Aristolochic acid CCAS# 4849-90-5 |
Quality Control & MSDS
3D structure
Package In Stock
Number of papers citing our products
| Cas No. | 4849-90-5 | SDF | Download SDF |
| PubChem ID | 165274 | Appearance | Yellow-orange powder |
| Formula | C16H9NO7 | M.Wt | 327.25 |
| Type of Compound | Alkaloids | Storage | Desiccate at -20°C |
| Synonyms | Aristolochic acid IIIa | ||
| Solubility | Sparingly soluble in water | ||
| Chemical Name | 10-hydroxy-6-nitronaphtho[2,1-g][1,3]benzodioxole-5-carboxylic acid | ||
| SMILES | C1OC2=C(O1)C3=C4C=C(C=CC4=CC(=C3C(=C2)C(=O)O)[N+](=O)[O-])O | ||
| Standard InChIKey | NBFGYDJKTHENDP-UHFFFAOYSA-N | ||
| 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 | 1. Aristolochic acid(AA) is a powerful nephrotoxic and carcinogenic substance with an extremely short latency period, not only in animals but also in humans, in particular, the highly similar metabolic pathway of activation and resultant DNA adducts of AA allows the extrapolation of carcinogenesis data from laboratory animals to the human situation; therefore, all products containing botanicals known to or suspected of containing AA should be banned from the market world wide. |
Aristolochic acid C Dilution Calculator
Aristolochic acid C Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 3.0558 mL | 15.2788 mL | 30.5577 mL | 61.1154 mL | 76.3942 mL |
| 5 mM | 0.6112 mL | 3.0558 mL | 6.1115 mL | 12.2231 mL | 15.2788 mL |
| 10 mM | 0.3056 mL | 1.5279 mL | 3.0558 mL | 6.1115 mL | 7.6394 mL |
| 50 mM | 0.0611 mL | 0.3056 mL | 0.6112 mL | 1.2223 mL | 1.5279 mL |
| 100 mM | 0.0306 mL | 0.1528 mL | 0.3056 mL | 0.6112 mL | 0.7639 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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Activating mutations at codon 61 of the c-Ha-ras gene in thin-tissue sections of tumors induced by aristolochic acid in rats and mice.[Pubmed:1884371]
Cancer Lett. 1991 Aug;59(2):139-43.
The plant extract aristolochic acid, which consists mainly of aristolochic acid I (AAI) and aristolochic acid II (AAII), induces tumors in rats and mice. Thin-tissue sections of rat tumors induced by AAI and of mouse tumors induced by aristolochic acid, were analyzed for c-Ha-ras mutations in codon 61. Areas of neoplastic and histologically normal tissue were manually scraped out and separated. Using the polymerase chain reaction (PCR) and mutation detection by selective oligonucleotide hybridization, we observed AT----TA transversion mutations in DNA of neoplastic portions, but not in DNA of adjacent normal tissue in both rat and mouse tumors.
Vitamin C attenuates the toxic effect of aristolochic acid on renal tubular cells via decreasing oxidative stressmediated cell death pathways.[Pubmed:26239057]
Mol Med Rep. 2015 Oct;12(4):6086-92.
Aristolochic acid (AA) is a component of Chinese medicinal herbs, including asarum and aristolochia and has been used in Traditional Chinese Medicine for a long time. Recent studies found that AA has a cytotoxic effect resulting in nephropathy. These studies indicated that AAinduced cytotoxicity is associated with increases in oxidative stress and caspase3 activation. The present study further demonstrated that AA mainly elevates the H2O2 ratio, leading to increases in oxidative stress. Furthermore, the results indicated that AA induces cell death can via caspasedependent and independent pathways. It is desirable to identify means of inhibiting AAinduced renal damage; therefore, the present study applied an antioxidative nutrient, vitamin C, to test whether it can be employed to reduce AAinduced cell cytotoxicity. The results showed that vitamin C decreased AAinduced H2O2 levels, caspase3 activity and cytotoxicity in renal tubular cells. In conclusion, the present study was the first to demonstrate that AAinduced increases of the H2O2 ratio resulted in renal tubular cell death via caspasedependent and independent pathways, and that vitamin C can decrease AAinduced increases in H2O2 levels and caspase3 activity to attenuate AAinduced cell cytotoxicity.
Targeting c-fms kinase attenuates chronic aristolochic acid nephropathy in mice.[Pubmed:26909597]
Oncotarget. 2016 Mar 8;7(10):10841-56.
Aristolochic acid nephropathy (AAN) is a progressive kidney disease caused by some Chinese herbal medicines, but treatment remains ineffective. Macrophage accumulation is an early feature in human and experimental AAN; however, the role of macrophages in chronic AAN is unknown. We report here that targeting macrophages with fms-I, a selective inhibitor of the tyrosine kinase activity of the macrophage colony-stimulating factor receptor, suppressed disease progression in a mouse model of chronic AAN. Treatment with fms-I (10mg/kg/BID) from day 0 to 28 (prevention study) or from day 14 to 28 (intervention study) substantially inhibited macrophage accumulation and significantly improved renal dysfunction including a reduction in proteinuria and tubular damage. Progressive interstitial fibrosis (myofibroblast accumulation and collagen deposition) and renal inflammation (increased expression of MCP-1, MIF, and TNF-alpha) were also attenuated by fms-I treatment. These protective effects involved inhibition of TGF-beta/Smad3 and NF-kB signaling. In conclusion, the present study establishes that macrophages are key inflammatory cells that exacerbates progressive tubulointerstitial damage in chronic AAN via mechanisms associated with TGF-beta/Smad3-mediated renal fibrosis and NF-kappaB-driven renal inflammation. Targeting macrophages via a c-fms kinase inhibitor may represent a novel therapy for chronic AAN.
