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    Vanillic acid
    CAS No. 121-34-6 Price $30 / 20mg
    Catalog No.CFN99331Purity>=98%
    Molecular Weight168.2 Type of CompoundPhenols
    FormulaC8H8O4Physical DescriptionPowder
    Download Manual    COA    MSDSSimilar structuralComparison (Web)
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    Biological Activity
    Description: Vanillic acid is a flavoring agent which has hepatoprotective, free radical scavenging, antioxidant and anti-inflammatory properties. It exerts protective effects in isoproterenol induced cardiotoxic rats, has inhibitory effect on methylglyoxal-mediated glycation in apoptotic Neuro-2A cells via inhibition of glycation mechanisms including ROS, p38 and JNK, PKC and p47(phox).
    Targets: TNF-α | ROS | p38MAPK | JNK | PKC | p47(phox) | IL Receptor | Fas | Caspase
    In vitro:
    Neurotoxicology. 2008 Nov;29(6):1016-22.
    Inhibitory effect of vanillic acid on methylglyoxal-mediated glycation in apoptotic Neuro-2A cells[Pubmed: 18706441]
    Methylglyoxal is a reactive dicarbonyl compound generated as an intermediate of glycolysis during the physical glycation in the diabetic condition. It is considered to be a potent precursor of advanced glycation end products (AGEs) formation. Methylglyoxal itself and methylglyoxal-derived AGEs have been commonly implicated in the development of diabetic neuropathy. Our previous study indicated that Vanillic acid showed an inhibitory effect against methylglyoxal-mediated Neuro-2A cell apoptosis, suggesting that Vanillic acid might possess cytoprotective properties in the prevention of diabetic neuropathy complication.
    In this study, the effects of Vanillic acid on the methylglyoxal-mediated glycation system involved in the progression of Neuro-2A cell apoptosis were further investigated. Our findings indicated that methylglyoxal-induced Neuro-2A cell apoptosis was mediated through the possible glycation mechanism of oxidative stress, activation of the MAPK signaling pathway (p38 and JNK) and oxidation-sensitive protein expression (PKC and p47(phox)) and methylglyoxal-derived N-epsilon-(carboxymethyl)lysine (CML) formation. Vanillic acid, however, suppressed methylglyoxal-induced Neuro-2A cell apoptosis via inhibition of glycation mechanisms including ROS, p38 and JNK, PKC and p47(phox), and methylglyoxal-derived CML formation.
    In the present study, we established the first evidence that Vanillic acid might contribute to the prevention of the development of diabetic neuropathy by blocking the methylglyoxal-mediated intracellular glycation system.
    In vivo:
    Eur J Pharmacol. 2011 Oct 1;668(1-2):233-40.
    Protective effects of vanillic acid on electrocardiogram, lipid peroxidation, antioxidants, proinflammatory markers and histopathology in isoproterenol induced cardiotoxic rats.[Pubmed: 21763302 ]
    Myocardial infarction affects a large proportion in the world. This study aims to evaluate the protective effects of Vanillic acid in isoproterenol induced cardiotoxic rats.
    Male Wistar rats were pretreated with Vanillic acid (5mg and 10mg/kg) daily for 10 days. After pretreatment, isoproterenol (100mg/kg) was subcutaneously injected to rats at an interval of 24h for 2 days to induce cardiotoxicity. Isoproterenol induced cardiotoxic rats showed significant increase in serum cardiac troponins, heart lipid peroxidation and significant decrease in the heart antioxidants. In addition, isoproterenol induced group electrocardiogram showed an elevation in ST segments and increased expressions of interleukin-1β, interleukin-6 and tumor necrosis factor-α genes in the myocardium. Pretreatment with Vanillic acid showed significant protective effects on cardiac troponins, lipid peroxidation, antioxidant system, electrocardiogram and expressions of interleukin-1β, interleukin-6 and tumor necrosis factor-α gene in the heart of isoproterenol induced cardiotoxic rats. Histopathology of myocardium correlated with these biochemical findings. The in vitro study also revealed that Vanillic acid is a potent free radical scavenger. Thus, Vanillic acid exerts protective effects in isoproterenol induced cardiotoxic rats due to its free radical scavenging, antioxidant and anti-inflammatory properties.
    Our study also showed that pretreatment with Vanillic acid at the dose of 10mg/kg was highly effective than 5mg/kg.
    Biol Pharm Bull. 2010;33(6):983-7.
    Hepatoprotective effect of syringic acid and vanillic acid on CCl4-induced liver injury.[Pubmed: 20522963]
    The mycelia of the edible mushroom Lentinula edodes can be cultured in solid medium containing lignin, and the hot-water extracts (L.E.M.) is commercially available as a nutritional supplement. During the cultivation, phenolic compounds, such as syringic acid and Vanillic acid, were produced by lignin-degrading peroxidase secreted from L. edodes mycelia. Since these compounds have radical scavenging activity, we examined their protective effect on oxidative stress in mice with CCl(4)-induced liver injury.
    We examined the hepatoprotective effect of syringic acid and Vanillic acid on CCl(4)-induced chronic liver injury in mice. The injection of CCl(4) into the peritoneal cavity caused an increase in the serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels. The intravenous administration of syringic acid and Vanillic acid significantly decreased the levels of the transaminases. Four weeks of CCl(4) treatment caused a sufficiently excessive deposition of collagen fibrils. An examination of Azan-stained liver sections revealed that syringic acid and Vanillic acid obviously suppressed collagen accumulation and significantly decreased the hepatic hydroxyproline content, which is the quantitative marker of fibrosis. Both of these compounds inhibited the activation of cultured hepatic stellate cells, which play a central role in liver fibrogenesis, and maintained hepatocyte viability.
    These data suggest that the administration of syringic acid and Vanillic acid could suppress hepatic fibrosis in chronic liver injury.
    Vanillic acid Description
    Source: The herbs of Cymbopogon javanensis
    Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
    Storage: Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).

    Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.

    Need more advice on solubility, usage and handling? Please email to: service@chemfaces.com

    After receiving: The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 5.9453 mL 29.7265 mL 59.453 mL 118.9061 mL 148.6326 mL
    5 mM 1.1891 mL 5.9453 mL 11.8906 mL 23.7812 mL 29.7265 mL
    10 mM 0.5945 mL 2.9727 mL 5.9453 mL 11.8906 mL 14.8633 mL
    50 mM 0.1189 mL 0.5945 mL 1.1891 mL 2.3781 mL 2.9727 mL
    100 mM 0.0595 mL 0.2973 mL 0.5945 mL 1.1891 mL 1.4863 mL
    * Note: If you are in the process of experiment, it's need to make the dilution ratios of the samples. The dilution data of the sheet for your reference. Normally, it's can get a better solubility within lower of Concentrations.
    Kinase Assay:
    Biochim Biophys Acta. 2014 Jan;1842(1):1-6.
    Effect of vanillic acid on COQ6 mutants identified in patients with coenzyme Q10 deficiency.[Pubmed: 24140869]
    Human COQ6 encodes a monooxygenase which is responsible for the C5-hydroxylation of the quinone ring of coenzyme Q (CoQ). Mutations in COQ6 cause primary CoQ deficiency, a condition responsive to oral CoQ10 supplementation. Treatment is however still problematic given the poor bioavailability of CoQ10.
    We employed S. cerevisiae lacking the orthologous gene to characterize the two different human COQ6 isoforms and the mutations found in patients. COQ6 isoform a can partially complement the defective yeast, while isoform b, which lacks part of the FAD-binding domain, is inactive but partially stable, and could have a regulatory/inhibitory function in CoQ10 biosynthesis. Most mutations identified in patients, including the frameshift Q461fs478X mutation, retain residual enzymatic activity, and all patients carry at least one hypomorphic allele, confirming that the complete block of CoQ biosynthesis is lethal. These mutants are also partially stable and allow the assembly of the CoQ biosynthetic complex. In fact treatment with two hydroxylated analogues of 4-hydroxybenzoic acid, namely, Vanillic acid or 3-4-hydroxybenzoic acid, restored the respiratory growth of yeast Δcoq6 cells expressing the mutant huCOQ6-isoa proteins.
    These compounds, and particularly Vanillic acid, could therefore represent an interesting therapeutic option for COQ6 patients.
    Animal Research:
    Chem Biol Interact. 2015 May 5;232:68-76.
    Vanillic acid prevents altered ion pumps, ions, inhibits Fas-receptor and caspase mediated apoptosis-signaling pathway and cardiomyocyte death in myocardial infarcted rats.[Pubmed: 25794854]
    Animal Models: Male albino Wistar rats
    Formulation: ---
    Dosages:5mg/kg and 10mg/kg/d for 10days
    Administration: p.o.