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AVE 0991 sodium salt

Ang-(1-7) receptor Mas agonist CAS# 306288-04-0

AVE 0991 sodium salt

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Chemical structure

AVE 0991 sodium salt

3D structure

Chemical Properties of AVE 0991 sodium salt

Cas No. 306288-04-0 SDF Download SDF
PubChem ID 78357809 Appearance Powder
Formula C29H32N4NaO5S2+ M.Wt 603.71
Type of Compound N/A Storage Desiccate at -20°C
Solubility DMSO : ≥ 55 mg/mL (91.26 mM)
*"≥" means soluble, but saturation unknown.
Chemical Name sodium;ethylcarbamoyl-[3-[4-[(5-formyl-4-methoxy-2-phenylimidazol-1-yl)methyl]phenyl]-5-(2-methylpropyl)thiophen-2-yl]sulfonylazanide
SMILES CCNC(=O)[N-]S(=O)(=O)C1=C(C=C(S1)CC(C)C)C2=CC=C(C=C2)CN3C(=C(N=C3C4=CC=CC=C4)OC)C=O.[Na+]
Standard InChIKey GABSTAFOMFJFOI-UHFFFAOYSA-M
Standard InChI InChI=1S/C29H32N4O5S2.Na/c1-5-30-29(35)32-40(36,37)28-24(16-23(39-28)15-19(2)3)21-13-11-20(12-14-21)17-33-25(18-34)27(38-4)31-26(33)22-9-7-6-8-10-22;/h6-14,16,18-19H,5,15,17H2,1-4H3,(H2,30,32,35);/q;+1/p-1
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Biological Activity of AVE 0991 sodium salt

DescriptionAVE 0991 sodium salt is a nonpeptide and orally active Ang-(1-7) agonist. AVE 0991 competes for high-affinity binding of [125I]-Ang-(1-7) to bovine aortic endothelial cell membranes with IC50 of 21±35 nM.In Vitro:AVE 0991 is a nonpeptide compound that evokes effects similar to Ang-(1-7) on the endothelium. AVE 0991 and unlabeled Ang-(1-7) compete for high-affinity binding of [125I]-Ang-(1-7) to bovine aortic endothelial cell membranes with IC50s of 21±35 and 220±280 nM, respectively. Peak concentrations of NO and O2- release by AVE 0991 sodium salt and Ang-(1-7) (both 10 μM) are not significantly different (NO: 295±20 and 270±25 nM; O2-: 18±2 and 20±4 nM). However, the released amount of bioactive NO is ≈5 times higher for AVE 0991 in comparison to Ang-(1-7)[1].In Vivo:AVE 0991 (0.58 nmol/g) produces a significant decrease of water diuresis in WT mice compared with vehicle-treated animals (0.06±0.03 mL versus 0.27±0.05; n=9 for each group; P<0.01). The antidiuretic effect of AVE 0991 (AVE) is associated with an increase in urine osmolality (1669±231.0 mOsm/KgH2O versus 681.1±165.8 mOsm/KgH2O in vehicle-treated mice; P<0.01). The genetic deletion of Mas abolishes the antidiuretic effect of AVE 0991 during water loading (0.37±0.10 mL [n=9] versus 0.27±0.03 mL [n=11] in AVE 0991-treated mice). As observed with C57BL/6 mice, administration of AVE 0991 (0.58 nmol/g) in water-loaded Swiss mice also produces a significant decrease of the urinary volume compared with vehicle-treated animals (0.13±0.05 mL [n=16] versus 0.51±0.04 mL [n=40]; P<0.01)[2]. One week of treatment with AVE-0991 produces a significant decrease in perfusion pressure (56.55±0.86 vs. 68.73±0.69 mmHg in vehicle-treated rats) and an increase in systolic tension (11.40±0.05 vs. 9.84±0.15 g in vehicle-treated rats), rate of tension rise (+dT/dt; 184.30±0.50 vs. 155.20±1.97 g/s in vehicle-treated rats), rate of tension fall (−dT/dt; 179.60±1.39 vs. 150.80±2.42 g/s in vehicle-treated rats). A slight increase in heart rate (HR) is also observed (220.40±0.71 vs. 214.20±0.74 beats/min in vehicle-treated rats[3].

