alpha-Mangostin
(Synonyms: α-倒捻子素; α-Mangostin) 目录号 : GC35306
A xanthone with diverse biological activities
Cas No.:6147-11-1
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.50%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
α-Mangostin is a xanthone that has been found in G. mangostana and has diverse biological activities.1,2,3,4,5 It inhibits fatty acid synthase and HIV-1 protease (IC50s = 5.54 and 5.12 μM, respectively).2,3 α-Mangostin is active against methicillin-sensitive and -resistant S. aureus strains (MICs = 1.57-12.5 μg/ml).1 It inhibits nitric oxide and prostaglandin E2 production in LPS-stimulated RAW 264.7 cells (IC50s = 12.4 and 11.08 μM, respectively).4 α-Mangostin is an agonist of stimulator of interferon genes (STING) that binds to the C-terminal domain of STING (H232 variant) with a Kd value of 137 μM and induces expression of an IFN-β-luciferase reporter in HEK293T cells transfected with human STING (H232 variant) to a greater extent than cells expressing murine STING or human STING (R232 variant) when used at a concentration of 25 μM.6 α-Mangostin (20 mg/kg) prevents carrageenan-induced paw edema in mice. It decreases the viability of LNCaP, 22Rv1, DU145, and PC3 prostate cancer cells in vitro (IC50s = 5.9, 6.9, 22.5, and 12.7 μM, respectively) and reduces tumor growth in a 22Rv1 mouse xenograft model when administered at a dose of 100 mg/kg.5
1.Iinuma, M., Tosa, H., Tanaka, T., et al.Antibacterial activity of xanthones from guttiferaeous plants against methicillin-resistant Staphylococcus aureusJ. Pharm. Pharmacol.48(8)861-865(1996) 2.Jiang, H.Z., Quan, X.F., Tian, W.X., et al.Fatty acid synthase inhibitors of phenolic constituents isolated from Garcinia mangostanaBioorg. Med. Chem. Lett.20(20)6045-6047(2010) 3.Chen, S.-X., Wan, M., and Loh, B.-N.Active constituents against HIV-1 protease from Garcinia mangostanaPlanta Med.62(4)381-382(1996) 4.Chen, L.-G., Yang, L.-L., and Wang, C.-C.Anti-inflammatory activity of mangostins from Garcinia mangostanaFood Chem. Toxicol.46(2)688-693(2008) 5.Johnson, J.J., Petiwala, S.M., Syed, D.N., et al.α-Mangostin, a santhone from mangosteen fruit, promotes cell cycle arrest in prostate cancer and decreases xenograft tumor growthCarcinogenesis33(2)413-419(2012) 6.Zhang, Y., Sun, Z., Pei, J., et al.Identification of α-mangostin as an agonist of human STINGChemMedChem13(19)2057-2064(2018)
| Cas No. | 6147-11-1 | SDF | |
| 别名 | α-倒捻子素; α-Mangostin | ||
| Canonical SMILES | O=C1C2=C(OC3=C1C(C/C=C(C)\C)=C(OC)C(O)=C3)C=C(O)C(C/C=C(C)\C)=C2O | ||
| 分子式 | C24H26O6 | 分子量 | 410.46 |
| 溶解度 | DMSO: ≥ 37 mg/mL (90.14 mM) | 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。 |
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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 | 2.4363 mL | 12.1815 mL | 24.3629 mL |
| 5 mM | 0.4873 mL | 2.4363 mL | 4.8726 mL |
| 10 mM | 0.2436 mL | 1.2181 mL | 2.4363 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。
alpha-Mangostin as an inhibitor of GSK3β in triple-negative breast cancer
J Biomol Struct Dyn 2022 Apr 23;1-7.PMID:35465844DOI:10.1080/07391102.2022.2068074.
