Tricarbonyldichlororuthenium(II) dimer, a pharmacological CO donor, prevents ischemia reperfusion (I R)-induced oxidative damage to the gastric mucosa by enhancing gastric blood flow (GBF) and reducing DNA oxidation and systemic inflammatory response.
Ethoxyquin dimer is an antioxidant and metabolite of ethoxyquin .1 It prevents oxidation of polyunsaturated fatty acids in fish meal and fish oil. Dietary administration of ethoxyquin dimer (0.1, 0.3, and 0.5% w/w) induces microvesicular steatosis and hepatocyte necrosis, as well as increases liver levels of oxidized glutathione and total lipids in mice.2
MSA-2 dimer is a selective, orally active non-nucleotide STING agonist (Kd=145 μM) with long-term antitumor and immunogenic activity. MSA-2 dimer is bound to STING as a non-covalent dimer exhibiting higher permeability than cyclic dinucleotide[1]. MSA-2 dimer (60 mg kg; p.o.; 50 days) inhibits tumor growth and prolongs overall survival[1]. MSA-2 dimer (40 mg kg; s.c.; 25 days) induces complete tumor regression[1].MSA-2 dimer (60 mg kg; p.o.; 4 hours) increases proinflammatory cytokine (IFN-β) level in tumors[1].MSA-2 dimer (60 mg kg; s.c.; 4 hours) concentrations is observed in tumors than in plasma or other nontumor tissues [1].MSA-2 dimer (THP-1 cells) induces phosphorylation of both TBK1 and IR. MSA-2 dimer (10 μM and 33 μM; macrophages) induces IFN-β[1].MSA-2 dimer also exhibits dose-dependent antitumor activity when administered by IT, SC, or PO routes[1]. [1]. Pan BS, et al. An orally available non-nucleotide STING agonist with antitumor activity. Science. 2020;369(6506):eaba6098.