1. Immunology/Inflammation
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    Metabolic Enzyme/Protease
  2. COX
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    Apoptosis
    Endogenous Metabolite
  3. Salicylic acid

Salicylic acid (Synonyms: 2-Hydroxybenzoic acid)

Cat. No.: HY-B0167 Purity: >98.0%
Handling Instructions

Salicylic acid (2-Hydroxybenzoic acid) inhibits cyclo-oxygenase-2 (COX-2) activity independently of transcription factor (NF-κB) activation.

For research use only. We do not sell to patients.

Salicylic acid Chemical Structure

Salicylic acid Chemical Structure

CAS No. : 69-72-7

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Based on 1 publication(s) in Google Scholar

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Description

Salicylic acid (2-Hydroxybenzoic acid) inhibits cyclo-oxygenase-2 (COX-2) activity independently of transcription factor (NF-κB) activation[1].

IC50 & Target[1]

Human Endogenous Metabolite

 

COX-2

 

Autophagy

 

Mitophagy

 

Apoptosis

 

In Vitro

Salicylic acid is an effective inhibitor of COX-2 activity at concentrations far below those required to inhibit NF-κB (20 mg/mL) activation. Salicylic acid inhibits prostaglandin E2 release when add together with interleukin 1β for 24 hr with an IC50 value of 5 μg/mL, an effect that is independent of NF-κB activation or COX-2 transcription or translation. Salicylic acid acutely (30 min) also causes a concentration-dependent inhibition of COX-2 activity measured in the presence of 0, 1, or 10 μM exogenous arachidonic acid. In contrast, when exogenous arachidonic acid is increased to 30 μM, Salicylic acid is a very weak inhibitor of COX-2 activity with an IC50 of >100 μg/mL. When added together with IL-1β for 24 hr, Salicylic acid causes a concentration-dependent inhibition of PGE2 release with an apparent IC50 value of approximately 5 μg/mL. The ability of Salicylic acid to directly inhibit COX-2 activity in A549 cells is tested after a 30-min exposure period, followed by the addition of different concentrations of exogenous arachidonic acid (1, 10, and 30 μM). Salicylic acid causes a concentration-dependent inhibition of COX-2 activity in the absence of added arachidonic acid or in the presence of 1 or 10 μM exogenous substrate with an apparent IC50 value of approximately 5 μg/mL. However, when the same experiments are performed using 30 μM arachidonic acid, Salicylic acid is an ineffective inhibitor of COX-2 activity, with an apparent IC50 value of more than 100 μg/mL, and achieves a maximal inhibition of less than 50%[1].

In Vivo

In C57Bl/6 DIO mice, Salicylic acid decreases both fasting and postprandial plasma glucose levels. Furthermore, there is a trend to reduce plasma triglyceride levels after Salicylic acid treatment in C57Bl/6 DIO mice (P=0.059). Salicylic acid significantly reduces 11β-HSD1 mRNA in omental adipose tissue in C57Bl/6 DIO mice, with a similar trend in mesenteric adipose (P=0.057). In mesenteric adipose of C57Bl/6 DIO mice, Salicylic acid also reduces 11β-HSD1 enzyme activity[2].

Clinical Trial
Molecular Weight

138.12

Formula

C₇H₆O₃

CAS No.

69-72-7

SMILES

O=C(O)C1=CC=CC=C1O

Shipping

Room temperature in continental US; may vary elsewhere.

Storage

4°C, protect from light

*In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)

Solvent & Solubility
In Vitro: 

DMSO : 100 mg/mL (724.01 mM; Need ultrasonic)

H2O : 1 mg/mL (7.24 mM; Need ultrasonic)

Preparing
Stock Solutions
Concentration Solvent Mass 1 mg 5 mg 10 mg
1 mM 7.2401 mL 36.2004 mL 72.4008 mL
5 mM 1.4480 mL 7.2401 mL 14.4802 mL
10 mM 0.7240 mL 3.6200 mL 7.2401 mL
*Please refer to the solubility information to select the appropriate solvent.
In Vivo:
  • 1.

    Add each solvent one by one:  10% DMSO    40% PEG300    5% Tween-80    45% saline

    Solubility: ≥ 2.5 mg/mL (18.10 mM); Clear solution

  • 2.

    Add each solvent one by one:  10% DMSO    90% (20% SBE-β-CD in saline)

    Solubility: ≥ 2.5 mg/mL (18.10 mM); Clear solution

  • 3.

    Add each solvent one by one:  10% DMSO    90% corn oil

    Solubility: ≥ 2.5 mg/mL (18.10 mM); Clear solution

*All of the co-solvents are provided by MCE.
References
Cell Assay
[1]

To assess the direct effect of Salicylic acid on COX-2 activity after induction has occurred, A549 cells are first treated with IL-1β for 24 hr, and the culture medium is replaced with DMEM containing different concentrations of Salicylic acid(10, 100 and 1000 μg/mL). Cells are incubated at 37°C for 30 min. Arachidonic acid (1-30 μM) is then added for 15 min, and the medium is removed for the measurement of PGE2[1].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Administration
[2]

Mice[2]
Adult male C57Bl/6 mice are at age 12 weeks. Diet-induced obese C57Bl/6 mice (C57Bl/6 DIO) are given 10 weeks of high-fat diet (58% fat, 12% sucrose) before treatment. Salicylic acid (120 mg/kg/day) is administered from 1 week after arriving (C57Bl/6 Lean), after 10 weeks of high-fat feeding (C57Bl/6 DIO), or after achieving target weight (HSD1KO-DIO) for 4 weeks to groups of n=8 via osmotic minipumps implant subcutaneously between the scapulae.

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

References
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Keywords:

Salicylic acid2-Hydroxybenzoic acidCOXAutophagyMitophagyApoptosisEndogenous MetaboliteCyclooxygenaseMitochondrial AutophagyInhibitorinhibitorinhibit

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Salicylic acid
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