AspalathinCAS# 6027-43-6 |
Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
Cas No. | 6027-43-6 | SDF | Download SDF |
PubChem ID | 11282394 | Appearance | White-beige powder |
Formula | C21H24O11 | M.Wt | 452.4 |
Type of Compound | Flavonoids | Storage | Desiccate at -20°C |
Solubility | Soluble in methanol and water | ||
Chemical Name | 3-(3,4-dihydroxyphenyl)-1-[2,4,6-trihydroxy-3-[(2S,3R,4R,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]phenyl]propan-1-one | ||
SMILES | C1=CC(=C(C=C1CCC(=O)C2=C(C(=C(C=C2O)O)C3C(C(C(C(O3)CO)O)O)O)O)O)O | ||
Standard InChIKey | VCPUQYKWJRESOC-VJXVFPJBSA-N | ||
Standard InChI | InChI=1S/C21H24O11/c22-7-14-17(28)19(30)20(31)21(32-14)16-13(27)6-12(26)15(18(16)29)10(24)4-2-8-1-3-9(23)11(25)5-8/h1,3,5-6,14,17,19-23,25-31H,2,4,7H2/t14-,17-,19+,20-,21+/m1/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. |
Aspalathin Dilution Calculator
Aspalathin Molarity Calculator
1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
1 mM | 2.2104 mL | 11.0522 mL | 22.1043 mL | 44.2087 mL | 55.2608 mL |
5 mM | 0.4421 mL | 2.2104 mL | 4.4209 mL | 8.8417 mL | 11.0522 mL |
10 mM | 0.221 mL | 1.1052 mL | 2.2104 mL | 4.4209 mL | 5.5261 mL |
50 mM | 0.0442 mL | 0.221 mL | 0.4421 mL | 0.8842 mL | 1.1052 mL |
100 mM | 0.0221 mL | 0.1105 mL | 0.221 mL | 0.4421 mL | 0.5526 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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Aspalathin Reverts Doxorubicin-Induced Cardiotoxicity through Increased Autophagy and Decreased Expression of p53/mTOR/p62 Signaling.[Pubmed:28937626]
Molecules. 2017 Sep 22;22(10). pii: molecules22101589.
Doxorubicin (Dox) is an effective chemotherapeutic agent used in the treatment of various cancers. Its clinical use is often limited due to its potentially fatal cardiotoxic side effect. Increasing evidence indicates that tumour protein p53 (p53), adenosine monophosphate-activated protein kinase (AMPK), nucleoporin p62 (p62), and the mammalian target of rapamycin (mTOR) are critical mediators of Dox-induced apoptosis, and subsequent dysregulation of autophagy. Aspalathin, a polyphenolic dihydrochalcone C-glucoside has been shown to activate AMPK while decreasing the expression of p53. However, the role that Aspalathin could play in the inhibition of Dox-induced cardiotoxicity through increased autophagy flux remained unexplored. H9c2 cardiomyocytes and Caov-3 ovarian cancer cells were cultured in Dulbecco's Modified Eagle's medium and treated with or without Dox for five days. Thereafter, cells exposed to 0.2 microM Dox were co-treated with either 20 microM Dexrazozane (Dexra) or 0.2 microM Aspalathin (ASP) daily for 5 days. Results obtained showed that ASP mediates its cytoprotective effect in a p53-dependent manner, by increasing the Bcl-2/Bax ratio and decreasing apoptosis. The latter effect was diminished through ASP-induced activation of autophagy-related genes (Atgs) with an associated decrease in p62 through induction of AMPK and Fox01. Furthermore, we showed that ASP was able to potentiate this effect without decreasing the anti-cancer efficacy of Dox, as could be observed in Caov-3 ovarian cancer cells. Taken together, the data presented in this study provides a credible mechanism by which ASP co-treatment could protect the myocardium from Dox-induced cardiotoxicity.
Inhibitory Interactions of Aspalathus linearis (Rooibos) Extracts and Compounds, Aspalathin and Z-2-(beta-d-Glucopyranosyloxy)-3-phenylpropenoic Acid, on Cytochromes Metabolizing Hypoglycemic and Hypolipidemic Drugs.[Pubmed:27845750]
Molecules. 2016 Nov 12;21(11). pii: molecules21111515.
