| Stereochemistry | ACHIRAL |
| Molecular Formula | C10H20N2O2 |
| Molecular Weight | 200.278 |
| Optical Activity | NONE |
| Defined Stereocenters | 0 / 0 |
| E/Z Centers | 0 |
| Charge | 0 |
SHOW SMILES / InChI
SMILES
CCCC(CCC)C(=O)NCC(N)=O
InChI
InChIKey=RALGCAOVRLYSMA-UHFFFAOYSA-N
InChI=1S/C10H20N2O2/c1-3-5-8(6-4-2)10(14)12-7-9(11)13/h8H,3-7H2,1-2H3,(H2,11,13)(H,12,14)
Valrocemide is an anticonvulsant agent which was under development by Teva and Acorda as a potential therapeutic for the treatment of epilepsy. Valrocemide is an N-valproyl derivative of GABAand glycine. It was found that 1 mM of valrocemide could drastically inhibit human brain crude homogenate MIP synthase activity. Furthermore, the mechanism of the effect of valrocemide was studied and results showed that valrocemide reduced the enzyme activity by an apparent competitive mode of inhibition. In October 2003, a phase II trial using valrocemide as an adjunct therapy in refractory epilepsy patients had been completed and phase III trials were being planned. Valrocemide was also being investigated for potential utility in the treatment of bipolar disorder and neuropathic pain. This compound was originally discovered by Yissum Research and Development Company of the Hebrew University of Jerusalem, then licensed and developed by Teva in collaboration with Acorda in 2003, then licensed to Shire the worldwide development, production and marketing rights in 2006. However, the development of Valrocemide was discontinued by Shire in 2009.
CNS Activity
Originator
Approval Year
PubMed
Sample Use Guides
After administration of single doses up to 4,000 mg and multiple daily doses between 250 and 1000 mg three times daily in healthy volunteers, valrocemide is absorbed rapidly.
Route of Administration:
Oral
ACTIVE MOIETY
