Lusianthridin
(Synonyms: 4,7-二羟基-2-甲氧基-9,10-二氢菲) 目录号 : GC61014
Lusianthridin是来自Dendrobiumvenustum的天然化合物，具有抗迁移作用。Lusianthridin通过抑制Src-STAT3信号，促进c-Myc的降解。
Cas No.:87530-30-1
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
Lusianthridin, a pure compound from Dendrobium venustum, have an anti-migratory effect. Lusianthridin enhances c-Myc degradation through the inhibition of Src-STAT3 signaling[1].
Lusianthridin (0-100 μM) inhibits cell viability at concentrations greater than 50 μM in both H460 and H292 cells[1].Lusianthridin significantly reduces the CSC populations in both H460 and H292 cells of the CSC spheres, with a significant decrease in the size of the H460 CSC spheres by approximately 10%, 63%, and 77% at day 3 at concentration 5, 10, and 20 μM Lusianthridin, respectively[1]. Cell Viability Assay[1] Cell Line: The human non-small cell lung cancer cell lines, NCI-H460, and NCI-H292 cells[1].0-100 μM.
[1]. Narumol Bhummaphan, et al. Targeting of Lung Cancer Stem Cells via Src-STAT3 Suppression. Phytomedicine. 2019 Sep;62:152932.
| Cas No. | 87530-30-1 | SDF | |
| 别名 | 4,7-二羟基-2-甲氧基-9,10-二氢菲 | ||
| Canonical SMILES | OC(C=C1CC2)=CC=C1C3=C2C=C(OC)C=C3O | ||
| 分子式 | C15H14O3 | 分子量 | 242.27 |
| 溶解度 | 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 | 4.1276 mL | 20.6381 mL | 41.2763 mL |
| 5 mM | 0.8255 mL | 4.1276 mL | 8.2553 mL |
| 10 mM | 0.4128 mL | 2.0638 mL | 4.1276 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。
Inhibitory Mechanisms of Lusianthridin on Human Platelet Aggregation
Int J Mol Sci 2021 Jun 25;22(13):6846.PMID:34202163DOI:10.3390/ijms22136846.
Lusianthridin is a phenanthrene derivative isolated from Dendrobium venustum. Some phenanthrene compounds have antiplatelet aggregation activities via undefined pathways. This study aims to determine the inhibitory effects and potential mechanisms of Lusianthridin on platelet aggregation. The results indicated that Lusianthridin inhibited arachidonic acid, collagen, and adenosine diphosphate (ADP)-stimulated platelet aggregation (IC50 of 0.02 ± 0.001 mM, 0.14 ± 0.018 mM, and 0.22 ± 0.046 mM, respectively). Lusianthridin also increased the delaying time of arachidonic acid-stimulated and the lag time of collagen-stimulated and showed a more selective effect on the secondary wave of ADP-stimulated aggregations. Molecular docking studies revealed that Lusianthridin bound to the entrance site of the cyclooxygenase-1 (COX-1) enzyme and probably the active region of the cyclooxygenase-2 (COX-2) enzyme. In addition, Lusianthridin showed inhibitory effects on both COX-1 and COX-2 enzymatic activities (IC50 value of 10.81 ± 1.12 µM and 0.17 ± 1.62 µM, respectively). Furthermore, Lusianthridin significantly inhibited ADP-induced suppression of cAMP formation in platelets at 0.4 mM concentration (p < 0.05). These findings suggested that possible mechanisms of Lusianthridin on the antiplatelet effects might act via arachidonic acid-thromboxane and adenylate cyclase pathways.
Protective Effect of Lusianthridin on Hemin-Induced Low-Density Lipoprotein Oxidation
Pharmaceuticals (Basel) 2021 Jun 14;14(6):567.PMID:34198641DOI:10.3390/ph14060567.
Oxidation of low-density lipoprotein (LDL) plays a crucial role in the pathogenesis of atherosclerosis. Hemin (iron (III)-protoporphyrin IX) is a degradation product of hemoglobin that can be found in thalassemia patients. Hemin is a strong oxidant that can cause LDL oxidation and contributes to atherosclerosis in thalassemia patients. Lusianthridin from Dendrobium venustrum is a phenolic compound that possesses antioxidant activity. Hence, Lusianthridin could be a promising compound to be used against hemin-induced oxidative stress. The major goal of this study is to evaluate the protective effect of Lusianthridin on hemin-induced low-density lipoprotein oxidation (he-oxLDL). Here, various concentrations of Lusianthridin (0.25, 0.5, 1, and 2 µM) were preincubated with LDL for 30 min, then 5 µM of hemin was added to initiate the oxidation, and oxidative parameters were measured at various times of incubation (0, 1, 3, 6, 12, 24 h). Lipid peroxidation of LDL was measured by thiobarbituric reactive substance (TBARs) assay and relative electrophoretic mobility (REM). The lipid composition of LDL was analyzed by using reverse-phase HPLC. Foam cell formation with he-oxLDL in RAW 264.7 macrophage cells was detected by Oil Red O staining. The results indicated that Lusianthridin could inhibit TBARs formation, decrease REM, decrease oxidized lipid products, as well as preserve the level of cholesteryl arachidonate and cholesteryl linoleate. Moreover, He-oxLDL incubated with Lusianthridin for 24 h can reduce the foam cell formation in RAW 264.7 macrophage cells. Taken together, Lusianthridin could be a potential agent to be used to prevent atherosclerosis in thalassemia patients.
