Triparanol
(Synonyms: 曲帕拉醇,MER-29) 目录号 : GC45090An inhibitor of DHCR24
Cas No.:78-41-1
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
Triparanol is a 24-dehydro cholesterol reductase (DHCR24) inhibitor (Ki = 0.523 µM), which is an enzyme involved in the biosynthesis of cholesterol. It has antitumor properties, such as decreasing proliferation and inducing apoptosis in many cancer cell lines and slowing tumor growth in a mouse xenograft model. It can also decrease Hedgehog pathway signaling in cancer cells. Formulations containing triparanol were discontinued in the 1960s due to serious adverse side effects, including rapid cataract development.
| Cas No. | 78-41-1 | SDF | |
| 别名 | 曲帕拉醇,MER-29 | ||
| Canonical SMILES | CC1=CC=C(C(CC2=CC=C(Cl)C=C2)(O)C3=CC=C(OCCN(CC)CC)C=C3)C=C1 | ||
| 分子式 | C27H32ClNO2 | 分子量 | 438 |
| 溶解度 | DMF: 30 mg/ml,DMSO: 20 mg/ml,Ethanol: 0.125 mg/ml | 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 | 2.2831 mL | 11.4155 mL | 22.8311 mL |
| 5 mM | 0.4566 mL | 2.2831 mL | 4.5662 mL |
| 10 mM | 0.2283 mL | 1.1416 mL | 2.2831 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。
Triggering of Erythrocyte Death by Triparanol
Toxins (Basel) 2015 Aug 24;7(8):3359-71.PMID:26305256DOI:10.3390/toxins7083359.
The cholesterol synthesis inhibitor Triparanol has been shown to trigger apoptosis in several malignancies. Similar to the apoptosis of nucleated cells, erythrocytes may enter eryptosis, the suicidal death characterized by cell shrinkage and cell membrane scrambling with phosphatidylserine translocation to the erythrocyte surface. Triggers of eryptosis include oxidative stress which may activate erythrocytic Ca(2+) permeable unselective cation channels with subsequent Ca(2+) entry and increase of cytosolic Ca(2+) activity ([Ca(2+)]i). The present study explored whether and how Triparanol induces eryptosis. To this end, phosphatidylserine exposure at the cell surface was estimated from annexin-V-binding, cell volume from forward scatter, hemolysis from hemoglobin release, [Ca(2+)]i from Fluo3-fluorescence, and ROS formation from 2',7'-dichlorodihydrofluorescein diacetate (DCFDA) dependent fluorescence. As a result, a 48 h exposure of human erythrocytes to Triparanol (20 µM) significantly increased DCFDA fluorescence and significantly increased Fluo3-fluorescence. Triparanol (15 µM) significantly increased the percentage of annexin-V-binding cells, and significantly decreased the forward scatter. The effect of Triparanol on annexin-V-binding was significantly blunted, but not abolished by removal of extracellular Ca(2+). In conclusion, Triparanol leads to eryptosis, the suicidal erythrocyte death characterized by cell shrinkage and phospholipid scrambling of the erythrocyte cell membrane. Triparanol is at least in part effective by stimulating ROS formation and Ca(2+) entry.
Triparanol suppresses human tumor growth in vitro and in vivo
Biochem Biophys Res Commun 2012 Aug 31;425(3):613-8.PMID:22877755DOI:10.1016/j.bbrc.2012.07.136.
Despite the improved contemporary multidisciplinary regimens treating cancer, majority of cancer patients still suffer from adverse effects and relapse, therefore posing a significant challenge to uncover more efficacious molecular therapeutics targeting signaling pathways central to tumorigenesis. Here, our study have demonstrated that Triparanol, a cholesterol synthesis inhibitor, can block proliferation and induce apoptosis in multiple human cancer cells including lung, breast, liver, pancreatic, prostate cancer and melanoma cells, and growth inhibition can be rescued by exogenous addition of cholesterol. Remarkably, we have proved Triparanol can significantly repress Hedgehog pathway signaling in these human cancer cells. Furthermore, study in a mouse xenograft model of human lung cancer has validated that Triparanol can impede tumor growth in vivo. We have therefore uncovered Triparanol as potential new cancer therapeutic in treating multiple types of human cancers with deregulated Hedgehog signaling.
