Background:

NCX 1000 is a liver-specific NO donor compound derived from ursodeoxycholic acid (UDCA).

NCX-1000 (15 mg/kg, p.o.) prevents ascite formation, reduces collagen deposition in CCl4-treated rats. NCX-1000 administration almost completely reverts portal hypertension induced by CCl4, and reduces portal pressure in cirrhotic rats. NCX-1000 reverts HSC contraction induced by FCS, and also inhibits MCP-1 release from HSCs stimulated with TNF-α and IFN-γ[1]. NCX-1000 (28 mg/kg, p.o.) decreases portal pressure without affecting mean arterial pressure and heart rate in rats. NCX-1000 also reduces vasoconstriction by 60% caused by 30 μM NE in rats. Administration of NCX-1000 to BDL and sham operated rats results in a similar increase of nitrite/nitrate and cGMP concentrations in the liver[2].

[1]. Fiorucci S, et al. NCX-1000, a NO-releasing derivative of ursodeoxycholic acid, selectively delivers NO to the liver and protects against development of portal hypertension. Proc Natl Acad Sci U S A. 2001 Jul 17;98(15):8897-902. Epub 2001 Jul 10. [2]. Fiorucci S, et al. NCX-1000, a nitric oxide-releasing derivative of ursodeoxycholic acid, ameliorates portal hypertension and lowers norepinephrine-induced intrahepatic resistance in the isolated and perfused rat liver. J Hepatol. 2003 Dec;39(6):932-9.