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China Factory Supply 99.5%Min Salicylic Acid Powder CAS 69-72-7

China Factory Supply 99.5%Min Salicylic Acid Powder CAS 69-72-7, Find details about China 69-72-7, Salicylic Acid from China Factory Supply 99.5%Min Salicylic Acid Powder CAS 69-72-7

Model NO.
69-72-7
Wickr
Bellachen
Common Name
Salicylic Acid
CAS Number
69-72-7
Molecular Weight
138.121
Density
1.4±0.1 g/cm3
Boiling Point
336.3±0.0 °c at 760 Mmhg
Melting Point
158-161 °c(Lit.)
Flash Point
144.5±19.1 °c
Molecular Formula
C7h6o3
Trademark
Hanhong
Transport Package
Customized
Specification
Customized
Origin
China
Model NO.
69-72-7
Wickr
Bellachen
Common Name
Salicylic Acid
CAS Number
69-72-7
Molecular Weight
138.121
Density
1.4±0.1 g/cm3
Boiling Point
336.3±0.0 °c at 760 Mmhg
Melting Point
158-161 °c(Lit.)
Flash Point
144.5±19.1 °c
Molecular Formula
C7h6o3
Trademark
Hanhong
Transport Package
Customized
Specification
Customized
Origin
China

Product Information

China Factory Supply 99.5%Min Salicylic Acid Powder CAS 69-72-7China Factory Supply 99.5%Min Salicylic Acid Powder CAS 69-72-7

Salicylic acid Biological Activity

DescriptionSalicylic acid inhibits cyclo-oxygenase-2 (COX-2) activity independently of transcription factor (NF-κB) activation.
Related Catalog
Signaling Pathways >> Autophagy >> Autophagy
Signaling Pathways >> Immunology/Inflammation >> COX
Signaling Pathways >> Autophagy >> Mitophagy
Research Areas >> Inflammation/Immun ology
Natural Products >> Phenols
Target

COX-2

Autophagy

Mitophagy

In VitroSalicylic 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 VivoIn 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].
Kinase AssayHuman purified COX-2 are and the cofactors Glutathione (5 mM), and Hematin (1 μM) are dissolved in 50 mM Tris buffer (pH 7.5). Hematin is first dissolved in a concentrated stock of 100 mM in 1 M NaOH before being further diluted in Tris buffer. Enzyme reactions are carried out in individual wells of 96-well plates with a final reaction volume of 200 μL. Different concentrations of Salicylic acid are added to the plate, followed by the addition of 10 units of enzyme (180 μL). The plates are incubated at 37° for 30 min before Arachidonic acid (10 nM to 30 μM) is added for a further 15 min. The reaction is stopped by heating the plate to 100°C for 5 min. The 96-well plate is then centrifuged at 10,000× g for 10 min, and appropriated samples are removed and added into the radioimmunoassay[1].
Cell AssayTo 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].
Animal AdminMice[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.

 Chemical & Physical Properties

Density1.4±0.1 g/cm3
Boiling Point336.3±0.0 °C at 760 mmHg
Melting Point158-161 °C(lit.)
Molecular FormulaC7H6O3
Molecular Weight138.121
Flash Point144.5±19.1 °C
Exact Mass138.031693
PSA57.53000
LogP2.06
Vapour density4.8 (vs air)
Vapour Pressure0.0±0.7 mmHg at 25°C
Index of Refraction1.616
Storage conditionStore at RT.
Water Solubility1.8 g/L (20 ºC)

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