Alisol BCAS# 18649-93-9 |
Quality Control & MSDS
3D structure
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| Cas No. | 18649-93-9 | SDF | Download SDF |
| PubChem ID | 189051 | Appearance | White powder |
| Formula | C30H48O4 | M.Wt | 472.7 |
| Type of Compound | Triterpenoids | Storage | Desiccate at -20°C |
| Synonyms | 16-Deoxoalisol C | ||
| Solubility | Soluble in chloroform, DMSO and methanol; insoluble in water | ||
| Chemical Name | (8S,9S,10S,11S,14R)-17-[(2R)-4-(3,3-dimethyloxiran-2-yl)-4-hydroxybutan-2-yl]-11-hydroxy-4,4,8,10,14-pentamethyl-1,2,5,6,7,9,11,12,15,16-decahydrocyclopenta[a]phenanthren-3-one | ||
| SMILES | CC(CC(C1C(O1)(C)C)O)C2=C3CC(C4C5(CCC(=O)C(C5CCC4(C3(CC2)C)C)(C)C)C)O | ||
| Standard InChIKey | GBJKHDVRXAVITG-DXYWBWDESA-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. Alisol B can suppress C3a induced epithelial-mesenchymal transition . 2. Alisol B may be a potential novel therapeutic molecule for bone disorders through targeting the differentiation of osteoclasts as well as their functions. 3. Alisol B also inhibited RANKL-induced expression of NFATc1 and c-Fos, which are key transcription factors for osteoclastogenesis. 4. The molecular target of Alisol B is the sarcoplasmic/endoplasmic reticulum Ca(2+) ATPase, it provides detailed insights into the cytotoxic mechanism of a novel antitumor compound. |
| Targets | TGF-β/Smad | JNK | AMPK | Calcium Channel | ATPase |
Alisol B Dilution Calculator
Alisol B Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 2.1155 mL | 10.5775 mL | 21.1551 mL | 42.3101 mL | 52.8877 mL |
| 5 mM | 0.4231 mL | 2.1155 mL | 4.231 mL | 8.462 mL | 10.5775 mL |
| 10 mM | 0.2116 mL | 1.0578 mL | 2.1155 mL | 4.231 mL | 5.2888 mL |
| 50 mM | 0.0423 mL | 0.2116 mL | 0.4231 mL | 0.8462 mL | 1.0578 mL |
| 100 mM | 0.0212 mL | 0.1058 mL | 0.2116 mL | 0.4231 mL | 0.5289 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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Alisol B is a potentially novel therapeutic compound for bone disorders by targeting the differentiation of osteoclasts as well as their functions. IC50 Value: Target: In vitro: The in vitro cultured human renal tubular epithelial HK-2 cells were intervened with 5 ng/mL transforming growth factor-beta (TGF-beta), 0.1 micromol C3a, and 0.1 micromol C3a + 10 micromol alisol B, respectively. Exogenous C3a could induce renal tubular EMT. Alisol B was capable of suppressing C3a induced EMT [1]. Alisol-B strongly inhibited RANKL-induced osteoclast formation when added during the early stage of cultures, suggesting that alisol-B acts on osteoclast precursors to inhibit RANKL/RANK signaling. Among the RANK signaling pathways, alisol-B inhibited the phosphorylation of JNK, which are upregulated in response to RANKL in bone marrow macrophages, alisol-B also inhibited RANKL-induced expression of NFATc1 and c-Fos, which are key transcription factors for osteoclastogenesis. In addition, alisol-B suppressed the pit-forming activity and disrupted the actin ring formation of mature osteoclasts [2]. Alisol B induced calcium mobilization from internal stores, leading to autophagy through the activation of the CaMKK-AMPK-mammalian target of rapamycin pathway. Moreover, the disruption of calcium homeostasis induces endoplasmic reticulum stress and unfolded protein responses in alisol B-treated cells, leading to apoptotic cell death. Finally, by computational virtual docking analysis and biochemical assays, it was showed that the molecular target of alisol B is the sarcoplasmic/endoplasmic reticulum Ca(2+) ATPase [3]. In vivo:
References:
[1]. Zhang RF, et al.[Alisol B inhibited complement 3a-induced human renal tubular epithelial to mesenchymal transition]. Zhongguo Zhong Xi Yi Jie He Za Zhi. 2012 Oct;32(10):1407-12.
[2]. Lee JW, et al. Alisol-B, a novel phyto-steroid, suppresses the RANKL-induced osteoclast formation and prevents bone loss in mice. Biochem Pharmacol. 2010 Aug 1;80(3):352-61.
[3]. Law BY, et al. Alisol B, a novel inhibitor of the sarcoplasmic/endoplasmic reticulum Ca(2+) ATPase pump, induces autophagy, endoplasmic reticulum stress, and apoptosis. Mol Cancer Ther. 2010 Mar;9(3):718-30.
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Alisol-B, a novel phyto-steroid, suppresses the RANKL-induced osteoclast formation and prevents bone loss in mice.[Pubmed:20412788]
Biochem Pharmacol. 2010 Aug 1;80(3):352-61.
