PRODUCT IDENTIFICATION

H.S. CODE

2915.90.0090

TOXICITY

SMILES

C(CCC)(CCC)C(=O)[O-].[Na+]

CLASSIFICATION

PHYSICAL AND CHEMICAL PROPERTIES

white to off-white crystalline powder, odorless

SOLVENT SOLUBILITY

AUTOIGNITION

NFPA RATINGS

REFRACTIVE INDEX

GENERAL DESCRIPTION & EXTERNAL LINKS

Valproic acid and its derivatives are used solely or in combination with other anticonvulsants to prevent seizures and migraines. Valproates are effective against the manic phase of bipolar disorder. A fatty acid with anticonvulsant properties used in the treatment of epilepsy. The mechanisms of its therapeutic actions are not well understood. It may act by increasing GAMMA-AMINOBUTYRIC ACID levels in the brain or by altering the properties of voltage dependent sodium channels.

Wikipedia Linking:http://en.wikipedia.org/wiki/Sodium_valproate

http://www.merck.com/
Special Alerts-Valproic Acid and Derivatives: Risk of Birth Defects - December 2009
The U.S. Food and Drug Administration (FDA) has issued a reminder to healthcare professionals and patients about the increased risk of neural tube defects (1 in 20 babies born exposed to valproic acid and derivatives compared to ~1 in 1500 not exposed), as well as, other major birth defects (eg, craniofacial defects, cardiovascular malformation), especially with exposure during the first 12 weeks of pregnancy. Information from the North American Antiepileptic Drug Pregnancy Registry notes a fourfold increase in congenital malformations with exposure to valproic acid monotherapy during the 1st trimester of pregnancy when compared to monotherapy with other antiepileptic drugs (AED)..........

http://www.ncbi.nlm.nih.gov/
.........Valproate mechanism-The mechanism by which valproate exerts its therapeutic effect is not well understood. Several hypotheses have been proposed concerning the mechanism of action in epilepsy and bipolar disorder. The most well studied and understood mechanism of valproate is its ability to potentiate or mimic the effects of the inhibitory neurotransmitter, gamma-aminobutyric acid (GABA) (Loscher 2002; Casey et al 2003; Salloum et al 2005). Indirectly, this potentiation of GABA has been hypothesized to produce inhibitory effects on central dopamine (Casey et al 2002; Loscher 2002). Some of the other and less well understood mechanisms involve the inhibition of neuronal excitability and a resultant anti-kindling effect (Loscher 2002). One specific area of study has focused on the inhibition of protein kinase C epsilon (PKC-epsilon) (Brunello 2004; Toth 2005). PKC-epsilon has been linked to the stimulation of intracellular calcium release and an increase in cortical excitation and instability. Valproate has also exhibited effects producing the blockade of voltage-dependent sodium channels (Loscher 2002; Owens and Nemeroff 2003). Another proposed mechanism, though controversial, is one likening valproate to lithium as a potential inhibitor of inositol synthesis through inhibition of myo-inositol-1phosphate (MIP) (Harwood and Agam 2003; Shaltiel et al 2004; Harwood 2005). It is not well understood if valproate inhibits MIP directly, but it has been shown to deplete inositol (Harwood and Agam 2003; Shaltiel et al 2004; Harwood 2005).........

APPEARANCE

white powder

CONTENT

98.0% min