Yang, Hsin-Ling et al. published their research in Biochimica et Biophysica Acta, Gene Regulatory Mechanisms in 2016 | CAS: 605-94-7

2,3-Dimethoxy-5-methylcyclohexa-2,5-diene-1,4-dione (cas: 605-94-7) belongs to ethers. Relative to alcohols, ethers are generally less dense, are less soluble in water, and have lower boiling points. They are relatively unreactive. Autoxidation is the spontaneous oxidation of a compound in air. In the presence of oxygen, ethers slowly autoxidize to form hydroperoxides and dialkyl peroxides. If concentrated or heated, these peroxides may explode. To prevent such explosions, ethers should be obtained in small quantities, kept in tightly sealed containers, and used promptly.Synthetic Route of C9H10O4

Coenzyme Q0 regulates NFκB/AP-1 activation and enhances Nrf2 stabilization in attenuation of LPS-induced inflammation and redox imbalance: Evidence from in vitro and in vivo studies was written by Yang, Hsin-Ling;Lin, Ming-Wei;Korivi, Mallikarjuna;Wu, Jia-Jiuan;Liao, Chun-Huei;Chang, Chia-Ting;Liao, Jiunn-Wang;Hseu, You-Cheng. And the article was included in Biochimica et Biophysica Acta, Gene Regulatory Mechanisms in 2016.Synthetic Route of C9H10O4 This article mentions the following:

Coenzyme Q (CoQ) analogs with variable number of isoprenoid units have been demonstrated as anti-inflammatory and antioxidant/pro-oxidant mols. In this study we used CoQ0 (2,3-dimethoxy-5-methyl-1,4-benzoquinone, zero isoprenoid side-chains), a novel quinone derivative, and investigated its mol. actions against LPS-induced inflammation and redox imbalance in murine RAW264.7 macrophages and mice. In LPS-stimulated macrophages, non-cytotoxic concentrations of CoQ0 (2.5-10 μM) inhibited iNOS/COX-2 protein expressions with subsequent reductions of NO, PGE2, TNF-α and IL-1β secretions. This inhibition was reasoned by suppression of NFκB (p65) activation, and inhibition of AP-1 (c-Jun., c-Fos, ATF2) translocation. Our findings indicated that IKKα-mediated I-κB degradation and MAPK-signaling are involved in regulation of NFκB/AP-1 activation. Furthermore, CoQ0 triggered HO-1 and NQO-1 genes through increased Nrf2 nuclear translocation and Nrf2/ARE-signaling. This phenomenon was confirmed by diminished CoQ0 protective effects in Nrf2 knockdown cells, where LPS-induced NO, PGE2, TNF-α and IL-1β productions remained high. Mol. evidence revealed that CoQ0 enhanced Nrf2 steady-state level at both transcriptional and translational levels. CoQ0-induced Nrf2 activation appears to be regulated by ROS-JNK-signaling cascades, as evidenced by suppressed Nrf2 activation upon treatment with pharmacol. inhibitors of ROS (N-acetylcysteine) and JNK (SP600125). Besides, oral administration of CoQ0 (5 mg/kg) suppressed LPS-induced (1 mg/kg) induction of iNOS/COX-2 and TNF-α/IL-1β through tight regulation of NFκB/Nrf2 signaling in mice liver and spleen. Our findings conclude that pharmacol. actions of CoQ0 are mediated via inhibition of NFκB/AP-1 activation and induction of Nrf2/ARE-signaling. Owing to its potent anti-inflammatory and antioxidant properties, CoQ0 could be a promising candidate to treat inflammatory disorders. In the experiment, the researchers used many compounds, for example, 2,3-Dimethoxy-5-methylcyclohexa-2,5-diene-1,4-dione (cas: 605-94-7Synthetic Route of C9H10O4).

2,3-Dimethoxy-5-methylcyclohexa-2,5-diene-1,4-dione (cas: 605-94-7) belongs to ethers. Relative to alcohols, ethers are generally less dense, are less soluble in water, and have lower boiling points. They are relatively unreactive. Autoxidation is the spontaneous oxidation of a compound in air. In the presence of oxygen, ethers slowly autoxidize to form hydroperoxides and dialkyl peroxides. If concentrated or heated, these peroxides may explode. To prevent such explosions, ethers should be obtained in small quantities, kept in tightly sealed containers, and used promptly.Synthetic Route of C9H10O4

Referemce:
Ether – Wikipedia,
Ether | (C2H5)2O – PubChem