| Size | Price | Stock | Qty |
|---|---|---|---|
| 1g |
|
||
| 2g |
|
||
| 5g |
|
||
| 10g |
|
||
| 100g |
|
||
| Other Sizes |
|
Purity: ≥98%
Valproic acid is an HDAC (Histone deacetylase) inhibitor used in the treatment of epilepsy, bipolar disorder and prevention of migraine headaches. Valproic Acid is a fatty acid with anticonvulsant properties by selectively inducing proteasomal degradation of HDAC2. It may act by increasing gamma-aminobutyric acid levels in the brain or by altering the properties of voltage dependent sodium channels. It is also under investigation for treatment of HIV and various cancers.
| ln Vitro |
In a dose- and time-dependent way, valproic acid (VPA) (0–15 mM; 24 and 72 h) suppresses the proliferation of Hela cells[1]. The activity of nuclear, cytosolic, and total HDACs is markedly reduced by valproic acid (10 mM; 24 h)[1]. The percentage of sub-G1 cells in HeLa cells rises when valproic acid (0–15 mM; 24 h) generates a G1/M phase arrest at 10 mM and a G1 phase arrest at 1-3 mM. Necrosis, apoptosis, and the release of lactate dehydrogenase (LDH) are additional effects of valproic acid[1]. Lithium works in concert with valproic acid (0–20 mM; 24 h) to stimulate Tcf/Lef-dependent transcription[2]. Neuro2A cells' β-catenin levels are elevated by valproic acid (0–5 mM; 0–18 h)[2]. Hepatocyte AMPK and ACC phosphorylation is stimulated by valproic acid (0–2 mM; 0–24 h)[5]. For two days, valproic acid (0 -10 mM) inhibits the generation of NE tumor markers in SCLC cells while inducing Notch1 signaling and morphologic differentiation[6].
|
|---|---|
| ln Vivo |
In mice transplanted with Kasumi-1 cells, valproic acid (VPA) (500 mg/kg; ip; daily for 12 days) suppresses tumor angiogenesis[3]. Rats with valproic acid (350 mg/kg; ip; once) exhibit improved social behavior [4]. In obese mice, valproic acid (0.26% w/v; po via drinking water; 14 days) reduces blood glucose, hepatic fat formation, and liver mass without causing hepatotoxicity[5].
|
| Cell Assay |
Cell Viability Assay[1]
Cell Types: HeLa cells Tested Concentrations: 0, 1, 3, 5, 10 and 15 mM Incubation Duration: 24 and 72 h Experimental Results: HeLa cell growth was dose- and time-dependently diminished with an IC50 of ~10 and 4 mM at 24 and 72 h. Western Blot Analysis[1][2][5] Cell Types: HeLa cells, Neuro2A cells or primary mouse hepatocytes Tested Concentrations: 10mM (HeLa); 0, 2, and 5mM (Neuro2A); 0.2, 0.4, 0.8, 1.2 and 2mM (hepatocytes) Incubation Duration: 10mM (HeLa ); 0, 2, and 5 mM (Neuro2A); 0.2, 0.4, 0.8, 1.2 and 2 Mm (hepatocytes) Experimental Results: Increased the form of acetylated histone 3. decreased PARP, induced cleavage PARP, and downregulated Bcl-2. Increased β-catenin levels. Increased the phosphorylation of AMPK and ACC. Cell Cycle Analysis[1] Cell Types: HeLa cells Tested Concentrations: 0, 1, 3, 5, 10 and 15 mM Incubation Duration: 24 h Experimental Results: Induced a G1 phase arrest at 1–3 mM, Dramatically induced a G2/M phase arrest at 10 mM, and increased the percentage of sub-G1 cells in HeLa cells in a dose-dependent manner at 24 |
| Animal Protocol |
Animal/Disease Models: Female BALB/c nude mice, Kasumi-1 tumor model[3]
Doses: 500 mg/kg Route of Administration: intraperitoneal (ip)injection, daily for 12 days Experimental Results: Inhibited tumor growth and tumor angiogenesis. Inhibited the mRNA and protein expression of VEGF, VEGFR2 and bFGF. Inhibited HDAC activity and increased acetylation of histone H3. Enhanced the accumulation of hyperacetylated histone H3 on VEGF promoters. Animal/Disease Models: Timed-pregnant Long Evans rats[4] Doses: 350 mg/kg Route of Administration: intraperitoneal (ip)injection, once Experimental Results: Demonstrated more social investigation and play fighting than control animals. Animal/Disease Models: Obese phenotype of ob/ob mice[5] Doses: 0.26% (w/v) Route of Administration: Oral via drinking water, 14 days Experimental Results: Revealed a marked reduction in the accumulation of fats in the liver as compared with the untreated mice, Dramatically diminished liver mass to body mass, diminished serum triglyceride concentrations, and did not induce hepatotoxicity. |
| References |
[1]. Han BR, et al. Valproic acid inhibits the growth of HeLa cervical cancer cells via caspase-dependent apoptosis. Oncol Rep. 2013 Dec;30(6):2999-3005.
