Chebulagic acidCAS# 23094-71-5 |
Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
| Cas No. | 23094-71-5 | SDF | Download SDF |
| PubChem ID | 442674 | Appearance | Beige powder |
| Formula | C41H30O27 | M.Wt | 954.7 |
| Type of Compound | Phenols | Storage | Desiccate at -20°C |
| Solubility | DMSO : 100 mg/mL (104.75 mM; Need ultrasonic) | ||
| SMILES | C1C2C3C(C(C(O2)OC(=O)C4=CC(=C(C(=C4)O)O)O)OC(=O)C5=CC(=C(C6=C5C(C(C(=O)O3)CC(=O)O)C(C(=O)O6)O)O)O)OC(=O)C7=CC(=C(C(=C7C8=C(C(=C(C=C8C(=O)O1)O)O)O)O)O)O | ||
| Standard InChIKey | HGJXAVROWQLCTP-YABCKIEDSA-N | ||
| Standard InChI | InChI=1S/C41H30O27/c42-13-1-8(2-14(43)24(13)49)35(56)68-41-34-33-31(64-39(60)12(6-19(47)48)22-23-11(38(59)67-34)5-17(46)27(52)32(23)65-40(61)30(22)55)18(63-41)7-62-36(57)9-3-15(44)25(50)28(53)20(9)21-10(37(58)66-33)4-16(45)26(51)29(21)54/h1-5,12,18,22,30-31,33-34,41-46,49-55H,6-7H2,(H,47,48)/t12-,18+,22-,30-,31+,33-,34+,41-/m0/s1 | ||
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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| About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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| Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. | ||
| Description | Chebulagic acid is a potent DNA topoisomerase inhibitor, and is also COX-2 and 5-LOX dual inhibitor. Chebulagic acid may be of value as broad-spectrum antivirals for limiting emerging/ recurring viruses known to engage host cell glycosaminoglycans for entry. Chebulagic acid can be used to control blood glucose and manage type 2 diabetes, although clinical trials are needed. |
| Targets | COX | LOX | Topoisomerase | HIV | AMPK | Autophagy | mTOR | ATPase | PPAR | GLUT | Bcl-2/Bax | Caspase | P450 (e.g. CYP17) | CDK | NF-kB | MMP(e.g.TIMP) | VEGFR | IkB | IKK |
| In vitro | Chebulagic acid from Terminalia chebula causes G1 arrest, inhibits NFκB and induces apoptosis in retinoblastoma cells.[Pubmed: 25169718]BMC Complement Altern Med. 2014 Aug 29;14:319.Plants are the valuable source of natural products with important medicinal properties. Most of the approved anti cancer drugs have a natural product origin or are natural products. Retinoblastoma is the most common ocular cancer of children. Although chemotherapy is the preferred mode of therapy, a successful treatment for retinoblastoma requires enucleation. Chebulagic acid (CA) from Terminalia chebula was shown to have anti-proliferative properties in the studies on cancerous cell lines. Due to anti cancer properties of CA and due to limitation in treatment options for retinoblastoma, the present study is undertaken to understand the role of CA on the proliferation of retinoblastoma cells.
The natural compound chebulagic acid inhibits vascular endothelial growth factor A mediated regulation of endothelial cell functions.[Pubmed: 25859636]Sci Rep. 2015 Apr 10;5:9642.Vascular endothelial growth factor A (VEGFA) plays an important role in tumour angiogenesis and its angiogenic action is mainly mediated through its VEGF receptor 2 (VEGFR-2). Therefore drugs targeting VEGFA/VEGFR-2 are being presently used in the clinics for treatment of several types of solid malignant tumours. |
| In vivo | Anti-hyperglycemic effect of chebulagic acid from the fruits of Terminalia chebula Retz.[Pubmed: 22754367]Int J Mol Sci. 2012;13(5):6320-33.
