Description

TRV120027, a β-arrestin-1-biased agonist of the angiotensin II receptor type 1 (AT1R), engages ß-arrestins while blocking G-protein signaling[1]. TRV120027 induces acute catecholamine secretion through cation channel subfamily C3 (TRPC3) coupling, promotes the formation of a macromolecular complex composed of AT1R–β-arrestin-1–TRPC3–PLCγ at the plasma membrane. TRV120027 inhibits angiotensin II–mediated vasoconstriction and increases cardiomyocyte contractility. TRV120027 has the potential for the acute decompensated heart failure (ADHF) treatment[2].–80°C, 2 years; -20°C, 1 year (Powder, sealed storage, away from moisture and light, under nitrogen)–Neuroscience-Neuromodulation–C43H67N13O10—Eur J Pharmacol. 2023 May 18;175780.|J Am Heart Assoc. 2022 Feb 15;11(4):e022070.|University of Medicine Berlin. 2023 Mar.-[1]Boerrigter G, et al. TRV120027, a novel β-arrestin biased ligand at the angiotensin II type I receptor, unloads the heart and maintains renal function when added to furosemide in experimental heart failure.Circ Heart Fail. 2012 Sep 1;5(5):627-34. Epub 2012 Aug 13.|[2]Liu CH, et al. Arrestin-biased AT1R agonism induces acute catecholamine secretion through TRPC3 coupling.Nat Commun. 2017 Feb 9;8:14335.–1234510-46-3–926.07–99.46–C[C@H](C(O)=O)NC([C@H]1N(C([C@H](CC2=CNC=N2)NC([C@H]([C@@H](C)CC)NC([C@H](CC3=CC=C(O)C=C3)NC([C@H](C(C)C)NC([C@H](CCCNC(N)=N)NC(CNC)=O)=O)=O)=O)=O)=O)CCC1)=O–Cardiovascular Disease–H2O : 100 mg/mL (ultrasonic;warming;heat to 60°C)–Angiotensin Receptor;Arrestin–AT1 Receptor–GPCR/G Protein–Peptides