In Vivo (Add solvents to the product individually and in order.)
Homogeneous suspension
CMC-NA
≥5mg/ml
Taking the 1 mL working solution as an example, add 5 mg of this product to 1 ml of CMC-Na solution, mix evenly to obtain a homogeneous suspension with a final concentration of 5 mg/ml.
* <1 mg/ml means slightly soluble or insoluble. * Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations. * Room temperature shipping (Stability testing shows this product can be shipped without any cooling measures.)
Preparing Stock Solutions
Biological Activity
Description
Valproic acid (VPA) is a fatty acid with anticonvulsant properties used in the treatment of epilepsy. It is also a histone deacetylase (HDAC) inhibitor and is under investigation for treatment of HIV and various cancers. This compound induces autophagy and mitophagy by upregulation of BNIP3 and mitochondrial biogenesis by upregulating PGC-1α. Additionally, it activates Notch-1 signalling.
Targets
HDAC
HDAC1 (Cell-free assay)
0.4 mM
In vitro
Like lithium, valproic acid (VPA) activates Wnt-dependent gene expression, but unlike lithium, it does not inhibit GSK-3β in vivo. This compound can inhibit GSK-3β-mediated phosphorylation of a CREB peptide in vitro. It may activate Wnt-dependent gene expression through inhibition of HDAC, which in turn leads to both increased expression of β-catenin and de-repression of Tcf/Lef (as well as activation of other HDAC-regulated genes). In vitro, VPA can stimulate glutamic acid decarboxylase, which is involved in GABA biosynthesis, and inhibit GABA transaminase, succinic semialdehyde dehydrogenase, and α-ketoglutarate dehydrogenase, enzymes involved in GABA degradation. It relieves HDAC-dependent transcriptional repression and causes hyperacetylation of histones in cultured cells and in vivo. VPA induces differentiation and/or apoptosis of carcinoma cells, PML-RAR-transformed hematopoietic progenitor cells and leukemic blasts from AML patients. In addition to selectively inhibiting the catalytic activity of class I HDACs, it also induces proteasomal degradation of HDAC2.
In Vivo
Valproic acid (VPA) increases the level of the inhibitory neurotransmitter γ-aminobutyric acid (GABA), with acute administration causing a 15-45% increase in GABA in the brains of rodents. It also inhibits tumour growth and metastasis in animal experiments, and is a well-tolerated drug even during long-term treatment.
Neuro2A cells are treated with VPA (0.5-5 mM) or with TSA (300 nm) for 24 h and then histones are isolated. Histone acetylation is assessed by immunoblotting with an antibody specific to acetylated histone H4.
Ginsenoside Rg1 Restores Sirt2/Foxo1 Expression and Alleviates Autism-Like Behaviors in a Valproic Acid Induced Male Mouse Model
[ Kaohsiung J Med Sci, 2025, e70078.]
Restoring sweat gland function in mice using regenerative sweat gland cells derived from chemically reprogrammed human epidermal keratinocytes
[ Sci Bull (Beijing), 2024, S2095-9273(24)00799-0]
RNA m6A modification regulates L1 retrotransposons in human spermatogonial stem cell differentiation in vitro and in vivo
[ Cell Mol Life Sci, 2024, 81(1):92]
Molecular mechanism underlying miR-204-5p regulation of adipose-derived stem cells differentiation into cells from three germ layers
[ Cell Death Discov, 2024, 10(1):95]
RETURN POLICY
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SHIPPING AND STORAGE
Selleck products are transported at room temperature. If you receive the product at room temperature, please rest assured, the Selleck Quality Inspection Department has conducted experiments to verify that the normal temperature placement of one month will not affect the biological activity of powder products. After collecting, please store the product according to the requirements described in the datasheet. Most Selleck products are stable under the recommended conditions.
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