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Activity Type | Relation | Activity value | Units | Action Type | Journal | PubMed Id | doi | Assay Aladdin ID |
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SKU | Size | Availability | Price | Qty |
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L651811-5mg | 5mg | Available within 8-12 weeks(?) Production requires sourcing of materials. We appreciate your patience and understanding. | $55.90 | |
L651811-10mg | 10mg | Available within 8-12 weeks(?) Production requires sourcing of materials. We appreciate your patience and understanding. | $88.90 | |
L651811-50mg | 50mg | Available within 8-12 weeks(?) Production requires sourcing of materials. We appreciate your patience and understanding. | $198.90 | |
L651811-100mg | 100mg | Available within 8-12 weeks(?) Production requires sourcing of materials. We appreciate your patience and understanding. | $308.90 |
Specifications & Purity | ≥98% |
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Biochemical and Physiological Mechanisms | L67 (DNA Ligase Inhibitor) is a competitive DNA ligase inhibitor that effectively inhibits DNA ligases I/III (both IC 50 are 10 μM). L67 (DNA Ligase Inhibitor) can cause nuclear DNA damage by reducing levels of mitochondrial DNA and increasing levels of m |
Storage Temp | Store at -20°C |
Shipped In | Ice chest + Ice pads |
Product Description | L67 (DNA Ligase Inhibitor) is a competitive DNA ligase inhibitor that effectively inhibits DNA ligases I/III (both IC 50 are 10 μM). L67 (DNA Ligase Inhibitor) can cause nuclear DNA damage by reducing levels of mitochondrial DNA and increasing levels of mitochondrially-generated ROS. L67 (DNA Ligase Inhibitor) also activates the Caspase 1 -dependent apoptosis pathway in cancer cells, can be used in cancer research. In Vitro L67 (10, 15 μM; 24 h) promotes nuclear DNA damage and (0-50 μM) increases level of mSOX by inhibiting mitochondrial LigIIIα in HeLa cells. L67 (10 μM; 24 h) induces changes in mitochondrial function that causes a reduction in OCR and mitochondrial DNA, and abnormal mitochondrial morphology in HeLa. L67 (10, 100 μM; 24 h) induces apoptosis in cancer cells. L67 (0-30 μM; 24 h) selectively induces cell death in cancer cells by activating a caspase 1-dependent apoptotic pathway. MCE has not independently confirmed the accuracy of these methods. They are for reference only. Cell Viability AssayCell Line: HeLa cells Concentration: 10, 15 μM; 0-50 μM Incubation Time: 24 h Result: Increased the formation of nuclear γH2AX foci and steady state levels of γH2AX when at 10 or 15 μM. (γH2AX: a sign of DNA double-strand breaks). Resulted in a concentration (0-50 μM)-dependent increase in mSOX (mitochondrial superoxide) levels. (mSOX is a major cause of the cellular oxidative damage). Cell Viability AssayCell Line: HeLa cells Concentration: 10 μM Incubation Time: 24 h Result: Reduced oxygen consumption rate (OCR) approximately 20%. Resulted in about a 25% reduction in mitochondrial DNA. Apoptosis AnalysisCell Line: HeLa cells Concentration: 10, 100 μM Incubation Time: 24 h Result: Result:Induced apoptosis, and at 100 μM with apoptotic cells constituting about 50% of the HeLa cell population. Cell Viability AssayCell Line: HeLa cells Concentration: 0-30 μM Incubation Time: 24 h Result: Activates a caspase 1-dependent cell death pathway in cancer cells. Form:Solid |
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Mechanism of Action | Action Type | target ID | Target Name | Target Type | Target Organism | Binding Site Name | References |
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IUPAC Name | 2-(3,5-dibromo-4-methylanilino)-N-[(E)-(2-hydroxy-5-nitrophenyl)methylideneamino]acetamide |
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INCHI | InChI=1S/C16H14Br2N4O4/c1-9-13(17)5-11(6-14(9)18)19-8-16(24)21-20-7-10-4-12(22(25)26)2-3-15(10)23/h2-7,19,23H,8H2,1H3,(H,21,24)/b20-7+ |
InChi Key | KFEPVFJQVOMODD-IFRROFPPSA-N |
Canonical SMILES | CC1=C(C=C(C=C1Br)NCC(=O)NN=CC2=C(C=CC(=C2)[N+](=O)[O-])O)Br |
Isomeric SMILES | CC1=C(C=C(C=C1Br)NCC(=O)N/N=C/C2=C(C=CC(=C2)[N+](=O)[O-])O)Br |
PubChem CID | 135419707 |
Molecular Weight | 486.11 |
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Solubility | DMSO : ≥ 33 mg/mL (67.89 mM) H2O : 1 mg/mL (2.06 mM; Need ultrasonic) |
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RIDADR | NONHforallmodesoftransport |
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