Olmesartan methyl ester is an intermediate in the synthesis of Olmesartan medoxomil. Olmesartan medoxomil is a potent and selective angiotensin AT1 receptor antagonist with IC50 of 66.2 μM[1][2].
Angiotensin II 5-valine is an agonist of angiotensin receptor.
Olmesartan is an angiotensin II receptor (AT1R) antagonist used to treat high blood pressure.
Olmesartan lactone impurity is a cyclic ester impurity of Olmesartan. Olmesartan is an angiotensin II receptor (AT1R) antagonist and has the potential for high blood pressure study[1][2].
Angiotensin II (5-8), human is an endogenous C-terminal fragment of the peptide vasoconstrictor angiotensin II[1]. Angiotensin II binds the AT II type 1 (AT1) receptor, stimulating GPCRs in vascular smooth muscle cells and increasing intracellular Ca2+ levels. Angiotensin II also acts at the Na+/H+ exchanger in the proximal tubules of the kidney[2][3].
BIBS 39 is a new nonpeptide angiotensin II (AII) receptor antagonist.Target: Angiotensin Receptorin vitro: BIBS 39 displaces [125I] AII from its specific binding sites with a Ki value of 29 ± 7 nM for the AII subtype 1 (AT1) receptor and a Ki value of 480 ± 110 nM for the AII subtype 2 (AT2) receptor. BIBS 222 shows a Ki value of 20 ± 7 nM for the AT1 subtype and a Ki value of 730 ± 170 nM for the AT2 subtype. BIBS 39 is 17 times more selective for the AT1 subtype and BIBS 222 37 times. BIBS 39 shifts the AII concentration-contractile response curves in isolated rabbit aorta to the right in a parallel fashion. [1]in vivo: In pithed rats, BIBS 39 dependently shifts the dose-response curve of AII to the right without affecting the maximal response. BIBS 222 also causes parallel shifts to the right but a significant reduction of the maximal responses was observed at 3 and 10 mg/kg i.v. These results show that the benzimidazole derivatives BIBS 39 is a potent and selective AII receptor antagonists. Substitution with a benzimidazole moiety results into a considerable loss of selectivity for the AT1 receptor subtype compared with an imidazole moiety as, for instance, in DuP 753.[1] BIBS 39 is a new nonpeptide angiotensin receptor blockers that has affinity for both AT1- and AT2-receptors, is also a potent antagonist of the cardiovascular effects of AII in pithed rabbits. [2]
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].
Azilsartan-d4 is the deuterium labeled Azilsartan[1]. Azilsartan is an orally active, potent, selective and specific angiotensin II type 1 receptor (AT1) antagonist. Azilsartan induces ROS formation and apoptosis in HepG2 cells. Azilsartan shows neuroprotective and anticancer activity. Azilsartan can be used for hypertension and stroke research[2][3][4][5][6].
Azilsartan D5 is the deuterium labeled Azilsartan(TAK-536), which is a specific and potent angiotensin II type 1 receptor antagonist.
A 779 is a specific antagonist of G-protein coupled receptor (Mas receptor), which is an Ang1-7 receptor distinct from the classical AngII.
Losartan-d2 is the deuterium labeled Losartan[1]. Losartan is an angiotensin II receptor antagonist, competing with the binding of angiotensin II to AT1 receptors with IC50 of 20 nM[2].
Saralasin ([Sar1,Ala8] Angiotensin II) acetate hydrate is an octapeptide analog of angiotensin II. Saralasin acetate hydrate is a competitive angiotensin II receptor antagonist with a Ki value of 0.32 nM for 74% of the binding sites, and has partial agonist activity as well. Saralasin acetate hydrate can be used for the research of renovascular hypertension, renin-dependent (angiotensinogenic) hypertension[1][3][6].
Sparsentan (RE-021; BMS-346567; PS433540; DARA-a) is a highly potent dual angiotensin II and endothelin A receptor antagonist with Kis of 0.8 and 9.3 nM, respectively.
Losartan is an angiotensin II receptor antagonist, competing with the binding of angiotensin II to AT1 receptors with IC50 of 20 nM.
ZD 7155 hydrochloride is an angiotensin II receptor type 1 (AT1 receptor) antagonist.
Azilsartan medoxomil(TAK 491) is an orally administered angiotensin II receptor type 1 antagonist with IC50 of 0.62 nM, which used in the treatment of adults with essential hypertension. IC50 Value: 0.62 nM [2]Target: AT1 receptorin vitro: In aortic endothelial cells, azilsartan inhibited cell proliferation at concentrations as low as 1 μmol/l, whereas valsartan showed little or no antiproliferative effects at concentrations below 10 μmol/l. Antiproliferative effects of azilsartan were also observed in cells lacking AT1 receptors[1].in vivo: Oral administration of 0.1-3 mg/kg olmesartan medoxomil reduced blood pressure; however, only the two highest doses significantly reduced blood pressure 24h after dosing. ED(25) values were 0.41 and 1.3 mg/kg for azilsartan medoxomil and olmesartan medoxomil, respectively [2]. Over a longer treatment period of 24 weeks, azilsartan medoxomil showed sustained BP-lowering efficacy, with the reduction in 24-hour mean SBP at week 24 significantly greater with azilsartan medoxomil 40 or 80 mg once daily than with valsartan 320 mg once daily. Mean reductions from baseline in mean clinic SBP and DBP as well as DBP by ABPM were also significantly greater with azilsartan medoxomil 40 or 80 mg once daily than with valsartan[3]. In 4 randomized controlled trials (3 published to date), azilsartan medoxomil/chlorthalidone 40 mg/12.5 mg and 40 mg/25 mg reduced blood pressure (BP) significantly more than comparators did, including an approximately 5-mm Hg greater BP reduction than olmesartan medoxomil/hydrochlorothiazide 40 mg/25 mg and azilsartan medoxomil/hydrochlorothiazide [4].
