SeSA-HCPT

SeSA-HCPT (48 h) exerts superior selective cytotoxicity against AR-positive (LNCaP) and AR-negative (PC3, DU145) human prostate cancer cells with IC50 values of 0.182, 0.198 and 0.175 μM, with minimal toxicity to normal human keratinocyte HaCaT cells (IC₅₀ =5.17 μM)^[1].
SeSA-HCPT (200 nM; 24-48 h) induces significantly higher apoptosis in PC3, DU145, and LNCaP human prostate cancer cells^[1].
SeSA-HCPT (0.175-5.17 μM; 24 h) induces S-phase cell cycle arrest in PC3, DU145, and LNCaP human prostate cancer cells, with no effect on normal human keratinocyte HaCaT cells, and upregulates Cyclin E expression in PC3 and DU145 cells^[1].
SeSA-HCPT (3-10 μM) inhibits Topo1-mediated DNA relaxation, and exhibits binding affinity for the Topo1-DNA complex than HCPT, enhancing its ability to block Topo1 catalytic function^[1].
SeSA-HCPT (1.25-5 nM) inhibits HDAC activity in PC3 and DU145 human prostate cancer cells^[1].
SeSA-HCPT (1.25-5 nM) induces dose-dependent DNA damage in PC3 and DU145 human prostate cancer cells, as measured by increased γ-H2AX levels^[1].
SeSA-HCPT (5 nM; 24-48 h) significantly inhibits proliferation and migration of PC3 and DU145 human prostate cancer cells^[1].
SeSA-HCPT (0-50 nM; 24 h) impairs homologous recombination-mediated DNA repair in PC3 and DU145 human prostate cancer cells by downregulating KIF4A and reducing Rad51 recruitment to DNA damage sites, while inducing a DNA damage response, and induces a dose-dependent decrease in KIF4A levels from 0 to 50 nM^[1].

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