Lusianthridin targeting of lung cancer stem cells via Src-STAT3 suppression
Phytomedicine 2019 Sep;62:152932.PMID:31100681DOI:10.1016/j.phymed.2019.152932.
Background: Cancer stem cells (CSCs) are well-recognized as a majority cause of treatment failure and can give rise to relapse. The discovery of compounds attenuating CSCs' properties is crucial for enabling advances in novel therapeutics to limit recurrence. CSCs' features in lung cancer are regulated through a reduction in Src-STAT3-c-Myc, which drives cancer progression, drug resistance, and metastasis. Methods: The effect of Lusianthridin suppresses CSC-like phenotypes was determined by 3D culture and anchorage independent growth. The expression of CSC markers and associated proteins were determined by Western blot analyses. Protein ubiquitination and degradation were assessed using immunoprecipitation. Results: Herein, we report that Lusianthridin, a pure compound from Dendrobium venustum, dramatically suppressed CSCs in lung cancer cells as verified by several CSC phenotype assessments and CSC markers. The CSC phenotypes in lusianthridin-treated cells were suppressed through downregulation of Src-STAT3-c-Myc pathways. Ectopic Src introduced by the transfection augmented CSC phenotypes in lung cancer cells through STAT3 (increased active p-STAT3Tyr705) and c-Myc signals, while the ShRNA-Src transfection or Src inhibitor dasatinib exhibited opposite results. Treatment of the Src-overexpressing cells with Lusianthridin resulted in the reversal of active STAT3 (p-STAT3Tyr705) and c-Myc as well as the CSC marker CD133. Importantly, we confirmed the CSC-targeted activity of Lusianthridin in CSC-rich primary lung cancer cells. The compound dramatically inhibited the formation of tumor spheres of primary lung cancer cells. Finally, we demonstrated that after CSC-attenuation by Lusianthridin, the lung cancer cells exhibited significantly higher susceptibility to chemotherapeutic drugs. Such a sensitizing effect caused by pro-survival suppression and pro-apoptotic induction together with the abolishment of stemness indicated by the decrease in CSC markers CD133, ABCG2, and ALDH1A1. Conclusion: These findings revealed a novel pharmacological action and the underlying mechanism of Lusianthridin in negatively regulating CSC-like phenotypes and sensitizing resistant cancer cells to cemetery.
Identification of Lusianthridin metabolites in rat liver microsomes by liquid chromatography combined with electrospray ionization time-of-flight mass spectrometry
Biomed Chromatogr 2021 Mar;35(3):e5001.PMID:33063881DOI:10.1002/bmc.5001.
Lusianthridin, a bioactive component isolated from Dendrobium venustum, has been demonstrated to have many biological properties such as antioxidant and anticancer activities. However, the metabolic profiles remain unknown. This study was carried out to investigate the metabolic profiles of Lusianthridin in liver microsomes. Lusianthridin was co-incubated with liver microsomes in the presence of nicotinamide adenine dinucleotide phosphate and UDP-glucuronic acid or glutathione at 37°C for 1 h. The incubation samples were analyzed by liquid chromatography combined with electrospray ionization high-resolution mass spectrometry. The data were acquired and processed. The structures of the metabolites were proposed by comparing their accurate mass and MS2 spectra with those of the parent compound. A total of 15 metabolites were detected in vitro, including two phase I and 13 phase II metabolites. The phase I metabolic pathways were oxidation, demethylation and dehydrogenation. The phase II metabolic pathways referred to glucuronidation and glutathione conjugation. The present study provides an overview pertaining to the metabolic profiles of Lusianthridin in vitro, which is indispensable for understanding the efficacy and safety of Lusianthridin, as well as the herbal medicine D. venustum.
Pharmacokinetic, bioavailability, and metabolism studies of Lusianthridin, a dihydrophenanthrene compound, in rats by liquid chromatography/electrospray ionization tandem mass spectrometry
J Pharm Biomed Anal 2021 Feb 20;195:113836.PMID:33358433DOI:10.1016/j.jpba.2020.113836.
Lusianthridin was reported to possess many biological properties such as anti-oxidant and anti-cancer activities. However, its metabolic profiles and pharmacokinetics in vivo remain unknown. This study was carried out to investigate the metabolic profiles and pharmacokinetics of Lusianthridin in rats. The metabolic profiles were obtained by an ultra-performance liquid chromatography quadrupole time-of-flight mass spectrometry (UPLC-Q/TOF-MS). A total of eighteen metabolites involved three phase I metabolites and fifteen phase II metabolites were detected and identified. The major metabolic pathways of Lusianthridin were demethylation, oxidation, sulfation, glucuronidation and glutathione conjugation. In addition, a simple and sensitive ultra-performance liquid chromatography tandem mass spectrometry (UPLC-MS/MS) method was established for determination of Lusianthridin in rat plasma. After extracted by protein precipitation, Lusianthridin was quantitated in positive ion mode. The method was linear over the range of 0.5-500 ng/mL (r ≥ 0.995) with the LLOQ of 0.5 ng/mL. The intra- and inter- precision and accuracy, extraction recovery, matrix effect and stability were within the acceptable limits. The validated method was applied to the pre-clinical pharmacokinetic study of Lusianthridin in rats. After oral administration, Lusianthridin was quickly absorbed into plasma and reached the max concentration of 236.22 ng/mL at 22.00 min. The elimination half life of Lusianthridin from plasma was approximately 83.05-104.47 min and the oral absolute bioavailability was calculated as 30.93 %.