SCR7-DataSheet-MedChemExpress

1、Hotline: 400-820-3792Inhibitors Agonists Screening Librarieswww.MedChemESCR7Cat. No.: HY-12742CAS No.: 1533426-72-0分式: CHNOS分量: 334.39作靶點: DNA/RNA Synthesis; CRISPR/Cas9作通路: Cell Cycle/DNA Damage儲存式: Powder -20C 3 years4C 2 yearsIn solvent -80C 6 months-20C 1 month溶解性數(shù)據(jù)體外實驗 DMSO : 45 mg/mL (134.57 m

2、M)* means soluble, but saturation unknown.Mass Solvent1 mg 5 mg 10 mg Concentration制備儲備液1 mM 2.9905 mL 14.9526 mL 29.9052 mL5 mM 0.5981 mL 2.9905 mL 5.9810 mL10 mM 0.2991 mL 1.4953 mL 2.9905 mL請根據(jù)產(chǎn)品在不同溶劑中的溶解度，選擇合適的溶劑配制儲備液，并請注意儲備液的保存式和期限。體內(nèi)實驗 請根據(jù)您的實驗動物和給藥式選擇適當(dāng)?shù)娜芙獍?，配制前請先配制澄清的儲備液，再依次添加助溶?為保證實驗結(jié)果的可靠性，體

3、內(nèi)實驗的作液，建議您現(xiàn)現(xiàn)配，當(dāng)天使；澄清的儲備液可以根據(jù)儲存條件，適當(dāng)保存；以下溶劑前的百分 指該溶劑在您配制終溶液中的體積占)：1. 請依序添加每種溶劑： 10% DMSO 40% PEG300 5% Tween-80 45% salineSolubility: 2.5 mg/mL (7.48 mM); Clear solutionBIOLOGICAL ACTIVITY1/3 Master of Small Molecules 您邊的抑制劑師www.MedChemE物活性 SCR7具有抗癌活性的 DNA 連接酶 IV 抑制劑， 也 CRISPR HDR 增強劑，可提 Cas9 介導(dǎo)的 HDR

4、 的效率 12。IC50 & Target DNA Ligase IV CRISPR/Cas9體外研究 SCR7 inhibits joining of double-strand breaks (DSBs) in cell-free repair system. SCR7 blocks Ligase IV-mediated joining by interfering with its DNA binding but not that of T4 DNA Ligase or Ligase I. SCR7 inhibitsNHEJ in a Ligase IV-dependent manner

5、 within cells, and activates the intrinsic apoptotic pathway. Resultsshow a dose-dependent decrease in cell proliferation of MCF7, A549, and HeLa with an IC50 of 40, 34, and 44M, respectively, which is further confirmed by DIC imaging in MCF7. T47D, A2780, and HT1080 are alsosensitive to SCR7, with

6、an IC50 of 8.5, 120, and 10 M, respectively 1.體內(nèi)研究 SCR7 treatment (10 mg/kg, six doses) significantly reduces breast adenocarcinoma-induced tumor. Untreatedtumor animals survived only for 52 days, whereas treated animals exhibit 4-fold increase in lifespan 1.PROTOCOLCell Assay 3 Wild-type, AAVS1TLR

7、HEK293 and mouse NIH3T3 cells are maintained in DMEM supplied with 15% FBS,cells are passaged three times per week. The mouse Burkitt lymphoma cell line, generated from a Burkitt-likemouse lymphoma is maintained in DMEM supplied with 15% FBS, 2 mM HEPES, 2 mM sodium pyruvate, 2mM L-glutamine, and 1

8、NAA, beta-mercaptoethanol and passaged four times per week. For puromycinselection, mCherry+ cells are sorted, seeded at 103 cells/well and selected with 3 mg/mL of Puromycin for 2weeks. Then colonies are counted and single cells are sorted. The SCR7 inhibitor is purchased, 12 h aftertransfection th

9、ese cells are maintained in complete medium supplied with 1 mM SCR7 inhibitor until analysis.At SCR7 concentrations of 60 mM and 10 mM, A reduction of transfection efficiency and of cell viability isobserved 3.MCE has not independently confirmed the accuracy of these methods. They are for reference

10、only.Animal Mice 1Administration 1 BALB/c mice are injected with DLA cells (0.25106) intraperitoneally for tumor development, after which twobatches of animals are divided into eight subgroups. Treatment is started after 5 days of DLA injection (d 0).Group I serves as tumor control (n=10). Group II

11、(IR, n=5) and III (IR+SCR7, n=5) receive two doses ofradiation (2 Gy) on day 0 and 4. Besides radiation, Group III also receives six doses of SCR7 (20 mg/kg) onalternate days from day 0. Group IV (Etoposide, n=5) and V (Etoposide+SCR7, n=5) received three doses ofEtoposide (10 mg/kg) intraperitoneal

12、ly on day 0, 4, and 8. In addition to Etoposide, Group V animals alsoreceive six doses of SCR7 (20 mg/kg) on alternate days from day 0. Group VI (3-ABA, n=5) and VII (3-ABA+SCR7, n=5) received three doses of 3-Aminobenzamide (10 mg/kg) on days 0, 4, and 8. Group VIIreceives six doses of SCR7. Group

13、VIII (SCR7, n=5) receives six doses of SCR7 alone (20 mg/kg) onalternate days (0, 2, 4, 6, 8, and 10) and serves as the control. Progression of tumor is monitored and dataare presented as a bar diagram. Error bars and levels of significance are indicated in respective figurelegends.MCE has not indep

14、endently confirmed the accuracy of these methods. They are for reference only.2/3 Master of Small Molecules 您邊的抑制劑師www.MedChemE戶使本產(chǎn)品發(fā)表的科研獻 EMBO Rep. 2019 Mar;20(3). pii: e46821. J Mol Med (Berl). 2019 Jun 14. Onco Targets Ther. 2018 Aug 17;11:4945-4953.See more customer validations on HYPERLINK / ww

15、w.MedChemEREFERENCES1. Srivastava M, et al. An inhibitor of nonhomologous end-joining abrogates double-strand break repair and impedes cancer progression.Cell. 2012 Dec 21;151(7):1474-87.2. Lin C, et al. Increasing the Efficiency of CRISPR/Cas9-mediated Precise Genome Editing of HSV-1 Virus in Human Cells. Sci Rep. 2016Oct 7;6:34531.3. Chu VT, et al. Increasing the efficiency of homology-directed repair for CRISPR-Cas9-induced precise gene editing inmammaliancells.Nat