TRV120027 is a β-arrestin-1-biased agonist of the angiotensin II receptor type 1. TRV120027 inhibits angiotensin II-mediated vasoconstriction and increases cardiomyocyte contractility.
Dehydro Olmesartan, deriving from Olmesartan, acts as an angiotensin II receptor (AT1R) antagonist and exhibits potential for the study of high blood pressure [1][2].
Olmesartan impurity, a compound related to Olmesartan, is an angiotensin II receptor (AT1R) antagonist utilized in the study of high blood pressure. Olmesartan (RNH-6270) is the parent compound with similar properties and functions as an AT1R antagonist.
TRV120055, a Gq-biased agonist, demonstrates a 10-fold higher molecular efficacy when tested against the AT1R-Gq fusion protein in comparison to the AT1R-βarr2 fusion protein.
TRV055 is a Gq-biased ligand of the angiotensin II receptor type 1 (AT1R). TRV055 is efficacious in stimulating cellular Gq-mediated signaling. TRV055 can be used to develop the Gq-biased AT1R agonists.
TRV120056 is a Gq-biased agonist that demonstrates a molecular efficacy ten times greater at the AT1R-Gq fusion protein than at the AT1R-βarr2 fusion protein.
TRV056 is a Gq-biased agonist of the angiotensin II type 1 receptor (AT1R), demonstrating efficacy in stimulating Gq-mediated cellular signaling. It can serve as a foundation for the development of Gq-biased AT1R agonists.
Olmesartan lactone impurity is a cyclic ester impurity derived from Olmesartan, which is an angiotensin II receptor (AT1R) antagonist with potential applications in the study of high blood pressure.
Angiotensin II human (Angiotensin II) TFA 作为肾素 血管紧张素系统中关键的生物活性肽,扮演着血管收缩剂的角色并在调节人体血压中发挥中心作用。其主要通过与 G 蛋白偶联受体 (GPCRs)、血管紧张素 II 1型受体 (AT1R) 和血管紧张素 II 2型受体 (AT2R) 的相互作用来介导效应,包括刺激交感神经系统、增加醛固酮的生物合成和肾脏功能。此外,Angiotensin II human TFA 促进血管平滑肌细胞的生长和 I 型及 III 型胶原在成纤维细胞中的合成,导致血管壁与心肌增厚及纤维化,并诱导细胞凋亡。还通过LOX-1依赖的氧化还原敏感路径诱导内皮细胞中的毛细血管形成。