Triparanol Inhibition of Sterol Biosynthesis in Chlorella ellipsoidea
Plant Physiol 1973 Sep;52(3):246-7.PMID:16658540DOI:10.1104/pp.52.3.246.
The sterol composition of C. ellipsoidea was markedly changed when this alga was grown in the presence of 1 mug/g Triparanol. Triparanol appears to inhibit the removal of 14alpha-methyl group, the second alkylation at C-24, Delta(7)-reductase, and Delta(8) --> Delta(7)-isomerase. The effect of Triparanol in Chlorella is much more diversified than the specific effect originally assigned to it in animals.
Functional and biochemical evidence of damage to enterocytes induced by Triparanol: role of lysosomes and the effect of gluten-free diet
Clin Sci Mol Med 1976 Jul;51(1):19-25.PMID:939062DOI:10.1042/cs0510019.
1. Functional and biochemical studies were performed on the small intestine of control rats, and the results were compared with similar studies on animals given Triparanol at a dosage of 0.114 mmol/kg daily for 10 days. The animals given Triparanol were fed with either standard rat food or a gluten-free diet. 2. By using a recirculating-perfusion technique in vivo, it was shown that absorption of galactose from an 8 mmol/l solution was impaired in the ileum but not in the jejunum of the triparanol-treated rats. 3. Assays of marker enzymes for the principal subcellular organelles were performed on isolated jejunal and ileal enterocytes. In the ileum there was a striking decrease in lysosomal enzyme activities and a smaller but significant decrease of lactate dehydrogenase, catalase and malate dehydrogenase activities. In the jejunum there was no significant change in the activities of these enzymes. 4. Measurements of lysosomal integrity indicated that ileal lysosomal fragility was markedly increased and that jejunal lysosomes were affected to a much smaller extent. 5. These effects of Triparanol could not be ameliorated by feeding with a gluten-free diet.
Probucol and the cholesterol synthesis inhibitors simvastatin and Triparanol regulate I ks channel function differently
Hum Exp Toxicol 2013 Oct;32(10):1028-37.PMID:23424208DOI:10.1177/0960327112474848.
Channels responsible for slowly activating delayed-rectifier potassium current (I(Ks)) are composed of KCNQ1 and KCNE1 subunits, and these channels play a role in the repolarization of cardiac action potentials. Recently, we showed that the antihyperlipidemic drug probucol, which induces QT prolongation, decreases the I(Ks) after 24-h treatment. In the present study, we investigated the effects of three cholesterol-lowering agents (probucol, an enhancer of cholesterol efflux; simvastatin, a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor; and Triparanol, a 3β-hydroxysterol-▵24-reductase inhibitor) on cholesterol synthesis, the KCNQ1 current (I KCNQ1), and the I(Ks) to clarify the differences in the modes of action of these agents on the I(Ks). Probucol did not inhibit cholesterol synthesis and had no effect on I KCNQ1, while I(Ks) decreased after 24-h treatment. Simvastatin inhibited cholesterol synthesis and decreased I KCNQ1 and I(Ks). Additionally, the activation kinetics of I(Ks) became faster, compared with that of control I(Ks). Triparanol inhibited cholesterol synthesis but did not reduce I KCNQ1 and I(Ks). However, the activation kinetics of I(Ks) became faster. Our data indicated that the mechanism by which probucol inhibits I(Ks) was not mediated by the inhibition of cholesterol synthesis but depended on an interaction with the KCNQ1/KCNE1 complex. Meanwhile, the reduction in cholesterol induced by simvastatin and Triparanol is one of the mechanisms that affects the kinetics of I(ks).