NJT-12
NJT-12 is a PARP-1 and CK2α inhibitor with IC50 values of 3.40 nM and 4.31 nM, respectively. NJT-12 blocks DNA single-strand break repair, promotes DNA damage, and interferes with tumor stemness signaling by inhibiting CK2α-mediated substrate phosphorylation. NJT-12 induces apoptosis through caspase signaling and G2-M phase arrest, inhibits migration and invasion, and reverses epithelial-mesenchymal transition. NJT-12 inhibits tumor growth in xenograft models with a favorable biosafety profile. NJT-12 can be used for research on ovarian cancer.
Nur für Forschungszwecke. Wir verkaufen nicht an Patienten.
- Formel: C20H17N5O3S
- Molecular Weight:407.45
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Speicherung:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biologische Aktivität
Beschreibung
NJT-12 is a PARP-1 and CK2α inhibitor with IC50 values of 3.40 nM and 4.31 nM, respectively. NJT-12 blocks DNA single-strand break repair, promotes DNA damage, and interferes with tumor stemness signaling by inhibiting CK2α-mediated substrate phosphorylation. NJT-12 induces apoptosis through caspase signaling and G2-M phase arrest, inhibits migration and invasion, and reverses epithelial-mesenchymal transition. NJT-12 inhibits tumor growth in xenograft models with a favorable biosafety profile. NJT-12 can be used for research on ovarian cancer[1].
IC50 & Target
[1]|
PARP-1 3.40 nM (IC50) |
CK2α 4.31 nM (IC50) |
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| SK-OV-3 | IC50 |
5.43 μM
|
Cytotoxicity against human SKOV3 cells assessed as viability reduction after 72 hrs incubation by MTT assay.
Cytotoxicity against human SKOV3 cells assessed as viability reduction after 72 hrs incubation by MTT assay.
|
Simultaneous-Inhibition-of-PARP-1-and-CK2-by-Novel |
| A2780 | IC50 |
4.69 μM
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Cytotoxicity against human A2780 cells assessed as viability reduction after 72 hrs incubation by MTT assay.
Cytotoxicity against human A2780 cells assessed as viability reduction after 72 hrs incubation by MTT assay.
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Simultaneous-Inhibition-of-PARP-1-and-CK2-by-Novel |
| MCF7 | IC50 |
9.57 μM
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Cytotoxicity against human MCF-7 cells assessed as viability reduction after 72 hrs incubation by MTT assay.
Cytotoxicity against human MCF-7 cells assessed as viability reduction after 72 hrs incubation by MTT assay.
|
Simultaneous-Inhibition-of-PARP-1-and-CK2-by-Novel |
| MDA-MB-231 | IC50 |
8.71 μM
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Cytotoxicity against human MDA-MB-231 cells assessed as viability reduction after 72 hrs incubation by MTT assay.
Cytotoxicity against human MDA-MB-231 cells assessed as viability reduction after 72 hrs incubation by MTT assay.
|
Simultaneous-Inhibition-of-PARP-1-and-CK2-by-Novel |
| PC-3 | IC50 |
9.26 μM
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Cytotoxicity against human PC-3 cells assessed as viability reduction after 72 hrs incubation by MTT assay.
Cytotoxicity against human PC-3 cells assessed as viability reduction after 72 hrs incubation by MTT assay.
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Simultaneous-Inhibition-of-PARP-1-and-CK2-by-Novel |
| L02 | IC50 |
59.57 μM
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Cytotoxicity against normal human L02 cells assessed as viability reduction after 72 hrs incubation by MTT assay.
Cytotoxicity against normal human L02 cells assessed as viability reduction after 72 hrs incubation by MTT assay.
|
Simultaneous-Inhibition-of-PARP-1-and-CK2-by-Novel |
In Vitro
Anti-cancerApoptosisCell Cycle RegulationOthers
Anti-cancer
NJT-12 (72 h) exhibits broad cytotoxicity against non-HRD cancer cell lines, with the greatest sensitivity observed in A2780 ovarian cancer cells (IC50 4.69 μM), while showing no significant effect on normal L02 cells[1].
