3-arylisoquinolinamine derivative (7b) shows more effective activity against Paclitaxel-resistant HCT-15 human colorectal cancer cell lines when compared to the original cytotoxic cancer drug, Paclitaxel. The cell cycle dynamics is analyzed by flow cytometry. Treatment of human HCT-15 cells with 3-arylisoquinolinamine derivative (7b) blocks or delays the progression of cells from the G0/G1 phase into the S phase, and induces cell death. 3-arylisoquinolinamine derivative (7b) inhibits the cell growth (IC50: 14 nM to 32 nM). In cell cycle analysis using HCT-15 cells, the treatment of 1 nM of 3-arylisoquinolinamine derivative (7b) displays a significant increase in G0/G1 phase at 24 h with a decrease in G2/M phase, but the increase of G0/G1 phase at 48 h is not significant. At a higher concentration of 3-arylisoquinolinamine derivative (7b) (10 nM), there are a significant increase in G0/G1 phase and a decrease in G2/M phase, and the emergence of sub-G1phase, at both 24 h and 48 h. 3-arylisoquinolinamine derivative (7b) blocks or delays the progression of cells from the G0/G1 phase into S phase, and induces cell death [1]. 3-arylisoquinolinamine derivative (compound 13; IC50: 15 nM in HCT-15 cells, 17 nM in HCT116 cells) shows potent antiproliferative activities with IC50 value in the low nanomolar range in both cells and higher antitumor activities than that of Paclitaxel against Paclitaxel-resistant HCT-15 colorectal cancer cells [2].

3-arylisoquinolinamine derivative has higher antitumor efficacy (69.2 % inhibition) than that of the control drug, Paclitaxel (48.8 % inhibition) in the inhibition of growth of tumor in an animal model [2].