Osteoclasts, bone-resorbing multinucleated cells, are differentiated from hemopoietic progenitors of the monocyte/macrophage lineage. Bone resorption by osteoclasts is considered a potential therapeutic target to the treatment of erosive bone diseases, including osteoporosis, rheumatoid arthritis, and periodontitis. In the present study, we found that alisol-B, a phyto-steroid from Alisma orientale Juzepczuk, exhibited inhibitory effects on osteoclastogenesis both in vitro and in vivo. Although RT-PCR analysis showed that alisol-B did not affect the 1alpha,25(OH)(2)D(3)-induced expressions of RANKL, OPG and M-CSF mRNAs in osteoblasts, addition of alisol-B to co-cultures of mouse bone marrow cells and primary osteoblasts with 10(-8)M 1alpha,25(OH)(2)D(3) caused significant inhibition of osteoclastogenesis. We further examined the direct effects of alisol-B on osteoclast precursors. Alisol-B strongly inhibited RANKL-induced osteoclast formation when added during the early stage of cultures, suggesting that alisol-B acts on osteoclast precursors to inhibit RANKL/RANK signaling. Among the RANK signaling pathways, alisol-B inhibited the phosphorylation of JNK, which are upregulated in response to RANKL in bone marrow macrophages, alisol-B also inhibited RANKL-induced expression of NFATc1 and c-Fos, which are key transcription factors for osteoclastogenesis. In addition, alisol-B suppressed the pit-forming activity and disrupted the actin ring formation of mature osteoclasts. In a hypercalcemic mouse model induced by 2-methylene-19-nor-(20S)-1alpha,25(OH)(2)D(3) (2MD), an analog of 1alpha,25(OH)(2)D(3), administration of alisol-B significantly suppressed 2MD-induced hypercalcemia as resulting from the inhibition of osteoclastogenesis. Taken together, these findings suggest that alisol-B may be a potential novel therapeutic molecule for bone disorders by targeting the differentiation of osteoclasts as well as their functions.
Alisol B, a novel inhibitor of the sarcoplasmic/endoplasmic reticulum Ca(2+) ATPase pump, induces autophagy, endoplasmic reticulum stress, and apoptosis.[Pubmed:20197400]
Mol Cancer Ther. 2010 Mar;9(3):718-30.
Emerging evidence suggests that autophagic modulators have therapeutic potential. This study aims to identify novel autophagic inducers from traditional Chinese medicinal herbs as potential antitumor agents. Using an image-based screen and bioactivity-guided purification, we identified Alisol B 23-acetate, alisol A 24-acetate, and Alisol B from the rhizome of Alisma orientale as novel inducers of autophagy, with Alisol B being the most potent natural product. Across several cancer cell lines, we showed that Alisol B-treated cells displayed an increase of autophagic flux and formation of autophagosomes, leading to cell cycle arrest at the G(1) phase and cell death. Alisol B induced calcium mobilization from internal stores, leading to autophagy through the activation of the CaMKK-AMPK-mammalian target of rapamycin pathway. Moreover, the disruption of calcium homeostasis induces endoplasmic reticulum stress and unfolded protein responses in Alisol B-treated cells, leading to apoptotic cell death. Finally, by computational virtual docking analysis and biochemical assays, we showed that the molecular target of Alisol B is the sarcoplasmic/endoplasmic reticulum Ca(2+) ATPase. This study provides detailed insights into the cytotoxic mechanism of a novel antitumor compound.
[Alisol B inhibited complement 3a-induced human renal tubular epithelial to mesenchymal transition].[Pubmed:23163157]
Zhongguo Zhong Xi Yi Jie He Za Zhi. 2012 Oct;32(10):1407-12.
OBJECTIVE: To study whether Alisol B could inhibit complement 3a (C3a) induced renal tubular epithelial-mesenchymal transition (EMT). METHODS: The in vitro cultured human renal tubular epithelial HK-2 cells were intervened with 5 ng/mL transforming growth factor-beta (TGF-beta), 0.1 micromol C3a, and 0.1 micromol C3a + 10 micromol Alisol B, respectively. The mRNA and protein expressions of alpha-SMA, E-cadherin, and C3 were detected using RT-PCR, Western blot, and immunofluorescence, respectively. RESULTS: The mRNA and protein expressions of C3 in HK-2 cells were up-regulated after intervention of C3a (P < 0.01), the mRNA and protein expressions of alpha-SMA in HK-2 cells were obviously enhanced (P < 0.01), the mRNA and protein expressions of E-cadherin obviously decreased (P < 0.01). When compared with the group intervened by exogenous C3a, after intervention of Alisol B, the mRNA and protein expressions of alpha-SMA in HK-2 cells were obviously reduced (P < 0.01), the mRNA and protein expressions of E-cadherin obviously increased (P < 0.05). CONCLUSIONS: Exogenous C3a could induce renal tubular EMT. Alisol B was capable of suppressing C3a induced EMT.