References:
[1]. Wiemer G, et al. AVE 0991, a nonpeptide mimic of the effects of angiotensin-(1-7) on the endothelium. Hypertension. 2002 Dec;40(6):847-52. [2]. Pinheiro SV, et al. Nonpeptide AVE 0991 is an angiotensin-(1-7) receptor Mas agonist in the mouse kidney. Hypertension. 2004 Oct;44(4):490-6. [3]. Ferreira AJ, et al. The nonpeptide angiotensin-(1-7) receptor Mas agonist AVE-0991 attenuates heart failure induced by myocardial infarction. Am J Physiol Heart Circ Physiol. 2007 Feb;292(2):H1113-9.

Protocol

Kinase Assay [1]
Binding of [125I]-Ang-(1-7) is performed. Briefly, 100 μg of membranes from primary cultured bovine aortic endothelial cells (BAECs, passage 1) are incubated in a total volume of 200 μL for 45 minutes at 25°C in HEPES-buffered saline (10 mM HEPES, 0.1 M NaCl, 5 mM MgCl2) containing 0.2% BSA and protease inhibitor cocktail Complete (Boehringer Mannheim). Saturable binding of [125I]-Ang-(1-7) is calculated by subtracting nonspecific binding (40% to 50%), determined in the presence of 10 μM unlabeled Ang-(1-7) from total binding. Competition experiments with increasing concentrations of AVE 0991 and unlabeled Ang-(1-7) are performed in the presence of 10 nM [125I]-Ang-(1-7). Assays are terminated by vacuum filtration (≤15 mm Hg) over Durapore filters (0.65 μm, Opak 96-well plates) presoaked with 1% BSA. The filters are washed 3 times with each 100 μL of PBS (50 mM, NaHPO4 and 0.15 M NaCl, pH 7.2). Radioactivity on dried filters is quantified with a gamma counter[1].

Animal Administration [2][3]
Mice[2] Swiss male mice, Mas-KO (Mas-/-) male mice on the pure genetic background C57BL/6, and WT C57BL/6 control mice (Mas+/+) are used. Water diuresis is induced by intraperitoneal water injection (0.05 mL/g of body weight [BW]) in conscious mice. Drugs are administered in the same injection with water load at prefixed volumes (0.01 mL/g BW). In the first set of experiments, WT mice (C57BL/6, control group) or Mas-KO mice are treated with: (1) 0.58 nmol/g AVE 0991 (n=9, control; n=11, Mas-KO mice); or (2) vehicle for AVE 0991 (10 μM KOH, 0.01 mL/g; n=9, control; n=9, Mas-KO). In the second set, Swiss mice are treated with: (1) vehicle (n=36); (2) 0.58 nmol/g AVE 0991 (n=16); (3) 46 pmol/g Ang-(1-7) antagonist A-779 (n=4); (4) 2 nmol/g losartan or valsartan (n=5); (5) 2 nmol/g AT2 receptor antagonists PD123319 or PD123177 (n=9); (6) AVE 0991 combined with A-779; (7) AVE 0991 combined with losartan or valsartan (n=4 for each); (8) or AVE 0991combined with PD123319 (n=5) or PD123177 (n=4). The urinary volume is measured for 60 minutes after water loading, and urine samples are obtained to determine the osmolality. The dose of AVE 0991is based in preliminary experiments performed in Swiss mice. Rats[3] Male Wistar rats weighting 250-300 g are used. Rats are treated either with AVE-0991 (1 mg/kg, n=9) or vehicle (0.9% NaCl, n=11) administered orally by gavage. At the end of the 7 day period of AVE-0991 treatment, the animals are decapitated 10-15 min after intraperitoneal injection of 400 IU of heparin. After the thorax is opened, the heart is carefully dissected, removed from the thoracic cavity, and placed in a plate containing ice-cold Krebs-Ringer solution (KRS) to attenuate any potential cardiac damage during dissection of aorta artery.

