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AVE 0991

产品编号 TQ0057 CAS 304462-19-9

AVE 0991 是血管紧张素-(1-7) [Ang-(1-7)] 的非肽类似物，是一种具有口服活性的 Mas 激动剂，对 [125I]-Ang-(1-7) 结合到牛主动脉内皮细胞膜有抑制作用，通过增强自噬来抑制星形胶质细胞介导的阿尔茨海默病神经炎症。

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AVE 0991, CAS 304462-19-9

规格	价格/CNY	货期
2 mg	￥ 782	现货
5 mg	￥ 1,570	现货
10 mg	￥ 2,480	现货
25 mg	￥ 4,280	现货
50 mg	￥ 6,220	现货
1 mL * 10 mM (in DMSO)	￥ 1,970	现货

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其他形式的 AVE 0991:

AVE 0991 sodium salt
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纯度: 98.69%

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生物活性

化学信息

存储 & 溶解度

参考文献

产品描述	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.
靶点活性	Ang (1-7) receptor:21±35 nM
体外活性	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].
体内活性	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].
激酶实验	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].
细胞实验	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].
动物实验	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].

分子量	580.72
分子式	C29H32N4O5S2
CAS No.	304462-19-9

存储

Powder: -20°C for 3 years | In solvent: -80°C for 1 year

溶解度

H2O: <0.1 mg/mL (Insoluble)

DMSO: 30 mg/mL(51.66 mM), Sonication is recommended.

溶液配制表

可选溶剂	浓度体积质量	1 mg	5 mg	10 mg	25 mg
DMSO	1 mM	1.722 mL	8.61 mL	17.22 mL	43.05 mL
	5 mM	0.3444 mL	1.722 mL	3.444 mL	8.61 mL
	10 mM	0.1722 mL	0.861 mL	1.722 mL	4.305 mL
	20 mM	0.0861 mL	0.4305 mL	0.861 mL	2.1525 mL
	50 mM	0.0344 mL	0.1722 mL	0.3444 mL	0.861 mL

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分子量计算器

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参考文献

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. Mo J, et al. AVE 0991 attenuates oxidative stress and neuronal apoptosis via Mas/PKA/CREB/UCP-2 pathway after subarachnoid hemorrhage in rats. Redox Biol. 2018 Sep 28;20:75-86. 4. 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.

剂量换算

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体内实验配液计算器

请在以下方框中输入您的动物实验信息后点击计算，可以得到母液配置方法和体内配方的制备方法：比如您的给药剂量是10 mg/kg，每只动物体重20 g，给药体积100 μL，一共给药动物10 只，您使用的配方为5% DMSO+30% PEG300+5% Tween 80+60% ddH2O。那么您的工作液浓度为2 mg/mL。

母液配置方法：2 mg 药物溶于 50 μL DMSO (母液浓度为 40 mg/mL)，如您需要配置的浓度超过该产品的溶解度，请先与我们联系。

体内配方的制备方法：取 50 μL DMSO 主液，加入 300 μL PEG300，混匀澄清，再加 50 μL Tween 80，混匀澄清，再加 600 μL ddH2O, 混匀澄清。

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