Aurora kinase-IN-15

Aurora kinase-IN-15 (compound 25; 48 h) exhibits potent antiproliferative activity against MCF-7, HepG-2, HCT-116, and PC-3 cells with IC₅₀ values of 7.72, 9.51, 13.49, and 17.80 μM, respectively, while showing reduced cytotoxicity toward normal WI-38 fibroblasts (IC₅₀ = 39.44 μM)^[1].
Aurora kinase-IN-15 significantly reduces intracellular Aurora A kinase levels from 53.96 to 42.21 pg/mg protein (~22% reduction) and Aurora B kinase levels from 63.84 to 36.48 pg/mg protein (~43% reduction) in MCF-7 cells^[1].
Aurora kinase-IN-15 induces G₂/M phase arrest in MCF-7 cells, increasing the G₂/M population from 26.46% to 46.10%^[1].
Aurora kinase-IN-15 induces significant apoptosis in MCF-7 cells, decreasing viable cells from 93.79% to 45.31%, with increases in early apoptotic cells (2.13% to 7.99%) and late apoptotic cells (3.67% to 25.39%)^[1].
Aurora kinase-IN-15 (7.72 μM; 48 h) activates Caspase 3 (7.6-fold increase), upregulates Bax (7.9-fold increase), and downregulates Bcl-2 (0.46-fold decrease) in MCF-7 cells^[1].
Aurora kinase-IN-15 is predicted to have extremely low blood‑brain barrier penetration, poor water solubility and intestinal absorption, no CYP2D6 inhibitory effect, and high plasma protein binding rate^[1].
Aurora kinase-IN-15 is predicted to have lower toxicity than Danusertib (HY‑10179) (reduced mutagenicity and developmental toxicity, with only mild eye irritation), with an oral LD₅₀ of 16.27 mg/kg and a chronic LOAEL of 0.031 mg/day in rats^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.