Polyporenic acid CCAS# 465-18-9 |
Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
| Cas No. | 465-18-9 | SDF | Download SDF |
| PubChem ID | 9805290 | Appearance | Powder |
| Formula | C31H46O4 | M.Wt | 482.7 |
| Type of Compound | Triterpenoids | Storage | Desiccate at -20°C |
| Solubility | Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc. | ||
| Chemical Name | (2R)-2-[(5R,10S,13R,14R,16R,17R)-16-hydroxy-4,4,10,13,14-pentamethyl-3-oxo-1,2,5,6,12,15,16,17-octahydrocyclopenta[a]phenanthren-17-yl]-6-methyl-5-methylideneheptanoic acid | ||
| SMILES | CC(C)C(=C)CCC(C1C(CC2(C1(CC=C3C2=CCC4C3(CCC(=O)C4(C)C)C)C)C)O)C(=O)O | ||
| Standard InChIKey | KPKYWYZPIVAHKU-WMNQUVFJSA-N | ||
| Standard InChI | InChI=1S/C31H46O4/c1-18(2)19(3)9-10-20(27(34)35)26-23(32)17-31(8)22-11-12-24-28(4,5)25(33)14-15-29(24,6)21(22)13-16-30(26,31)7/h11,13,18,20,23-24,26,32H,3,9-10,12,14-17H2,1-2,4-8H3,(H,34,35)/t20-,23-,24+,26+,29-,30-,31+/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. | ||
| Description | 1. Polyporenic acid C shows inhibitory activity against human collagenase. 2. Polyporenic acid C induces apoptosis through the death receptor-mediated apoptotic pathway where the activation of caspase-8 leads to the direct cleavage of execution caspases without the involvement of the mitochondria. |
| Targets | PARP | Caspase | PI3K | Akt | p53 |
Polyporenic acid C Dilution Calculator
Polyporenic acid C Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 2.0717 mL | 10.3584 mL | 20.7168 mL | 41.4336 mL | 51.792 mL |
| 5 mM | 0.4143 mL | 2.0717 mL | 4.1434 mL | 8.2867 mL | 10.3584 mL |
| 10 mM | 0.2072 mL | 1.0358 mL | 2.0717 mL | 4.1434 mL | 5.1792 mL |
| 50 mM | 0.0414 mL | 0.2072 mL | 0.4143 mL | 0.8287 mL | 1.0358 mL |
| 100 mM | 0.0207 mL | 0.1036 mL | 0.2072 mL | 0.4143 mL | 0.5179 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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Polyporenic acid C induces caspase-8-mediated apoptosis in human lung cancer A549 cells.[Pubmed:18973184]
Mol Carcinog. 2009 Jun;48(6):498-507.
Lung cancer continues to be the leading cause of cancer-related mortality worldwide. This warrants the search for new and effective agents against lung cancer. We and others have recently shown that lanostane-type triterpenoids isolated from the fungal species Poria cocos (P. cocos) can inhibit cancer growth. However, the mechanisms responsible for the anticancer effects of these triterpenoids remain unclear. In this study, we investigated the effect of Polyporenic acid C (PPAC), a lanostane-type triterpenoid from P. cocos, on the growth of A549 nonsmall cell lung cancer cells (NSCLC). The results demonstrate that PPAC significantly reduced cell proliferation via induction of apoptosis as evidenced by sub-G1 analysis, annexin V-FITC staining, and increase in cleavage of procaspase-8, -3, and poly(ADP-ribose)-polymerase (PARP). However, unlike our previously reported lanostane-type triterpenoid, pachymic acid, treatment of cells with PPAC was not accompanied by disruption of mitochondrial membrane potential and increase in cleavage of procaspase-9. Further, PPC-induced apoptosis was inhibited by caspase-8 and pan caspase inhibitors but not by a caspase-9 inhibitor. Taken together, the results suggest that PPAC induces apoptosis through the death receptor-mediated apoptotic pathway where the activation of caspase-8 leads to the direct cleavage of execution caspases without the involvement of the mitochondria. Furthermore, suppressed PI3-kinase/Akt signal pathway and enhanced p53 activation after PPAC treatment suggests this to be an additional mechanism for apoptosis induction. Together, these results encourage further studies of PPAC as a promising candidate for lung cancer therapy.
