| Identification | Back Directory | [Name]
Alisol B | [CAS]
18649-93-9 | [Synonyms]
ALISOL B
Alisol B Standard
(23S,24R)-24,25-Epoxy-11b,23-dihydroxy-8a,9b,14b-dammar-13(17)-en-3-one
(8α,9β,14β,23S,24R)-11β,23-Dihydroxy-24,25-epoxy-5α-dammar-13(17)-en-3-one
Dammar-13(17)-en-3-one, 24,25-epoxy-11,23-dihydroxy-, (8α,9β,11β,14β,23S,24R)- | [Molecular Formula]
C30H48O4 | [MDL Number]
MFCD06798979 | [MOL File]
18649-93-9.mol | [Molecular Weight]
472.7 |
| Chemical Properties | Back Directory | [Melting point ]
166-168 °C | [Boiling point ]
575.1±50.0 °C(Predicted) | [density ]
1.12±0.1 g/cm3(Predicted) | [storage temp. ]
Inert atmosphere,2-8°C | [solubility ]
Soluble in chloroform, DMSO and methanol; | [form ]
powder | [pka]
14.35±0.20(Predicted) | [color ]
White | [Water Solubility ]
insoluble in water |
| Hazard Information | Back Directory | [Uses]
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: | [Definition]
ChEBI: Alisol B is a triterpenoid. | [target]
TGF-β/Smad | JNK | AMPK | Calcium Channel | ATPase | [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. PMID:23163157
[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. DOI:10.1016/j.bcp.2010.04.014
[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. DOI:10.1158/1535-7163.MCT-09-0700 |
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