NJT-12 (5.0-15.0 μM; 12 h) inhibits PARP-1 activity, induces γH2AX, and inhibits CK2α substrate phosphorylation in A2780 cells in a dose-dependent manner[1].
NJT-12 (2.5-7.5 μM; 24 h) inhibits colony formation of A2780 cells in a concentration-dependent manner[1].
NJT-12 (2.5-7.5 μM; 24 h) inhibits A2780 cell invasion and migration in a concentration-dependent manner[1].
NJT-12 (10.0 μM; 24 h) reverses the EMT phenotype of A2780 cells by upregulating E-cadherin and downregulating N-cadherin[1].
NJT-12 (15.0 μM; 24 h) inhibits the CSC-related transcription factors OCT4, SOX2, and Nanog in A2780 cells more strongly than CX-4945[1].
NJT-12 (5.0 μM; 10 days) inhibits 3D tumor sphere formation in A2780ALDH1A1+ ovarian cancer stem-like cells[1].
NJT-12 inhibits ALDH1A1 expression in A2780 cells more strongly than CX-4945[1].
NJT-12 regulates the Wnt/β-catenin pathway in A2780 cells by increasing DKK1 and decreasing p-GSK-3βSer9 and β-catenin[1].
NJT-12 (5.0-15.0 μM; 12 h) inhibits PARP-1 activity, induces γH2AX, and inhibits CK2α substrate phosphorylation in A2780 cells in a dose-dependent manner[1].
NJT-12 (2.5-7.5 μM; 24 h) inhibits colony formation of A2780 cells in a concentration-dependent manner[1].
NJT-12 (2.5-7.5 μM; 24 h) inhibits A2780 cell invasion and migration in a concentration-dependent manner[1].
NJT-12 (10.0 μM; 24 h) reverses the EMT phenotype of A2780 cells by upregulating E-cadherin and downregulating N-cadherin[1].
NJT-12 (15.0 μM; 24 h) inhibits the CSC-related transcription factors OCT4, SOX2, and Nanog in A2780 cells more strongly than CX-4945[1].
NJT-12 (5.0 μM; 10 days) inhibits 3D tumor sphere formation in A2780ALDH1A1+ ovarian cancer stem-like cells[1].
NJT-12 inhibits ALDH1A1 expression in A2780 cells more strongly than CX-4945[1].
NJT-12 regulates the Wnt/β-catenin pathway in A2780 cells by increasing DKK1 and decreasing p-GSK-3βSer9 and β-catenin[1].
Anti-cancer
Apoptosis
Anti-cancer
Cell Cycle Regulation
NJT-12 (5.0-15.0 μM; 24 h) induces G2-M phase cell cycle arrest in A2780 cells in a concentration-dependent manner[1].
Others
NJT-12 (0.1 nM-2 μM) is a potent dual PARP-1/CK2α inhibitor in cell-free enzyme assays, with IC50 values of 3.40 nM and 4.31 nM for PARP-1 and CK2α, respectively, and exhibits selectivity for PARP-1 over PARP-2[1].
NJT-12 (1.0 μM; 0-45 min) is metabolically stable in human, rat, and mouse liver microsomes, with T1/2 values of 51.38 min, 55.58 min, and 26.16 min, respectively[1].
NJT-12 (1.0 μM; 0-45 min) is metabolically stable in human, rat, and mouse liver microsomes, with T1/2 values of 51.38 min, 55.58 min, and 26.16 min, respectively[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Western Blot Analysis[1]
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Cell Line:A2780 human ovarian cancer cells
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Concentration:5.0, 10.0, 15.0 μM
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Incubation Time:12 h
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Result:Dose-dependently diminished intracellular PAR polymers; at 15.0 μM, PAR polymer expression was inhibited by over 90%.
γH2AX expression was upregulated with increasing concentration; at 10.0 μM, γH2AX levels were higher than in the Olaparib group.
Also dose-dependently downregulated p-Akt1S129 and p-Cdc37S13, with stronger inhibition than CX-4945 under identical dosing conditions.
