| Name | PLK1-IN-4 |
| Description | PLK1-IN-4 (compound 31) is a selective PLK1 inhibitor (IC50 < 0.51 nM) exhibiting antiproliferative activity against multiple cancer cell lines including A549, HT-29, and HCT-116. It induces cell cycle arrest and apoptosis, making it suitable for hepatocellular carcinoma research. |
| In vitro | PLK1-IN-4 (compound 31) (0–5 μM, 48 h) exhibits excellent antiproliferative activity against hepatocellular carcinoma (HCC) cells [1].
PLK1-IN-4 (60 and 100 nM, 24 h) induces abnormal spindle formation in the human hepatocellular carcinoma cell line HepG2 and the human colorectal cancer cell line HT-29 [1].
PLK1-IN-4 (10–300 nM, 0–48 h) can induce cancer cell apoptosis by arresting the cell cycle at the G2/M phase [1].
PLK1-IN-4 (0–120 nM, 24 h) dose-dependently increases the phosphorylation levels of PLK1, histone H3, and nucleophosmin (NPM), while decreasing the phosphorylation level of Cdc2 [1]. |
| In vivo | PLK1-IN-4 shows low metabolic stability in humans, mice, dogs and monkeys, with its hepatic clearance (CLhep) values of 74.3, 330.9, 61.5 and 196.5 mL/min/kg, respectively [1].
At a dose of 30 mg/kg administered via tail vein injection (once or twice daily for 12 consecutive days), PLK1-IN-4 suppresses tumour growth in a dose-dependent manner [1]. |
| Storage | Shipping with blue ice/Shipping at ambient temperature. |
| Inhibitors Related | Stavudine | Aceglutamide | Urea | Tamoxifen | Cysteamine hydrochloride | Metronidazole | Citric Acid Triammonium | Formamide | Dimethyl phthalate | Alginic acid | Sodium Molybdate | Sildenafil citrate |
| Related Compound Libraries | Bioactive Compound Library | Bioactive Compounds Library Max | Fluorochemical Library |
United States
