SCR7

Description	in vitro: SCR7 does not induce DSBs directly to the genome and is Ligase IV dependent. Besides, upon incubation of oligomeric dsDNA or supercoiled plasmid DNA with increasing concentrations of SCR7, there was no evidence for DNA breaks. Accumulation of DSBs leads to cell death upon SCR7 treatment with a dose-dependent decrease in cell proliferation of MCF7, A549, and HeLa with an IC50 of 40, 34, and 44 μM, respectively, which was further confirmed by DIC imaging in MCF7. T47D, A2780, and HT1080 were also sensitive to SCR7, with an IC50 of 8.5, 120, and 10 μM, respectively. SCR7 encapsulated micelles (ES) were also characterized by small-angle neutron scattering (SANS). Encapsulated SCR7 treatment resulted in accumulation of DNA breaks within the cells, resulting in cell cycle arrest at G1 phase and activation of apoptosis. in vivo: SCR7 treatment (10 mg/kg, six doses) significantly reduced breast adenocarcinoma-induced tumor in mice. Untreated tumor animals survived only for 52 days, w
Pathways	Cell Cycle/DNA Damage
Targets	DNA/RNA Synthesis

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