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Triparanol

(Synonyms: 曲帕拉醇,MER-29) 目录号 : GC45090

An inhibitor of DHCR24

Triparanol Chemical Structure

Cas No.:78-41-1

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500μg
¥720.00
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1mg
¥1,302.00
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5mg
¥2,518.00
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10mg
¥4,317.00
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产品描述

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.

Chemical Properties

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
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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
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Research Update

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).