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| Kinase Assay | Chebulagic acid from Terminalia chebula enhances insulin mediated glucose uptake in 3T3-L1 adipocytes via PPARγ signaling pathway.[Pubmed: 25529897]Neuroprotective Effect of Chebulagic Acid via Autophagy Induction in SH-SY5Y Cells.[Pubmed: 25143804]Biomol Ther (Seoul). 2014 Jul;22(4):275-81.Autophagy is a series of catabolic process mediating the bulk degradation of intracellular proteins and organelles through formation of a double-membrane vesicle, known as an autophagosome, and fusing with lysosome. Autophagy plays an important role of death-survival decisions in neuronal cells, which may influence to several neurodegenerative disorders including Parkinson's disease. Chebulagic acid, the major constituent of Terminalia chebula and Phyllanthus emblica, is a benzopyran tannin compound with various kinds of beneficial effects. This study was performed to investigate the autophagy enhancing effect of Chebulagic acid on human neuroblastoma SH-SY5Y cell lines. Biofactors. 2014 Nov-Dec;40(6):646-57.The thiazolidinedione (TZDs) class of drugs are very effective for the treatment of type 2 diabetes mellitus (T2DM). But due to the adverse effects of synthetic TZDs, their use is strictly regulated. The therapeutic actions of TZDs are mediated via modulation of peroxisome proliferator-activated receptor gamma (PPARγ). Naturally occurring PPARγ modulators are more desirable as they lack the serious adverse effects caused by TZDs. This has prompted the exploitation of medicinal plants used in traditional medicine, for their potential PPARγ activity. |
Chebulagic acid Dilution Calculator
Chebulagic acid Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 1.0474 mL | 5.2372 mL | 10.4745 mL | 20.949 mL | 26.1862 mL |
| 5 mM | 0.2095 mL | 1.0474 mL | 2.0949 mL | 4.1898 mL | 5.2372 mL |
| 10 mM | 0.1047 mL | 0.5237 mL | 1.0474 mL | 2.0949 mL | 2.6186 mL |
| 50 mM | 0.0209 mL | 0.1047 mL | 0.2095 mL | 0.419 mL | 0.5237 mL |
| 100 mM | 0.0105 mL | 0.0524 mL | 0.1047 mL | 0.2095 mL | 0.2619 mL |
| * Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. | |||||
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Chebulagic acid is a COX-LOX dual inhibitor isolated from the fruits of Terminalia chebula Retz, on angiogenesis. target: COX-LOX [1] In vitro: Chebulagic acid can enhance the autophagy. Chebulagic acid exert anti-inflammatory and anti-infective effects. [1] [2] Chebulagic acid also show a protective effect against 1-methyl-4-phenylpyridinium (MPP+) - induce cytotoxicity which mimics the pathological symptom of Parkinson's disease. Chebulagic acid inhibit the LPS-induced upregulation of TNF-α and IL-1β in a dose- and time-dependent manner. Furthermore, LPS-activated MAPK signaling is inhibited by CA treatment in the EA.hy926 cells. [3]
References:
[1]. Kim HJ et al. Neuroprotective Effect of Chebulagic Acid via Autophagy Induction in SH-SY5Y Cells. Biomol Ther (Seoul). 2014 Jul;22(4):275-81.
[2]. Liu Y et al. Chebulagic acid inhibits the LPS-induced expression of TNF-α and IL-1β in endothelial cells by suppressing MAPK activation. Exp Ther Med. 2015 Jul;10(1):263-268.
[3]. Athira AP et al. Inhibition of Angiogenesis In Vitro by Chebulagic Acid: A COX-LOX Dual Inhibitor. Int J Vasc Med. 2013;2013:843897.
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Anti-hyperglycemic effect of chebulagic acid from the fruits of Terminalia chebula Retz.[Pubmed:22754367]
Int J Mol Sci. 2012;13(5):6320-33.
