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Description: DNA-PK inhibitor
Chemical Name: 4,5-Dimethoxy-2-nitrobenzaldehyde
Purity: ≥98% (HPLC)
Biological Activity for DMNB
Inhibitor of DNA-dependent protein kinase (DNA-PK) (IC50 = 15 μM), an enzyme involved in the non-homologous end-joining (NHEJ) pathway of double-stranded DNA break (DSB) repair in human cells. Displays 100-fold higher potency than its analog vanillin and does not affect PKC activity. Produces lethal effects on cisplatin-treated D5037 cells upon continuous exposure.
Technical Data for DMNB
| M. Wt | 211.15 |
| Formula | C9H9NO5 |
| Storage | Store at -20°C |
| Purity | ≥98% (HPLC) |
| CAS Number | 20357-25-9 |
| PubChem ID | 88505 |
| InChI Key | YWSPWKXREVSQCA-UHFFFAOYSA-N |
| Smiles | COC1=C(OC)C=C(C(C=O)=C1)[N+]([O-])=O |
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
Product Datasheets for DMNB
References for DMNB
References are publications that support the biological activity of the product.
Durant and Karran (2003) Vanillins - a novel family of DNA-PK inhibitors. Nucleic Acids Res. 31 5501 PMID: 14500812
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Keywords: DMNB, DMNB supplier, DNA-dependent, protein, kinases, inhibitors, inhibits, Checkpoint, Control, Kinases, DNA-PK, Protein, Kinase, 2088, Tocris Bioscience
Citations for DMNB
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Currently there are no citations for DMNB.
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Literature in this Area
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Cell Cycle and DNA Damage Research Product Guide
This product guide provides a review of the cell cycle and DNA damage research area and lists over 150 products, including research tools for:
- Cell Cycle and Mitosis
- DNA Damage Repair
- Targeted Protein Degradation
- Ubiquitin Proteasome Pathway
- Chemotherapy Targets
Cell Cycle & DNA Damage Repair Poster
In normal cells, each stage of the cell cycle is tightly regulated, however in cancer cells many genes and proteins that are involved in the regulation of the cell cycle are mutated or over expressed. This poster summarizes the stages of the cell cycle and DNA repair. It also highlights strategies for enhancing replicative stress in cancer cells to force mitotic catastrophe and cell death.