Description

TRV120027 TFA, a β-arrestin-1-biased agonist of the angiotensin II receptor type 1 (AT1R), engages ß-arrestins while blocking G-protein signaling[1]. TRV120027 TFA 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 TFA inhibits angiotensin II–mediated vasoconstriction and increases cardiomyocyte contractility. TRV120027 TFA 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)–COVID-19-immunoregulation–C45H68F3N13O12—J Am Heart Assoc. 2022 Feb 15;11(4):e022070.|University of Medicine Berlin. 2023 Mar.|Eur J Pharmacol. 2023 May 18;175780.-[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.—-1040.10–98.34–OC(C(F)(F)F)=O.CC[C@@H]([C@@H](C(N[C@H](C(N1CCC[C@H]1C(N[C@@H](C(O)=O)C)=O)=O)CC2=CNC=N2)=O)NC([C@@H](NC([C@H](C(C)C)NC([C@@H](NC(CNC)=O)CCCNC(N)=N)=O)=O)CC3=CC=C(O)C=C3)=O)C–Cardiovascular Disease–DMSO : 100 mg/mL (ultrasonic)–Angiotensin Receptor;Arrestin–AT1 Receptor–GPCR/G Protein–Peptides