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AVE-3085 Catalog No.GC32486

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1mg
$92.00
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5mg
$184.00
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10mg
$313.00
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20mg
$552.00
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Sample solution is provided at 25 µL, 10mM.

Quality Control

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Protocol

Animal experiment:

Male C57BL/6J mice (8-10 weeks old; 24-26 g) are housed in individual cages on a 12 h light-dark cycle in a temperature- (24 ± 2°C) and humidity-controlled room with ad libitum access to tap water and standard rodent chow. The mice are anesthetized via an intraperitoneal injection of 1.5% pentobarbital (W*0.06), and cardiac hypertrophy is induced by pressure overload, which is achieved via descending aortic banding (AB). Similar surgeries that do not include aortic banding are performed on the sham-operated. Twenty-four hours after ligation, the surviving mice are randomly divided into the following three groups (n=8 per group): (1) a sham-operated group (Sham group), (2) a vehicle-treated AB group (vehicle-treated group), and (3) an AB group treated with AVE 3085 (AVE 3085 group). AVE 3085 is administered orally once daily at a dose of 10 mg kg day−1 for 4 weeks, and isovolumic sodium chloride is administered in the same manner to the sham-operated and vehicle-treated groups.

References:

[1]. Chen Y, et al. AVE 3085, a novel endothelial nitric oxide synthase enhancer, attenuates cardiac remodeling in mice through the Smad signaling pathway. Arch Biochem Biophys. 2015 Mar 15;570:8-13.
[2]. Xue HM, et al. AVE3085 protects coronary endothelium from the impairment of asymmetric dimethylarginine by activation and recoupling of eNOS. Cardiovasc Drugs Ther. 2012 Oct;26(5):383-92.
[3]. Yang Q, et al. AVE3085, an enhancer of endothelial nitric oxide synthase, restores endothelial function and reduces blood pressure in spontaneously hypertensive rats. Br J Pharmacol. 2011 Jul;163(5):1078-85

Chemical Properties

Cas No. 450348-85-3 SDF Download SDF
Synonyms N/A
Chemical Name N/A
Canonical SMILES O=C(C1=CC=C(OC(F)(F)O2)C2=C1)NC3CC4=C(C=CC=C4)C3
Formula C17H13F2NO3 M.Wt 317.29
Solubility Soluble in DMSO Storage Store at -20°C
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.
Shipping Condition Evaluation sample solution : ship with blue ice
All other available size: ship with RT , or blue ice upon request
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Background

AVE-3085 is a potent endothelial nitric oxide synthase enhancer, used for cardiovascular disease treatment.

Pre-incubation with AVE3085 restores the bradykinin-induced relaxation, reverses the decrease of p-eNOSSer1177, and loares the level of p-eNOSThr495 and nitrotyrosine. NO release in response to bradykinin is significantly reduced by ADMA and such reduction is restored by AVE3085. AVE3085 also prevents the elevation of O2.- and ONOO- levels in coronary arteries exposed to ADMA[2]. AVE3085 (10 μM) markedly increases ACh-induced relaxations in SHR aortae without affecting those in WKY aortae, and also increases the eNOS expression in WKY aortae[3].

AVE 3085 (10 mg/kg/day, p.o.) treatment prevents the increases in the left ventricular weight, left ventricular weight/body weight ratio, mean myocyte diameter, and the expression of the hypertrophic markers ANP and β-MHC compared to the vehicle-treated mice. AVE 3085 treatment also attenuates the collagen volume fraction levels compared to the vehicle-treated mice. In the AVE 3085-treated mice, the EFs, FSs, mitral E velocity, E/A ratio and LVDds are significantly improved compared to the vehicle-treated mice. AVE 3085 treatment attenuates the increase in the expression of Smad2 mRNA. Furthermore, the levels of the eNOS protein expression are significantly up-regulated in the AVE 3085 group than in the vehicle-treated AB group[1]. AVE3085 (10 mg/kg, p.o.) significantly improves ACh-induced endothelium-dependent relaxations in the aortae of SHRs, and reduces systolic blood pressure in SHRs. AVE3085 treatment for 4 weeks increases levels of p-eNOS and eNOS in SHR aortae without affecting levels of eNOS and p-eNOS in WKY aortae[3].

[1]. Chen Y, et al. AVE 3085, a novel endothelial nitric oxide synthase enhancer, attenuates cardiac remodeling in mice through the Smad signaling pathway. Arch Biochem Biophys. 2015 Mar 15;570:8-13. [2]. Xue HM, et al. AVE3085 protects coronary endothelium from the impairment of asymmetric dimethylarginine by activation and recoupling of eNOS. Cardiovasc Drugs Ther. 2012 Oct;26(5):383-92. [3]. Yang Q, et al. AVE3085, an enhancer of endothelial nitric oxide synthase, restores endothelial function and reduces blood pressure in spontaneously hypertensive rats. Br J Pharmacol. 2011 Jul;163(5):1078-85