| Stereochemistry | MIXED |
| Molecular Formula | C8H17NO |
| Molecular Weight | 143.2267 |
| Optical Activity | UNSPECIFIED |
| Defined Stereocenters | 0 / 2 |
| E/Z Centers | 0 |
| Charge | 0 |
SHOW SMILES / InChI
SMILES
CCC(C)C(CC)C(N)=O
InChI
InChIKey=QRCJOCOSPZMDJY-UHFFFAOYSA-N
InChI=1S/C8H17NO/c1-4-6(3)7(5-2)8(9)10/h6-7H,4-5H2,1-3H3,(H2,9,10)
| Molecular Formula | C8H17NO |
| Molecular Weight | 143.2267 |
| Charge | 0 |
| Count |
MOL RATIO
1 MOL RATIO (average) |
| Stereochemistry | MIXED |
| Additional Stereochemistry | No |
| Defined Stereocenters | 0 / 2 |
| E/Z Centers | 0 |
| Optical Activity | UNSPECIFIED |
Valnoctamide is a valproic acid derivative associated with a decreased risk for congenital abnormalities and developed by Beersheva Mental Health Center for treatment mania. Valnoctamide has been marketed as an anxiolytic and sedative in several European countries (as Nirvanil), including Italy, Holland, and Switzerland, until the year 2000 but was not actively promoted as an anticonvulsant. It was marketed in the U.S. as Axiquel by McNeil Laboratories in the 1970s. In mice, valnoctamide has been shown to be distinctly less teratogenic than valproic acid. Injection of 3 mkmol ⁄ kg at day 8 of gestation produced only 1% exencephaly (as compared to 0–1% in control mice and 53% in valproate-treated mice). Embryolethality rates showed similar results: 52% with valproate versus 5% in the controls and 2% with valnoctamide. Valnoctamide's patent is expired, and it is not the property of any major pharmaceutical company. Valnoctamide has potential as a therapy in epilepsy including status epilepticus (SE) and neuropathic pain and is currently being developed for the treatment of mania and Schizoaffective Disorder. In clinical trials, Valnoctamide was well tolerated but lacked efficacy in the treatment of symptoms in patients with acute mania.
CNS Activity
Originator
Approval Year
Doses
PubMed
Patents
Sample Use Guides
600 mg ⁄ day (200 mg three times daily) and increased to 1200 mg (400 mg three times daily) after four days. Each patient received valnoctamideor for five weeks
Route of Administration:
Oral
Whole-cell recordings of mIPSCs were obtained by voltage clamping the cell at −70 mV (with series resistance compensation) while blocking excitatory currents with 3 mM kynurenic acid (Sigma-Aldrich, St. Louis, MO, USA) and Na+ channel-dependent release with 1 μM TTX (Abcam, Cambridge, UK). Following a 4-min baseline, perfusion solution was switched to an identical solution containing 1 mM valnoctamide (VCD). Drug was applied for 10 min and then washed out in normal recording solution for another 10 min. Flumazenil (FMZ) competition and diazepam (DZP) occlusion experiments were conducted similarly, with the first perfusion change to 500 μM VCD followed by 500 μM VCD + 10 μM FMZ or 1 μM DZP followed by 1 μM DZP + 1 mM VCD, respectively. FMZ and DZP were purchased from Tocris Bioscience (Bristol, UK) and VCD was purchased from Santa Cruz Biotechnology (Dallas, TX, USA). These drugs were dissolved in DMSO at stock concentrations of 1 M (VCD), 10 mM (FMZ and DZP). The final concentration of DMSO then ranged from 0.05–0.2% and was kept constant throughout each experiment.