In the present study, we firstly compared rat intestinal alpha-glucosidase inhibitory activity by different ethanol-aqueous extractions from the dried fruits of Terminalia chebula Retz. The enzymatic assay showed that the 80% ethanol extract was more potent against maltase activity than both 50% and 100% ethanol extracts. By HPLC analysis, it was determined that the 80% ethanol extract had a higher content of Chebulagic acid than each of 50% or 100% ethanol extract. Next, we investigated how efficiently Chebulagic acid could inhibit sugar digestion by determining the glucose level on the apical side of the Caco-2 cell monolayer. The result showed that the maltose-hydrolysis activity was down-regulated by Chebulagic acid, which proved to be a reversible inhibitor of maltase in Caco-2 cells. On the other hand, Chebulagic acid showed a weak inhibition of sucrose-hydrolysis activity. Meanwhile, Chebulagic acid did not have an obvious influence on intestinal glucose uptake and was not effective on glucose transporters. Further animal studies revealed that the oral administration of Chebulagic acid (100 mg/kg body weight) significantly reduced postprandial blood glucose levels by 11.1% in maltose-loaded Sprague-Dawley (SD) rats compared with the control group, whereas the oral administration of Chebulagic acid did not show a suppressive effect on postprandial hyperglycemia in sucrose- or glucose-loaded SD-rats. The results presented here suggest that Chebulagic acid from T. chebula can be used to control blood glucose and manage type 2 diabetes, although clinical trials are needed.
Chebulagic acid from Terminalia chebula causes G1 arrest, inhibits NFkappaB and induces apoptosis in retinoblastoma cells.[Pubmed:25169718]
BMC Complement Altern Med. 2014 Aug 29;14:319.
BACKGROUND: Plants are the valuable source of natural products with important medicinal properties. Most of the approved anti cancer drugs have a natural product origin or are natural products. Retinoblastoma is the most common ocular cancer of children. Although chemotherapy is the preferred mode of therapy, a successful treatment for retinoblastoma requires enucleation. Chebulagic acid (CA) from Terminalia chebula was shown to have anti-proliferative properties in the studies on cancerous cell lines. Due to anti cancer properties of CA and due to limitation in treatment options for retinoblastoma, the present study is undertaken to understand the role of CA on the proliferation of retinoblastoma cells. METHODS: Anti proliferative potential of CA was determined by MTT assay. The expression levels of various cell death mediators in retinoblastoma cells with CA treatment were assessed by Western blotting. Flowcytometer analysis was used to estimate the mitochondrial membrane potential (MMP) and to determine the percentage of cells undergoing apoptosis. RESULTS: The present study showed CA inhibited the proliferation of retinoblastoma cells in a dose dependent manner. CA modulated MMP, induced release of Cytochrome c, activated caspase 3 and shifted the ratio of BAX and Bcl2 towards cell death. G1 arrest, noticed in CA treated cells, is mediated by the increase in the expression of CDK inhibitor p27. CA treatment also decreased the levels of NFkappaB in the nucleus. This decrease is mediated by suppression in degradation of IkappaBalpha. CONCLUSION: CA has shown significant anti proliferative potential on retinoblastoma cells. Our findings clearly demonstrate that CA induces G1 arrest, inhibits NFkappaB and induces apoptosis of retinoblastoma cells.
Neuroprotective Effect of Chebulagic Acid via Autophagy Induction in SH-SY5Y Cells.[Pubmed:25143804]
Biomol Ther (Seoul). 2014 Jul;22(4):275-81.
