BRCA2-RAD51-IN-3

BRCA2-RAD51-IN-3 (compound 19) inhibits the RAD51-BRCA2 protein-protein interaction in an in vitro ELISA assay with a EC₅₀ of 29.35 μM and a maximum inhibition of 76%^[1].
BRCA2-RAD51-IN-3 binds directly to recombinant human RAD51 with a K_d of 75.14 μM, as measured by MST^[1].
BRCA2-RAD51-IN-3 (50 μM; 1 μM RAD51 plus 2-5 μM BRC4 peptide) binds to the RAD51-BRCA2 interaction interface, as confirmed by NMR displacement assays^[1].
BRCA2-RAD51-IN-3 (10-80 μM) dose-dependently inhibits homologous recombination in BxPC-3 cells with an IC₅₀ of 21.74 μM, reaching 81% inhibition at 80 μM^[1].
BRCA2-RAD51-IN-3 (10-60 μM) inhibits homologous recombination in HEK-293 cells, reducing HR-proficient cells at 40 μM^[1].
BRCA2-RAD51-IN-3 disrupts RAD51 foci formation in BxPC-3 cells after Cisplatin (HY-17394)-induced DNA damage, consistent with inhibition of RAD51-BRCA2-mediated DNA repair^[1].
BRCA2-RAD51-IN-3 (40 μM; 6 days, in combination with 10 μM Olaparib (HY-10162) ) reduced cell viability synergistically in 2D BxPC-3 and HPAC cells (Interaction Index = 0.77 and 0.72, respectively), had no significant effect on the viability of normal H-6037 pancreatic epithelial cells, and induced apoptosis in BxPC-3 and HPAC cells as evidenced by a significantly increased BAX/BCL2 ratio.
BRCA2-RAD51-IN-3 (40-60 μM; 144 hours, in combination with 10 μM Olaparib) synergizes with Olaparib to reduce viability, inhibit growth, and induce cell death in BxPC-3 3D spheroids, with a 3D Interaction Index of 0.85 after 144 hours of treatment^[1].

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