Shopping Cart
  • Remove All
  • TargetMol
    Your shopping cart is currently empty

AVE 0991

🥰Excellent
Catalog No. TQ0057Cas No. 304462-19-9

AVE 0991, a nonpeptide analog of angiotensin-(1-7) [Ang-(1-7)], is an orally active Mas agonist with inhibitory effects on [125I]-Ang-(1-7) binding to bovine aortic endothelial cell membranes, and inhibits astrocyte-mediated neuroinflammation in Alzheimer's disease by enhancing autophagy.

AVE 0991

AVE 0991

🥰Excellent
Purity: 98.69%
Catalog No. TQ0057Cas No. 304462-19-9
AVE 0991, a nonpeptide analog of angiotensin-(1-7) [Ang-(1-7)], is an orally active Mas agonist with inhibitory effects on [125I]-Ang-(1-7) binding to bovine aortic endothelial cell membranes, and inhibits astrocyte-mediated neuroinflammation in Alzheimer's disease by enhancing autophagy.
Pack SizePriceAvailabilityQuantity
2 mg$82 In Stock
5 mg$147 In Stock
10 mg$239 In Stock
25 mg$459 In Stock
50 mg$718 In Stock
1 mL x 10 mM (in DMSO)$189 In Stock
Bulk & Custom
Add to Cart
Questions
View More

Related Compound Libraries of "AVE 0991"

Select Batch
Purity:98.69%
Contact us for more batch information
Resource Download
All TargetMol products are for research purposes only and cannot be used for human consumption. We do not provide products or services to individuals. Please comply with the intended use and do not use TargetMol products for any other purpose.

Product Introduction

Bioactivity
Description
AVE 0991, a nonpeptide analog of angiotensin-(1-7) [Ang-(1-7)], is an orally active Mas agonist with inhibitory effects on [125I]-Ang-(1-7) binding to bovine aortic endothelial cell membranes, and inhibits astrocyte-mediated neuroinflammation in Alzheimer's disease by enhancing autophagy.
Targets&IC50
Ang (1-7) receptor:21±35 nM
In vitro
AVE 0991 is a nonpeptide compound that elicits effects on the endothelium similar to Angiotensin-(1-7) [Ang-(1-7)]. 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. The peak concentrations of NO and O2- release induced by AVE 0991 sodium salt and Ang-(1-7) (both at 10 μM) show no significant difference (NO: 295±20 and 270±25 nM; O2-: 18±2 and 20±4 nM); however, the amount of bioactive NO released is approximately 5 times higher for AVE 0991 compared to Ang-(1-7) [1].
In vivo
In wild-type (WT) mice, the administration of AVE 0991 at a dose of 0.58 nmol/g leads to a significant reduction in water diuresis compared to vehicle-treated mice (0.06±0.03 mL versus 0.27±0.05; n=9 for each group; P<0.01). This antidiuretic effect of AVE 0991 is accompanied by 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, a receptor associated with the effects of AVE 0991, eliminates the antidiuretic impact 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). Similar to observations in C57BL/6 mice, the administration of AVE 0991 (0.58 nmol/g) in water-loaded Swiss mice also results in a significant reduction in urinary volume compared to vehicle-treated animals (0.13±0.05 mL [n=16] versus 0.51±0.04 mL [n=40]; P<0.01).Furthermore, a one-week treatment with AVE-0991 induces a notable 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). Additionally, there is an elevation in the rate of tension rise (+dT/dt; 184.30±0.50 vs. 155.20±1.97 g/s in vehicle-treated rats) and the 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) [4].
Kinase Assay
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. 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 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].
Cell Research
COS cells and CHO cells are stably transfected with rat Mas cDNA driven by a cytomegalovirus promoter and selected by neomycin. 125I-Ang-(1-7) (0.5×10^-9 mol/L) is incubated in 24-well plates for 60 minutes at 4°C in 0.3 mL of serum-free medium (DMEM) supplemented with 0.2% BSA, 0.005% bacitracin, 0.1 mol/L PMSF, and 0.5 mol/L orthophenanthroline with Mas-transfected COS cells in the presence or absence of AVE 0991 (AVE, 10-10 to -5 mol/L). After 2 ishes with ice-cold serum-free DMEM, cells are disrupted with 0.1% Triton X-100. Bound radioactivity is measured in a gamma counter. Binding of rhodamine-Ang-(1-7) in Mas-transfected CHO cells is performed under similar conditions using 2×10^-9 mol/L rhodamine-labeled-Ang-(1-7) in the presence or absence of AVE (10^-6 mol/L), CV11974 (10^-6 mol/L), or PD123319 (10^-6 mol/L). NSB is determined in the presence of 10-6 mol/L Ang-(1-7) [1].
Animal Research
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 [2]. Male Wistar rats weighing 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 [3].
Chemical Properties
Molecular Weight580.72
FormulaC29H32N4O5S2
Cas No.304462-19-9
SmilesCCNC(=O)NS(=O)(=O)c1sc(CC(C)C)cc1-c1ccc(Cn2c(C=O)c(OC)nc2-c2ccccc2)cc1
Relative Density.1.31 g/cm3 (Predicted)
Storage & Solubility Information
StoragePowder: -20°C for 3 years | In solvent: -80°C for 1 year | Shipping with blue ice.
Solubility Information
H2O: <0.1 mg/mL (Insoluble)
DMSO: 30 mg/mL (51.66 mM), Sonication is recommended.
Solution Preparation Table
DMSO
1mg5mg10mg50mg
1 mM1.7220 mL8.6100 mL17.2200 mL86.1000 mL
5 mM0.3444 mL1.7220 mL3.4440 mL17.2200 mL
10 mM0.1722 mL0.8610 mL1.7220 mL8.6100 mL
20 mM0.0861 mL0.4305 mL0.8610 mL4.3050 mL
50 mM0.0344 mL0.1722 mL0.3444 mL1.7220 mL

