Divalproex Sodium (Valproate semisodium) binds to and inhibits gamma-aminobutyric acid (GABA) transaminase and its anticonvulsant activity may be exerted by increasing brain concentration of GABA and by inhibiting enzymes that catabolize GABA or block the reuptake of GABA into glia and nerve endings. It also is an HDAC inhibitor， Comprised of sodium valproate and valproic acid with anticonvulsant and antiepileptic activities. Divalproex may also work by suppressing repetitive neuronal firing through the inhibition of voltage-sensitive sodium channels.

Divalproex sodium enhances apoptosis, IM-induced cell growth inhibition and cell cycle arrest in K562-G and K562-S cells. It enhances the inhibitory effects of IM on SIRT1 expression in K562-G and K562-S cells. Divalproex sodium enhances the effect of IM on apoptosis in K562-G cells partly through SIRT1.

Divalproex (500 mg/kg) significantly increases dopamine (DA) and acetylcholine (ACh) efflux in the rat hippocampus, and DA, but not ACh, efflux in the rat medial prefrontal cortex (mPFC), whereas 50 mg/kg has no effect on DA or ACh in either region. Divalproex (50 mg/kg) combined with the atypical APDs Olanzapine (1.0 mg/kg) or Aripiprazole (0.3 mg/kg) significantly potentiates the effect of both antipsychotic drugs (APDs) on DA, but not ACh efflux in the HIP and mPFC.