Rosuvastatin Calcium
(Synonyms: 瑞舒伐他汀钙; Rosuvastatin hemicalcium; ZD 4522 Calcium) 目录号 : GC15736
Rosuvastatin Calcium是一种竞争性HMG-CoA还原酶抑制剂，IC50值为11nM。
Cas No.:147098-20-2
Sample solution is provided at 25 µL, 10mM.
_1-3.$$$39978408@51.jpg');)
_1-9.$$$38538795@65.jpg');)
_1-9.$$$39112701@51.jpg');)
_1-7.$$$37316672@70.jpg');)
_366-372.$$$36198801@70.jpg');)
.$$$38565142@65.jpg');)
_1867-1883.$$$33248023@67.jpg');)
_eads6055.$$$39977546@45.jpg');)
_eadm9805.$$$40080571@45.jpg');)
_eadj3020.$$$39666821@45.jpg');)
_1-20.$$$39757301@28.jpg');)
_1-24.$$$38898113@28.jpg');)
_273-287.$$$36806353@46.jpg');)
_1-16.$$$37156877@44.jpg');)
_1-19.$$$37460805@44.jpg');)
_1291-1307.$$$34518654@46.jpg');)
Rosuvastatin Calcium is a competitive HMG-CoA reductase inhibitor with an IC50 value of 11nM[1]. HMG-CoA reductase is the rate-limiting enzyme in mevalonate biosynthesis, a key step in cholesterol synthesis[2]. Rosuvastatin Calcium potently blocks human ether-a-go-related gene (hERG) currents (IC50=195nM), leading to delayed cardiac repolarization, prolonged action potential duration (APD), and QT interval prolongation (QTc)[3]. Rosuvastatin Calcium effectively reduces low-density lipoprotein (LDL) cholesterol, triglyceride, and C-reactive protein levels[4].
In vitro, treatment of microglia with Rosuvastatin Calcium (1μM) for 6, 24, and 72h significantly inhibited cell proliferation and adhesion, and reduced the expression of pro-inflammatory genes such as IL-1β and TNF-α induced by LPS[5]. Rosuvastatin Calcium (10nM) treatment of human promyelocytic leukemia cells (HL-60 cells) significantly reduced PMA- or hydrogen peroxide-induced DNA damage, decreased reactive oxygen species (ROS) production, and upregulated γ-glutamylcysteine synthetase expression[6].
In vivo, intravenous administration of Rosuvastatin Calcium (0.2mg/kg) to mice with acute stroke significantly reduced brain infarct area 4 hours after middle cerebral artery occlusion (MCAO)[7].
References:
[1] Watanabe M, Koike H, Ishiba T, et al. Synthesis and biological activity of methanesulfonamide pyrimidine-and N-methanesulfonyl pyrrole-substituted 3, 5-dihydroxy-6-heptenoates, a novel series of HMG-CoA reductase inhibitors[J]. Bioorganic & medicinal chemistry, 1997, 5(2): 437-444.
[2] Schumacher M M, DeBose-Boyd R A. Posttranslational regulation of HMG CoA reductase, the rate-limiting enzyme in synthesis of cholesterol[J]. Annual review of biochemistry, 2021, 90(1): 659-679.
[3] Plante I, Vigneault P, Drolet B, et al. Rosuvastatin Calcium blocks hERG current and prolongs cardiac repolarization[J]. Journal of pharmaceutical sciences, 2012, 101(2): 868-878.
[4] Glynn R J, Koenig W, Nordestgaard B G, et al. Rosuvastatin Calcium for primary prevention in older persons with elevated C-reactive protein and low to average low-density lipoprotein cholesterol levels: exploratory analysis of a randomized trial[J]. Annals of internal medicine, 2010, 152(8): 488-496.
[5] Kata D, Földesi I, Feher L Z, et al. Rosuvastatin Calcium enhances anti-inflammatory and inhibits pro-inflammatory functions in cultured microglial cells[J]. Neuroscience, 2016, 314: 47-63.
[6] Schupp N, Schmid U, Heidland A, et al. Rosuvastatin Calcium protects against oxidative stress and DNA damage in vitro via upregulation of glutathione synthesis[J]. Atherosclerosis, 2008, 199(2): 278-287.
[7] Prinz V, Laufs U, Gertz K, et al. Intravenous Rosuvastatin Calcium for acute stroke treatment: an animal study[J]. Stroke, 2008, 39(2): 433-438.
