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SML1546

Sigma-Aldrich

SCR7 pyrazine

≥98% (HPLC)

Synonyme(s) :

2,3-Dihydro-6,7-diphenyl-2-thioxo-4(1H)-pteridinone, 6,7-Diphenyl-2-thio-lumazine (8CI)

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About This Item

Formule empirique (notation de Hill):
C18H12N4OS
Numéro CAS:
Poids moléculaire :
332.38
Numéro MDL:
Code UNSPSC :
12352200
ID de substance PubChem :
Nomenclature NACRES :
NA.77

Niveau de qualité

Pureté

≥98% (HPLC)

Forme

powder

Couleur

faintly yellow to dark yellow

Solubilité

DMSO: 10 mg/mL, clear

Température de stockage

room temp

Chaîne SMILES 

O=C(C1=C(N2)N=C(C3=CC=CC=C3)C(C4=CC=CC=C4)=N1)NC2=S

InChI

1S/C18H12N4OS/c23-17-15-16(21-18(24)22-17)20-14(12-9-5-2-6-10-12)13(19-15)11-7-3-1-4-8-11/h1-10H,(H2,20,21,22,23,24)

Clé InChI

GSRTWXVBHGOUBU-UHFFFAOYSA-N

Description générale

SCR7 pyrazine is an inhibitor of DNA ligase IV.

Application

SCR7 pyrazine has been used as a non-homologous end joining (NHEJ) modulator to study its effect on CRISPR/Cas9-mediated editing.
SCR7 pyrazine has been shown to enhance CRISPR genome editing efficiency. To see other small molecule CRISPR enhancers, visit sigma.com/CRISPR-enhancers.

Actions biochimiques/physiologiques

SCR7 pyrazine is reported to be an inhibitor of non-homologous end joining (NHEJ) and has been shown to enhance the efficiency of CRISPR-Cas9 genome editing. The effect of SCR7 pyrazine on the efficiency and targeting precision of CRISPR applications has been shown to be cell type specific and context dependent. SCR7 pyrazine is a product of spontaneous cyclization of SCR7, first reported by Srivastava, M., et al.

Pictogrammes

Exclamation mark

Mention d'avertissement

Warning

Mentions de danger

Classification des risques

Acute Tox. 4 Oral

Code de la classe de stockage

11 - Combustible Solids

Classe de danger pour l'eau (WGK)

WGK 3

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable


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Consulter la Bibliothèque de documents

Yuanwu Ma et al.
RNA biology, 13(7), 605-612 (2016-05-11)
Precise modifications such as site mutation, codon replacement, insertion or precise targeted deletion are needed for studies of accurate gene function. The CRISPR/Cas9 system has been proved as a powerful tool to generate gene knockout and knockin animals. But the
Disruption of diphthamide synthesis genes and resulting toxin resistance as a robust technology for quantifying and optimizing CRISPR/Cas9-mediated gene editing.
Killian T, et al.
Scientific Reports, 7(1), 15480-15480 (2017)
Diane Yang et al.
Scientific reports, 6, 21264-21264 (2016-02-19)
Efficient gene editing is essential to fully utilize human pluripotent stem cells (hPSCs) in regenerative medicine. Custom endonuclease-based gene targeting involves two mechanisms of DNA repair: homology directed repair (HDR) and non-homologous end joining (NHEJ). HDR is the preferred mechanism
Justin Moser et al.
Proceedings of the National Academy of Sciences of the United States of America, 115(35), E8219-E8227 (2018-08-17)
The Restriction Point was originally defined as the moment that cells commit to the cell cycle and was later suggested to coincide with hyperphosphorylation of the retinoblastoma protein (Rb). Current cell cycle models posit that cells exit mitosis into a
Mrinal Srivastava et al.
Cell, 151(7), 1474-1487 (2012-12-25)
DNA Ligase IV is responsible for sealing of double-strand breaks (DSBs) during nonhomologous end-joining (NHEJ). Inhibiting Ligase IV could result in amassing of DSBs, thereby serving as a strategy toward treatment of cancer. Here, we identify a molecule, SCR7 that

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