iCRT3

901751-47-1

C23H26N2O2S

DMSO : 150 mg/mL (380.20 mM; Need ultrasonic and warming)

Stem Cell/Wnt

iCRT3 is an inhibitor of both Wnt and beta-catenin-responsive transcription. IC50 & Target: Wnt^[1], beta-catenin-responsive transcription^[2] In Vitro: iCRT3 is an inhibitor of both Wnt and beta-catenin-responsive transcription. iCRT3 significantly decreases TOP Flash activity and reduces the level of NTSR1. The anti-apoptotic effects of Neurotensin (NTS) and Wnt3a can be largely abrogated by iCRT3^[1]. Cells maintained long term with iCRT3 show enhanced expression of classic pluripotency genes compare with the DMSO control, whereas expression of differentiation markers and T-cell factor (TCF) target genes is concomitantly reduced^[2]. Treatment with iCRT3 at doses of 12.5, 25, 50, and 75 uM decreases TNF-alpha levels by 14.7%, 18.5%, 44.9% and 61.3%, respectively. With iCRT3 treatment, IkappaB levels are increased in a dose-dependent manner compare to the vehicle^[3]. In Vivo: 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-1beta 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].