Rooibos extract, due to its glucose and lipid lowering effects, has potential as a nutraceutical for improvement of metabolic dysfunction. Potential herb-drug interactions as a result of the use of natural products are of increasing concern. Cytochrome P450 enzymes, CYP2C8, CYP2C9, and CYP3A4, are important in the metabolism of hypoglycemic drugs, such as thiazolidinediones (TZDs) and sulfonylureas, and hypocholesterolemic drugs, such as atorvastatin. This study investigated the effects of rooibos extracts, prepared from "unfermented" and "fermented" rooibos plant material and two of the major bioactive compounds, Z-2-(beta-d-glucopyranosyloxy)-3-phenylpropenoic acid (PPAG) and Aspalathin (ASP), on Vivid((R)) recombinant CYP450 enzymes. Unfermented (GRT) and fermented (FRE) rooibos extracts inhibited the activity of CYP2C8 (7.69 +/- 8.85 microg/mL and 8.93 +/- 8.88 microg/mL, respectively) and CYP3A4 (31.33 +/- 4.69 microg/mL and 51.44 +/- 4.31 microg/mL, respectively) based on their respective IC50 concentrations. Both extracts dose- and time-dependently inhibited CYP2C8 activity, but only time-dependently inhibited CYP2C9. CYP3A4 showed concentration-dependent inhibition by ASP, GRT, and FRE at 25, 50, and 100 microg/mL concentrations. ASP, GRT, and FRE time-dependently inhibited CYP3A4 activity with GRT and FRE showing a more potent time-dependent inhibition, comparable to erythromycin. These findings suggest that herb-drug interactions may occur when nutraceuticals containing rooibos extracts are co-administered with hypoglycemic drugs such as TZDs, sulfonylureas, and dyslipidemic drug, atorvastatin.
Myocardial Glucose Clearance by Aspalathin Treatment in Young, Mature, and Obese Insulin-Resistant Rats.[Pubmed:28772334]
Planta Med. 2018 Jan;84(2):75-82.
Rooibos, an indigenous South African plant ingested as herbal tea, is well known for its antioxidant effects. This in vitro study investigated Aspalathin (C21H24O11), a dihydrochalcone unique to rooibos, for hypoglycemic effects in the context of age- and obesity-induced insulin resistance and the mechanisms involved. Male Wistar rats were allocated into three groups: 16 - 30 weeks feeding with either standard rat chow or a high-caloric diet, or 6 - 10 weeks feeding with standard rat chow. Ventricular cardiomyocytes were isolated by collagenase perfusion digestion, and glucose uptake was determined by 2-[(3)H]-deoxyglucose accumulation. Viability was tested by trypan blue exclusion or propidium iodide staining. The high-caloric diet significantly increased body weight gain (508.5 +/- 50.0 vs. 417.3 +/- 40.0 g), visceral adiposity (42.30 +/- 10.1 vs. 21.75 +/- 7.0 g), and fasting blood glucose (5.7 +/- 0.4 vs. 4.7 +/- 0.1 mM). Aspalathin (10 microM for 90 min) induced 2-[(3)H]-deoxyglucose uptake in young cardiomyocytes (37.2 +/- 13.9 vs. 25.7 +/- 2.5 pmol 2-[(3)H]-deoxyglucose/mg protein) and enhanced insulin-mediated 2-[(3)H]-deoxyglucose uptake in control cells (32.4 +/- 6.4 vs. 23.5 +/- 10.0 pmol 2-[(3)H]-deoxyglucose/mg protein), but failed to induce 2-[(3)H]-deoxyglucose uptake in high-caloric diet cells. Aspalathin induced glucose uptake in insulin-sensitive cardiomyocytes from young and aged rats, but not in high-caloric diet animals and enhanced the actions of insulin through a PI3K-dependent mechanism, resulting in an additive response.
Intestinal Transport Characteristics and Metabolism of C-Glucosyl Dihydrochalcone, Aspalathin.[Pubmed:28358310]
Molecules. 2017 Mar 30;22(4). pii: molecules22040554.
Insight into the mechanisms of intestinal transport and metabolism of Aspalathin will provide important information for dose optimisation, in particular for studies using mouse models. Aspalathin transportation across the intestinal barrier (Caco-2 monolayer) tested at 1-150 microM had an apparent rate of permeability (Papp) typical of poorly absorbed compounds (1.73 x 10(-6) cm/s). Major glucose transporters, sodium glucose linked transporter 1 (SGLT1) and glucose transporter 2 (GLUT2), and efflux protein (P-glycoprotein, PgP) (1.84 x 10(-6) cm/s; efflux ratio: 1.1) were excluded as primary transporters, since the Papp of Aspalathin was not affected by the presence of specific inhibitors. The Papp of Aspalathin was also not affected by constituents of Aspalathin-enriched rooibos extracts, but was affected by high glucose concentration (20.5 mM), which decreased the Papp value to 2.9 x 10(-7) cm/s. Aspalathin metabolites (sulphated, glucuronidated and methylated) were found in mouse urine, but not in blood, following an oral dose of 50 mg/kg body weight of the pure compound. Sulphates were the predominant metabolites. These findings suggest that Aspalathin is absorbed and metabolised in mice to mostly sulphate conjugates detected in urine. Mechanistically, we showed that Aspalathin is not actively transported by the glucose transporters, but presumably passes the monolayer paracellularly.
Aspalathin Protects the Heart against Hyperglycemia-Induced Oxidative Damage by Up-Regulating Nrf2 Expression.[Pubmed:28098811]
Molecules. 2017 Jan 14;22(1). pii: molecules22010129.
