Fluvastatin
(Synonyms: 氟伐他汀; XU 62-320 free acid) 目录号 : GC13535
An HMG-CoA reductase inhibitor
Cas No.:93957-54-1
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
| Cell experiment [1-3]: | |
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Cell lines |
Human smooth muscle cells, human monocyte U937 cell line |
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Preparation method |
The solubility of this compound in DMSO is >20.6 mg/mL. General tips for obtaining a higher concentration: Please warm the tube at 37 ℃ for 10 minutes and/or shake it in the ultrasonic bath for a while. Stock solution can be stored below -20℃ for several months. |
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Reacting condition |
40 mg, 6 days |
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Applications |
In human smooth muscle cells, addition of serum from patients (40 mg of fluvastatin a day for the 6 days) treated with fluvastatin caused a significant reduction in cell proliferation. Fluvastatin (100 nM) attenuated the expression of both ICAM-1 and LFA-1. Fluvastatin (10 μM) showed no effect on cell viability. Fluvastatin induced apoptosis in cardiac myocytes in a time- and dose-dependent manner. Fluvastatin decreased RhoA protein in the membrane fraction, whereas there were no significant changes of the RhoA protein in the cytosol fraction. Fluvastatin completely inhibited interleukin-1β-stimulated 3H-leucine incorporation. |
| Animal experiment [4-6]: | |
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Animal models |
Sprague–Dawley male rats |
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Dosage form |
Oral administration, 5, 10 and 20 mg/kg |
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Application |
In hypercholesterolemic rats, treatment with fluvastatin (10 mg/kg/day) significantly attenuated the leukocyte-adherence responses to PAF and LTB4 as well as the leukocyte emigration response to LTB4. Fluvastatin treatment inhibited the PAF- and LTB4-induced reductions in leukocyte rolling velocity. Oral administration of fluvastatin (5, 10 and 20 mg/kg) significantly prevented almost all the parameters of isoproterenol-induced heart failure and myocardial injury. Compared with control group, any indexes in sham rats treated with fluvastatin (20 mg/kg) alone were unaltered. Treatment with fluvastatin resulted in a significant decrease in the urinary protein excretion. Fluvastatin treatment significantly ameliorated the decreased expression of nephrin in PAN nephrosis rats. Fluvastatin markly attenuated tubulointerstitial damage in the presence of moderate proteinuria. |
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Other notes |
Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal. |
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References: [1]. Buemi M, Allegra A, Senatore M, et al. Pro-apoptotic effect of fluvastatin on human smooth muscle cells[J]. European journal of pharmacology, 1999, 370(2): 201-203. [2]. Niwa S, Totsuka T, Hayashi S. Inhibitory effect of fluvastatin, an HMG-CoA reductase inhibitor, on the expression of adhesion molecules on human monocyte cell line[J]. International journal of immunopharmacology, 1996, 18(11): 669-675. [3]. Ogata Y, Takahashi M, Takeuchi K, et al. Fluvastatin induces apoptosis in rat neonatal cardiac myocytes: a possible mechanism of statin-attenuated cardiac hypertrophy[J]. Journal of cardiovascular pharmacology, 2002, 40(6): 907-915. [4]. Zhou R, Xu Q, Zheng P, et al. Cardioprotective effect of fluvastatin on isoproterenol-induced myocardial infarction in rat[J]. European journal of pharmacology, 2008, 586(1): 244-250. [5]. Kimura M, Kurose I, Russell J, et al. Effects of fluvastatin on leukocyte–endothelial cell adhesion in hypercholesterolemic rats[J]. Arteriosclerosis, Thrombosis, and Vascular Biology, 1997, 17(8): 1521-1526. [6]. Shibata S, Nagase M, Fujita T. Fluvastatin ameliorates podocyte injury in proteinuric rats via modulation of excessive Rho signaling[J]. Journal of the American Society of Nephrology, 2006, 17(3): 754-764. |
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Fluvastatin (XU 62-320 free acid) is a first fully synthetic, competitive HMG-CoA reductase inhibitor with an IC50 of 8 nM. Fluvastatin protects vascular smooth muscle cells against oxidative stress through the Nrf2-dependent antioxidant pathway[1][2][3].
Fluvastatin (XU 62-320 free acid) is a competitive inhibitor of hydroxymethylglutaryl-coenzyme A reductase (HMGCR), the enzyme that catalyzes the conversion of HMG-CoA to mevalonic acid, the rate-limiting step in cholesterol biosynthesis. Human hepatocellular carcinoma cell (HCC) studies indicate that Fluvastatin induces G2/M phase arrest. In the presence of Fluvastatin (XU 62320), HCC cells show a decrease of Bcl-2 and procaspase-9 expression, and an increase in Bax, cleaved caspase-3, and cytochrome c. Fluvastatin (XU 62320) is antilipemic and is used to reduce plasma cholesterol levels and prevent cardiovascular disease.
References:
[1]. Araújo FA, Rocha MA, Capettini LS, et al. 3-Hydroxy-3-methylglutaryl coenzyme A reductase inhibitor (fluvastatin) decreases inflammatory angiogenesis in mice. APMIS. 2012 24. [Epub ahead of print]
[2]. Makabe S, Takahashi Y, Watanabe H, et al. Fluvastatin protects vascular smooth muscle cells against oxidative stress through the Nrf2-dependent antioxidant pathway. Atherosclerosis. 2010 Dec;213(2):377-84.
[3]. Zhang W, Wu J, Zhou L, et al. Fluvastatin, a lipophilic statin, induces apoptosis in human hepatocellular carcinoma cells through mitochondria-operated pathway. Indian J Exp Biol. 2010 Dec;48(12):1167-74.
[4]. Scripture CD, Pieper JA. Clinical pharmacokinetics of fluvastatin. Clin Pharmacokinet. 2001;40(4):263-81.
| Cas No. | 93957-54-1 | SDF | |
| 别名 | 氟伐他汀; XU 62-320 free acid | ||
| 化学名 | (E,3R,5S)-7-[3-(4-fluorophenyl)-1-propan-2-ylindol-2-yl]-3,5-dihydroxyhept-6-enoic acid | ||
| Canonical SMILES | CC(C)N1C2=CC=CC=C2C(=C1C=CC(CC(CC(=O)O)O)O)C3=CC=C(C=C3)F | ||
| 分子式 | C24H26FNO4 | 分子量 | 411.47 |
| 溶解度 | ≥ 20.57 mg/mL in DMSO, ≥ 42.2 mg/mL in EtOH with gentle warming, ≥ 32.53 mg/mL in Water with gentle warming | 储存条件 | Store at -20°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。 |
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| 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 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 2.4303 mL | 12.1516 mL | 24.3031 mL |
| 5 mM | 0.4861 mL | 2.4303 mL | 4.8606 mL |
| 10 mM | 0.243 mL | 1.2152 mL | 2.4303 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。