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Calenduloside E

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].

Product Specifications

CAS Number

26020-14-4

UNSPSC

12352005

Target

AMPK; Apoptosis; Bcl-2 Family; Calcium Channel; Interleukin Related; JAK; PPAR; Pyroptosis; Reactive Oxygen Species (ROS) ; SOD; STAT; TNF Receptor

Type

Natural Products

Related Pathways

Apoptosis; Cell Cycle/DNA Damage; Epigenetics; Immunology/Inflammation; JAK/STAT Signaling; Membrane Transporter/Ion Channel; Metabolic Enzyme/Protease; Neuronal Signaling; NF-κB; PI3K/Akt/mTOR; Protein Tyrosine Kinase/RTK; Stem Cell/Wnt; Vitamin D Related/Nuclear Receptor

Field of Research

Inflammation/Immunology; Cardiovascular Disease

Assay Protocol

https://www.medchemexpress.com/calenduloside-e.html

Purity

99.07

Solubility

DMSO : 100 mg/mL (ultrasonic)

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

Molecular Formula

C36H56O9

Molecular Weight

632.82

References & Citations

[1]Tian Y, et al. The clickable activity-based probe of anti-apoptotic calenduloside E. Pharm Biol. 2019 Dec;57 (1) :133-139.|[2]Lanfang Li, et al. "Calenduloside e modulates macrophage polarization via KLF2-regulated glycolysis, contributing to attenuates atherosclerosis." International Immunopharmacology 117 (2023) : 109730.|[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.|[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.|[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.|[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.

Shipping Conditions

Room Temperature

Storage Conditions

-20°C, 3 years; 4°C, 2 years (Powder)

Scientific Category

Natural Products

Clinical Information

No Development Reported

Available Sizes

Frequently Asked Questions

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