SCR7 pyrazine
SCR7 pyrazine structure
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Common Name | SCR7 pyrazine | ||
|---|---|---|---|---|
| CAS Number | 14892-97-8 | Molecular Weight | 332.37900 | |
| Density | N/A | Boiling Point | N/A | |
| Molecular Formula | C18H12N4OS | Melting Point | 209 °C | |
| MSDS | Chinese USA | Flash Point | N/A | |
| Symbol |
GHS07 |
Signal Word | Warning | |
Use of SCR7 pyrazineSCR7 pyrazine is a DNA ligase IV inhibitor that blocks nonhomologous end-joining (NHEJ) in a ligase IV-dependent manner. SCR7 pyrazine is also a CRISPR/Cas9 enhancer which increases the efficiency of Cas9-mediated homology-directed repair (HDR). SCR7 pyrazine induces cell apoptosis and has anticancer activity[1][2]. |
| Name | 6,7-diphenyl-2-sulfanylidene-1H-pteridin-4-one |
|---|---|
| Synonym | More Synonyms |
| Description | SCR7 pyrazine is a DNA ligase IV inhibitor that blocks nonhomologous end-joining (NHEJ) in a ligase IV-dependent manner. SCR7 pyrazine is also a CRISPR/Cas9 enhancer which increases the efficiency of Cas9-mediated homology-directed repair (HDR). SCR7 pyrazine induces cell apoptosis and has anticancer activity[1][2]. |
|---|---|
| Related Catalog | |
| Target |
DNA Ligase IV[1] CRISPR/Cas9[2] |
| In Vitro | SCR7 pyrazine (20-100 μM; 24 hours; MCF7 cells) treatment interferes with NHEJ in cells, leading to accumulation of unrepaired double-strand breaks (DSBs)[1]. SCR7 pyrazine treatment shows a dose-dependent decrease in cell proliferation with IC50 values of 40 μM, 34 μM, 44 μM, 8.5 μM, 120 μM, 10 μM and 50 μM for MCF7, A549, HeLa, T47D, A2780, HT1080 and Nalm6 cells, respectively[1]. In MCF7 cells, SCR7 pyrazine (20, 40 μM) treatment increases phosphorylation of ATM and activates p53, decreases MDM2, BCL2, resulting in activation of proapoptotic proteins, PUMA and BAX. And the shorter fragments of MCL1, PARP1, Caspase 3, and Caspase 9 cleavage are upregulated in a dose-dependent manner[1]. Western Blot Analysis[1] Cell Line: MCF7 cells Concentration: 20 μM, 40 μM, 100 μM Incubation Time: 24 hours Result: Showed an increase in levels of gH2AX foci and protein. |
| In Vivo | SCR7 pyrazine (10 mg/kg; intraperitoneal injection; six doses; BALB/c mice) treatment significantly reduces breast adenocarcinoma-induced tumor and increases lifespan[1]. Animal Model: BALB/c mice injected with breast adenocarcinoma cells[1] Dosage: 10 mg/kg Administration: Intraperitoneal injection; on alternate days (0, 2, 4, 6, 8, and 10) Result: Significantly reduced breast adenocarcinoma-induced tumor and increased lifespan. |
| References |
| Melting Point | 209 °C |
|---|---|
| Molecular Formula | C18H12N4OS |
| Molecular Weight | 332.37900 |
| Exact Mass | 332.07300 |
| PSA | 110.59000 |
| LogP | 3.74810 |
| Symbol |
GHS07 |
|---|---|
| Signal Word | Warning |
| Hazard Statements | H302 |
| Precautionary Statements | P301 + P312 + P330 |
| RIDADR | NONH for all modes of transport |
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Increasing the efficiency of CRISPR/Cas9-mediated precise genome editing in rats by inhibiting NHEJ and using Cas9 protein.
.PubMed ID 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 pow... |
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Enrichment of G2/M cell cycle phase in human pluripotent stem cells enhances HDR-mediated gene repair with customizable endonucleases.
Sci. Rep. 6 , 21264, (2016) 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: homo... |
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Increasing the efficiency of precise genome editing with CRISPR-Cas9 by inhibition of nonhomologous end joining.
Nat. Biotechnol. 33(5) , 538-42, (2015) Methods to introduce targeted double-strand breaks (DSBs) into DNA enable precise genome editing by increasing the rate at which externally supplied DNA fragments are incorporated into the genome thro... |
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| 2-Thioxo-4-oxo-6,7-diphenyl-1H,3H-pteridin |
| 6,7-diphenyl-2-thioxo-2,3-dihydro-1H-pteridin-4-one |
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| SCR7 pyrazine |