MEG hemisulfate (Mercaptoethylguanidine hemisulfate) acts as a highly potent and selective suppressor of inducible NO synthase (iNOS), demonstrating EC50 values of 11.5 μM for iNOS, 110 μM for ecNOS, and 60 μM for bNOS in tissue homogenates. It is notably effective as a peroxynitrite scavenger and blocks peroxynitrite-triggered oxidative mechanisms. Furthermore, this compound offers protective benefits across various experimental inflammation prototypes, such as ischemia/reperfusion injury, hemorrhagic shock, periodontitis, inflammatory bowel disease, and both endotoxic and septic shock.

MEG (0.1-1000 μM; 18 h) reduces nitrite accumulation in the supernatant of cultured J774.2 macrophages activated with LPS (10 μg/mL) and INF (50 μg/mL). MEG inhibits iNOS activity in homogenates of lungs taken from LPS-treated rats[1]. MEG (1 μM-3 mM; 3 min) dose-dependently inhibits the peroxynitrite-induced oxidation of cytochrome c2+ and hydroxylation of benzoate. MEG (1-300 μM) inhibits the suppression of mitochondrial respiration and DNA single strand breakage in response to peroxynitrite in J774 cells. MEG (300 μM; 30 min) inhibits the suppression of vascular contractility in response to peroxynitrite in thoracic aortic rings[2].

MEG (30-60 mg/kg; a single i.p.) decreases mean arterial blood pressure (MAP) of normal rats[1]. MEG (10 mg/kg; i.p. for 5 d) attenuates the degree of lipid peroxidation, protein oxidation, and peroxynitrites level and ameliorated the decrease of antioxidant enzymes activities in the esophagus of rats subjected to caustic burn injury[3]. MEG (10 mg/kg; a single i.p.) improves the renal dysfunction and tissue injury induced by ischemia/reperfusion (I/R) of rat kidney[4].