References:
[1]. Wiemer G, et al. AVE 0991, a nonpeptide mimic of the effects of angiotensin-(1-7) on the endothelium. Hypertension. 2002 Dec;40(6):847-52. [2]. Pinheiro SV, et al. Nonpeptide AVE 0991 is an angiotensin-(1-7) receptor Mas agonist in the mouse kidney. Hypertension. 2004 Oct;44(4):490-6. [3]. Ferreira AJ, et al. The nonpeptide angiotensin-(1-7) receptor Mas agonist AVE-0991 attenuates heart failure induced by myocardial infarction. Am J Physiol Heart Circ Physiol. 2007 Feb;292(2):H1113-9.

AVE 0991 sodium salt Dilution Calculator

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AVE 0991 sodium salt Molarity Calculator

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Preparing Stock Solutions of AVE 0991 sodium salt

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 1.6564 mL 8.2821 mL 16.5642 mL 33.1285 mL 41.4106 mL
5 mM 0.3313 mL 1.6564 mL 3.3128 mL 6.6257 mL 8.2821 mL
10 mM 0.1656 mL 0.8282 mL 1.6564 mL 3.3128 mL 4.1411 mL
50 mM 0.0331 mL 0.1656 mL 0.3313 mL 0.6626 mL 0.8282 mL
100 mM 0.0166 mL 0.0828 mL 0.1656 mL 0.3313 mL 0.4141 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

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Background on AVE 0991 sodium salt

IC50: AVE 0991 and Ang-(1–7) competitively bind to bovine aortic endothelial cell membranes with IC50 values of 21 ± 35 and 220 ± 280 nM, respectively.

Angiotensin-(1–7) (Ang-[1–7]) acts as a crucial component of the renin-angiotensin system which can regulate and maintain the blood pressure by offsetting effects of Ang II, a typical vasoconstrictor in vivo. AVE 0991, a nonpeptide mimic of Ang-(1–7), performs as an agonist of angiotensin-(1-7) receptor. It plays an important role in exploring effects of Ang-(1-7) and evaluating the potential of Ang-(1-7) as a cardiovascular drug. [1]

In vitro: AVE 0991 was found to compete with Ang-(1-7) for bovine aortic endothelial cell membrane receptors with an IC50 of 21±35 nM. There was no significant difference in peak concentrations of NO and O2- released from AVE 0991 treated group and Ang-(1-7) treated group. However, the released amount of NO was approximately 5 times higher in AVE 0991 group than that in Ang-(1-7) group. Moreover, AVE 0091 significantly displaced the binding of I-Ang-(1-7) in both Mas-transfected monkey kidney cells (COS) and Mas-transfected Chinese hamster ovary (CHO) cells. [1]

In vivo: AVE 0091 at a dosage of 0.58 nmol/g resulted in a significant decrease in urinary volume, together with an increase in urinary osmolality in water-loaded C57BL/6 mice. [2] The antidiuretic effect of AVE was completely offset by the Ang II antagonists, which indicting a high specificity of AVE 0991. Since Ang II induced atherogenesis and ang-(1–7) offset Ang II action, it was proved that AVE 0991 blocked atherogenesis in apolipoprotein E (apoE)-knockout mice model. [3]

Clinical trial: So far, no clinical trial has been conducted.

References:
[1]Wiemer G, Dobrucki LW, Louka FR, Malinski T, Heitsch H.  AVE 0991, a nonpeptide mimic of the effects of angiotensin-(1–7) on the endothelium. Hypertension. 2002 Dec; 40: 847-52.
[2] Pinheiro SV, Silva AC, Sampaio WO, Paula RD, Mendes EP, Bontempo ED, Pesquero JB, Walther T, Alenina N, Bader M, Bleich M and Santos RA.  Nonpeptide AVE 0991 is an angiotensin-(1-7) receptor Mas agonist in the mouse kidney. Hypertension. 2004 Oct; 44(4):490-6.
[3]Toton-Zuranska J, Gajda M, Pyka-Fosciak G, Kus K, Pawlowska M, Niepsuj A, Wolkow P, Olszanecki R, Jawien J and Korbut R.  AVE 0991- angiotensin-(1-7) receptor agonist, inhibits atherogenesis in APOE-knockout mice. J Physiol Pharm. 2010, 61(2):181-183.

