SCR7 is a potent and selective inhibitor of non-homologous
end 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 that
of T4 DNA Ligase or Ligase I, thereby leading to accumulation of DSBs within
the cells, culminating into cytotoxicity. SCR7 inhibits NHEJ in a Ligase
IV-dependent manner within cells, and activates the intrinsic apoptotic
pathway. More importantly, SCR7 impedes tumor progression in mouse models, and
when co-administered with DSB-inducing therapeutic modalities it enhances their
sensitivity significantly. In addition, SCR7 can promote the efficiency of HDR
4–5-fold for CRISPR editing in both human and mouse cell lines.
How to Use:
In vitro:? SCR7
was used at 20-150 μM final concentration in vitro and in cellular assays for
anti-cancer. SCR7 was used at 1 μM final concentration in CRISPR editing.
In vivo: ?SCR7 was intraperitoneally (IP) dosed to mice
at 20 mg/kg once per day.
Reference:
1. Srivastava
M, et al. An inhibitor of nonhomologous end-joining abrogates double-strand
break repair and impedes cancer progression. (2012) Cell. 151(7):1474-87.
2. Chu
VT, et al. Increasing the efficiency of homology-directed repair for
CRISPR-Cas9-induced precise gene editing in mammalian cells. (2015) Nat
Biotechnol. In press.
Products are for research use only. Not for human use.