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Propyl gallate PPAR inhibitor

Cat.No.S5113

Propyl gallate (Gallic acid propyl esterZ, n-Propyl gallate) is an antioxidant used in foods especially animal fats and vegetable oils, also in a wide variety of cosmetics and beauty care products.
Propyl gallate PPAR inhibitor Chemical Structure

Chemical Structure

Molecular Weight: 212.20

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Quality Control

Batch: S511301 DMSO]42 mg/mL]false]]]false]]]false Purity: 99.92%
99.92

Solubility

In vitro
Batch:

DMSO : 42 mg/mL (197.92 mM)
(Moisture-contaminated DMSO may reduce solubility. Use fresh, anhydrous DMSO.)

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In vivo
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Method for preparing DMSO master liquid: mg drug pre-dissolved in μL DMSO ( Master liquid 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 master liquid, next addμL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O, mix and clarify.

Method for preparing in vivo formulation: Take μL DMSO master liquid, next add μL Corn oil, mix and clarify.

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Chemical Information, Storage & Stability

Molecular Weight 212.20 Formula

C10H12O5

Storage (From the date of receipt)
CAS No. 121-79-9 Download SDF Storage of Stock Solutions

Synonyms Gallic acid propyl esterZ, n-Propyl gallate Smiles CCCOC(=O)C1=CC(=C(C(=C1)O)O)O

Mechanism of Action

In vitro
Propyl gallate (PG) could modulate heme oxygenase-1 (HO-1) activation and decrease lung cancer cell survival. This compound also induces apoptosis in human leukemia cells and HeLa cells by increasing reactive oxygen species (ROS) levels and glutathione (GSH) depletion. It inhibits the expression of MMP-2 and MMP-9 and exerts an antimigration effect on TMZ-treated U87MG cells. This chemical also possesses anti-inflammatory activity via downregulation of the NF-κB pathway. It could reduce the proliferation and augment the chemosensitivity of a THP-1 leukemia cell line via extrinsic and intrinsic apoptotic pathways.
In vivo
In brain ischemia, Propyl gallate inhibits the activity of NF-κB, reduces COX-2 and TNF-alpha G expression, and decreases ischemic-reperfusion injury.
References

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