Aspalathin (ASP) can protect H9c2 cardiomyocytes against high glucose (HG)-induced shifts in myocardial substrate preference, oxidative stress, and apoptosis. The protective mechanism of ASP remains unknown. However, as one of possible, it is well known that phytochemical flavonoids reduce oxidative stress via nuclear factor (erythroid-derived 2)-like 2 (Nrf2) activation resulting in up-regulation of antioxidant genes and enzymes. Therefore, we hypothesized that ASP protects the myocardium against HG- and hyperglycemia-induced oxidative damage by up-regulating Nrf2 expression in H9c2 cardiomyocytes and diabetic (db/db) mice, respectively. Using an oxidative stress RT(2) Profiler PCR array, ASP at a dose of 1 microM was demonstrated to protect H9c2 cardiomyocytes against HG-induced oxidative stress, but silencing of Nrf2 abolished this protective response of ASP and exacerbated cardiomyocyte apoptosis. Db/db mice and their non-diabetic (db/+) littermate controls were subsequently treated daily for six weeks with either a low (13 mg/kg) or high (130 mg/kg) ASP dose. Compared to nondiabetic mice the db/db mice presented increased cardiac remodeling and enlarged left ventricular wall that occurred concomitant to enhanced oxidative stress. Daily treatment of mice with ASP at a dose of 130 mg/kg for six weeks was more effective at reversing complications than both a low dose ASP or metformin, eliciting enhanced expression of Nrf2 and its downstream antioxidant genes. These results indicate that ASP maintains cellular homeostasis and protects the myocardium against hyperglycemia-induced oxidative stress through activation of Nrf2 and its downstream target genes.
The Transcription Profile Unveils the Cardioprotective Effect of Aspalathin against Lipid Toxicity in an In Vitro H9c2 Model.[Pubmed:28146135]
Molecules. 2017 Jan 31;22(2). pii: molecules22020219.
Aspalathin, a C-glucosyl dihydrochalcone, has previously been shown to protect cardiomyocytes against hyperglycemia-induced shifts in substrate preference and subsequent apoptosis. However, the precise gene regulatory network remains to be elucidated. To unravel the mechanism and provide insight into this supposition, the direct effect of Aspalathin in an isolated cell-based system, without the influence of any variables, was tested using an H9c2 cardiomyocyte model. Cardiomyocytes were exposed to high glucose (33 mM) for 48 h before post-treatment with or without Aspalathin. Thereafter, RNA was extracted and RT2 PCR Profiler Arrays were used to profile the expression of 336 genes. Results showed that, 57 genes were differentially regulated in the high glucose or high glucose and Aspalathin treated groups. Search Tool for the Retrieval of Interacting Genes/Proteins (STRING) analysis revealed lipid metabolism and molecular transport as the biological processes altered after high glucose treatment, followed by inflammation and apoptosis. Aspalathin was able to modulate key regulators associated with lipid metabolism (Adipoq, Apob, CD36, Cpt1, Ppargamma, Srebf1/2, Scd1 and Vldlr), insulin resistance (Igf1, Akt1, Pde3 and Map2k1), inflammation (Il3, Il6, Jak2, Lepr, Socs3, and Tnf13) and apoptosis (Bcl2 and Chuk). Collectively, our results suggest that Aspalathin could reverse metabolic abnormalities by activating Adipoq while modulating the expression of Ppargamma and Srebf1/2, decreasing inflammation via Il6/Jak2 pathway, which together with an observed increased expression of Bcl2 prevents myocardium apoptosis.
Aspalathin from Rooibos (Aspalathus linearis): A Bioactive C-glucosyl Dihydrochalcone with Potential to Target the Metabolic Syndrome.[Pubmed:29388183]
Planta Med. 2018 Jul;84(9-10):568-583.
Aspalathin is a C-glucosyl dihydrochalcone that is abundantly present in Aspalathus linearis. This endemic South African plant, belonging to the Cape Floristic region, is normally used for production of rooibos, a herbal tea. Aspalathin was valued initially only as precursor in the formation of the characteristic red-brown colour of "fermented" rooibos, but the hype about the potential role of natural antioxidants to alleviate oxidative stress, shifted interest in Aspalathin to its antioxidant properties and subsequently, its potential role to improve metabolic syndrome, a disease condition interrelated with oxidative stress. The potential use of Aspalathin or Aspalathin-rich rooibos extracts as a condition-specific nutraceutical is hampered by the limited supply of green rooibos (i.e., "unfermented" plant material) and low levels in "fermented" rooibos, providing incentive for its synthesis. In vitro and in vivo studies relating to the metabolic activity of Aspalathin are discussed and cellular mechanisms by which Aspalathin improves glucose and lipid metabolism are proposed. Other aspects covered in this review, which are relevant in view of the potential use of Aspalathin as an adjunctive therapy, include its poor stability and bioavailability, as well as potential adverse herb-drug interactions, in particular interference with the metabolism of certain commonly prescribed chronic medications for hyperglycaemia and dyslipidaemia.