13585831301
021-59541103 021-60443211
3004967995
13585831301021-59541103 021-604432113004967995
聯系人:高小姐
電話:021-59541103 021-60443211
手機:13585831301
Q Q： 3004967995
Email:3004967995@qq.com
詳細地址：上海嘉定區嘉羅公路1661
化學性質：
| 規格 | 1mg 5mg 10mg 20mg |
| CAS | 450348-85-3 |
| 別名 | N/A |
| 化學名 | N/A |
| 分子式 | C17H13F2NO3 |
| 分子量 | 317.29 |
| 溶解度 | Soluble in DMSO |
| 儲存條件 | 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. |
| Shipping Condition | Evaluation sample solution : ship with blue ice |
產品描述：
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.
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原創作者：上海莼試生物技術有限公司
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普票匯款信息
賬 戶 名：上海生物
開 戶 行：中國銀行山東省分行營業部
賬 號：2169 2341 6278
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