John Franklin, George Jinu, Srivastava Mrinal, Hassan P A, Aswal V K, Karki Subhas S, Raghavan Sathees C
Biotechnology Laboratory, PG and Research Department of Chemistry, Sacred Heart College, Kochi 682 013, India.
Faraday Discuss. 2015;177:155-61. doi: 10.1039/c4fd00176a.
Nonhomologous end joining (NHEJ) of DNA double strand breaks (DSBs) inside cells can be selectively inhibited by 5,6-bis-(benzylideneamino)-2-mercaptopyrimidin-4-ol (SCR7) which possesses anticancer properties. The hydrophobicity of SCR7 decreases its bioavailability which is a major setback in the utilization of this compound as a therapeutic agent. In order to circumvent the drawback of SCR7, we prepared a polymer encapsulated form of SCR7. The physical interaction of SCR7 and Pluronic® copolymer is evident from different analytical techniques. The in vitro cytotoxicity of the drug formulations is established using the MTT assay.
细胞内DNA双链断裂(DSB)的非同源末端连接(NHEJ)可被具有抗癌特性的5,6-双-(亚苄基氨基)-2-巯基嘧啶-4-醇(SCR7)选择性抑制。SCR7的疏水性降低了其生物利用度,这是将该化合物用作治疗剂的一个主要障碍。为了克服SCR7的缺点,我们制备了SCR7的聚合物包封形式。通过不同的分析技术可以明显看出SCR7与普朗尼克®共聚物之间的物理相互作用。使用MTT法确定了药物制剂的体外细胞毒性。