Triple-negative breast cancer (TNBC) is a breast cancer subtype that does not express the estrogen receptor, the progesterone receptor, or the human epidermal growth factor receptor 2 and that is characterized by high invasiveness, high metastatic potential, and poor prognosis. TNBC lacks receptors and hence cannot be treated by using targeted therapies; as such, the therapeutic potential of Indonesian herbal plants against this disease is worth exploring. Herein, we explore the molecular docking and the molecular dynamics simulations of α-mangostin on glycogen synthase kinase 3β (GSK3β; PDB ID: 4ACC). Our findings reveal that α-mangostin has a weaker binding affinity to GSK3β than the native ligand (-8.22kcal/mol), while the latter binds to GSK3β with a stronger binding affinity of -8.92kcal/mol. According to the binding site analysis, the hydrogen bonds of the native ligand on Asp133 and Arg141, while α-mangostin only appeared to form a hydrogen bond on the enzyme's Asp133. On the other hand, α-mangostin shares similar docking sites with the native ligand (namely, Ile62, Phe67, Val70, and Thr138), thus leading to the conclusion that the native ligand and α-mangostin might share a similar molecular mechanism. The molecular dynamics simulation by using the molecular mechanics Poisson-Boltzmann and surface area (MM-PBSA) calculations' method shows that α-mangostin maintains a better affinity (with a value of ΔGTotal at -114.463kJ/mol) as compared with the native ligand (with a respective ΔGTotal value of -75.158kJ/mol). Our findings are suggestive of α-mangostin possessing a valuable potential as an anti-TNBC agent through GSK3β inhibition.Communicated by Ramaswamy H. Sarma.
Alpha-Mangostin-Loaded Transferrin-Conjugated Lipid-Polymer Hybrid Nanoparticles: Development and Characterization for Tumor-Targeted Delivery
ScientificWorldJournal 2022 Aug 30;2022:9217268.PMID:36081606DOI:10.1155/2022/9217268.
alpha-Mangostin, a natural xanthone mainly extracted from the pericarp of Garcinia mangostana, has been shown to have promising anticancer properties in many types of cancer. However, the therapeutic potential of α-mangostin has been limited so far due to its poor aqueous solubility and low oral bioavailability, which limited its biopharmaceutical applications. Furthermore, α-mangostin failed to specifically reach tumors at a therapeutic concentration due and rapid elimination in vivo. We hypothesized that this drawback could be overcome by loading the drug within a delivery system conjugated to transferrin (Tf), whose receptors are overexpressed on many cancer cells and would enhance the specific delivery of α-mangostin to cancer cells, thereby enhancing its therapeutic efficacy. The objectives of this study were therefore to prepare and characterize transferrin-conjugated lipid-polymer hybrid nanoparticles (LPHN) entrapping α-mangostin, as well as to evaluate their therapeutic efficacy in vitro. We successfully prepared α-mangostin loaded LPHN using a one-step nanoprecipitation method with high drug entrapment efficiency. The conjugation of Tf to the LPHN was achieved by using the thiol-maleimide "click" reaction, leading to an increase in the particle hydrodynamic size of Tf-LPHN compared to that of unconjugated (control) LPHN (Ctrl-LPHN). Both Tf-LPHN and Ctrl-LPHN were bearing negative surface charges. Tf-LPHN and Ctrl-LPHN exhibited a sustained release of α-mangostin at pH 7.4, following an initial burst release, unlike rapid release of drug solution. The entrapment of α-mangostin in the LPHN led to an increase in α-mangostin uptake by cancer cells, and thus improved its antiproliferative activity compared to that observed with the drug solution. In conclusion, α-mangostin entrapped in the Tf-LPHN is therefore a highly promising therapeutic system that should be further optimized as therapeutic tools for cancer treatment.
alpha-Mangostin Protects PC12 Cells Against Neurotoxicity Induced by Cadmium and Arsenic
Biol Trace Elem Res 2022 Nov 29.PMID:36445559DOI:10.1007/s12011-022-03498-8.
Arsenic and cadmium are nonessential elements that are of importance in public health due to their high toxicity. Contact with these toxic elements, even in very small amounts, can induce various side effects, including neurotoxicity. Oxidative stress and apoptosis are part of the main mechanisms of arsenic- and cadmium-induced toxicity. alpha-Mangostin is the main xanthone derived from mangosteen, Garcinia mangostana, with anti-oxidative properties.In this study, PC12 cells were selected as a nerve cell model, and the protective effects of alpha-Mangostin against neurotoxicity induced by arsenic and cadmium were investigated. PC12 cells were exposed to cadmium (5-80 µM) and arsenic (2.5-180 µM) for 24 h. Cytotoxicity, reactive oxygen species (ROS) production, and the protein expression of Bax, Bcl2, and cleaved caspase 3 were determined using MTT assay, fluorimetry, and western blot, respectively.Arsenic (10-180 µM) and cadmium (50-80 µM) significantly reduced cell viability. IC50 values were 10.3 ± 1.09 and 45 ± 4.63 µM, respectively. Significant increases in ROS, Bax/Bcl-2 ratio, and cleaved caspase-3 were observed after arsenic and cadmium exposures. Cell viability increased and ROS production decreased when cells were pretreated with alpha-Mangostin for 2 h. alpha-Mangostin reduced the increased level of cleaved caspase-3 induced by cadmium and decreased the elevated level of the Bax/Bcl-2 ratio after arsenic exposure.alpha-Mangostin significantly increased cell viability and reduced oxidative stress caused by cadmium and arsenic in PC12 cells. Moreover, alpha-Mangostin reduced cadmium-induced apoptosis through the reduction in the level of cleaved caspase 3. Further studies are required to determine the different mechanisms of alpha-Mangostin against neurotoxicity induced by these elements.