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References on AVE 0991 sodium salt

Acute and chronic angiotensin-(1-7) restores vasodilation and reduces oxidative stress in mesenteric arteries of salt-fed rats.[Pubmed:21803946]

Am J Physiol Heart Circ Physiol. 2011 Oct;301(4):H1341-52.

This study determined the effect of ANG-(1-7) on salt-induced suppression of endothelium-dependent vasodilatation in the mesenteric arteries of male Sprague-Dawley rats. Chronic intravenous infusion of ANG-(1-7), oral administration of the nonpeptide mas receptor agonist AVE-0991, and acute preincubation of the arteries with ANG-(1-7) and AVE-0991 all restored vasodilator responses to both ACh and histamine that were absent in the arteries of rats fed a high-salt (4% NaCl) diet. The protective effects of ANG-(1-7) and AVE-0991 were inhibited by acute or chronic administration of the mas receptor antagonist A-779, the ANG II type 2 (AT(2)) receptor blocker PD-123319, or N-nitro-l-arginine methyl ester, but not the ANG II type 1 receptor antagonist losartan. Preincubation with the antioxidant tempol or the nitric oxide (NO) donor diethylenetriamine NONOate and acute and chronic administration of the AT(2) receptor agonist CGP-42112 mimicked the protective effect of ANG-(1-7) to restore vascular relaxation. Acute preincubation with ANG-(1-7) and chronic infusion of ANG-(1-7) ameliorated the elevated superoxide levels in rats fed a high-salt diet, but the expression of Cu/Zn SOD and Mn SOD enzyme proteins in the vessel wall was unaffected by ANG-(1-7) infusion. These results indicate that both acute and chronic systemic administration of ANG-(1-7) or AVE-0991 restore endothelium-dependent vascular relaxation in salt-fed Sprague-Dawley rats by reducing vascular oxidant stress and enhancing NO availability via mas and AT(2) receptors. These findings suggest a therapeutic potential for mas/AT(2) receptor activation in preventing the vascular oxidant stress and endothelial dysfunction associated with elevated dietary salt intake.

Angiotensin-(1-7) Selectively Induces Relaxation and Modulates Endothelium-Dependent Dilation in Mesenteric Arteries of Salt-Fed Rats.[Pubmed:27676088]

J Vasc Res. 2016;53(1-2):105-118.

This study investigated the acute effects of angiotensin-(1-7) and AVE0991 on active tone and vasodilator responses to bradykinin and acetylcholine in isolated mesenteric arteries from Sprague-Dawley rats fed a high-salt (HS; 4% NaCl) versus a normal salt (NS; 0.4% NaCl) diet. Angiotensin-(1-7) and AVE0991 elicited relaxation, and angiotensin-(1-7) unmasked vasodilator responses to bradykinin in arteries from HS-fed rats. These effects of angiotensin-(1-7) and AVE0991 were inhibited by endothelium removal, A779, PD123319, HOE140 and L-NAME. Angiotensin-(1-7) also restored the acetylcholine-induced relaxation that was suppressed by the HS diet. Vasodilator responses to bradykinin and acetylcholine in the presence of angiotensin-(1-7) were mimicked by captopril and the AT2 receptor agonist CGP42112 in arteries from HS-fed rats. Thus, in contrast to salt-induced impairment of vascular relaxation in response to vasodilator stimuli, angiotensin-(1-7) induces endothelium-dependent and NO-mediated relaxation, unmasks bradykinin responses via activation of mas and AT2 receptors, and restores acetylcholine-induced vasodilation in HS-fed rats. AT2 receptor activation and angiotensin-converting enzyme (ACE) inhibition shared the ability of angiotensin-(1-7) to enhance bradykinin and acetylcholine responses in HS-fed rats. These findings suggest a therapeutic potential for mas and/or AT2 receptor activation and ACE inhibition in restoring endothelial function impaired by elevated dietary salt intake or other pathological conditions.

Description

AVE 0991 sodium salt is a nonpeptide and orally active Ang-(1-7) receptor Mas agonist. AVE 0991 competes for high-affinity binding of [125I]-Ang-(1-7) to bovine aortic endothelial cell membranes with IC50 of 21±35 nM.

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