26020-14-4
Chemical Structure
Calenduloside E
- CAS No.: 26020-14-4
- Formula:C36H56O9
- Molecular Weight:632.82
IUPAC Name: (2S,3S,4S,5R,6R)-6-(((3S,4aR,6aR,6bS,8aS,12aS,14aR,14bR)-8a-carboxy-4,4,6a,6b,11,11,14b-heptamethyl-1,2,3,4,4a,5,6,6a,6b,7,8,8a,9,10,11,12,12a,14,14a,14b-icosahydropicen-3-yl)oxy)-3,4,5-trihydroxytetrahydro-2H-pyran-2-carboxylic acid
InChIKey: IUCHKMAZAWJNBJ-RCYXVVTDSA-N
SMILES: C[C@]12[C@]3(C([C@@]4([H])[C@](C(O)=O)(CCC(C)(C)C4)CC3)=CC[C@]1([H])[C@@]5([C@@](C(C)([C@@H](O[C@]6([H])O[C@@H]([C@@H](O)[C@H](O)[C@H]6O)C(O)=O)CC5)C)([H])CC2)C)C
Biological Activity: Calenduloside E is a pentacyclic triterpenoid saponin that can be extracted from the bark and roots of Aralia ovata, and has anti-inflammatory and anti-apoptotic activities. Calenduloside E alleviates atherosclerosis by regulating macrophage polarization, improves mitochondrial function by regulating the AMPK-SIRT3 pathway, and alleviates acute liver injury. In addition, Calenduloside E promotes the interaction between L-type calcium channels and Bcl-2 related apoptosis genes, inhibits calcium overload, and alleviates myocardial ischemia/reperfusion injury. Calenduloside E also improves non-alcoholic fatty liver disease by regulating heat shock-dependent pathways, and inhibits ROS mediated JAK1-STAT3 pathways to reduce cellular inflammatory responses[1][2][3][4][5][6].
| Cat. No. | Product Name | Purity | Description | Pricing | |||||||||||||||||||
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Calenduloside E | 98.92% | Calenduloside E is a pentacyclic triterpenoid saponin that can be extracted from the bark and roots of Aralia ovata, and has anti-inflammatory and anti-apoptotic activities. Calenduloside E alleviates atherosclerosis by regulating macrophage polarization, improves mitochondrial function by regulating the AMPK-SIRT3 pathway, and alleviates acute liver injury. In addition, Calenduloside E promotes the interaction between L-type calcium channels and Bcl-2 related apoptosis genes, inhibits calcium overload, and alleviates myocardial ischemia/reperfusion injury. Calenduloside E also improves non-alcoholic fatty liver disease by regulating heat shock-dependent pathways, and inhibits ROS mediated JAK1-STAT3 pathways to reduce cellular inflammatory responses. | ||||||||||||||||||||
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References
- [1]. Tian Y, et al. The clickable activity-based probe of anti-apoptotic calenduloside E. Pharm Biol. 2019 Dec;57(1):133-139. [Content Brief]
- [2]. Lanfang Li, et al. "Calenduloside e modulates macrophage polarization via KLF2-regulated glycolysis, contributing to attenuates atherosclerosis." International Immunopharmacology 117 (2023): 109730. [Content Brief]
- [3]. Pengli Guo, et al. "Isolation of Calenduloside E from achyranthes bidentata blume and its effects on LPS/D-GalN-induced acute liver injury in mice by regulating the AMPK-SIRT3 signaling pathway." Phytomedicine 125 (2024): 155353. [Content Brief]
- [4]. Ruiying Wang, et al. "Calenduloside E suppresses calcium overload by promoting the interaction between L-type calcium channels and Bcl2-associated athanogene 3 to alleviate myocardial ischemia/reperfusion injury." Journal of Advanced Research 34 (2021): 173-186. [Content Brief]
- [5]. Yifei Le, et al. "Calenduloside E ameliorates non-alcoholic fatty liver disease via modulating a pyroptosis-dependent pathway." Journal of Ethnopharmacology 319 (2024): 117239. [Content Brief]
- [6]. Min Wang, et al. "Calenduloside E ameliorates myocardial ischemia‐reperfusion injury through regulation of AMPK and mitochondrial OPA1." Oxidative Medicine and Cellular Longevity 2020.1 (2020): 2415269. [Content Brief]
