| Name | 2,5-dimethyl Celecoxib |
| Description | 2,5-dimethyl Celecoxib is a celecoxib derivative and a targeted inhibitor of microsomal prostaglandin E synthase-1 (mPGES-1), a key enzyme in the PGE2 synthesis pathway of inflammatory mediators. |
| In vitro | 2,5-dimethyl Celecoxib(1–100?μM) decreased the viability of GBM cell lines in a dose-dependent manner. 2,5-dimethyl Celecoxib downregulated β-catenin target genes expression in A-172, T98G and U-138 MG cell lines. Apoptosis was induced, and cell cycle distribution was altered after the treatment with 2,5-dimethyl Celecoxib in T98G cell line.2,5-dimethyl Celecoxib downregulated β-catenin target genes expression in patient-derived primary GBM cell lines P1 and P6[1]. |
| In vivo | 2,5-dimethyl Celecoxib prevented cardiac remodeling and markedly reduced urinary albumin excretion without altering blood pressure in mice. 2,5-dimethyl Celecoxib prevented podocyte injury, glomerulosclerosis, and interstitial fibrosis in the kidney of mice loaded with angiotensin II and high-salt load. 2,5-dimethyl Celecoxib reduced the phosphorylation level of Akt and activated glycogen synthase kinase-3, which led to the suppression of the Wnt/β-catenin signal in the heart and kidney. 2,5-dimethyl Celecoxib also reduced the expression level of snail, a key transcription factor for the epithelial–mesenchymal transition and of which gene is a target of the Wnt/β-catenin signal[2]. |
| Storage | Powder: -20°C for 3 years | In solvent: -80°C for 1 year | Shipping with blue ice. |
| Solubility Information | Ethanol : 3 mg/mL
DMSO : 60 mg/mL (151.75 mM)
DMF : 5 mg/mL
DMSO:PBS (pH 7.2) (1:3) : 0.25 mg/mL
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| Keywords | 2,5-dimethyl Celecoxib | 2,5dimethyl Celecoxib | 2,5 dimethyl Celecoxib |
| Inhibitors Related | Stavudine | Sodium 4-phenylbutyrate | Tributyrin |
| Related Compound Libraries | Anti-Colorectal Cancer Compound Library | Pain-Related Compound Library | Bioactive Compound Library | Membrane Protein-targeted Compound Library | Anti-Ovarian Cancer Compound Library | Neuroprotective Compound Library | Inhibitor Library | Bioactive Compounds Library Max | GPCR Compound Library |
United States
