Cell experiment:

HeLa and mouse melanoma B16F-10 cells are treated with 5, 10, 20 μM kinetin riboside for 48 h. 15 μL of MTT solution (5 mg/mL) is added to each well and cells are maintained for 4 h at 37℃. Hundred microlitres of solubilizing solution is then added. After an overnight incubation at room temperature, absorbance at 490 nm is measured[2].

Animal experiment:

Mice: Male C57BL/6 mice are injected B16 F-10 cells. After 5 days for tumor growth, kinetin riboside (10, 20, 40 mg/kg) is injected to tumor mass directly. Drug injection is performed once a 3 days for three times. After third injection of drug, mice are kept for 3 days with no injection and tumor mass is removed from each mouse and weighed[2].

Kinetin riboside, a cytokinin analog, can induce apoptosis in cancer cells. It inhibits the proliferation of HCT-15 cells with an IC50 of 2.5 μM. IC50: 2.5 μM (HCT-15 cells)[1]

Kinetin riboside displays antiproliferative and apoptogenic activity against various human cancer cell lines. Kinetin riboside is able to inhibit the proliferation in HCT-15 human colon cancer cells in a dose-dependent manner (IC50=2.5 μM)[1]. Kinetin riboside induces apoptosis in HeLa and mouse melanoma B16F-10 cells. Kinetin riboside disrupts the mitochondrial membrane potential and induces the release of cytochrome c and activation of caspase-3. Bad are up-regulated while Bcl-2 is down-regulated under kinetin riboside exposure[2].

Kinetin riboside significantly suppresses tumor growth. The most effective anti-melanoma response is elicited at 40 mg/kg[2].

[1]. Rajabi M, et al. Antiproliferative activity of kinetin riboside on HCT-15 colon cancer cell line. Nucleosides Nucleotides Nucleic Acids. 2012;31(6):474-81. [2]. Choi BH, et al. Kinetin riboside preferentially induces apoptosis by modulating Bcl-2 family proteins and caspase-3 in cancer cells. Cancer Lett. 2008 Mar 8;261(1):37-45.