| Size | Price | Stock | Qty |
|---|---|---|---|
| 5g |
|
||
| 25g |
|
||
| Other Sizes |
| Targets |
Vanillic acid exhibits anti-inflammatory and analgesic effects through mechanisms involving the inhibition of the transcription factor NFκB and subsequent reduction of pro-inflammatory cytokine production (e.g., TNF-α, IL-1β, IL-6, IL-33). It also demonstrates antioxidant activity and inhibits cyclooxygenase-2 (COX-2) expression. [1]
|
|---|---|
| ln Vitro |
All three doses of vanillic acid (50, 100, and 200 μM) were non-toxic to HT22 cells; co-treating vanillic acid with Aβ1-42 resulted in a considerable increase in cell survival (1.5-fold, 1.9-fold, and 2-fold, respectively) [2].
Previous in vitro studies (referenced but not detailed in this study) indicate that vanillic acid reduces lipopolysaccharide (LPS)-induced TNF-α and IL-6 production, decreases LPS-induced COX-2 expression and PGE2 production in mouse peritoneal macrophages, and inhibits LPS-induced phosphorylation of IκB and NFκB p65 subunit expression in macrophages. [1] This study mentions that the antioxidant mechanisms of vanillic acid in vitro include free radical scavenging activity, reducing power, and inhibition of lipid peroxidation. [1] |
| ln Vivo |
Paw edema, neutrophil and macrophage recruitment, and carrageenan-induced mechanical hyperalgesia are all inhibited by vanillic acid (3–30 mg/kg; i.p.; 5 hours) [1].
Vanillic acid (3-30 mg/kg, intraperitoneal, 1 h pretreatment) significantly inhibited acetic acid-induced writhing response in mice, with doses of 10 and 30 mg/kg showing efficacy. Maximal inhibition was observed with 30 mg/kg. A pretreatment time of 60 minutes was found to be optimal. [1] Vanillic acid (10 and 30 mg/kg, ip) also inhibited phenyl-p-benzoquinone (PBQ)-induced writhing response. [1] Vanillic acid (30 mg/kg, ip, 1 h pretreatment) inhibited the second phase of formalin-induced paw licking behavior. [1] Vanillic acid (30 mg/kg, ip, 1 h pretreatment) significantly inhibited carrageenan-induced mechanical hyperalgesia and paw edema in mice over a 1-5 hour period. It also reduced carrageenan-induced recruitment of neutrophils (measured by myeloperoxidase/MPO activity) and macrophages (measured by N-acetyl-β-D-glucosaminidase/NAG activity) in paw skin tissue. [1] In a persistent inflammation model, daily post-treatment with vanillic acid (30 mg/kg, ip, for 7 days, starting 24 h after induction) inhibited complete Freund's adjuvant (CFA)-induced mechanical hyperalgesia and paw edema over the 7-day period. It also reduced CFA-induced neutrophil and macrophage recruitment in paw tissue at day 7. [1] Vanillic acid (30 mg/kg, ip, 1 h pretreatment) prevented carrageenan-induced oxidative stress in paw tissue, as evidenced by the reversal of reduced antioxidant capacity (FRAP assay, ABTS radical scavenging, GSH levels) and inhibition of lipid peroxidation (TBARS assay). [1] Vanillic acid (30 mg/kg, ip, 1 h pretreatment) inhibited carrageenan-induced production of pro-inflammatory cytokines IL-1β, TNF-α, and IL-33 in paw skin tissue. [1] Vanillic acid (30 mg/kg, ip, 1 h pretreatment) suppressed carrageenan-induced activation of the transcription factor NFκB (p65 subunit) in paw skin tissue, as determined by ELISA. [1] |
| Cell Assay |
Cell viability assay [2]
Cell Types: HT22 Cell Tested Concentrations: 50, 100 and 200 μM Incubation Duration: 24 hrs (hours) Experimental Results: The viability of HT22 cells increased after 24 hrs (hours) at three different concentrations (50, 100 and 200 μM). This study references previous in vitro work where vanillic acid inhibited LPS-induced cytokine production, COX-2 expression, and NFκB activation in mouse peritoneal macrophages. [1] |
| Animal Protocol |
Animal/Disease Models: Male Swiss mouse (25-30 g) [1]
Doses: 3, 10 or 30 mg/kg Route of Administration: intraperitoneal (ip) injection; 5 hrs (hrs (hours)) Experimental Results: Inhibition of carrageenan-induced mechanical hyperalgesia, paw Edema and recruitment of neutrophils and macrophages. Acetic acid/PBQ writhing test: Male Swiss mice (25-30 g) were treated with vanillic acid (dissolved in 5% Tween 80 saline, 3-30 mg/kg) or vehicle via intraperitoneal (ip), subcutaneous (sc), or per oral (po) routes, 1 hour before ip injection of the nociceptive stimulus (0.8% acetic acid or PBQ). The writhing response (abdominal contortions) was counted over 20 minutes. [1] Formalin test: Mice were treated with vanillic acid (30 mg/kg, ip, 5% Tween 80 saline, 1 h pretreatment) before intraplantar injection of formalin (1.5%). Paw flinching and licking time were recorded over 30 minutes, analyzing the first (0-5 min) and second (10-30 min) phases. [1] Carrageenan-induced acute inflammation: Mice were pretreated with vanillic acid (3-30 mg/kg, ip, 5% Tween 80 saline, 1 h) before intraplantar