[2]. Valproic acid, et al. Histone deacetylase is a direct target of valproic acid, a potent anticonvulsant, mood stabilizer, and teratogen. J Biol Chem. 2001 Sep 28;276(39):36734-41. [3]. Zhang ZH, et al. Valproic acid inhibits tumor angiogenesis in mice transplanted with Kasumi 1 leukemia cells. Mol Med Rep. 2013 Nov 28. [4]. Cohen OS, et al. Acute prenatal exposure to a moderate dose of valproic acid increases social behavior and alters gene expression in rats. Int J Dev Neurosci. 2013 Dec;31(8):740-50. [5]. Avery LB, et al. Valproic Acid Is a Novel Activator of AMP-Activated Protein Kinase and Decreases Liver Mass, Hepatic Fat Accumulation, and Serum Glucose in Obese Mice. Mol Pharmacol. 2014 Jan;85(1):1-10. [6]. Platta CS, et al. Valproic acid induces Notch1 signaling in small cell lung cancer cells. J Surg Res. 2008 Jul;148(1):31-7. [7]. Routy JP, et al. Valproic acid in association with highly active antiretroviral therapy for reducing systemic HIV-1 reservoirs: results from a multicentre randomized clinical study. HIV Med. 2012 May;13(5):291-6. |
| Molecular Formula |
C8H16O2
|
|
|---|---|---|
| Molecular Weight |
144.21144
|
|
| CAS # |
99-66-1
|
|
| Related CAS # |
Valproic acid sodium;1069-66-5;Valproic acid-d4;87745-17-3;Valproic acid-d6;87745-18-4;Valproic acid-d15;362049-65-8;Valproic acid (sodium)(2:1);76584-70-8;Valproic acid-d4 sodium;Valproic acid-d4-1;345909-03-7
|
|
| SMILES |
CCCC(CCC)C(O)=O
|
|
| Synonyms |
|
|
| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month |
|
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
|
| Solubility (In Vitro) |
|
|||
|---|---|---|---|---|
| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.5 mg/mL (17.34 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: ≥ 2.5 mg/mL (17.34 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly. Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution. View More
Solubility in Formulation 3: ≥ 2.5 mg/mL (17.34 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. Solubility in Formulation 4: 2 mg/mL (13.87 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with ultrasonication. Solubility in Formulation 5: 20 mg/mL (138.69 mM) in 0.5% CMC/saline water (add these co-solvents sequentially from left to right, and one by one), suspension solution; with ultrasonication. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 6.9343 mL | 34.6717 mL | 69.3433 mL | |
| 5 mM | 1.3869 mL | 6.9343 mL | 13.8687 mL | |
| 10 mM | 0.6934 mL | 3.4672 mL | 6.9343 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
Products are for research use only; We do not sell to patients
Copyright 2020 InvivoChem LLC | All Rights Reserved
COA
