SCR7 inhibits end joining of double strand breaks in diverse cell types resulting in tumour regression by activation of p53 mediated apoptosis.SCR7 blocks Ligase IV-mediated joining by interfering with its DNA binding but not that of T4 DNA Ligase or Ligase I. 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 coadministered with DSB-inducing therapeutic modalities enhances their sensitivity significantly.SCR7 is a new anti cancer molecule having capability to selectively inhibit non-homologous end joining (NHEJ), one of the DNA double strand break (DSB) repair pathways inside the cells.
|Body Surface Area (m2)||0.007||0.025||0.15||0.05||0.02||0.5|
|Animal A (mg/kg) = Animal B (mg/kg) multiplied by||Animal B Km|
|Animal A Km|
For example, to modify the dose of resveratrol used for a mouse (22.4 mg/kg) to a dose based on the BSA for a rat, multiply 22.4 mg/kg by the Km factor for a mouse and then divide by the Km factor for a rat. This calculation results in a rat equivalent dose for resveratrol of 11.2 mg/kg.
Pluronic copolymer encapsulated SCR7 as a potential anticancer agent.
John F, et al. Faraday Discuss. 2015;177:155-61. PMID: 25608025.
Enhanced efficacy of pluronic copolymer micelle encapsulated SCR7 against cancer cell proliferation.
John F, et al. Macromol Biosci. 2015 Apr;15(4):521-34. PMID: 25515310.
An inhibitor of nonhomologous end-joining abrogates double-strand break repair and impedes cancer progression.
Srivastava M, et al. Cell. 2012 Dec 21;151(7):1474-87. PMID: 23260137.
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