Effect of alpha-Mangostin on olanzapine-induced metabolic disorders in rats
Iran J Basic Med Sci 2022 Feb;25(2):198-207.PMID:35655598DOI:10.22038/IJBMS.2022.58734.13047.
Objectives: As olanzapine has side effects such as weight gain and metabolic disorders, and alpha-Mangostin has been shown to control metabolic disorders, the effects of alpha-Mangostin on metabolic disorders induced by olanzapine were investigated in this study. Materials and methods: Obesity was induced in female Wistar rats by daily administration of olanzapine (5 mg/kg/day, IP, 14 days). Rats were divided into 6 groups:1) vehicle (control); 2) olanzapine (5 mg/kg/day); 3,4,5) olanzapine+ alpha-Mangostin (10, 20, 40 mg/kg/day, IP); 6) alpha-Mangostin (40 mg/kg/day). Weight changes were measured every 3 days and food intake was assessed every day. Systolic blood pressure, plasma levels of blood sugar, triglycerides, total cholesterol, HDL, LDL, leptin, oxidative stress markers (MDA, GSH), AMPK, and P-AMPK protein levels in liver tissue were assessed on the last day of the study. Results: Administration of olanzapine significantly increased weight gain, food intake, blood pressure, triglycerides, LDL, blood sugar, leptin, and MDA in rat liver tissue and also decreased GSH, AMPK, and P-AMPK in liver tissue compared with the control group. Different doses of alpha-Mangostin significantly reduced weight gain, food intake, systolic blood pressure, triglycerides, LDL, blood sugar, leptin, and MDA. Also, they significantly increased GSH, AMPK, and P-AMPK in liver tissue compared with the olanzapine group. Conclusion: Olanzapine increases leptin levels, food intake, and weight, induces oxidative stress, decreases the levels of AMPK and P-AMPK proteins in liver tissue, and causes metabolic disorders. But, alpha-Mangostin reduces the negative effects of olanzapine by activation of AMPK.
alpha-Mangostin dephosphorylates ERM to induce adhesion and decrease surface stiffness in KG-1 cells
Hum Cell 2022 Jan;35(1):189-198.PMID:34817798DOI:10.1007/s13577-021-00651-8.
Surface stiffness is a unique indicator of various cellular states and events and needs to be tightly controlled. α-Mangostin, a natural compound with numerous bioactivities, reduces the mechanical stiffness of various cells; however, the mechanism by which it affects the actin cytoskeleton remains unclear. We aimed to elucidate the mechanism underlying α-mangostin activity on the surface stiffness of leukocytes. We treated spherical non-adherent myelomonocytic KG-1 cells with α-mangostin; it clearly reduced their surface stiffness and disrupted their microvilli. The α-mangostin-induced reduction in surface stiffness was inhibited by calyculin A, a protein phosphatase inhibitor. α-Mangostin also induced KG-1 cell adhesion to a fibronectin-coated surface. In KG-1 cells, a decrease in surface stiffness and the induction of cell adhesion are largely attributed to the dephosphorylation of ezrin/radixin/moesin proteins (ERMs); α-mangostin reduced the levels of phosphorylated ERMs. It further increased protein kinase C (PKC) activity. α-Mangostin-induced KG-1 cell adhesion and cell surface softness were inhibited by the PKC inhibitor GF109203X. The results of the present study suggest that α-mangostin decreases stiffness and induces adhesion of KG-1 cells via PKC activation and ERM dephosphorylation.