SCR7 is a potent and selective inhibitor of non-homologousend joining (NHEJ). It inhibits joining of DSBs in cell-free DNA repair system,blocks Ligase IV-mediated joining by interfering with its DNA binding but not thatof T4 DNA Ligase or Ligase I, thereby leading to accumulation of DSBs withinthe cells, culminating into cytotoxicity. SCR7 inhibits NHEJ in a LigaseIV-dependent manner within cells, and activates the intrinsic apoptoticpathway. More importantly, SCR7 impedes tumor progression in mouse models, andwhen co-administered with DSB-inducing therapeutic modalities it enhances theirsensitivity significantly. In addition, SCR7 can promote the efficiency of HDR4–5-fold for CRISPR editing in both human and mouse cell lines.

How to Use:

In vitro: SCR7was used at 20-150 µM final concentration in vitro and in cellular assays foranti-cancer. SCR7 was used at 1 µM final concentration in CRISPR editing.

In vivo: SCR7 was intraperitoneally (IP) dosed to miceat 20 mg/kg once per day.

Reference:

1. 1. SrivastavaM, et al. An inhibitor of nonhomologous end-joining abrogates double-strandbreak repair and impedes cancer progression. (2012) Cell. 151(7):1474-87.
2. 2. ChuVT, et al. Increasing the efficiency of homology-directed repair forCRISPR-Cas9-induced precise gene editing in mammalian cells. (2015) NatBiotechnol. In press.

SCR7_spec.pdf

SCR7_MSDS.pdf

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