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  • Brand : BIOFRON

  • Catalogue Number : BF-I2001

  • Specification : 98%

  • CAS number : 20784-50-3

  • Formula : C20H20O4

  • Molecular Weight : 324.37

  • PUBCHEM ID : 5281255

  • Volume : 20mg

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Catalogue Number


Analysis Method






Molecular Weight



Yellow crystalline powder

Botanical Source

Cullen corylifolium,Glycyrrhiza uralensis

Structure Type



Standards;Natural Pytochemical;API




(2E)-1-[2,4-Dihydroxy-3-(3-methyl-2-buten-1-yl)phenyl]-3-(4-hydroxyphenyl)-2-propen-1-one/4-Hydroxyisocordoim/2',4',4-trihydroxy-3'-prenylchalcone/4-Hydroxyisocordoin/Isobacachalcone/4,2',4'-trihydroxy-3'-prenylchalcone/(E)-1-[2,4-dihydroxy-3-(3-methylbut-2-enyl)phenyl]-3-(4-hydroxyphenyl)prop-2-en-1-one/2-Propen-1-one, 1-[2,4-dihydroxy-3-(3-methyl-2-buten-1-yl)phenyl]-3-(4-hydroxyphenyl)-, (2E)-/Corylifolinin




1.2±0.1 g/cm3



Flash Point

299.9±26.6 °C

Boiling Point

549.0±50.0 °C at 760 mmHg

Melting Point


InChl Key

WGK Germany


HS Code Reference


Personal Projective Equipment

Correct Usage

For Reference Standard and R&D, Not for Human Use Directly.

Meta Tag

provides coniferyl ferulate(CAS#:20784-50-3) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate




Aberrant activation of the extracellular signal‑regulated kinases (ERKs)/ribosomal S6 kinase 2 (RSK2) signaling pathway is frequently determined in various human tumor types, including liver cancer, and has been considered as a promising target for cancer chemoprevention and therapy. In the present study, using computer‑aided virtual screening and molecular docking, isobavachalcone (IBC), a natural chalcone compound, was identified to be an ATP‑competitive inhibitor targeting ERK1/2 and RSK2. Cell Counting Kit‑8, EdU incorporation and colony formation assays were used to detect the effects of IBC on cell viability and proliferation, and the results demonstrated that IBC effectively inhibited the proliferation of liver cancer HepG2 and Hep3B cells, whereas it had no notable cytotoxic effect on immortal liver L02 cells. Flow cytometric analysis and western blotting further revealed that IBC caused significant levels of apoptosis on liver cancer cells via the caspase‑dependent mitochondria pathway. The computer prediction was confirmed with pull‑down and in vitro kinase assays, in which IBC directly bound with ERK1/2 and RSK2, and dose‑dependently blocked RSK2 kinase activity in liver cancer cells. Treatment of HepG2 or Hep3B cells with IBC significantly attenuated epidermal growth factor‑induced phosphorylation of RSK2 and resulted in the reduced activation of its downstream substrates including cAMP response element‑binding protein, activating transcription factor 1, histone H3 and activating protein‑1. Enforced RSK2 expression in L02 cells could increase the effect of IBC on suppressing cell growth. Conversely, knockdown of RSK2 reduced the inhibitory effect of IBC on HepG2 cell proliferation. Overall, the present data indicated that ERKs/RSK2 signaling serves a pivotal role in IBC‑induced suppression of liver cancer cells and that IBC may be a potential therapeutic candidate for human cancer with elevated ERKs/RSK2 activity.


Isobavachalcone exerts anti‑proliferative and pro‑apoptotic effects on human liver cancer cells by targeting the ERKs/RSK2 signaling pathway.


Li B1, Xu N2, Wan Z3, Ma L4, Li H2, Cai W2, Chen X2, Huang Z2, He Z1.

Publish date

2019 Jun




Non-apoptotic cell-death induction is a potential strategy for cancer treatment. Cytoplasmic vacuolation-associated cell death represents a novel type of non-apoptotic cell-death. Here, we showed that isobavachalcone (IBC), a naturally occurring chalcone compound, selectively induced cell death with massive cytoplasmic vacuolation in some leukemic cells but not in normal peripheral blood cells. Although the IBC-induced cell death displayed certain apoptotic changes, the caspase inhibitor Z-VAD-FMK did not significantly suppress IBC-induced cell death. IBC-induced vacuoles are acidic in nature, as revealed by neutral red staining. However, these vacuoles could not be labeled by lysosome or mitochondrial trackers. Moreover, the knockdown of several autophagy-related genes, such as LC3, Beclin-1, and ATG7, did not inhibit IBC-induced vacuolation. Transmission electron microscope examination revealed that these vacuoles mainly derived from the endosome. Surprisingly, Vacuolar-type H + -ATPase inhibitors, weak bases, such as chloroquine and AKT inhibitors, markedly abrogated vacuolization but enhance IBC-induced cell death, suggesting that IBC-induced vacuolation and cell death go into different direction and the vacuolization is a protective action rather than a part of the death mechanism. In conclusion, by using IBC as a chemical probe, we provide new characteristics of methuosis-like cell death. Inducing methuosis-like cell death may represent a novel strategy to combat leukemia.

Copyright © 2019 Elsevier B.V. All rights reserved.


Isobavachalcone reveals novel characteristics of methuosis-like cell death in leukemia cells.


Yang L1, Song L2, Zhao S2, Ma C2, Wu D3, Wu YL4.

Publish date

2019 May 1




The aim of this study is to investigate the protective effect and underlying molecular mechanisms of isobavachalcone on Sephadex-induced lung injury in rats. The result showed isobavachalcone inhibited massive granulomas, decreased inflammatory cells infiltration and oxidative stress markers level, but it can increase antioxidant enzymes level. The ELISA assay exhibited isobavachalcone decreased TNF-α production in BALF and lung tissue. Western blotting analysis showed isobavachalcone can inhibit NF-κB pathway that may be mediated by upregulation of A20. Furthermore, we also found isobavachalcone can activate NRF2/HO-1 pathway and inhibit adhesion molecule expression. Taken together, the present results suggested that isobavachalcone can attenuate Sephadex-induced lung injury that may be related to inhibition of NF-κB mediated by upregulation of A20 and activation of NRF2/HO-1 signaling pathway.

Copyright © 2019 Elsevier B.V. All rights reserved.


A20; Isobavachalcone; Lung injury; NF-κB; NRF2/HO-1


Isobavachalcone attenuates Sephadex-induced lung injury via activation of A20 and NRF2/HO-1 in rats.


Gao D1, Liu F2, Li Z3, Guan Y4.

Publish date

2019 Apr 5

Description :

Isobavachalcone(Corylifolinin) is a chalcone constituent of Angelica keiskei, induces apoptosis in neuroblastoma.IC50 value:Target: Isobavachalcone inhibits platelet aggregation. Inhibitor of Epstein-Barr virus early antigen (EBV-EA) induction. Isobavachalcone exhibits potent inhibitory effect on skin tumor promotion. Potent inhibitor of MMP-2. Displays DNA strand-scission (cleaving) activity. Isobavachalcone hows antifungal activity.