AVE3085 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-eNOS^Ser1177, and loares the level of p-eNOS^Thr495 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. 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.

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

AVE3085 (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 AVE3085-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 AVE3085 group than in the vehicle-treated AB group. 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.

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

AVE3085 (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 AVE3085-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 AVE3085 group than in the vehicle-treated AB group. 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.

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

• . 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.  [Content Brief]

  . 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.  [Content Brief]

  . 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  [Content Brief]