产品
编 号：F511884
分子式：C23H26N2O2S
分子量：394.53
分子式：C23H26N2O2S
分子量：394.53
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是否有货
10mM*1mL in DMSO
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1mg
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5mg
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10mg
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25mg
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50mg
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100mg
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CAS No: 901751-47-1
产品详情
生物活性：
iCRT3 is an inhibitor of both Wnt and β-catenin-responsive transcription.
体内研究：
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. 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.
体外研究：
iCRT3 is an inhibitor of both Wnt and β-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. 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. Treatment with iCRT3 at doses of 12.5, 25, 50, and 75 μM decreases TNF-α levels by 14.7%, 18.5%, 44.9% and 61.3%, respectively. With iCRT3 treatment, IκB levels are increased in a dose-dependent manner compare to the vehicle.
iCRT3 is an inhibitor of both Wnt and β-catenin-responsive transcription.
体内研究：
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. 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.
体外研究：
iCRT3 is an inhibitor of both Wnt and β-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. 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. Treatment with iCRT3 at doses of 12.5, 25, 50, and 75 μM decreases TNF-α levels by 14.7%, 18.5%, 44.9% and 61.3%, respectively. With iCRT3 treatment, IκB levels are increased in a dose-dependent manner compare to the vehicle.
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