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Calenduloside E

MCE China：Calenduloside E

Brand：MedChemExpress (MCE)

Cat. No.HY-N6850

CAS：26020-14-4

Purity：99.07%

Storage：Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month

Shipping：Room temperature in continental US; may vary elsewhere.

Description：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.

In Vitro：Calenduloside E (1.25 μg/mL; 24 h) inhibits glycolysis-mediated M1 macrophage polarization[2]. Calenduloside E (1 μM; 2 h) alleviates LPS (HY-D1056)/D-galn-induced AML12 and LX2 cell damage and AMPK-SIRT3 signaling pathway protein expression[3]. Calenduloside E (0-16 μM; 24 h) inhibits inflammasome activation and pyroptosis in AML-12 cells stimulated by lipid mixture[5].

In Vivo：Calenduloside E (11 mg/kg; i.g.; once daily for 16 weeks) reduces atherosclerotic plaque size, enhanced plaque stability, and reduced inflammatory responses in ApoE-/- mice[2]. Calenduloside E (15 and 30 mg/kg; i.g.; once daily for 7 days) inhibits hepatocyte apoptosis and reduced oxidative stress and immune inflammation in mice with acute liver injury induced by LPS (HY-D1056) and D-GalN[3]. Calenduloside E (7.5-30 mg/kg; i.g.; once daily for 3 days) restores sarcomere contraction and calcium transients in adult rat ventricular myocytes (ARVMs)[4]. Calenduloside E (5 and 10 mg/kg; i.g.; once daily for 4 weeks) improves liver injury, lipid accumulation, and profibrotic phenotypes in nonalcoholic fatty liver disease model mice and inhibits inflammasome activation and pyroptosis in the liver of mice[5].

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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]