| 包装 | 价格(元) |
| 10mM (in 1mL DMSO) | 电议 |
| 2mg | 电议 |
| 5mg | 电议 |
| 10mg | 电议 |
| 100mg | 电议 |
Preparation Method | Competition experiments with increasing concentrations of AVE 0991 and unlabeled Ang-(1 7) were performed in the presence of 10 nmol/L [125I]-Ang-(1-7). Assays were terminated by vacuum filtration ( 15 mm Hg) over Durapore filters (0.65 |, Opak 96-well plates, Millipore) presoaked with 1% BSA. |
Applications | AVE 0991 and unlabeled Ang-(1-7) competed the specific binding of [125I]-Ang-(1-7), with IC50 values of 21 !A35 and 220 !A 280 nmol/L, respectively (each n=3). The Ang-(1-7) analogue [D-Ala7]-Ang-(1 7) totally competed the specific binding of [125I]-Ang-(1-7), with an IC50 value of 0.41 !A3.0 |ol/L (n=3). |
Cell lines | Chinese hamster ovary (CHO) cells |
Preparation Method | Binding of rhodamine Ang-(1-7) in Mas-transfected CHO cells was performed under similar conditions using 2*10 -9 mol/L rhodamine-labeled Ang-(1-7) in the presence or absence of AVE 0991(10 -6 mol/L), CV11974, or PD123319 |
Reaction Conditions | AVE 0991 (10-6mol/L) |
Applications | AVE 0991 displaced the binding of 125I-Ang-(1-7) in Mas-transfected monkey kidney cells (COS) cells (IC50=4.75x10(-8) mol/L) and of rhodamine-Ang-(1-7) in Mas-transfected Chinese hamster ovary (CHO) cells. It also produced NO release in Mas-transfected CHO cells blocked by A-779 but not by angiotensin II type-1 (AT1) and AT2 antagonists. |
Animal models | Male C57BL/6J mice (8¨C10 weeks old; 24¨C26 g) |
Preparation Method | Twenty-four h after ligation, the surviving mice were randomly divided into four groups: 1) sham-operated group, 2) vehicle-treated AB group (vehicle-treated group ), 3) AB mice treated with AVE 0991 ( AVE 0991 group ). AVE 0991 group was administered orally once a day at AVE 0991 (20 mg kg/day) for 4 weeks while isovolumic sodium chloride was administrated in the same manner for the sham-operated and vehicle-treated group. |
Dosage form | AVE 0991 (20 mg kg/day) for 4 weeks |
Applications | AVE 0991 treatment could attenuate cardiac hypertrophy and improve heart function, which may be due to reduce oxidative stress./p> |
| 产品描述 | AVE 0991 is a Nonpeptide Mimic of the Effects of Angiotensin-(1-7) on the Endothelium. AVE 0991 and unlabeled Ang-(1-7) competed for high-affinity binding of [125I]-Ang-(1-7) to bovine aortic endothelial cell membranes with IC50 values of 21+/-35 and 220+/-280 nM, respectively[4]. AVE 0991 displaced the binding of 125I-Ang-(1-7) in Mas-transfected monkey kidney cells (COS) cells (IC50=4.75x10(-8) mol/L) and of rhodamine-Ang-(1-7) in Mas-transfected Chinese hamster ovary (CHO) cells. It also produced NO release in Mas-transfected CHO cells blocked by A-779 but not by angiotensin II type-1 (AT1) and AT2 antagonists[7]. AVE 0991 attenuates oxidative stress and neuronal apoptosis via Mice were underwent aortic banding to induce cardiac hypertrophy followed by the administration of AVE 0991 (20 mg kg.day (-1)) for 4 weeks. It was shown that AVE 0991 reduced left ventricular hypertrophy and improved heart function, characterized by decreases in left ventricular weight and left ventricular end-diastolic diameter, and increases in ejection fraction. Moreover, AVE 0991 significantly down-regulated mean myocyte diameter and attenuate the gene expression of the hypertrophic markers[2].Mas/PKA/CREB/UCP-2 pathway after subarachnoid hemorrhage in rats[1]. Enhanced Ang II and attenuated Ang-(1-7) levels were also observed in the liver tissue of heatstroke rats, which were consistent with their receptors and converting enzymes. Hepatic damage associated with increased ROS and protein expression levels of NOX4, NLRP3, caspase-1, and IL-1β was attenuated by AVE 0991, an analogue of Ang-(1-7)[3]. Oral treatment with AVE 0991 reduces blood-pressure cardiac remodeling and improves baroreflex sensitivity in 2K1C renovascular hypertensive rats[5]. AVE 0991 prevented AngII-inducing myocardial hypertrophy in a dose-dependent fashion, a process that may be associated with the inhibition of TGF-beta1/Smad2 signaling[6]. References: |
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