Autophagy is a series of catabolic process mediating the bulk degradation of intracellular proteins and organelles through formation of a double-membrane vesicle, known as an autophagosome, and fusing with lysosome. Autophagy plays an important role of death-survival decisions in neuronal cells, which may influence to several neurodegenerative disorders including Parkinson's disease. Chebulagic acid, the major constituent of Terminalia chebula and Phyllanthus emblica, is a benzopyran tannin compound with various kinds of beneficial effects. This study was performed to investigate the autophagy enhancing effect of Chebulagic acid on human neuroblastoma SH-SY5Y cell lines. We determined the effect of Chebulagic acid on expression levels of autophago-some marker proteins such as, DOR/TP53INP2, Golgi-associated ATPase Enhancer of 16 kDa (GATE 16) and Light chain 3 II (LC3 II), as well as those of its upstream pathway proteins, AMP-activated protein kinase (AMPK), mammalian target of rapamycin (mTOR) and Beclin-1. All of those proteins were modulated by Chebulagic acid treatment in a way of enhancing the autophagy. Additionally in our study, Chebulagic acid also showed a protective effect against 1-methyl-4-phenylpyridinium (MPP(+)) - induced cytotoxicity which mimics the pathological symptom of Parkinson's disease. This effect seems partially mediated by enhanced autophagy which increased the degradation of aggregated or misfolded proteins from cells. This study suggests that Chebulagic acid is an attractive candidate as an autophagy-enhancing agent and therefore, it may provide a promising strategy to prevent or cure the diseases caused by accumulation of abnormal proteins including Parkinson's disease.
The natural compound chebulagic acid inhibits vascular endothelial growth factor A mediated regulation of endothelial cell functions.[Pubmed:25859636]
Sci Rep. 2015 Apr 10;5:9642.
Vascular endothelial growth factor A (VEGFA) plays an important role in tumour angiogenesis and its angiogenic action is mainly mediated through its VEGF receptor 2 (VEGFR-2). Therefore drugs targeting VEGFA/VEGFR-2 are being presently used in the clinics for treatment of several types of solid malignant tumours. We here in report that low dose of Chebulagic acid (CA), a hydrolysable tannin found in myrobalan fruits can inhibit VEGFA induced vascular permeability, endothelial cell proliferation, migration, tube formation and thereby, angiogenesis by suppressing VEGFR-2 phosphorylation. CA may thus be an effective and useful natural inhibitor of VEGFA mediated angiogenesis.
Chebulagic acid from Terminalia chebula enhances insulin mediated glucose uptake in 3T3-L1 adipocytes via PPARgamma signaling pathway.[Pubmed:25529897]
Biofactors. 2014 Nov-Dec;40(6):646-57.
The thiazolidinedione (TZDs) class of drugs are very effective for the treatment of type 2 diabetes mellitus (T2DM). But due to the adverse effects of synthetic TZDs, their use is strictly regulated. The therapeutic actions of TZDs are mediated via modulation of peroxisome proliferator-activated receptor gamma (PPARgamma). Naturally occurring PPARgamma modulators are more desirable as they lack the serious adverse effects caused by TZDs. This has prompted the exploitation of medicinal plants used in traditional medicine, for their potential PPARgamma activity. In the present work, we studied Chebulagic acid (CHA) isolated from fruits of Terminalia chebula with respect to its effect on adipogenesis, glucose transport, and endocrine function of adipocyte. The mRNA expression profile of PPARgamma target gene CCAAT/enhancer-binding protein alpha (C/EBP-alpha) was analyzed by qRT-PCR. The putative binding mode and the potential ligand-target interactions of CHA, with PPARgamma was analyzed using docking software (Autodock and iGEMDOCKv2). The results showed that CHA enhances PPARgamma signaling and adipogenesis dose dependently but in a moderate way, less than rosiglitazone. GLUT4 expression and adiponectin secretion was increased by CHA treatment. The mRNA expression of PPARgamma target gene C/EBP-alpha was increased in CHA -treated adipocytes. The comparison of results of various parameters of adipogenesis, insulin sensitivity, endocrine function and molecular docking experiments of roziglitazone and Chebulagic acid indicate that the latter behaves like partial PPARgamma agonist which could be exploited for phytoceutical development against T2DM.
