The tumor growth rates are markedly retarded by iCRT3 treatment. Consistently, the tumor-suppressive role of iCRT3 is accompanied with a reduction in Ki67 index, a proliferation marker[1]. The IL-6 levels in the 10 mg/kg iCRT3 treatment group are 82.9% lower than those in the vehicle group. IL-1β levels are undetectable in the sham but reach 371 pg/mL in septic mice and are down by 30.2% and 53.2%, respectively, with 5 and 10 mg/kg iCRT3. With iCRT3 treatment at doses of 5 and 10 mg/kg, AST levels in these septic mice are 15.4% and 44.2% lower, respectively, than those in the vehicle-treated mice. After treatment with 10 mg/kg iCRT3, lung morphology is improved with much reduced microscopic deterioration, compare to the vehicle group. The number of apoptotic cells in the lung tissues of the iCRT3-treated mice is significantly reduced by 92.7% in comparison with the vehicle group[3].
![2-[[[2-(4-ethylphenyl)-5-methyl-4-oxazolyl]methyl]thio]-N-(2-phenylethyl)acetamide Structure](https://www.chemicalbook.com/CAS/20180703/GIF/901751-47-1.gif)