Cell Cycle Analysis[1]
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Cell Line:A2780 human ovarian cancer cells
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Concentration:5.0, 10.0, 15.0 μM
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Incubation Time:24 h
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Result:Downregulated the proportions of cells in G0-G1 and S phases and concentration-dependently elevated the G2-M population.
The control G2-M percentage was 15.30%; after 5.0 μM, G2-M increased to 28.55%; at 15.0 μM, G2-M increased to 38.74%.
Apoptosis Analysis[1]
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Cell Line:A2780 human ovarian cancer cells
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Concentration:5.0, 10.0, 15.0 μM
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Incubation Time:24 h
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Result:Induced apoptosis in a dose-dependent manner.
At 15.0 μM, the apoptotic ratio was 50.2%; at 10.0 μM, the apoptosis rate was 33.20%.
At 10.0 μM, positive controls CX-4945 and Olaparib induced apoptosis at rates of 22.78% and 29.80%, respectively.
Western Blot Analysis[1]
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Cell Line:A2780 human ovarian cancer cells
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Concentration:5.0, 10.0, 15.0 μM
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Incubation Time:24 h
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Result:Downregulated Bcl-2, pro-caspase-3, and pro-caspase-9, and upregulated Bax, cleaved-caspase-3, cleaved-caspase-9, and cleaved-PARP in a dose-dependent pattern.
At the same concentration, had stronger modulatory effects than positive control agents.
Western Blot Analysis[1]
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Cell Line:A2780 human ovarian cancer cells
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Concentration:10.0 μM
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Incubation Time:24 h
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Result:Upregulated E-cadherin and downregulated N-cadherin relative to the control group.
Exerted superior efficacy in reversing the EMT phenotype compared with CX-4945 and Olaparib.
Real Time qPCR[1]
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Cell Line:A2780 cancer cells
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Concentration:15.0 μM
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Incubation Time:24 h
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Result:Inhibited the transcriptional levels of OCT4, SOX2, and Nanog more strongly than CX-4945, with the most significant inhibition nearly twice or higher than CX-4945.
Cell Invasion Assay[1]
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Cell Line:A2780 cancer cells
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Concentration:2.5, 5 and 7.5 μM
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Incubation Time:24 h
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Result:Inhibited the invasion and migration of A2780 cells in a concentration-dependent manner; at 7.5 μM, the inhibition rates for invasion and migration were 84.47% and 82.20%, respectively.
Parmacokinetics
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:BALB/c nude (female, 5 weeks old, body weight 16-18 g)[1]
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Dosage:25.0 mg/kg, 50.0 mg/kg, and 100.0 mg/kg
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Administration:i.g. (intragastric gavage); once daily; 21 consecutive days
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Result:Tumor growth inhibition rate was 43.20% at 25.0 mg/kg, 68.86% at 50.0 mg/kg, and 79.66% at 100.0 mg/kg.
No substantial body weight loss was observed during the whole administration cycle, including in the high-dose group.
Related Protocols :
- Western Blot
- Annexin V plus membrane-impermeant dye apoptosis staining
- Cell migration
- Patient-Derived Orthotopic Xenograft (PDOX)
- Kinase activity and phosphorylation assays
- Detection of Apoptosis
- TUNEL staining for apoptotic DNA fragmentation
- Patient-Derived Xenograft (PDX)
- Apoptosis Solutions
- Cell invasion
- Splenic/Portal-Vein Liver Metastasis Xenograft
- Protocol for Kinase activity and phosphorylation assays
- Subcutaneous Cell-Line-Derived Xenograft
- Genotoxicity/Mutagenicity Study
- Orthotopic Cell-Line Xenograft
- Intraperitoneal/Peritoneal Dissemination Xenograft
Chemical Information
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Molecular Weight 407.45
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Formel C20H17N5O3S
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SMILES
N/C(SC)=N\N=C\C1=CC=C(C2=NC3=C(OC4=CC(OC)=CC=C43)C(N2)=O)C=C1
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Please store the product under the recommended conditions in the Certificate of Analysis.
Reinheit & Dokumentation
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Calculators
Molaritätsrechner
Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)
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Verdünnungsrechner
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)
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