Powder: -20°C for 3 years | In solvent: -80°C for 1 year
Cantrixil (TRX-E-002-1) is a second-generation super-benzopyran (SBP) compound, derived from TRX-E-002. It elicits an increase in phosphorylated c-Jun levels, leading to caspase-mediated apoptosis in ovarian cancer cells. Cantrixil exhibits potent pan anti-cancer activity against various cancer phenotypes.
产品描述 | Cantrixil (TRX-E-002-1) is a second-generation super-benzopyran (SBP) compound, derived from TRX-E-002. It elicits an increase in phosphorylated c-Jun levels, leading to caspase-mediated apoptosis in ovarian cancer cells. Cantrixil exhibits potent pan anti-cancer activity against various cancer phenotypes. |
体外活性 | TRX-E-002-1 shows broad cytotoxic activity against ovarian, prostate and lung cancer cells, with IC 50 values of ≤0.1 μM (SK-OV-3, JAM, OVCAR-3 cells: IC 50 =0.023-0.065 μM; DU145, PC3; C4-2B cells: IC 50 =0.014-0.096 μM; A549 cells: IC 50 =0.058 μM). Activity in pancreatic and colorectal cancer cells and glioblastoma cells are more variable[1]. Cantrixil (0.2 μM; 2-24 hours) shows high levels of phosphorylated c-Jun (p-c-Jun) and low levels of phosphorylated-ERK (p-ERK)[2]. Cantrixil (2.45 μM; 2-24 hours) induces a significant increase in both caspase-3/7 and caspase-9 activity at 16 and 24 hours[2]. TRX-E-002-1 inhibits multiple cytochrome P450 drug-metabolizing enzymes, including CYP2C9, CYP2C8, CYP2C19, CYP2B6, CYP3A4, CYP2D6, CYP2A6 and CYP1A2. IC 50 values ranges from 1.5 to 75 μM (612-30,600 ng/mL)[1]. Western Blot Analysis[2]Cell Line: Ovarian cancer stem cells (OCSCs) Concentration: 0.2 μM Incubation Time: 2, 4, 8, 16, 24 hours Result: Showed higher levels of phosphorylated c-Jun (p-c-Jun) and lower levels of phosphorylated-ERK (p-ERK). Showed a time-dependent increase in p-c-Jun accompanied by a time-dependent increase in total c-Jun. |
体内活性 | TRX-E-002-1 (100 mg/kg/day; IP; for 13-14 days) significantly inhibits tumour growth in disseminated ovarian cancer mouse model[1]. TRX-E-002-1 (100 mg/kg/day; IP; for 4 weeks) inhibits tumour growth and reduces terminal tumour burden by 77% in the recurrent ovarian cancer mouse model[1]. TRX-E-002-1 (100 mg/kg/day; IP; for 18 days) significantly reduces terminal pancreatic tumour burden in a mouse model of pancreatic cancer (human Panc-1 pancreatic tumour cells implanted orthotopically into female NOD-SCID mice)[1]. TRX-E-002-1 (100 mg/kg; IP) has a T 1/2 of 2.5 hours, a C max of 8355 ng/mL and an AUC 0-∞ of 40600 ng?h/mL[1]. Animal Model: Disseminated ovarian cancer mouse model[1]Dosage: 100 mg/kg (dissolved in 20% SBECD) Administration: IP; once daily; for 13-14 days Result: Significantly inhibited tumour growth and reduced excised tumour weight at termination by 50-72%. Animal Model: Male female Sprague-Dawley rats[1]Dosage: 100 mg/kg (Pharmacokinetic Analysis) Administration: IP Result: Had a T 1/2 of 2.5 hours, a C max of 8355 ng/mL and an AUC 0-∞ of 40600 ng?h/mL. |
别名 | TRX-E-002-1 |
分子量 | 408.45 |
分子式 | C24H24O6 |
CAS No. | 2135511-22-5 |
Powder: -20°C for 3 years | In solvent: -80°C for 1 year
对于不同动物的给药剂量换算,您也可以参考 更多...
请在以下方框中输入您的动物实验信息后点击计算,可以得到母液配置方法和体内配方的制备方法: 比如您的给药剂量是10 mg/kg,每只动物体重20 g,给药体积100 μL,一共给药动物10 只,您使用的配方为5% DMSO+30% PEG300+5% Tween 80+60% ddH2O。那么您的工作液浓度为2 mg/mL。
母液配置方法:2 mg 药物溶于 50 μL DMSO (母液浓度为 40 mg/mL), 如您需要配置的浓度超过该产品的溶解度,请先与我们联系。
体内配方的制备方法:取 50 μL DMSO 主液,加入 300 μL PEG300, 混匀澄清,再加 50 μL Tween 80,混匀澄清,再加 600 μL ddH2O, 混匀澄清。
您可能有的问题的答案可以在抑制剂处理说明中找到,包括如何准备库存溶液,如何存储产品,以及基于细胞的分析和动物实验需要特别注意的问题。
Cantrixil 2135511-22-5 TRX-E-002-1 Inhibitor inhibitor inhibit