2,5-dimethyl Celecoxib

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].

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].

Ethanol:3 mg/mL,DMSO:5 mg/mL,DMF:5 mg/mL,DMSO:PBS (pH 7.2) (1:3):0.25 mg/mL