3-Arylisoquinolinylamine derivative is a 3-arylisoquinolinylamine derivative that was taken out of compound 7b in reference [1]. The initial phase and its derivative (7b) of 3-arylisoquinolinylamine are the same. In comparison to paclitaxel, the more strong active cytotoxic anticancer medication paclitaxel is exhibited by the paclitaxel-resistant HCT-15 human colorectal cancer cell line. use of flow cytometry for the analysis of cell cycle dynamics. When 3-arylisoquinolinylamine derivatives (7b) are administered to human HCT-15 cells, they cause cell death and inhibit or impede the cells' transition from the G0/G1 phase into the S phase. In addition, treatment with 3-arylisoquinolinamine derivatives (7b) dramatically reduced tumor growth and improved tumor regression in an HCT-15 xenograft model resistant to paclitaxel. 3. With IC50 values ranging from 14 nM to 32 nM, 3-Arylisoquinolinylamine derivatives (7b) suppressed cell proliferation in tested human cancer cells. Using HCT-15 cells for cell cycle analysis, 1 nM treatment The 3-arylisoquinolinylamine derivative (7b) demonstrated a considerable rise in the G0/G1 phase and a decrease in the G2/M phase at 24 hours, but not the G0/G1 phase. The G1 phase did not significantly increase at 48 hours. The G0/G1 phase rose dramatically after 24 and 48 hours, the G2/M phase reduced, and a sub-G1 phase appeared at a greater concentration of 3-arylisoquinolinylamine derivative (7b) (10 nM). 3-Arylisoquinolinamine derivatives (7b) cause cell death by preventing or delaying the entry of cells from G0/G1 phase into S phase [1]. The 3-arylisoquinolinylamine derivative, or 3-arylisoquinolinylamine derivative 13, was taken from reference [1]. In colon cancer cells, a 3-arylisoquinolinamine derivative (compound 13) was evaluated, and its anticancer efficacy was contrasted with that of paclitaxel. Using IC50 values in the low nanomolar range, 3-Arylisoquinolinylamine derivatives (IC50: 15 nM in HCT-15 cells, 17 nM in HCT116 cells) shown strong antiproliferative activity in both cells. Additionally, on 15 colorectal cancer cells, paclitaxel-resistant HCT exhibited greater antitumor efficacy than paclitaxel [2].

In animal tests, the 3-arylisoquinolinamine derivative (compound 13) inhibits tumor growth more effectively than the control medication paclitaxel (48.8% inhibition) with a 69.2% inhibition rate [2].

[1]. Synthesis, in vitro and in vivo evaluation of 3-arylisoquinolinamines as potent antitumor agents. Bioorg Med Chem Lett. 2010 Sep 1;20(17):5277-81.

[2]. 5, 6, or 7-substituted-s- (hetero)arylisoquinolinamine derivatives as antitumor agents. WO 2008063548 A2.

293.153

1029008-71-6

24801853

Light yellow to yellow solid powder

4.139

1

4

3

22

362

0

SSNNAZIMPALQIR-UHFFFAOYSA-N

InChI=1S/C18H19N3O/c1-21(2)14-8-7-12-10-17(20-18(19)16(12)11-14)13-5-4-6-15(9-13)22-3/h4-11H,1-3H3,(H2,19,20)

3-(3-methoxyphenyl)-7-N,7-N-dimethylisoquinoline-1,7-diamine

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ≥ 50 mg/mL (~170.44 mM)

Solubility in Formulation 1: ≥ 2.75 mg/mL (9.37 mM) (saturation unknown) in 10% DMSO + 40% PEG300 +5% Tween-80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 27.5 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 + to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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 (Please use freshly prepared in vivo formulations for optimal results.)