- ￥526 - 4954
- Solarbio
- 北京
- IM2850
- 2025年07月23日
企业认证
相关产品推荐更多 >
万千商家帮你免费找货
0 人在求购买到急需产品
- 详细信息
- 文献和实验
- 技术资料
- 保存条件：
Powder:2-8℃，2 years;Insolvent(母液):-20℃，6 months;-80℃，1 year
- 保质期：
Powder:2-8℃，2 years;Insolvent(母液):-20℃，6 months;-80℃，1 year
- 英文名：
Maraviroc
- 库存：
现询
- 供应商：
北京索莱宝科技有限公司
- CAS号：
376348-65-1
- 规格：
100mg/50mg/10mg/5mg
| 规格： | 100mg | 产品价格： | ￥4954.0 |
|---|---|---|---|
| 规格： | 50mg | 产品价格： | ￥3290.0 |
| 规格： | 10mg | 产品价格： | ￥890.0 |
| 规格： | 5mg | 产品价格： | ￥526.0 |
| 基本信息 | |
| CAS | No.376348-65-1 |
| 中文名称 | 马拉维若 |
| 英文名称 | Maraviroc |
| 别名 | UK-427857;Selzentry;Celsentri |
| 分子式 | C29H41F2N5O |
| 分子量 | 513.67 |
| 溶解性 | Soluble in DMSO ≥5mg/mL |
| 纯度 | ≥98% |
| 外观(性状) | White to off-white Solid |
| 储存条件 | Powder:2-8℃，2 years;Insolvent(母液):-20℃，6 months;-80℃，1 year |
| EC | EINECS 609-456-0 |
| MDL | MFCD13188530 |
| SMILES | O=C(C1CCC(F)(F)CC1)N[C@H](C2=CC=CC=C2)CCN3[C@H]4C[C@@H](N5C(C)=NN=C5C(C)C)C[C@@H]3CC4 |
| InChIKey | GSNHKUDZZFZSJB-HLMSNRGBSA-N |
| InChI | InChI=1S/C29H41F2N5O/c1-19(2)27-34-33-20(3)36(27)25-17-23-9-10-24(18-25)35(23)16-13-26(21-7-5-4-6-8-21)32-28(37)22-11-14-29(30,31)15-12-22/h4-8,19,22-26H,9-18H2,1-3H3,(H,32,37)/t23-,24+,25 ,26-/m0/s1 |
| PubChem CID | 3002977 |
| 靶点 | CCR5 |
| 通路 | Immunology & Inflammation;GPCR & G Protein |
| 背景说明 | Maraviroc是选择性的CCR5拮抗剂,具有抑制 HIV 的活性。 |
| 生物活性 | Maraviroc is a selective?CCR5?antagonist with activity against human?HIV.[1-4] |
| IC50 | IC50:3.3 nM (MIP-1α-CCR5， in HEK-293 cell membrane);5.2 nM (RANTES-CCR5， in HEK-293 cell membrane);7.2 nM (MIP-1β-CCR5， in HEK-293 cell membrane);1.1 nM (HIV-1 (Ba-L)， in PM-1 cells)[1] |
| In Vitro | Maraviroc demonstrated potent Antiviral activity against all CCR5-tropic HIV-1 viruses tested， including 43 primary isolates from various clades and diverse geographic origin (geometric mean 90% inhibitory concentration of 2.0 nM). Maraviroc was active against 200 clinically derived HIV-1 envelope-recombinant pseudoviruses， 100 of which were derived from viruses resistant to existing drug classes. There was little difference in the sensitivity of the 200 viruses to maraviroc， as illustrated by the biological cutoff in this assay (= geometric mean plus two standard deviations [SD] of 1.7-fold). The mechanism of action of maraviroc was established using cell-based assays， where it blocked binding of viral envelope， gp120， to CCR5 to prevent the membrane fusion events necessary for viral entry. Maraviroc did not affect CCR5 cell surface levels or associated intracellular signaling， confirming it as a functional antagonist of CCR5. Maraviroc has no detectable in vitro cytotoxicity and is highly selective for CCR5， as confirmed against a wide range of receptors and Enzymes， including the hERG ion channel (50% inhibitory concentration， >10 microM)， indicating potential for an excellent clinical safety profile.[1]。 |
| 细胞实验 | Acute and chronic colitis were induced by administration of DSS or TNBS to wild-type and CCR5(-/-) mice or adoptive transfer of splenic na?ve CD4(+) T-cells from wild type or CCR5(-/-) mice into RAG-1(-/-). CCR5 gene ablation reduced the mucosal recruitment and activation of CCR5-bearing CD4(+) and CD11b(+) leukocytes， resulting in profound attenuation of signs and symptoms of inflammation in the TNBS and transfer models of colitis. In the DSS/TNBS colitis and in the transfer model， maraviroc attenuated development of intestinal inflammation by selectively reducing the recruitment of CCR5 bearing leukocytes.[2] |
| 细胞实验 | HEK-293 cell aliquots (100 μL at 1×106 cells/mL) are plated into poly-D-lysine-coated plates and incubated at 37°C overnight. A 1:1 mix of soluble recombinant human CD4 (sCD4) (diluted to 4.5 nM in culture medium) and HIV-1 gp120 is incubated at room temperature for 15 min prior to its addition to PBS-washed cells in the presence of dilutions of maraviroc to enable IC50 determination. The assay plates are incubated at 37°C for 1 h and washed. Eu3+-labeled anti-gp120 antibody (1/500 dilution in assay buffer) is added to each well (50 μL) and incubated for 1 h. The plate is washed three times with wash buffer prior to the addition of enhancement solution (200 μL/well) and measurement of Eu3+ fluorescence (Victor2multilabel counter; “Europium” protocol). Nonspecific binding is taken as the fluorescence measured for gp120 incubated with cells in the absence of preincubation with sCD4[1]. |
