CAS 18649-93-9|Alisol B

Introduction：Basic information about CAS 18649-93-9|Alisol B, including its chemical name, molecular formula, synonyms, physicochemical properties, and safety information, etc.

Table of Contents

1. Names
2. Alisol B BiologicalActivity
3. Chemical & Physical Properties
4. Synonyms

Common Name	Alisol B
CAS Number	18649-93-9	Molecular Weight	472.70
Density	1.1±0.1 g/cm3	Boiling Point	567.1±50.0 °C at 760 mmHg
Molecular Formula	C₃₀H₄₈O₄	Melting Point	/
MSDS	/	Flash Point	181.2±23.6 °C

Names

Name	Alisol B
Synonym	More Synonyms

Alisol B BiologicalActivity

Description	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:
Related Catalog	Signaling Pathways >>Others >>OthersResearch Areas >>OthersNatural Products >>Terpenoids and Glycosides
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.

Description

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:

Related Catalog

Signaling Pathways >>Others >>OthersResearch Areas >>OthersNatural Products >>Terpenoids and Glycosides

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.

Chemical & Physical Properties

Density	1.1±0.1 g/cm3
Boiling Point	567.1±50.0 °C at 760 mmHg
Molecular Formula	C₃₀H₄₈O₄
Molecular Weight	472.70
Flash Point	181.2±23.6 °C
PSA	70.06000
LogP	4.37
Vapour Pressure	0.0±3.5 mmHg at 25°C
Index of Refraction	1.560
InChIKey	GBJKHDVRXAVITG-CHCGYSKXSA-N
SMILES	CC(CC(O)C1OC1(C)C)C1=C2CC(O)C3C4(C)CCC(=O)C(C)(C)C4CCC3(C)C2(C)CC1
Storage condition	-20℃

Synonyms

Gon-13(17)-en-3-one, 17-[(1R,3S)-3-[(2S)-3,3-dimethyloxiranyl]-3-hydroxy-1-methylpropyl]-11-hydroxy-8,10,14-trimethyl-, (5α,8α,9β,11β,14β)-

(5α,8α,9β,11β,14β,23S,24S)-11,23-Dihydroxy-8,14-dimethyl-24,25-epoxy-18-norcholest-13(17)-en-3-one

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