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  • Brand : BIOFRON

  • Catalogue Number : BF-R4003

  • Specification : 98%(HPLC)

  • CAS number : 34221-41-5

  • Formula : C16H14O4

  • Molecular Weight : 270.28

  • PUBCHEM ID : 6442675

  • Volume : 25mg

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Catalogue Number


Analysis Method






Molecular Weight



White crystalline powder

Botanical Source

Dracaena cochinchinensis,Astragalus membranaceus,Glycyrrhiza uralensis,Glycyrrhiza inflata

Structure Type



Standards;Natural Pytochemical;API




Echinatin/Retrochalcone/(2E)-3-(4-Hydroxy-2-methoxyphenyl)-1-(4-hydroxyphenyl)-2-propen-1-one/Echinantin/2-Propen-1-one, 3-(4-hydroxy-2-methoxyphenyl)-1-(4-hydroxyphenyl)-, (2E)-/2-methoxy-4,4'-dihydroxychalcone/(2E)-3-(4-hydroxy-2-methoxyphenyl)-1-(4-hydroxyphenyl)prop-2-en-1-one/loureirin C/(E)-4,4'-Dihydroxy-2-methoxychalcone/4',4-dihydroxy-2-methoxychalcone




1.3±0.1 g/cm3


Methanol; DMF

Flash Point

193.3±23.6 °C

Boiling Point

509.8±50.0 °C at 760 mmHg

Melting Point

210ºC (dec.)



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#:34221-41-5) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate




Esophageal squamous cell carcinoma (ESCC) is a poor prognostic cancer with a low five-year survival rate. Echinatin (Ech) is a retrochalone from licorice. It has been used as a herbal medicine due to its anti-inflammatory and anti-oxidative effects. However, its anticancer activity or underlying mechanism has not been elucidated yet. Thus, the objective of this study was to investigate the anti-tumor activity of Ech on ESCC by inducing ROS and ER stress dependent apoptosis. Ech inhibited ESCC cell growth in anchorage-dependent and independent analysis. Treatment with Ech induced G2/M phase of cell cycle and apoptosis of ESCC cells. It also regulated their related protein markers including p21, p27, cyclin B1, and cdc2. Ech also led to phosphorylation of JNK and p38. Regarding ROS and ER stress formation associated with apoptosis, we found that Ech increased ROS production, whereas its increase was diminished by NAC treatment. In addition, ER stress proteins were induced by treatment with Ech. Moreover, Ech enhanced MMP dysfunction and caspases activity. Furthermore, it regulated related biomarkers. Taken together, our results suggest that Ech can induce apoptosis in human ESCC cells via ROS/ER stress generation and p38 MAPK/JNK activation.


Echinatin; Esophageal squamous cell carcinoma; Reactive oxygen species; c-Jun N-terminal kinase; p38.


Retrochalcone Echinatin Triggers Apoptosis of Esophageal Squamous Cell Carcinoma via ROS- And ER Stress-Mediated Signaling Pathways


Ah-Won Kwak 1 , Joon-Seok Choi 2 , Mee-Hyun Lee 3 4 , Ha-Na Oh 1 , Seung-Sik Cho 1 , Goo Yoon 1 , Kangdong Liu 3 4 , Jung-Il Chae 5 , Jung-Hyun Shim 1 3

Publish date

2019 Nov 9




Background and purpose: Flavonoids, important plant pigments, have been shown to allosterically modulate brain GABA(A) receptors (GABA(A)Rs). We previously reported that trans-6,4′-dimethoxyretrochalcone (Rc-OMe), a hydrolytic derivative of the corresponding flavylium salt, displayed nanomolar affinity for the benzodiazepine binding site of GABA(A)Rs. Here, we evaluate the functional modulations of Rc-OMe, along with two other synthetic derivatives trans-6-bromo-4′-methoxyretrochalcone (Rc-Br) and 4,3′-dimethoxychalcone (Ch-OMe) on GABA(A)Rs.
Experimental approach: Whole-cell patch-clamp recordings were made to determine the effects of these derivatives on GABA(A)Rs expressed in HEK-293 cells and in hippocampal CA1 pyramidal and thalamic neurones from rat brain.
Key results: Rc-OMe strongly potentiated GABA-evoked currents at recombinant α(1-4)β(2)γ(2s) and α(4)β(3)δ receptors but much less at α(1)β(2) and α(4)β(3). Rc-Br and Ch-OMe potentiated GABA-evoked currents at α(1)β(2)γ(2s). The potentiation by Rc-OMe was only reduced at α(1)H101Rβ(2)γ(2s) and α(1)β(2)N265Sγ(2s), mutations known to abolish the potentiation by diazepam and loreclezole respectively. The modulation of Rc-OMe and pentobarbital as well as by Rc-OMe and the neurosteroid 3α,21-dihydroxy-5α-pregnan-20-one was supra-additive. Rc-OMe modulation exhibited no apparent voltage-dependence, but was markedly dependent on GABA concentration. In neurones, Rc-Br slowed the decay of spontaneous inhibitory postsynaptic currents and both Rc-OMe and Rc-Br positively modulated synaptic and extrasynaptic diazepam-insensitive GABA(A)Rs.
Conclusions and implications: The trans-retrochalcones are powerful positive allosteric modulators of synaptic and extrasynaptic GABA(A)Rs. These novel modulators act through an original mode, thus making them putative drug candidates in the treatment of GABA(A)-related disorders in vivo.
© 2011 The Authors. British Journal of Pharmacology © 2011 The British Pharmacological Society.


Echinatin; Esophageal squamous cell carcinoma; Reactive oxygen species; c-Jun N-terminal kinase; p38.


Retrochalcone Derivatives Are Positive Allosteric Modulators at Synaptic and Extrasynaptic GABA(A) Receptors in Vitro


Ruotian Jiang 1 , Akiko Miyamoto, Adeline Martz, Alexandre Specht, Hitoshi Ishibashi, Marie Kueny-Stotz, Stefan Chassaing, Raymond Brouillard, Lia Prado de Carvalho, Maurice Goeldner, Junichi Nabekura, Mogens Nielsen, Thomas Grutter

Publish date

2011 Mar




Three O-methyltransferases which catalyze S-adenosyl-L-methionine (SAM)-dependent O-methylation of licodione (LMT), flavone/flavonol (FMT), and caffeic acid (CMT) were separated from the callus culture of Glycyrrhiza echinata, and characteristic differences between their pH optima and Mg(2+) requirement for activity were demonstrated. The activity of LMT, which is involved in retrochalcone (echinatin) biosynthesis, but not of FMT or CMT, was found to be stimulated when suspension-cultured G. echinata cells were treated with yeast extract (YE), which causes rapid production of echinatin in the cells. Cycloheximide suppressed both the YE-induced echinatin formation and LMT enhancement. The results indicate a selective induction of retrochalcone pathway in Glycyrrhiza cells in response to stress.


Regulation of Retrochalcone Biosynthesis: Activity Changes of O-methyltransferases in the Yeast Extract-Induced Glycyrrhiza Echinata Cells


S Ayabe 1 , A Udagawa, K Iida, T Yoshikawa, T Furuya

Publish date

1987 Feb

Description :

Echinatin is a chalcone isolated from the Chinese herbal medicine Gancao with hepatoprotective and anti-inflammatory effects. Echinatin may undergo an electron transfer (ET) and a proton transfer (PT) to cause the antioxidant action in aqueous solution[1]. Echinatin can be quickly absorbed and eliminated and extensively distributed with an absolute bioavailability of approximately 6.81% in Rat[2].