1. GPCR/G Protein
  2. Angiotensin Receptor
  3. AVE 0991 sodium salt

AVE 0991 sodium salt 

Cat. No.: HY-15778A Purity: 98.42%
Handling Instructions

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 nM.

For research use only. We do not sell to patients.

AVE 0991 sodium salt Chemical Structure

AVE 0991 sodium salt Chemical Structure

CAS No. : 306288-04-0

Size Price Stock Quantity
10 mM * 1  mL in DMSO USD 398 In-stock
Estimated Time of Arrival: December 31
5 mg USD 300 In-stock
Estimated Time of Arrival: December 31
10 mg USD 456 In-stock
Estimated Time of Arrival: December 31
50 mg USD 1080 In-stock
Estimated Time of Arrival: December 31
100 mg USD 1680 In-stock
Estimated Time of Arrival: December 31
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Customer Review

Based on 7 publication(s) in Google Scholar

Other Forms of AVE 0991 sodium salt:

Top Publications Citing Use of Products

    AVE 0991 sodium salt purchased from MCE. Usage Cited in: PLoS One. 2015 Nov 5;10(11):e0142087.

    The effect of AVE0991 on neuronal cell death following glucose deprivation. Data are shown for cells exposed to normal conditions (control) or glucose deprivation (vehicle) for 24 h or with (A) AVE0991 or (B) AVE0991+A779.

    AVE 0991 sodium salt purchased from MCE. Usage Cited in: Redox Biol. 2019 Jan;20:75-86.

    AVE 0991 (AVE) treatment increases the expression of PKA-Cα, p-CREB, UCP-2, and Bcl-2, but the expression of Bax and Romo-1 are decreased in SAH+AVE group when compared with SAH+vehicle group.
    • Biological Activity

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    • References

    • Customer Review

    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 nM[1].

    IC50 & Target

    IC50: 21±35 nM (Ang-(1-7) receptor)[1]

    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].

    Molecular Weight

    602.70

    Formula

    C₂₉H₃₁N₄NaO₅S₂

    CAS No.

    306288-04-0

    SMILES

    O=S(C1=C(C2=CC=C(CN3C(C=O)=C(OC)N=C3C4=CC=CC=C4)C=C2)C=C(CC(C)C)S1)([N-]C(NCC)=O)=O.[Na+]

    Shipping

    Room temperature in continental US; may vary elsewhere.

    Storage
    Powder -20°C 3 years
      4°C 2 years
    In solvent -80°C 6 months
      -20°C 1 month
    Solvent & Solubility
    In Vitro: 

    DMSO : ≥ 55 mg/mL (91.26 mM)

    *"≥" means soluble, but saturation unknown.

    Preparing
    Stock Solutions
    Concentration Solvent Mass 1 mg 5 mg 10 mg
    1 mM 1.6592 mL 8.2960 mL 16.5920 mL
    5 mM 0.3318 mL 1.6592 mL 3.3184 mL
    10 mM 0.1659 mL 0.8296 mL 1.6592 mL
    *Please refer to the solubility information to select the appropriate solvent.
    In Vivo:
    • 1.

      Add each solvent one by one:  10% DMSO    40% PEG300    5% Tween-80    45% saline

      Solubility: ≥ 2.08 mg/mL (3.45 mM); Clear solution

    • 2.

      Add each solvent one by one:  10% DMSO    90% (20% SBE-β-CD in saline)

      Solubility: ≥ 2.08 mg/mL (3.45 mM); Clear solution

    • 3.

      Add each solvent one by one:  10% DMSO    90% corn oil

      Solubility: ≥ 2.08 mg/mL (3.45 mM); Clear solution

    *All of the co-solvents are provided by MCE.
    References
    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 DuP-753 or CGP 48933 (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 DuP-753 or CGP 48933 (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.

    MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    References

    Purity: 98.42%

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    Keywords:

    AVE 0991AVE0991AVE-0991Angiotensin ReceptorInhibitorinhibitorinhibit

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    Product Name:
    AVE 0991 sodium salt
    Cat. No.:
    HY-15778A
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