| 动物实验 | Rats and Dogs[1]：Preclinical pharmacokinetic studies are carried out with maraviroc following a single intravenous and oral administration to both male Sprague-Dawley rats (1 mg/kg of body weight given intravenously [i.v.] and 10 mg/kg given orally [p.o.]; n=2) and male beagle dogs (0.5 mg/kg i.v. and 2 mg/kg p.o; n=4). Plasma samples are taken for up to 24 h postdose， and the concentrations of unchanged maraviroc are determined using a specific high-performance liquid chromatography-tandem mass spectrum assay.Mice[2]：Splenocytes are collected from 6-10 week old CCR5-/- mice or wild-type controlmice (n=8 per group) and naive CD4+ CD45RBhigh T-cells are isolated by cell sorting. A total of 3×105 CD45RBhigh cells are then injected intravenously into Rag1-/- mice that are subsequently weighed and assessed for fecal score every 20 days to evaluate IBD development. To investigate whether Maraviroc rescues from intestinal inflammation induced by transfer colitis， Rag1-/- mice are injected with CD4+ CD45RB-/- T-cells and 34 days later randomized into either a control group (no further treatment， n=6) or treatment with Maraviroc， 50 mg/kg/d Maraviroc per os (n=4) for 3 weeks， 5 d/week. |
| 激酶实验 | Binding of 125I-labeled MIP-1α， MIP-1β， and RANTES to CCR5 is measured essentially using intact HEK-293 cells stably expressing the receptor or membrane preparations thereof. Briefly， cells are resuspended in binding buffer (50 mM HEPES containing 1 mM CaCl2， 5 mM MgCl2， and 0.5% bovine serum albumin [BSA] and adjusted to pH 7.4) to a density of 2×106 cells/mL. For membrane preparations， phosphate-buffered saline (PBS)-washed cells are resuspended in lysis buffer (20 mM HEPES， 1 mM CaCl2， 1 tablet COMPLETE per 50 mL， pH 7.4; Boehringer) prior to homogenization in a Polytron hand-held homogenizer， ultracentrifugation (40，000× g for 30 min)， and resuspension in binding buffer to a protein concentration of 0.25 mg/mL (12.5 μg of membrane protein is used in each well of a 96-well plate). 125I-radiolabeled MIP-1α， MIP-1β， and RANTES are prepared and diluted in binding buffer to a final concentration of 400 pM in the assay. Appropriate maraviroc dilutions are added to each well to a final volume of 100 μL， the assay plates incubated for 1 h， and the contents filtered through preblocked and washed Unifilter plates which are counted following overnight drying[1]. |
| 数据来源文献 | [1]. Dorr P， et al. 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 [2]. Mencarelli 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. [3]. Romero-Sánchez MC， et al. Effect of maraviroc on HIV-disease progression-related biomarkers. Antimicrob Agents Chemother. 2012 Nov;56(11):5858-64. [4]. Huilin Mou， et al. NRSF and CCR5 Established Neuron-glia Communication during Acute and Chronic Stresses. Journal of Drug Metabolism & Toxicology. January 10， 2016. |
| 单位 | 瓶 |
风险提示：丁香通仅作为第三方平台，为商家信息发布提供平台空间。用户咨询产品时请注意保护个人信息及财产安全，合理判断，谨慎选购商品，商家和用户对交易行为负责。对于医疗器械类产品，请先查证核实企业经营资质和医疗器械产品注册证情况。
文献和实验相关实验
2F+DwTquooTcizAj6Sh40arj1e+iWJ2ispgsbT801bWi9OaaVDQ0u7N9Rf22Q7je3ypEkT/aXtAx/4gHh20RbetchuWXizve3YY/3L0LGHHqt8Cva+97zf/vEfvyYb4imWXpTxLz8m4rvgjodswc3X26Xnn2o3LbjZPv/Fv5GGuGa33/ZzO2n2HD17NAEWeUXwmQh44uy32U+uutL+69e+6jjedfsddvSxx3m8xNNFQ67wipqQKHyESZ35
5+YiLLj4HREBXstjztk7uH3PDncf2sPhxRlMq6wGF+vZ2OlE8VGoBH85gWn/XYBn2ck48eAqDu+xwjbrU7h2Zz2aZ3fD6YWWeBFuzJv2yfAMMyYBFj4y5r7yqpgAE0jPBFRyolzbpihAeo1X9z5K2o2YlqOUxRTN25rQLQ+8+x4oVfFzvgFHklZM2raEadaIsxjVfI0wedUizB5fB7r8yR8TTr6mQAL8FlQgbB6KCTABJiAfgWD8ev0cIrh
BL/6J X SJL/J）F1代雌鼠的受精卵中，并引起插入突变（Im）,这是Edward H.Birkenmeier (Bir) 实验室命名的第一只转基因小鼠。 根据转基因动物命名的原则，如果转基因动物的遗传背景是由不同的近交系或远交群之间混合而成时，则该转基因符号应不使用动物品系或种群的名称。 转基因符号的缩写：转基因符号可以缩写，即去掉插入片段标示部分，例如TgN（GPDHIm）1 Bir可缩写为TgN 1 Bir。一般在文章中第一次出现时使用全称，以后再出现时可使用缩写名称。
技术资料暂无技术资料 索取技术资料
IM2850 马拉维若 免疫学/炎症 索莱宝
￥526 - 4954
