and superfused in the presence of the GABA transport inhibitor nipecotic and GABA aminotransferase inhibitor aminooxyacetic acids. GABA efflux was estimated by monitoring the efflux of [3H]GABA. The overflow of GABA evoked by electrical field stimulation was blocked by 0.5 - 10 microM of SCH 23390.
