Valproic acid (sodium) (2:1)

Valproic acid (VPA) sodium (2:1) is an orally active HDAC inhibitor, with IC₅₀ in the range of 0.5 and 2 mM, also inhibits HDAC1 (IC₅₀, 400 μM), and induces proteasomal degradation of HDAC2. Valproic acid sodium (2:1) activates Notch1 signaling and inhibits proliferation in small cell lung cancer (SCLC) cells. Valproic acid sodium (2:1) is used in the treatment of epilepsy, bipolar disorder, metabolic disease, HIV infection and prevention of migraine headaches^{[1][2][3][4][5][6][7]}. In Vitro: Valproic acid (VPA) (0-15 mM; 24 and 72 h) inhibits Hela cell growth in a dose- and time- dependent manner^[1].
Valproic acid (10 mM; 24 h) significantly attenuates the activities of total, cytosol and nuclear HDACs^[1].
Valproic acid (0-15 mM; 24 h) induces a G1 phase arrest at 1–3 mM and a G2/M phase arrest at 10 mM, and increases the percentage of sub-G1 cells in HeLa cells. Valproic acid also induces necrosis, apoptosis and lactate dehydrogenase (LDH) release^[1].
Valproic acid (0-20 mM; 24 h) activates Tcf/Lef-dependent transcription and synergizes with lithium^[2].
Valproic acid (0-5 mM; 0-18 h) increases β-catenin levels in Neuro2A cells^[2].
Valproic acid (0-2 mM; 0-24 h) stimulates phosphorylation of AMPK and ACC in hepatocytes^[5].
Valproic acid (0-10 mM; 2 days) induces Notch1 signaling and morphologic differentiation, suppresses production of NE tumor markers in SCLC cells^[6]. In Vivo: Valproic acid (VPA) (500 mg/kg; i.p.; daily for 12 days) inhibits tumor angiogenesis in mice transplanted with Kasumi-1 cells^[3].
Valproic acid (350 mg/kg; i.p.; once) enhances social behavior in rats^[4].
Valproic acid (0.26% (w/v); p.o. via drinking water; 14 days) decreases liver mass, hepatic fat accumulation, and serum glucose in obese mice without hepatotoxicity^[5].