Tranilast is an antiallergic agent.Target: Angiotensin ReceptorTranilast has been approved in Japan and South Korea, since 1982, for the treatment of bronchial asthma, with indications for keloids and hypertrophic scar added in 1993. Tranilast is also used to treat asthma, autoimmune diseases, atopic and fibrotic pathologies, and can also inhibit angiogenesis. The antiproliferative properties of tranilast were found that tranilast elicited an inhibitory effect on fibroblast proliferation in vitro and also suppressed collagen production both in vitro and in vivo . Tranilast also reduced the release of chemical mediators from mast cells and suppressed hypersensitivity reactions. [1]Three-week-old C57Bl/10 and mdx mice received tranilast (~300 mg/kg) in their food for 9 weeks, after which fibrosis was assessed through histological analyses, and functional properties of tibialis anterior muscles were assessed in situ and diaphragm muscle strips in vitro. Tranilast administration did not significantly alter the mass of any muscles in control or mdx mice, but it decreased fibrosis in the severely affected diaphragm muscle by 31% compared with untreated mdx mice (P< 0.05) [2].
FK-739 (free base) is an angiotensin II type 1 (AT1) receptor antagonist used in the study of hypertension[1].
TRV056 is a Gq-biased ligand of the angiotensin II receptor type 1 (AT1R). TRV056 is efficacious in stimulating cellular Gq-mediated signaling. TRV056 can be used to develop the Gq-biased AT1R agonists[1].
AVE 0991 is a nonpeptide and orally active angiotensin-(1-7) receptor agonist with an IC50 of 21 nM.
Azilsartan medoxomil(TAK 491) is an orally administered angiotensin II receptor type 1 antagonist with IC50 of 0.62 nM, which used in the treatment of adults with essential hypertension. IC50 Value: 0.62 nM [2]Target: AT1 receptorin vitro: In aortic endothelial cells, azilsartan inhibited cell proliferation at concentrations as low as 1 μmol/l, whereas valsartan showed little or no antiproliferative effects at concentrations below 10 μmol/l. Antiproliferative effects of azilsartan were also observed in cells lacking AT1 receptors[1].in vivo: Oral administration of 0.1-3 mg/kg olmesartan medoxomil reduced blood pressure; however, only the two highest doses significantly reduced blood pressure 24h after dosing. ED(25) values were 0.41 and 1.3 mg/kg for azilsartan medoxomil and olmesartan medoxomil, respectively [2]. Over a longer treatment period of 24 weeks, azilsartan medoxomil showed sustained BP-lowering efficacy, with the reduction in 24-hour mean SBP at week 24 significantly greater with azilsartan medoxomil 40 or 80 mg once daily than with valsartan 320 mg once daily. Mean reductions from baseline in mean clinic SBP and DBP as well as DBP by ABPM were also significantly greater with azilsartan medoxomil 40 or 80 mg once daily than with valsartan[3]. In 4 randomized controlled trials (3 published to date), azilsartan medoxomil/chlorthalidone 40 mg/12.5 mg and 40 mg/25 mg reduced blood pressure (BP) significantly more than comparators did, including an approximately 5-mm Hg greater BP reduction than olmesartan medoxomil/hydrochlorothiazide 40 mg/25 mg and azilsartan medoxomil/hydrochlorothiazide [4].Clinical trial: Effect of Azilsartan on Aldosterone in Post-menopausal Females . Phase not specified
Irbesartan-d6-1 is the deuterium labeled Irbesartan[1]. Irbesartan (SR-47436) is an orally active Ang II type 1 (AT1) receptor blocker (ARB). Irbesartan can relax the blood vessels, low blood pressure and increase the supply of blood and oxygen to the heart. Irbesartan can be used for the research of high blood pressure, heart failure, and diabetic kidney disease[2].
EMD 66684 is an antagonist of Angiotensin II Type 1 (AT1) receptor. EMD 66684 shows potent binding affinities for the AT1 subtype Ang II receptor with an IC50 value of 0.7 nM. EMD 66684 also serves as an antiischemic cytoprotectant [1]-[5].
C-Type Natriuretic Peptide (1-53), human is the 1-53 fragment of C-Type Natriuretic Peptide. C-Type Natriuretic Peptide is natriuretic peptide family peptide that is involved in the maintenance of electrolyte-fluid balance and vascular tone[1].
Olmesartan impurity is an Olmesartan impurity. Olmesartan (RNH-6270) is an angiotensin II receptor (AT1R) antagonist has the potential for high blood pressure study[1][2].
Elisartan is an orally active non-peptide pro-drug of angiotensin II AT1 receptor antagonist HN-12206, and shows anti-hypertension activities.
LY285434 is a suitable angiotensin II receptor antagonist.
Aclerastide (DSC-127) is an angiotensin receptor agonist. Aclerastide also is a peptide analog of angiotensin II. Aclerastide can be used for the research of tissue regeneration in diabetic ulcers[1][2].
L162389 is a potent antagonist of angiotensin AT1 receptor with Ki of 28 nM.
SL910102 is a nonpeptide angiotensin AT1 receptor antagonist.