IBR120

IBR120 (4 days) exhibited growth inhibitory activity in MBA-MD-468 cells with an IC₅₀ of 3.1 μM^[1].
IBR120 (4 days) selectively inhibits the growth of multiple cancer cell lines (K562, MCF7, MDA-MB-231, MDA-MB-361, MDA-MB-435, MDA-MB-468, Hs578-T, T47D, U2OS, T98G, HeLa) with IC₅₀ values of 3~5 μM, while exhibiting significantly lower toxicity to normal MCF10A cells, with IC₅₀ > 30 μM^[1].
IBR120 (10-20 µM; 24) inhibits homologous recombination repair in HeLa cells stably expressing DR-GFP in a dose-dependent manner^[1].
IBR120 (4 days) significantly enhances the killing effect of various chemotherapeutic agents on cancer cells, such as Osimertinib (HY-15772), Afatinib (HY-10261), Lapatinib (HY-50898), Imatinib (HY-15463), Vemurafenib (HY-12057), Regorafenib (HY-10331), Enzalutamide (HY-70002), and Vincristine (HY-N0488A), reducing the IC₅₀ of these anticancer agents by up to 90%^[2].
IBR120 (24 h) reduced RAD51 protein levels by more than 80% in NSCLC cell lines^[2].
IBR120 inhibits HR, SSA, and Alt-EJ, but not NHEJ, in U2OS cells^[3].
IBR120 inhibits RAD51 foci formation in TNBC cells^[3].
IBR120 (1:10 molar ratio; 30 min) disrupts RAD51 multimerization, as shown by gel filtration profiles, with a major monomer peak appearing in the presence of IBR120^[1].
IBR120 eliminated the RAD51-DNA interaction in an FP-based cell-free assay^[3].

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