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Alisol B
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Product Name Alisol B
Price: $118 / 20mg
CAS No.: 18649-93-9
Catalog No.: CFN92406
Molecular Formula: C30H48O4
Molecular Weight: 472.7 g/mol
Purity: >=98%
Type of Compound: Triterpenoids
Physical Desc.: Powder
Source: The tubers of Alisma plantago-aquatica Linn.
Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
Download: COA    MSDS    SDF    Manual
Similar structural: Comparison (Web)  (SDF)
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Size /Price /Stock 10 mM * 1 mL in DMSO / $33.8 / In-stock
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Related Screening Libraries
Size /Price /Stock 10 mM * 100 uL in DMSO / Inquiry / In-stock
10 mM * 1 mL in DMSO / Inquiry / In-stock
Related Libraries
Biological Activity
Description: Alisol B, a novel inhibitor of the sarcoplasmic/endoplasmic reticulum Ca(2+) ATPase pump, induces autophagy, endoplasmic reticulum stress, and apoptosis.Alisol B may be a potential novel therapeutic molecule for bone disorders through targeting the differentiation of osteoclasts as well as their functions. Alisol B also inhibited RANKL-induced expression of NFATc1 and c-Fos, which are key transcription factors for osteoclastogenesis.
Targets: TGF-β/Smad | JNK | AMPK | Calcium Channel | ATPase
In vitro:
Zhongguo Zhong Xi Yi Jie He Za Zhi. 2012 Oct;32(10):1407-12.
Alisol B inhibited complement 3a-induced human renal tubular epithelial to mesenchymal transition[Pubmed: 23163157]
To study whether Alisol B could inhibit complement 3a (C3a) induced renal tubular epithelial-mesenchymal transition (EMT).
METHODS AND RESULTS:
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. 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.
In vivo:
Biochem Pharmacol. 2010 Aug 1;80(3):352-61.
Alisol-B, a novel phyto-steroid, suppresses the RANKL-induced osteoclast formation and prevents bone loss in mice.[Pubmed: 20412788]
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.
METHODS AND RESULTS:
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.
CONCLUSIONS:
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 Description
Source: The tubers of Alisma plantago-aquatica Linn.
Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
Storage: Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).

Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.

Need more advice on solubility, usage and handling? Please email to: service@chemfaces.com

After receiving: The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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Recently, ChemFaces products have been cited in many studies from excellent and top scientific journals

Cell. 2018 Jan 11;172(1-2):249-261.e12.
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Calculate Dilution Ratios(Only for Reference)
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 need to make the dilution ratios of the samples. The dilution data of the sheet for your reference. Normally, it's can get a better solubility within lower of Concentrations.
Protocol
Kinase Assay:
Mol Cancer Ther. 2010 Mar;9(3):718-30.
Alisol B, a novel inhibitor of the sarcoplasmic/endoplasmic reticulum Ca(2+) ATPase pump, induces autophagy, endoplasmic reticulum stress, and apoptosis.[Pubmed: 20197400]
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.
METHODS AND RESULTS:
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.
CONCLUSIONS:
This study provides detailed insights into the cytotoxic mechanism of a novel antitumor compound.
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