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的活性。",{"key":228,"value":229},"相关类别","信号通路\n>>\nG 蛋白偶联受体\u002FG 蛋白\n>>\nCCR\n信号通路\n>>\n免疫及炎症\n>>\nCCR\n信号通路\n>>\n抗感染\n>>\nHIV\n研究领域\n>>\n炎症\u002F免疫",{"key":231,"value":232},"靶点","MIP-1α-CCR5:3.3 nM (IC50, in HEK-293 cell membrane)\nRANTES-CCR5:5.2 nM (IC50, in HEK-293 cell membrane)\nMIP-1β-CCR5:7.2 nM (IC50, in HEK-293 cell membrane)\nHIV-1 (Ba-L):1.1 nM (IC50, in PM-1 cells)",{"key":234,"value":235},"体外研究","Maraviroc是一种选择性CCR5拮抗剂,具有强效的抗人类免疫缺陷病毒1型(HIV-1)活性。 Maraviroc抑制趋化因子诱导的细胞内钙重新分布的下游事件,针对MIP-1β,MIP-1α和RANTES获得的IC50为7至30nM。当使用分离的多个(合并的)供体PBMC(IC90,3.1 nM)在5天抗病毒测定中测量时,Maraviroc在低纳摩尔浓度下对HIV-1 Ba-L(实验室适应的R5菌株)具有活性(IC90),单供体PBMC(IC90,1.8 nM)或PM-1细胞(IC90,1.1 nM)[1]。",{"key":237,"value":238},"体内研究","静脉内给药后,大鼠和狗的清除值均为中等至高(分别为74和21mL\u002Fmin\u002Fkg)。 Maraviroc在两个物种中的分布均适中(4.3至6.5升\u002F kg)。 maraviroc的半衰期值在大鼠中为0.9小时,在狗中为2.3小时。口服给药(2mg\u002Fkg)后,Cmax(256ng\u002FmL)发生1.5小时。给药后,生物利用度为40％。对于大鼠,口服给药后在门静脉中获得的浓度的研究表明,约30％的给药剂量是从肠道吸收的[1]。在DSS\u002FTNBS结肠炎和转移模型中,Maraviroc通过选择性地减少携带CCR5的白细胞的募集来减弱肠道炎症的发展[2]",{"key":240,"value":241},"激酶实验","基本上使用稳定表达受体或其膜制剂的完整HEK-293细胞测量125 I标记的MIP-1α，MIP-1β和RANTES与CCR5的结合。简而言之，将细胞重悬于结合缓冲液（含有1mM CaCl 2,5mM MgCl 2和0.5％牛血清白蛋白[BSA]的50mM HEPES并调节至pH 7.4）至2×10 6个细胞\u002F mL的密度。对于膜制剂，将磷酸盐缓冲盐水（PBS）洗涤的细胞重悬于裂解缓冲液（20mM HEPES，1mM CaCl 2,1片剂，每50mL，pH 7.4; Boehringer）中，然后在Polytron手持式均质器中均质化。 ，超速离心（40,000×g，30分钟），并在结合缓冲液中重新悬浮至蛋白质浓度为0.25mg \u002F mL（在96孔板的每个孔中使用12.5μg膜蛋白）。制备125 I-放射性标记的MIP-1α，MIP-1β和RANTES，并在测定中在结合缓冲液中稀释至终浓度为400pM。向每个孔中加入适当的maraviroc稀释液至终体积为100μL，将测定板温育1小时，并通过预封闭和洗涤的Unifilter板过滤内容物，在过夜干燥后计数[1]。",{"key":243,"value":244},"细胞实验","将HEK-293细胞等分试样（100μL，1×10 6个细胞\u002F mL）接种到聚-D-赖氨酸包被的板中，并在37℃下孵育过夜。将可溶性重组人CD4（sCD4）（在培养基中稀释至4.5nM）和HIV-1 gp120的1：1混合物在室温下孵育15分钟，然后在稀释的存在下加入PBS洗涤的细胞中。 maraviroc能够确定IC50。将测定板在37℃下孵育1小时并洗涤。将Eu3 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Maraviroc (UK-427,857), a potent, orally bioavailable, and selective small-molecule inhibitor of chemokine receptor CCR5 with broad-spectrum anti-human immunodeficiency virus type 1 activity. Antimicrob Agents Chemother. 2005 Nov;49(11):472\n[2].\nMencarelli A, et al. Highly specific blockade of CCR5 inhibits leukocyte trafficking and reduces mucosal inflammation in murine colitis. Sci Rep. 2016 Aug 5;6:30802.\n[3].\nRomero-Sánchez MC, et al. Effect of maraviroc on HIV-disease progression-related biomarkers. Antimicrob Agents Chemother. 2012 Nov;56(11):5858-64.\n[4].\nHuilin Mou, et al. NRSF and CCR5 Established Neuron-glia Communication during Acute and Chronic Stresses. Journal of Drug Metabolism & Toxicology. 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