Calculator

  • Molarity Calculator
  • Dilution Calculator
  • Reconstitution Calculator
  • Molecular Weight Calculator

In Vivo Formulation Calculator (Clear solution)

Please enter your animal experiment information in the following box and click Calculate to obtain the mother liquor preparation method and in vivo formula preparation method:
TargetMol | Animal experimentsFor example, your dosage is 10 mg/kg Each animal weighs 20 g, and the dosage volume is 100 μL . TargetMol | Animal experiments A total of 10 animals were administered, and the formula you used is 5% TargetMol | reagent DMSO+30% PEG300+5% Tween 80+60% ddH2O. So your working solution concentration is 2 mg/mL。
Mother liquor preparation method: 2 mg of drug dissolved in 50 μL DMSOTargetMol | reagent (mother liquor concentration of 40 mg/mL), if you need to configure a concentration that exceeds the solubility of the product, please contact us first.
Preparation method for in vivo formula: Take 50 μL DMSOTargetMol | reagent main solution, add 300 μLPEG300TargetMol | reagent mix well and clarify, then add 50 more μL Tween 80, mix well and clarify, then add 600 more μLddH2OTargetMol | reagent mix well and clarify
For Reference Only. Please develop an appropriate dissolution method based on your laboratory animals and route of administration.
1 Enter information below:
mg/kg
g
μL
2 Enter the in vivo formulation:
% DMSO
%
%Tween 80
%ddH2O

Dose Conversion

You can also refer to dose conversion for different animals. More Dose Conversion

Tech Support

Please see Inhibitor Handling Instructions for more frequently ask questions. Topics include: how to prepare stock solutions, how to store products, and cautions on cell-based assays & animal experiments, etc

Keywords

Related Tags: buy AVE 0991 | purchase AVE 0991 | AVE 0991 cost | order AVE 0991 | AVE 0991 chemical structure | AVE 0991 in vivo | AVE 0991 in vitro | AVE 0991 formula | AVE 0991 molecular weight