SCR7 pyrazine | CRISPR enhancer

SCR7 pyrazine (14892-97-8) enhances the efficiency of precise genome editing with CRISPR/Cas9 up to 19-fold via inhibition of nonhomologous end joining (NHEJ).^1,2 May be employed in an optimized CRISPR/Cas9 method to target methylation in a site-specific manner enabling maintenance of gene silencing in vitro and in vivo.³ SCR7 pyrazine exhibits greater activity against DNA ligases I and III than DNA ligase IV.⁴  Induces cancer cell death via inhibition of NHEJ and potentiates the effect of double strand break-inducing therapeutic modalities.^4,5

References/Citations:

1. Maruyama et al. (2015), Increasing the efficiency of precise genome editing with CRISPR-Cas9 by inhibition of nonhomologous end joining; Nat. Biotechnol. 33 538
2. Chu et al. (2015), Increasing the efficiency of homology-directed repair for CRISPR-Cas9-induced precise gene editing in mammalian cells; Nat. Biotechnol. 33 543
3. Wang et al. (2022), CRISPR/Cas9-mediated epigenetic editing tool: An optimized strategy for targeting de novo DNA methylation with stable status via homology directed repair pathway; Nat. Med. 202 190
4. Greco et al. (2016), SCR7 is neither a selective nor a potent inhibitor of human DNA ligase IV; DNA Repair (Amst) 43 18
5. Vartak et al. (2018), Autocyclized and oxidized forms of SCR7 induce cancer cell death by inhibiting nonhomologous DNA end joining in a Ligase IV dependent manner; FEBS J. 285 3959