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SML1546

Sigma-Aldrich

SCR7 pyrazine

≥98% (HPLC)

Sinónimos:

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

Fórmula empírica (notación de Hill):
C18H12N4OS
Número de CAS:
14892-97-8
Peso molecular:
332.38
MDL number:
MFCD02167478
UNSPSC Code:
12352200
PubChem Substance ID:
329825955
NACRES:
NA.77

Quality Level

100

assay

≥98% (HPLC)

form

powder

color

faintly yellow to dark yellow

solubility

DMSO: 10 mg/mL, clear

storage temp.

room temp

SMILES string

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)

InChI key

GSRTWXVBHGOUBU-UHFFFAOYSA-N

General description

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.

Biochem/physiol Actions

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.

pictograms

Exclamation mark
GHS07

signalword

Warning

hcodes

H302

Hazard Classifications

Acute Tox. 4 Oral

Storage Class

11 - Combustible Solids

wgk_germany

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

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Certificados de análisis (COA)

Lot/Batch Number
026M4608V

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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
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
pRB-Depleted Pluripotent Stem Cell Retinal Organoids Recapitulate Cell State Transitions of Retinoblastoma Development and Suggest an Important Role for pRB in Retinal Cell Differentiation.
Rozanska, et al.
Stem Cells Translational Medicine, 11, 415-433 (2023)
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
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Modulation of homology-directed repair (HDR) within the context of CRISPR-genome editing has led to the identification of small molecules that enhance CRISPR-mediated HDR efficiency in various cell types.

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Modulation of homology-directed repair (HDR) within the context of CRISPR-genome editing has led to the identification of small molecules that enhance CRISPR-mediated HDR efficiency in various cell types.

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Modulation of homology-directed repair (HDR) within the context of CRISPR-genome editing has led to the identification of small molecules that enhance CRISPR-mediated HDR efficiency in various cell types.

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