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Chemical Structure
DMNQ [6956-96-3]
![Research Use Only](static/images/certificates/ruo.jpg)
AG-CR1-3598
CAS Number6956-96-3
Product group Chemicals
Estimated Purity>99%
Molecular Weight218.2
Overview
- SupplierAdipoGen Life Sciences
- Product NameDMNQ [6956-96-3]
- Delivery Days Customer10
- CAS Number6956-96-3
- CertificationResearch Use Only
- Estimated Purity>99%
- Hazard InformationWarning
- Molecular FormulaC12H10O4
- Molecular Weight218.2
- Scientific DescriptionCell permeable, non-alkylating, non-thiol, adduct-forming, redox cycling quinone. Intracellular superoxide anion formation/ROS generation inducer. Anticancer agent. Shown to induce cell proliferation, apoptosis, necrosis and necroptosis in vitro, dependent on concentration, time, temperature and cell type. Valuable tool for the generation of reactive oxygen species (ROS) in order to study the role of ROS in cell toxicity, apoptosis and necrosis. Useful as reference compound in characterizing the effects of oxidative stress. Can be used to eliminate any mechanistic ambiguity involving redox cycling quinoids as the source of reactive oxidant species/oxidative stress in biological studies. - Chemical. CAS: 6956-96-3. Formula: C12H10O4. MW: 218.2. Cell permeable, non-alkylating, non-thiol, adduct-forming, redox cycling quinone. Intracellular superoxide anion formation/ROS generation inducer. Anticancer agent. Shown to induce cell proliferation, apoptosis, necrosis and necroptosis in vitro, dependent on concentration, time, temperature and cell type. Valuable tool for the generation of reactive oxygen species (ROS) in order to study the role of ROS in cell toxicity, apoptosis and necrosis. Useful as reference compound in characterizing the effects of oxidative stress. Can be used to eliminate any mechanistic ambiguity involving redox cycling quinoids as the source of reactive oxidant species/oxidative stress in biological studies.
- SMILESCOC1=C(OC)C(=O)C2=C(C=CC=C2)C1=O
- Storage Instruction2°C to 8°C,-20°C
- UNSPSC12352200
References
- The role of oxidative processes in the cytotoxicity of substituted 1,4-naphthoquinones in isolated hepatocytes: D. Ross, et al.; Arch. Biochem. Biophys. 248, 460 (1986)
- Redox cycling and sulphydryl arylation; their relative importance in the mechanism of quinone cytotoxicity to isolated hepatocytes: T.W. Gant, et al.; Chem. Biol. Interact. 65, 157 (1988)
- Quinone-induced DNA single strand breaks in rat hepatocytes and human chronic myelogenous leukaemic K562 cells: W.A. Morgan, et al.; Biochem. Pharmacol. 44, 215 (1992)
- Quinone-induced oxidative stress elevates glutathione and induces gamma-glutamylcysteine synthetase activity in rat lung epithelial L2 cells: M.M. Shi, et al.; J. Biol. Chem. 269, 26512 (1994)
- Different prooxidant levels stimulate growth, trigger apoptosis, or produce necrosis of insulin-secreting RINm5F cells: J.M. Dypbukt, et al.; J. Biol. Chem. 269, 30553 (1994)
- DNA single-strand breakage in mammalian cells induced by redox cycling quinones in the absence of oxidative stress: W.A. Morgan; J. Biochem. Toxicol. 10, 227 (1995)
- Naphthoquinone-induced DNA damage in the absence of oxidative stress: W.A. Morgan; Biochem. Soc. Trans. 23, 225S (1995)
- Differential mechanisms of cell killing by redox cycling and arylating quinones: T.R. Henry & K.B. Wallace; Arch. Toxicol. 70, 482 (1996)
- Naphthazarin derivatives: synthesis, cytotoxic mechanism and evaluation of antitumor activity: Y.J. You, et al.; Arch. Pharm. Res. 21, 595 (1998)
- Temperature-dependent quinone cytotoxicity in platelets involves arylation: Y.A. Kang, et al.; J. Toxicol. Environ. Health A 65, 1367 (2002)