Angiotensin II human (Ang II) is a biologically active peptide, a vasoconstrictor. Angiotensin II interacts with AT1R and AT2R to regulate blood pressure, stimulate sympathetic nerves, and increase aldosterone biosynthesis and renal activity in humans.

Angiotensin II 5-valine TFA is an agonist of angiotensin receptor.

Angiotensin I/II (1-5) is a peptide (ASP-ARG-VAL-TYR-ILE) that contains the amino acids 1-5 and is converted from Angiotensin I/II.

[Sar1, Ile8]-Angiotensin II acetate activates both the NADPH and NADH oxidases, and stimulates superoxide anion formation in vascular smooth muscle cells. [Sar1, Ile8]-Angiotensin II acetate has multiple effects on vascular smooth muscle, including contra

[Sar1, Ile8]-Angiotensin II 3TFA ([Sar1, Ile8]-Angiotensin II 3TFA (37827-06-8(free base))) is a peptide that has multiple effects on vascular smooth muscle.

Angiotensin I/II (1-6) is a peptide (ASP-ARG-VAL-TYR-ILE-HIS) that contains the amino acids 1-6 and is converted from Angiotensin I/II peptide.

Angiotensin II (5-8) is an endogenous C-terminal fragment of the peptide vasoconstrictor angiotensin II

[Sar1, Ile8]-Angiotensin II(3TFA) is a peptide that has multiple effects on vascular smooth muscle.

Angiotensin II is a potent direct vasoconstrictor, causing arteries and veins to constrict, so leading to an increase in blood pressure. Angiotensin also potentiates the release of norepinephrine by a direct action on postganglionic sympathetic fibers.

[Tyr(P)4] Angiotensin II is a peptide that exerts a multitude of effects on vascular smooth muscle. These effects include the contraction of normal arteries, as well as the induction of hypertrophy or hyperplasia in cultured cells or diseased vessels.

The substitution with Sar at position 1 of angiotensin II resulted in a partial agonistic activity.

ngiotensin II 5-valine is an angiotensin II analog which is an agonist at angiotensin receptors.

[Sar1, Ile8]-Angiotensin II (TFA) is a peptide compound that exerts various effects on vascular smooth muscle. These effects include the contraction of normal arteries as well as the hypertrophy or hyperplasia of cultured cells or diseased vessels.

Angiotensin II human acetate (DRVYIHPF acetate) is a vasoconstrictor that mainly acts on the AT1 receptor.

Angiotensin II (3-8), human is a less effective agonist at the angiotensin AT1 receptor.

Angiotensin II human TFA, a potent vasoconstrictor within the renin/angiotensin system, plays a pivotal role in human blood pressure regulation primarily through interactions with the G-protein-coupled receptors Angiotensin II type 1 receptor (AT1R) and Angiotensin II type 2 receptor (AT2R). It not only prompts sympathetic nervous stimulation, aldosterone biosynthesis, and renal effects but also fosters growth in vascular smooth muscle cells and boosts collagen type I and III synthesis in fibroblasts. This action results in the thickening of the vascular wall and myocardium, alongside fibrosis. Additionally, Angiotensin II human TFA triggers apoptosis and encourages capillary formation from endothelial cells through the LOX-1 dependent redox-sensitive pathway [1] [2] [3] [4].

(Sar1,Ile4,8)-Angiotensin II is a functionally selective agonist for the angiotensin II type 1 receptor (AT1R), enhancing insulin-stimulated signaling of the insulin receptor (IR) and glycogen synthesis. It boosts the insulin-induced phosphorylation of Akt and GSK3α/β [1].

Angiotensin II is a potent direct vasoconstrictor, causing arteries and veins to constrict, so leading to an increase in blood pressure.

Angiotensin pentapeptide is a peptide.

Angiotensin I/II (1-6) TFA is a chemical compound comprising amino acids 1-6. It is derived from the Angiotensin I/II peptide, which is formed by the cleavage of the precursor angiotensinogen by renin. The resulting Angiotensin I is then hydrolyzed by angiotensin-converting enzyme (ACE) to produce biologically active Angiotensin II. Angiotensin II has been extensively studied for its potential applications in the treatment of Hypertension, Renin Angiotensin System, and Idiopathic Membranous Nephropathy[1][2][3].

Pentasarcosyl angiotensin II is a synthetic analog of angiotensin II.

TRV055 acetate is a ligand of angiotensin II type 1 receptor and stimulates cellular Gq-mediated signaling.

TRV-120027 acetate is a β-arrestin-1-biased agonist of the angiotensin II receptor type 1 (AT1 receptor) and engages -arrestins while blocking G-protein signaling.

Angiotensin 1/2 (1-9)TFA is containing the amino acids 1-9 that are converted from Angiotensin I/II peptide.

