GEA 3162 (hydrochloride)

GEA 3162 hydrochloride is an orally active compound that acts as a NO/ONOO⁻ donor. GEA 3162 hydrochloride significantly inhibits the activation of human polymorphonuclear leukocytes (PMNs) through the cGMP pathway, inhibits the release of inflammatory mediators, and exerts anti-inflammatory and protective effects. GEA 3162 hydrochloride induces apoptosis of neutrophils and bone marrow cells by activating caspase-2/3/8/9 through the ONOO⁻ pathway. GEA 3162 hydrochloride has a bidirectional effect in the rat gastric ulcer model: at low doses, it significantly reduces gastric mucosal damage, while at high doses, it aggravates the ulcer area. GEA 3162 hydrochloride can be used for research on inflammatory conditions such as gastric ulcers[1][2][3][4].

Product Specifications

UNSPSC

12352005

Target

Apoptosis; Caspase; Endogenous Metabolite

Related Pathways

Apoptosis; Metabolic Enzyme/Protease

Field of Research

Inflammation/Immunology

Smiles

ClC1=CC=C([N+]2=NOC([NH-])=N2)C=C1Cl.Cl

Molecular Formula

C7H5Cl3N4O

Molecular Weight

267.50

References & Citations

[1]Moilanen E, et al. Inhibition by nitric oxide-donors of human polymorphonuclear leucocyte functions. Br J Pharmacol. 1993;109 (3) :852-858. |[2]Taylor EL, et al. GEA 3162 hydrochloride decomposes to co-generate nitric oxide and superoxide and induces apoptosis in human neutrophils via a peroxynitrite-dependent mechanism. Br J Pharmacol. 2004 Sep;143 (1) :179-85. |[3]Taylor EL, et al. GEA 3162, a peroxynitrite donor, induces Bcl-2-sensitive, p53-independent apoptosis in murine bone marrow cells. Biochem Pharmacol. 2007 Oct 1;74 (7) :1039-49|[4]Asmawi MZ, Moilanen E, Annala K, Rahkonen P, Kankaanranta H. Effects of nitric oxide donors GEA 3162 and SIN-1 on ethanol-induced gastric ulceration in rats. Eur J Pharmacol. 1999 Jul 28;378 (1) :123-7.