injection of carrageenan (300 μg/paw). Mechanical hyperalgesia (electronic pressure meter) and paw edema (caliper) were measured at 1-5 hours post-carrageenan. At the 5th hour, paw skin samples were collected for MPO and NAG activity assays. For oxidative stress and cytokine analysis, samples were collected 3 hours post-carrageenan. For NFκB activation, samples were also collected 3 hours post-carrageenan. [1] CFA-induced persistent inflammation: Mice received an intraplantar injection of CFA (10 μL). Starting 24 hours later, they were treated daily with vanillic acid (3-30 mg/kg, ip, 5% Tween 80 saline) for 7 days. Mechanical hyperalgesia and paw edema were assessed daily. On day 7, after behavioral tests, paw skin samples were collected for MPO and NAG activity assays. [1] Toxicity assessment: Mice were treated daily with vanillic acid (30 mg/kg, ip, 5% Tween 80 saline) for 7 days. Plasma was collected for AST and ALT measurement, and stomach tissue was collected for MPO activity assay. [1] |
| Toxicity/Toxicokinetics |
In a 7-day repeated-dose study, daily intraperitoneal injection of vanillic acid (30 mg/kg) did not cause liver injury, as evidenced by no significant changes in plasma aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels compared to the control group. In contrast, the positive control drug indomethacin significantly increased AST and ALT levels. [1] Under the same 7-day treatment regimen, intraperitoneal injection of vanillic acid (30 mg/kg) did not cause gastric injury, as evidenced by no changes in myeloperoxidase (MPO) activity in gastric tissue. Indomethacin significantly increased gastric MPO activity, indicating gastric injury. [1]
|
| References |
|
| Additional Infomation |
Vanillic acid is a monohydroxybenzoic acid, a compound in which 4-hydroxybenzoic acid is substituted with a methoxy group at the 3-position. It is a plant metabolite. It is both monohydroxybenzoic acid and methoxybenzoic acid. It is the conjugate acid of vanillic acid esters. It is a flavoring agent. It is an intermediate in the two-step bioconversion of ferulic acid to vanillin (J Biotechnol 1996;50(2-3):107-13). Vanillic acid has been reported in tea (Camellia sinensis), peony (Paeonia obovata), and other organisms with relevant data. Vanillic acid is a metabolite found or produced in Saccharomyces cerevisiae. It is a flavoring agent. It is an intermediate in the two-step bioconversion of ferulic acid to vanillin (J Biotechnol 1996;50(2-3):107-13). Vanillic acid (4-hydroxy-3-methoxybenzoic acid) is a phenolic compound found in edible plants and fruits. It is the oxidized form of vanillin and is used as a flavoring agent. [1] This study shows that the anti-inflammatory and analgesic mechanisms of vanillic acid involve multiple target pathways: inhibiting the recruitment of neutrophils and macrophages to sites of inflammation, reducing oxidative stress (maintaining antioxidant capacity and inhibiting lipid peroxidation), inhibiting the production of pro-inflammatory cytokines (IL-1β, TNF-α, IL-33), and inhibiting the activation of the transcription factor NFκB. [1] This study concludes that vanillic acid is effective in various mouse models of inflammatory pain (acetic acid, PBQ, formalin, carrageenan, CFA) and shows good hepatotoxicity and gastric toxicity safety in short-term treatment regimens, which distinguishes it from classic nonsteroidal anti-inflammatory drugs (NSAIDs) such as indomethacin. [1]
|
| Molecular Formula |
C8H8O4
|
|---|---|
| Molecular Weight |
168.1467
|
| Exact Mass |
168.042
|
| CAS # |
121-34-6
|
| PubChem CID |
8468
|
| Appearance |
White to yellow solid powder
|
| Density |
1.4±0.1 g/cm3
|
| Boiling Point |
353.4±27.0 °C at 760 mmHg
|
| Melting Point |
208-210 °C(lit.)
|
| Flash Point |
149.4±17.2 °C
|
| Vapour Pressure |
0.0±0.8 mmHg at 25°C
|
| Index of Refraction |
1.586
|
| LogP |
1.33
|
| Hydrogen Bond Donor Count |
2
|
| Hydrogen Bond Acceptor Count |
4
|
| Rotatable Bond Count |
2
|
| Heavy Atom Count |
12
|
| Complexity |
168
|
| Defined Atom Stereocenter Count |
0
|
| InChi Key |
WKOLLVMJNQIZCI-UHFFFAOYSA-N
|
| InChi Code |
InChI=1S/C8H8O4/c1-12-7-4-5(8(10)11)2-3-6(7)9/h2-4,9H,1H3,(H,10,11)
|
| Chemical Name |
4-hydroxy-3-methoxybenzoic acid
|
| HS Tariff Code |
2934.99.9001
|
| 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) |
DMSO : ≥ 100 mg/mL (~594.71 mM)
|
|---|---|
| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.5 mg/mL (14.87 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 (14.87 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 (14.87 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 5.9471 mL | 29.7354 mL | 59.4707 mL | |
| 5 mM | 1.1894 mL | 5.9471 mL | 11.8941 mL | |
| 10 mM | 0.5947 mL | 2.9735 mL | 5.9471 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