Alamandine can be formed from angiotensin A by action of ACE-2 or directly from angiotensin-(1-7) by decarboxylation of its aspartate residue. The angiotensin A analog produces effects resembling those of Ang II (1-7). However, it acts independently of the two known vasodilators receptors of the RAS (Mas and angiotensin II type 2). To produce its effects, alamandine binds to the Mas-related receptor, MrgD. A novel orally active formulation of alamandine produced a long-term antihypertensive effect in spontaneously hypertensive rats and cardioprotective effects. These novel findings will be helpful for developing a new understanding of the RAS, a key regulator of blood pressure and fluid balance. The heptapeptide could serve as a model peptide, e.g. in the development and evaluation of analytical methods.

Angiotensin 1/2 (1-9) is containing the amino acids 1-9 that are converted from Angiotensin I/II peptide.

Competitive non-selective angiotensin II antagonist.

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.

Angiotensin-converting enzyme (ACE), a dicarboxypeptidase, converts inactive Angiotensin I (Ang I) to its active form, Angiotensin II (Ang II), and degrades active bradykinin (BK), functioning as a potent vasoconstrictor frequently utilized in biochemical studies [1].

Saralasin TFA ([Sar1,Ala8] Angiotensin II) is a synthetic octapeptide analog of angiotensin II, functioning as a competitive antagonist at angiotensin II receptors with a K i value of 0.32 nM for 74% of its binding sites, while also exhibiting partial agonist activity. It is utilized in the study of renovascular and renin-dependent (angiotensinogenic) hypertension [1] [3] [6].

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.

TRV120027 TFA is a β-arrestin-1-biased agonist of the angiotensin II receptor type 1 (AT1R) and engages ß-arrestins while blocking G-protein signaling.

Angiotensin III, human, mouse (Angiotensin III, human, mouse(3TFA))(3TFA) is an endogenous angiotensin II receptor (AT2R) agonist(IC50s of 0.648 nM).

Angiotensin 1-7 (Ang-(1-7)) acetate, an endogenous heptapeptide from the renin-angiotensin system (RAS), exhibits cardioprotective effects through its anti-inflammatory and anti-fibrotic activities in cardiac cells. It effectively inhibits purified canine ACE activity (IC 50 =0.65 μM) and serves as a local synergistic modulator of kinin-induced vasodilation by hindering ACE and facilitating nitric oxide release. Additionally, this compound prevents Ang II-induced proliferation and hypertrophy in smooth muscle cells, alongside demonstrating antiangiogenic and growth-inhibitory effects on the endothelium [1] [2] [3].

Angiotensin 1/2 (1-8) amide (H2N-Asp-Arg-Val-Tyr-Ile-His-Pro-Phe-amide) is a peptide analog to angiotensin II that is used as a vasopressor agent in the treatment of certain types of shock and circulatory collapse. It is a potent vasoconstrictor and is us

Apelin-13 is a 13-amino acid peptide sequence found in the central and peripheral nervous system that is an endogenous ligand for the G protein-coupled receptor angiotensin II protein J (APJ), with an EC50 value of 0.37 nM for APJ.Apelin-13 has vasodilatory and antihypertensive activity and can be used to study type 2 diabetic syndrome. Apelin-13 has vasodilatory and antihypertensive activities and can be used to study type 2 diabetes syndrome.

Angiotensin (1-7) (ASP-ARG-VAL-TYR-ILE-HIS-PRO) is a synthetic heptapeptide identical to endogenous angiotensin-(1-7) , inhibits purified canine ACE activity (IC50=0.65 μM) with vasodilator and antiproliferative activities.

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.

Saralasin acetate is a Non-selective angiotensin II antagonist.

Nitrosoglutathione (GSNO) is an endogenous transnitrosation donor involved in S-nitrosation of a variety of cellular proteins. GSNO, an exogenous NO donor and substrate of rat alcohol dehydrogenase class III isoenzyme, inhibits cerebral angiotensin II-dependent and -independent AT1 receptor responses.

Adrenomedullin (13-52) is a truncated form of adrenomedullin (1-52) . It induces nitric oxide-dependent relaxation of and inhibits release of angiotensin II and endothelin-1 from isolated rat aorta. In vivo, adrenomedullin (13-52) decreases mean arterial pressure (MAP) in spontaneously and renal hypertensive rats in a dose-dependent manner. Adrenomedullin (13-52) (10-3,000 ng per animal) reverses increases in lobar arterial pressure induced by U-46619 in a dose-dependent manner in cats but has no effect on basal lobar arterial pressure or systemic arterial pressure. It also potentiates inflammatory edema and neutrophil accumulation in rats.

TRV055 hydrochloride, a Gq-biased ligand and G-protein-biased agonist of the angiotensin II receptor type 1 (AT1R), effectively stimulates cellular Gq-mediated signaling [1].

Angiotensin I (human, mouse, rat) is the precursor to the vasoconstrictor peptide angiotensin II, cleaved by the angiotensin-converting enzyme (ACE).Angiotensin is a peptide hormone that causes vasoconstriction and an increase in blood pressure. It is part of the renin–angiotensin system, which regulates blood pressure. Angiotensin also stimulates the release of aldosterone from the adrenal cortex to promote sodium retention by the kidneys.