1. Immunology/Inflammation
  2. NO Synthase
  3. MEG hemisulfate

MEG hemisulfate (Synonyms: Mercaptoethylguanidine hemisulfate)

Cat. No.: HY-138454
Handling Instructions

MEG (Mercaptoethylguanidine) hemisulfate is a potent and selective inhibitor of the inducible NO synthase (iNOS), with EC50s of 11.5, 110, and 60 μM for iNOS, ecNOS, and bNOS respectively in tissue homogenates. MEG hemisulfate is also a potent scavenger of peroxynitrite and inhibits peroxynitrite-induced oxidative processes. MEG hemisulfate has a protective effect in many experimental models of inflammation, including ischemia/reperfusion injury, periodontitis, hemorrhagic shock, inflammatory bowel disease, and endotoxic and septic shock.

For research use only. We do not sell to patients.

MEG hemisulfate Chemical Structure

MEG hemisulfate Chemical Structure

CAS No. : 3979-00-8

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Description

MEG (Mercaptoethylguanidine) hemisulfate is a potent and selective inhibitor of the inducible NO synthase (iNOS), with EC50s of 11.5, 110, and 60 μM for iNOS, ecNOS, and bNOS respectively in tissue homogenates. MEG hemisulfate is also a potent scavenger of peroxynitrite and inhibits peroxynitrite-induced oxidative processes. MEG hemisulfate has a protective effect in many experimental models of inflammation, including ischemia/reperfusion injury, periodontitis, hemorrhagic shock, inflammatory bowel disease, and endotoxic and septic shock[1][2][3][4].

IC50 & Target

IC50: 11.5 μM (iNOS), 110 μM (ecNOS), 60 μM (bNOS)[1]

In Vitro

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[2].
MEG (1-300 μM) inhibits the suppression of mitochondrial respiration and DNA single strand breakage in response to peroxynitrite in J774 cells[2].
MEG (300 μM; 30 min) inhibits the suppression of vascular contractility in response to peroxynitrite in thoracic aortic rings[2].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

In Vivo

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 (30-60 mg/kg; a single i.p.) decreases mean arterial blood pressure (MAP) of normal rats[1].
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].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Sprague-Dawley rats (200-250 g) were injured the esophagus[3]
Dosage: 10 mg/kg
Administration: I.p. for 5 days
Result: Reduced the stenosis index (SI) and the histopathologic damage score.
Decreased the malondialdehyde and protein carbonyl content and increased the activities of superoxide dismutase and glutathione peroxidase.
Regulated the nitrate and nitrite level.
Molecular Weight

168.23

Formula

C₃H₉N₃S.₁/₂H₂O₄S

CAS No.

3979-00-8

SMILES

NC(NCCS)=N.O=S(O)(O)=O.[1/2]

Shipping

Room temperature in continental US; may vary elsewhere.

Storage

Please store the product under the recommended conditions in the Certificate of Analysis.

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Keywords:

MEG hemisulfateMercaptoethylguanidine hemisulfateNO SynthaseNitric oxide synthasesNOSinducibleNOsynthaseiNOSecNOSbNOSscavengerperoxynitriteoxidativeinflammationischemiareperfusioninjuryperiodontitishemorrhagicshockendotoxicsepticInhibitorinhibitorinhibit

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MEG hemisulfate
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