Rosuvastatin Calcium是一种竞争性HMG-CoA还原酶抑制剂，IC50值为11nM[1]。HMG-CoA还原酶是甲羟戊酸生物合成的限速酶，是直接参与胆固醇合成的关键步骤[2]。Rosuvastatin Calcium能够强力阻断人醚-α-Go相关基因（hERG）电流，IC50值为195nM，导致延迟心脏复极化，从而延长动作电位持续时间（APDs）和校正QT间期（QTc）[3]。Rosuvastatin Calcium能够有效降低低密度脂蛋白（LDL）胆固醇、甘油三酯和C反应蛋白水平[4]。
在体外，Rosuvastatin Calcium（1μM）处理小胶质细胞6、24、72h，显著抑制了细胞的增殖和细胞黏附，降低了LPS刺激的细胞内IL-1β、TNF-α等促炎基因的表达[5]。Rosuvastatin Calcium（10nM）处理人类早幼粒细胞（HL-60细胞），显著减少了由佛波醇12-肉豆蔻酸13-乙酸（PMA）或由过氧化氢诱导的DNA损伤，降低了细胞内活性氧的产生，上调了γ-谷氨酰半胱氨酸合成酶的表达[6]。
在体内，Rosuvastatin Calcium（0.2mg/kg）通过静脉注射治疗急性中风模型小鼠，显著降低了丝状中大动脉闭塞（MCAO）后4小时内的脑损伤面积[7]。
| Cell experiment [1]: | |
Cell lines | Microglial cells |
Preparation Method | On the fourth day of subcloning (subDIV4), the DMEM medium was replaced, and the expanded pure microglia cells were treated for 24h with either LPS, Rosuvastatin Calcium (1μM final concentration, dissolved in sterile distilled water), or a combination of LPS and Rosuvastatin Calcium. The effects were compared using a variety of morphological and functional tests. LPS treatment served as an immune challenge. Four treatment regimens were used: (1) control cultures; (2) LPS-challenged cultures (20ng/mL LPS); (3) Rosuvastatin Calcium-treated cultures (1μM Rosuvastatin Calcium); (4) LPS-challenged+Rosuvastatin Calcium-treated cultures (both drugs at the indicated doses). Depending on the experiment, the treatments lasted for 6, 24, or 72h at 37°C. |
Reaction Conditions | 1μM; 6, 24, or 72h |
Applications | Rosuvastatin Calcium inhibited proliferation and cell adhesion in control microglia. Rosuvastatin Calcium inhibited IL-1β, TNF-α synthesis and other pro-inflammatory genes in LPS-treated cells. Rosuvastatin Calcium elevated IL-10 production and the expression of other anti-inflammatory genes in both groups. |
| Animal experiment [2]: | |
Animal models | 129/SV wild-type mice |
Preparation Method | Mice were subjected to 1-hour filamentous middle cerebral artery occlusion (MCAo), followed by reperfusion, and were postevent treated with i.v. Rosuvastatin Calcium given up to 6h after MCAo (0.02, 0.2, 2mg/kg). After 24h or 5 days, animals were euthanized by a pentobarbital overdose, and brains were quickly removed from the skull and snap-frozen in isopentane on dry ice for cryostat sectioning. |
Dosage form | 0.02, 0.2, 2mg/kg; i.v. |
Applications | Rosuvastatin Calcium, when administered i.v., significantly reduced lesion size when given up to 4h after MCAo and in doses as low as 0.2mg/kg. |
References: | |
| Cas No. | 147098-20-2 | SDF | |
| 别名 | 瑞舒伐他汀钙; Rosuvastatin hemicalcium; ZD 4522 Calcium | ||
| 化学名 | calcium;(E,3R,5S)-7-[4-(4-fluorophenyl)-2-[methyl(methylsulfonyl)amino]-6-propan-2-ylpyrimidin-5-yl]-3,5-dihydroxyhept-6-enoate | ||
| Canonical SMILES | CC(C)C1=NC(=NC(=C1C=CC(CC(CC(=O)[O-])O)O)C2=CC=C(C=C2)F)N(C)S(=O)(=O)C.CC(C)C1=NC(=NC(=C1C=CC(CC(CC(=O)[O-])O)O)C2=CC=C(C=C2)F)N(C)S(=O)(=O)C.[Ca+2] | ||
| 分子式 | C22H27Ca0.5FN3O6S | 分子量 | 500.57 |
| 溶解度 | ≥ 28.55mg/mL in DMSO | 储存条件 | Store at 2-8°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
||
| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
 |
1 mg | 5 mg | 10 mg |
| 1 mM | 1.9977 mL | 9.9886 mL | 19.9772 mL |
| 5 mM | 399.5 μL | 1.9977 mL | 3.9954 mL |
| 10 mM | 199.8 μL | 998.9 μL | 1.9977 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Quality Control & SDS
- View current batch:
- Purity: >99.50%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet