SCR7

SCR7 is a small molecule inhibitor of DNA ligase IV that prevents nonhomologous end-joining by interfering with ligase binding and activating apoptosis.¹ It also inhibits ligase III, but does not affect the activity of T4 DNA ligase or ligase I. SCR7 has been used to increase the rate of homology directed repair triggered by DNA double-strand breaks and to inhibit cancer cell growth in vitro (IC₅₀s = 8-120 µM) and in mouse models when co-administered with double-strand break-inducing therapeutic compounds.^1,2,3,4

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1. Srivastava, M., Nambiar, M., Sharma, S., et al. An inhibitor of nonhomologous end-joining abrogates double-strand break repair and impedes cancer progression. Cell 151(7), 1474-1487 (2012).

2. Chu, V.T., Weber, T., Wefers, B., et al. Increasing the efficiency of homology-directed repair for CRISPR-Cas9-induced precise gene editing in mammalian cells. Nat. Biotechnol. 33(5), 543-550 (2015).

3. John, F., George, J., Srivastava, M., et al. Pluronic copolymer encapsulated SCR7 as a potential anticancer agent. Faraday Discussions 177, 1-7 (2014).

4. Maruyama, T., Dougan, S.K., Truttmann, M.C., et al. Increasing the efficiency of precise genome editing with CRISPR-Cas9 by inhibition of nonhomologous end joining. Nat. Biotechnol. 33(5), 538-542 (2015).