SCR7 pyrazine (SCR7) enhances CRISPR-Cas9-mediated homology-directed repair (HDR) efficiency in vitro up to 19-fold. Inhibits nonhomologous end-joining (NHEJ).

SCR7在200μM及以上浓度下有效抑制多聚体的形成。SCR7成功抑制了MCF7、A549、HeLa、T47D、A2780、HT1080和Nalm6细胞的增殖，其IC50分别为40、34、44、8.5、120、10和50μM。[1] SCR7抑制了CRISPR-Cas9诱导的DSBs的NHEJ修复。[2]

SCR7处理（10 mg/kg，肌肉注射）显著减少了乳腺腺癌诱导的肿瘤，并且与对照组相比，生命期增加了4倍。然而，在携带Dalton's淋巴瘤肿瘤模型的瑞士白鼠中，SCR7（20 mg/kg，腹腔注射）既不表现出肿瘤退缩也不增加生命期。在BALB/c小鼠中，SCR7（20 mg/kg，腹腔注射）显著增强了辐射、依托泊苷和3-氨基苯甲酰胺对源自Dalton's淋巴瘤（DLA）细胞的肿瘤的细胞毒作用。[1]

Complementation of SCR7 Inhibition with Puri?ed Ligase IV: Complementation experiment is carried out by adding increasing concentrations of puri?ed Ligase IV/XRCC4 complex (30, 60, and 120 fmol) along with the oligomeric DNA substrates (5' compatible and 5'-5' noncompatible ends) to the SCR7-treatedextracts. Reactions are incubated for 2 h at 25℃. The reaction products are then resolved on 8% denaturing PAGE. The gel is dried and exposed and the signal is detected with a PhosphorImager and analyzed with Multi Gauge (V3.0) software.

Cell proliferation of cancer cells are determined by MTT and trypan blue assays. Briefly, MCF7, CEM, HeLa, A549, HT1080, A2780, T47D, Nalm6, N114 and K562 cells are grown in presence of SCR7 (10, 50, 100, and 250?μM) for 24 or 48?h, and subjected to MTT or trypan blue assays. Each experiment is repeated a minimum of three independent times. (Only for Reference)