Agaric acidCAS# 666-99-9 |
Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
| Cas No. | 666-99-9 | SDF | Download SDF |
| PubChem ID | 12629 | Appearance | Powder |
| Formula | C22H40O7 | M.Wt | 416.5 |
| Type of Compound | N/A | Storage | Desiccate at -20°C |
| Solubility | Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc. | ||
| Chemical Name | 2-hydroxynonadecane-1,2,3-tricarboxylic acid | ||
| SMILES | CCCCCCCCCCCCCCCCC(C(=O)O)C(CC(=O)O)(C(=O)O)O | ||
| Standard InChIKey | HZLCGUXUOFWCCN-UHFFFAOYSA-N | ||
| Standard InChI | InChI=1S/C22H40O7/c1-2-3-4-5-6-7-8-9-10-11-12-13-14-15-16-18(20(25)26)22(29,21(27)28)17-19(23)24/h18,29H,2-17H2,1H3,(H,23,24)(H,25,26)(H,27,28) | ||
| 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. | ||
Agaric acid Dilution Calculator
Agaric acid Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 2.401 mL | 12.0048 mL | 24.0096 mL | 48.0192 mL | 60.024 mL |
| 5 mM | 0.4802 mL | 2.401 mL | 4.8019 mL | 9.6038 mL | 12.0048 mL |
| 10 mM | 0.2401 mL | 1.2005 mL | 2.401 mL | 4.8019 mL | 6.0024 mL |
| 50 mM | 0.048 mL | 0.2401 mL | 0.4802 mL | 0.9604 mL | 1.2005 mL |
| 100 mM | 0.024 mL | 0.12 mL | 0.2401 mL | 0.4802 mL | 0.6002 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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Agaric acid induces mitochondrial permeability transition through its interaction with the adenine nucleotide translocase. Its dependence on membrane fluidity.[Pubmed:16050990]
Mitochondrion. 2005 Aug;5(4):272-81.
The effect of Agaric acid as inducer of mitochondrial permeability transition was studied. It was found that: (i) Agaric acid (AA) promoted efflux of accumulated Ca2+, collapse of transmembrane potential, and mitochondrial swelling; (ii) these effects depend on membrane fluidity; (iii) ADP inhibited the effect of AA on Ca2+ efflux, and (iv) AA blocked binding of the sulfhydryl reagent, eosin-5-maleimide, to the adenine nucleotide translocase. It is proposed that AA induces pore opening through binding of the citrate moiety to the ADP/ATP carrier; this interaction must be stabilized by insertion of the alkyl chain in the lipid milieu of the membrane.
Glucocorticoid induction of fatty-acid synthase mediates the stimulatory effect of the hormone on choline-phosphate cytidylyltransferase activity in fetal rat lung.[Pubmed:2160286]
Biochim Biophys Acta. 1990 May 1;1044(1):70-6.
Fetal lung fatty-acid synthase and choline-phosphate cytidylyltransferase activities are increased by glucocorticoids. There is evidence that the hormone increases synthesis of fatty-acid synthase but only increases the catalytic activity of the cytidylyltransferase. Free fatty acids and a number of phospholipids have been reported to stimulate cytidylyltransferase activity in several organs, including the lung. We have addressed the question of whether glucocorticoid induction of fatty-acid synthase mediates the stimulatory effect of the hormone on choline-phosphate cytidylyltransferase activity. Explants of 18-day fetal rat lung were cultured for 48 h with dexamethasone and inhibitors of de novo fatty acid biosynthesis (Agaric acid and hydroxycitric acid) being included in the medium for the final 20 h. Dexamethasone increased the activities of fatty acid synthase and choline-phosphate cytidylyltransferase by 84% and 60%, respectively. Agaric acid and hydroxycitric acid completely abolished the stimulatory effect of the hormone on cytidylyltransferase but not on fatty-acid synthase. The inhibitors had no effect on cytidylyltransferase activity in control cultures. Fetal lung choline-phosphate cytidylyltransferase can be maximally stimulated by inclusion of phosphatidylglycerol in the assay mixture and under this condition, cytidylyltransferase activity in control and dexamethasone-treated cultures in the presence and absence of the inhibitors were all increased to the same level. Therefore, the inhibitors did not diminish the capacity of cytidylyltransferase to be fully activated. We suggest that the glucocorticoid induction of fatty-acid synthase in fetal lung results in increased synthesis of fatty acids which in turn, either as free acids or after incorporation into phospholipids, activate choline-phosphate cytidylyltransferase.
