High impact information on Ro-46-2005

• We report here evidence for the pathophysiological role of endothelin-1 as brought by the first synthetic orally active nonpeptide antagonist of endothelin receptors, Ro 46-2005 [1].
• 5. The novel non-peptide ligands, Ro 46-2005, SB 209670 and BMS 182874, were found to inhibit [125I]-ET-1 binding to human recombinant ETA and ETB receptors.(ABSTRACT TRUNCATED AT 250 WORDS)[2]
• In contrast to Ro 46-2005, the selective peptide ETA antagonists BQ-123 and FR-139317 had no effect on plasma ET-1 concentrations [3].
• In vitro characterization of Ro 46-2005, a novel synthetic non-peptide endothelin antagonist of ETA and ETB receptors [4].
• Ro 46-2005 had no effect on plasma concentrations of big ET-1 and only a minor effect on those of ET-3 [3].

Biological context of Ro-46-2005

• In binding experiments, Ro 46-2005 proved to be equipotent (IC50 200-500 nM) for inhibition of [125]ET-1 binding on the two known ET receptor subtypes (ETA and ETB) [4].

Anatomical context of Ro-46-2005

• Characterisation of the endothelin receptor mediating contraction of human pulmonary artery using BQ123 and Ro 46-2005 [5].
• The specific [125I]-ET-1 binding in non-pregnant and pregnant myometrium was completely inhibited by unlabelled ET-1 and Ro 46-2005 [6].

Gene context of Ro-46-2005

• ET-1 binding was completely inhibited by a nonselective antagonist (Ro-46-2005) or a combination of ETA-selective and ETB-selective ligands (BQ-123 and ET-3) [7].
• Effect of different endothelin receptor antagonists and of the novel non-peptide antagonist Ro 46-2005 on endothelin levels in rat plasma [3].

References